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Hill AT, Sullivan AL, Chalmers JD, et al. British Thoracic Society guideline for Pleural Disease bronchiectasis in adults. BMI Open Respir Res. 2018;5:e000348. [PMID: Dugan KC, Laxmanan B, Murgrr S, et al. Management of persistent air leaks. 306875021 doi:10.1136/bmjresp 2018 000348 Chest. 2017;152:417-423. [PMID: 282674361 doi:10.1016/j.chest.2017.02.o2o Ramsahai JM, Hansbro PM, Wark PAB. Mechanisms and management of Feller Kopman D, Light R. Pleural disease. N Engl J Med. 2018;378:740 751. asthma exacerbations. Am J Respir Crit Care Med.2019;799:423-432. IPMID: 294661461 doi:10.1056/NElMral4o3503 IPMID: 30562041] doi:10.1164/rccm.20l810-l931CI : Feller-Kopman DJ, Reddy CB, Decamp MM, et al. Management of malignant : Rusznak M1, Peebles RS. Aspirin exacerbated respiratory disease. N Engl J pleural effusions. an official ATS/STS/STR clinical practice guideline. Am J Med. 2018 Dec 6:379(23\:2280 2281. Respir Crit Care Med. 2018;198:839 849. [PMID: 30272503) doi:10.1164/ i Skloot GS, Busse PJ, Braman SS, et al; ATS ad hoc Committee on Asthma in the rccm.201807-1415ST Elderly. An official american thoracic society workshop report: evaluation Iyer NP, Reddy CB, Wahidi MM, et al. Indwelling pleural catheter versus l and management of asthma in the elderly. Ann Am Thorac Soc. 2016; pleurodesis for malignant pleural effusions. A systematic review and 13 :2061 2077. [PMID: 27831798] meta anab/sis. Ann Am Thorac Soc. 2019;16:124-137. [PMID: 30272486] Siu AL, Bibbins Domingo K, Grossman DC. et all US Preventive Services Task doi:l o.l 5l 3/AnnalsATS.2O1807-495OC I.brce (USPSTF). Screening for chronic obstructive pulmonary disease: US Khemasuwan D, Sorensen J, Griffin DC. Predictive variables for failure in preventive services task force recommendation statement. IAMA. administration of intrapleural tissue plasminogen activator/deoxyribonu- 2Ol6;315:1372 7. [PMIDT 27046365] doi:10.1001/iama.2016.2638 clease in patients with complicated parapneumonic effusions/empyema. Walshaw Ml. Cystic fibrosis: diagnosis and management-NlcE guideline 78. Chest.2o18;154:550-556. [PMID:29425674)doi:7O.1016/i.chest.2018.01.037 Paediatr Respir Rev. 2019;31:12 14. [PMID: 30962150] doi:10.1016/j.prrv. Nayak R, Brogly SB, Lajkosz K, et al. Outcomes ofoperative and nonoperative 2019.02.006 treatment ofthoracic empyema: A population-based sftrdy Arm Thorac Surg. Dillirse Parenchymal Lung Disease 2019;108;1456 1463. [PMID: 31356799] doi:1o.1016/j.athoracsur.2019.05.090

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Mira-Avendano I, Abril A, Burger CD, et al. lnterstitial lung disease and other Puhnonary vascular Disease pulmonary manifestations in connective tissue diseases. Mayo Clin Proc. Frost A, Badesch D, Gibbs JSR, et al. Diagnosis ofpulmonary hypertension. Eur 2019;94:309 325. [PMID: 3055S827] doi:10.1016/j.mayocp.2018.O9.OO2 Respir J. 2019j53:1801904. doi:10.1183/13993003.01904 2018 Noe MH, Rosenbach M. Cutaneous sarcoidosis. Curr Opin Pulm Med. 2017; GaliC N, Humbert M, Vachiery JL. et al; ESC Scientific Document Group. 2015 23:482 486. IPMID: 28598873] doi:1O.1097/MCPOO0OOOOO00000402 ESC/ERS guidelines for the diagnosis and treatment of pulmonary hyper- Raghu G, Remy Jardin M, Myers lL. et ali American Thoracic Societ1,, tension: the Joint Task Force for the Diagnosis and Treatment ofPulmonary European Respiratory Society, Japanese Respiratory SocieBl and Latin Hypertension of the European Society of Cardiolory (ESC) and the American Thoracic Society. Diagnosis ofidiopathic pulmonary fibrosis. an European Respiratory Society (ERS)r endorsed by: Association for European official ATS/ERS/JRS/ALAT clinical practice guideline. Am J Respir Crit Paediatric and Congenital Cardiologr (AEPC), Intemational Society for Care Med. 2018;198:e44-e68. IPMID: 30168753] doi:10.i164lrccm.201807 Heart and Lung Tnnsplantation (ISHLI). Eur Heart J.2016;37:67 119. l255ST IPMID: 26320113] doi:10.1093/eurheartj/ehv317 Raghu C, Rochwerg B, Zhang Y, et al; American Thoracic Society. An official Kim NH, Delcroix M, Jais X, et al. Chronic thromboembolic pulmonary hyper- ATS/ERS/JRS/ALAT clinical practice guideline: treatment of idiopathic tension. Eur Respir J. 2019;53. [PMID: 30545969] doir10.1183/i3993003. pulmonary fibrosis. an update ofthe 20ll clinical practice guideline. Am J olgls-2018 Respir Crit Care Med. 2O15:192:e3 19. IPMID: 2617718ts) doi:10.1164/ rccm.201506 10635T Klinger JR, Elliott CG, Levine Dl, et al. Therapy for pulmonary arterial hyper tension in adults: update ofthe CHEST guideline and expert panel report. Tomassetti S, Ravaglia C, Poletti V Diffuse parenchymal lung disease. Eur Chest. 2019t155:565-586. [PMID: 306607831 doi:10.1016/j.chest.2018.U.030 Respir Rev 2017; 26. [PMID : 28446 601l doi : I 0. I I 83 / I 600 0677 .OO O 4 2017 Simonneau G, Montani D, Celermajer DS, et al. Haemodynamic definitions Witt U. Curran JJ, Strek ME. The diagnosis and treatment of antisynthetase and updated clinical classification of pulmonary hypertension. Eur Respir syndrome. Clin Pulm Med. 2016;23:218 226. [PMID: 27594777] J. 2019;53. [PMID: 30545968] doi:10.1183/13993003.01913 2018 Yoon HY, Kim TH, Seo lB, et al. Effects of emphysema on physiological and Simonneau G, Montani D, Celermajer DS, et al. Haemodynamic definitions prognostic characteristics of lung function in idiopathic pulrnonary fibro- and updated clinical classification of pulmonary hypertension. Eur Respir sis. Respirologr. 2019 ;24:55-62. IPMID: 30136753] doi:10.1111/resp.13387 J. 2O19;53:18O1913. doi:10.1183/13993003.01913 2018 Occupational Lung Disease Lung Tumors Bacchus L, Shah RD, Chung JH, et al; Expert Panel on Thoracic Imaging. ACR Carter BW Marom EM, Detterbeck FC. Approaching the patient with an ante appropriateness criteria review ACR appropriateness criteria- occupational rior mediastinal mass: a guide for clinicians. J Thorac Oncol. 2014;9:5102 9. Iung diseases. J Thorac Imaging. 2016;31:W1-3. [PMID: 26656194] IPMID: 25396306] doi:10.1097/1TO.0000000000000294 doi:l 0.1097/RTI.0000000000000194 Gould MK, Donington J, Lynch WR, et al. Evaluation of individuals with pul De Matteis S, Heederik D, Burdorf A, et al; European Respiratory Society monary nodules: when is it lung cancer? Diagnosis and management of Environment and Health Committee. Current and new challenges in occu lung cancer, 3rd ed: American College of Chest Physicians evidence-based pational lung diseases. Eur Respir Rev 2017;26. [PMID: 29141963] clinical practice guidelines. Chest. 2013r143:e93S-e120S. IPMID: 236494561 doi:10.1183 i 16000617.OO80 2017 doi:10.1378/chest.12 2351 Perlman DM, Maier LA. Occupational lung disease. Med Clin North Am. Kindler HL, Ismaila N, Armato SG 3rd, et al. Treatment of malignant pleural 2019;103:535-548. IPMID, 30955520] doi:10.10161j.mcna.2018.12.012 mesothelioma: American Society of Clinical Oncolory clinical practice Seaman DM, Meyer CA, Kanne JP Occupational and environmental lung guideline. J Clin Oncol. 2018;36 1343 - 1373. [PMID, 29346042) doi:lO.l2OO I :

Occupational Lung Disease Lung Tumors Bacchus L, Shah RD, Chung JH, et al; Expert Panel on Thoracic Imaging. ACR Carter BW Marom EM, Detterbeck FC. Approaching the patient with an ante appropriateness criteria review ACR appropriateness criteria- occupational rior mediastinal mass: a guide for clinicians. J Thorac Oncol. 2014;9:5102 9. Iung diseases. J Thorac Imaging. 2016;31:W1-3. [PMID: 26656194] IPMID: 25396306] doi:10.1097/1TO.0000000000000294 doi:l 0.1097/RTI.0000000000000194 Gould MK, Donington J, Lynch WR, et al. Evaluation of individuals with pul De Matteis S, Heederik D, Burdorf A, et al; European Respiratory Society monary nodules: when is it lung cancer? Diagnosis and management of Environment and Health Committee. Current and new challenges in occu lung cancer, 3rd ed: American College of Chest Physicians evidence-based pational lung diseases. Eur Respir Rev 2017;26. [PMID: 29141963] clinical practice guidelines. Chest. 2013r143:e93S-e120S. IPMID: 236494561 doi:10.1183 i 16000617.OO80 2017 doi:10.1378/chest.12 2351 Perlman DM, Maier LA. Occupational lung disease. Med Clin North Am. Kindler HL, Ismaila N, Armato SG 3rd, et al. Treatment of malignant pleural 2019;103:535-548. IPMID, 30955520] doi:10.10161j.mcna.2018.12.012 mesothelioma: American Society of Clinical Oncolory clinical practice Seaman DM, Meyer CA, Kanne JP Occupational and environmental lung guideline. J Clin Oncol. 2018;36 1343 - 1373. [PMID, 29346042) doi:lO.l2OO I : disease. CIin Chest Med. 2015:36:249 68, viii ix. [PMID: 26024603] JCO.2017.76.6394 doi:10.1016/j.ccm.2015.02.008 MacMahon H, Naidich DP Goo lM, et al. Guidelines for management of inci van der Molen HF, de Groene GJ, HulshofCTJ, et al. Association between work dental pulmonary nodules detected on CT images: from the Fleischner and chronic obstructive pulmonary disease (COPD). J Clin Med. 2018;7. Society 20U. Radiolory. 2017;284:228 243. [PMID: 282405621 doi:10.1148/ IPMID: 303047641 doi:10.339O/jcm71O0335 radio1.2017161659

disease. CIin Chest Med. 2015:36:249 68, viii ix. [PMID: 26024603] JCO.2017.76.6394 doi:10.1016/j.ccm.2015.02.008 MacMahon H, Naidich DP Goo lM, et al. Guidelines for management of inci van der Molen HF, de Groene GJ, HulshofCTJ, et al. Association between work dental pulmonary nodules detected on CT images: from the Fleischner and chronic obstructive pulmonary disease (COPD). J Clin Med. 2018;7. Society 20U. Radiolory. 2017;284:228 243. [PMID: 282405621 doi:10.1148/ IPMID: 303047641 doi:10.339O/jcm71O0335 radio1.2017161659 l 90 I ]

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IPMID: 28162150] doi:10.5664/jcsm.6506 Contract No. 290-2015 00006 l-2.) AHRQ Publication No. 19 EHC019 EF. Rockville, MD: Agency for Healthcare Research and Quality; September Mokhlesi B, Masa JE, Brozek JL, et al. Evaluation and management ofobesity 2019. doi:IO.23970/AHRQEPCCER2l9 hypoventilation syndrome. an official American Thoracic Society clinical practice guideline. Am J Respir Crit Care Med. 2019;200:e6 e24. [PMID: Ouellette DR, Patel S, Girard TD, et al. Liberation from mechanical ventilation 313687981 doi:10.1164/rccm.2O19O5-1071ST in critically ill adults: An official American College of Chest Physicians/ American Thoracic Society clinical practice guideline: inspiratory pressure Patil SP, Ayappa lA, Caples SM, et al. Treatment ofadult obstructive sleep apnea augmentation during spontaneous breathing trials, orotocols minimizing with positive airway pressure: an American Academy of Sleep Medicine sedation, and noninvasive ventilation immediately after extubation. Chest. systematic review meta analysis, and GRADE assessment. J Clin Sleep 2017;151:166-180. [PMID: 27818331] doi:10.1016/j.chest.2016.10.036 Med. 2019;15:301 334. [PMID: 307368881 doi:10.5664/jcsm.7638 Rochwerg B, Brochard L, Elliott MW et al. Offlicial ERS/ATS clinical practice Ramar K, Dort LC, Katz SG, et al. Clinical practice guideline for the treatment guidelines: noninvasive ventilation for acute respiratory failure. Eur Respir of obstructive sleep apnea and snoring with oral appliance therapy: an J. 2017:50. [PMID: 28860265] doi:10.1183/13993003.02426 2076 update fbr 2015. J Clin Sleep Med. 2015:17:773-827. [PMID, 26094920] doi:10.5664/jcsm.4858 Rochwerg B, Einav S, Chaudhuri D, et al. The role for high flow nasal cannula as a respiratory support strateS/ in adults: a clinical practice guideline. High-Altitude - Related Illnesses lntensive Care Med. 2020:46:2226-2237. [PMID: 33201321] doi:1O.1007/ Ahmedzai S, Balfour Lynn IM, Bewick T, et al; British Thoracic Society s00134-020-06312 y Standards ofCare Committee. Managing passengers with stable respiratory Taylor BE, McClave SA, Martindale RG, et al; Society of Critical Care Medicine. disease planning air travel: British Thoracic Society recommendations. GuideLines for the provision and assessment ofnukition support therapy in the Thorax. 2011;66 Suppl 1;i1 30. IPMID; 21856702] doi:10.1136/thoraxjnl 2011 adult critically ill patient: Society of Critical Care Medicine (SCCM) and 20029s American Society for Parenteral and Enteral Nutrition (AS.PE.N.). Crit Care Med. 2016;44:390 438.IPMID :26nfi861 doi:10.1097/CCM.0000O00000001525 Bartsch P Swenson ER. Clinical practice: acute high-altitude illnesses. N Engl J Med. 2013;368:2294 3O2. IPMID: 23758234] doi:10.1056/NEJMcpl214870 Thille AW, Muller G, Gacouin A, et al; HIGH WEAN Study Group and the REVA Ergan B, Akgun M, Pacilli AMG, et al. Should I stay or should I go? COPD and Research Network. Effect of postexhrbation high flow nasal orygen with air travel. Eur Respir Rev 2018;27. [PMID: 29898904] doi:10.1183/16000617. noninvasive ventilation vs high flow nasal oxygen alone on reintubation 0030 2018 among patients at high risk ofextubation failure: A randomized clinical trial. JAMA. 2019;322:1465 7475. [PMID: 31577036] doi:10.1001/jama.2019 74907 Hu X, Cowl CT, Baqir M, et al. Air travel and pneumothorax. Chest. 2014; Ye Z, Reintam Blaser A, Lytlyn L, et al. Gastrointestinal bleeding prophylaxis 145:688-694. IPMID: 24687705] doi:10.1378/chest.13 2363 for critically il1 patients: a clinical practice guideline. BMl.202o36a:16722. Luks AM, Auerbach PS, Freer L, et al. Wildemess Medical Society clinical IPMID: 319072231 doi:10.1136/bmj.16722 practice guidelines for the prevention and treatment of acute altitude ill hess' ZOig update. Wilderness Environ Med. 2019;30:53-518. IPMID: Zorowitz RD. ICU-acquired weakness: a rehabilitation perspective of diagno 312488181 doi:i0.1016/i.wem.2o19.04.006 sis, treatment, and functional management. Chest. 2016;150:966 971. lP MID : 27 3727 37) doi 1 0. 10 1 6 / j. chest. 20 16. 0 6. 006 :

Kapur VK, Auckley DH, Chowdhuri S, et al. Clinical practice guideline for Neufeld KJ, Needham DM, Oh ES, et al. Antipsychotics for the prevention and diagnostic testing for adult obstructive sleep apnea: an American Academy treatment ofdelirium. Comparative Effectiveness Review No. 219. (Prepared ol Sleep Medicine clinical practice guideline. J Clin SleepMed.2077:13:479- by the Johns Hopkins University Evidence-based Practice Center under 504. IPMID: 28162150] doi:10.5664/jcsm.6506 Contract No. 290-2015 00006 l-2.) AHRQ Publication No. 19 EHC019 EF. Rockville, MD: Agency for Healthcare Research and Quality; September Mokhlesi B, Masa JE, Brozek JL, et al. Evaluation and management ofobesity 2019. doi:IO.23970/AHRQEPCCER2l9 hypoventilation syndrome. an official American Thoracic Society clinical practice guideline. Am J Respir Crit Care Med. 2019;200:e6 e24. [PMID: Ouellette DR, Patel S, Girard TD, et al. Liberation from mechanical ventilation 313687981 doi:10.1164/rccm.2O19O5-1071ST in critically ill adults: An official American College of Chest Physicians/ American Thoracic Society clinical practice guideline: inspiratory pressure Patil SP, Ayappa lA, Caples SM, et al. Treatment ofadult obstructive sleep apnea augmentation during spontaneous breathing trials, orotocols minimizing with positive airway pressure: an American Academy of Sleep Medicine sedation, and noninvasive ventilation immediately after extubation. Chest. systematic review meta analysis, and GRADE assessment. J Clin Sleep 2017;151:166-180. [PMID: 27818331] doi:10.1016/j.chest.2016.10.036 Med. 2019;15:301 334. [PMID: 307368881 doi:10.5664/jcsm.7638 Rochwerg B, Brochard L, Elliott MW et al. Offlicial ERS/ATS clinical practice Ramar K, Dort LC, Katz SG, et al. Clinical practice guideline for the treatment guidelines: noninvasive ventilation for acute respiratory failure. Eur Respir of obstructive sleep apnea and snoring with oral appliance therapy: an J. 2017:50. [PMID: 28860265] doi:10.1183/13993003.02426 2076 update fbr 2015. J Clin Sleep Med. 2015:17:773-827. [PMID, 26094920] doi:10.5664/jcsm.4858 Rochwerg B, Einav S, Chaudhuri D, et al. The role for high flow nasal cannula as a respiratory support strateS/ in adults: a clinical practice guideline. High-Altitude - Related Illnesses lntensive Care Med. 2020:46:2226-2237. [PMID: 33201321] doi:1O.1007/ Ahmedzai S, Balfour Lynn IM, Bewick T, et al; British Thoracic Society s00134-020-06312 y Standards ofCare Committee. Managing passengers with stable respiratory Taylor BE, McClave SA, Martindale RG, et al; Society of Critical Care Medicine. disease planning air travel: British Thoracic Society recommendations. GuideLines for the provision and assessment ofnukition support therapy in the Thorax. 2011;66 Suppl 1;i1 30. IPMID; 21856702] doi:10.1136/thoraxjnl 2011 adult critically ill patient: Society of Critical Care Medicine (SCCM) and 20029s American Society for Parenteral and Enteral Nutrition (AS.PE.N.). Crit Care Med. 2016;44:390 438.IPMID :26nfi861 doi:10.1097/CCM.0000O00000001525 Bartsch P Swenson ER. Clinical practice: acute high-altitude illnesses. N Engl J Med. 2013;368:2294 3O2. IPMID: 23758234] doi:10.1056/NEJMcpl214870 Thille AW, Muller G, Gacouin A, et al; HIGH WEAN Study Group and the REVA Ergan B, Akgun M, Pacilli AMG, et al. Should I stay or should I go? COPD and Research Network. Effect of postexhrbation high flow nasal orygen with air travel. Eur Respir Rev 2018;27. [PMID: 29898904] doi:10.1183/16000617. noninvasive ventilation vs high flow nasal oxygen alone on reintubation 0030 2018 among patients at high risk ofextubation failure: A randomized clinical trial. JAMA. 2019;322:1465 7475. [PMID: 31577036] doi:10.1001/jama.2019 74907 Hu X, Cowl CT, Baqir M, et al. Air travel and pneumothorax. Chest. 2014; Ye Z, Reintam Blaser A, Lytlyn L, et al. Gastrointestinal bleeding prophylaxis 145:688-694. IPMID: 24687705] doi:10.1378/chest.13 2363 for critically il1 patients: a clinical practice guideline. BMl.202o36a:16722. Luks AM, Auerbach PS, Freer L, et al. Wildemess Medical Society clinical IPMID: 319072231 doi:10.1136/bmj.16722 practice guidelines for the prevention and treatment of acute altitude ill hess' ZOig update. Wilderness Environ Med. 2019;30:53-518. IPMID: Zorowitz RD. ICU-acquired weakness: a rehabilitation perspective of diagno 312488181 doi:i0.1016/i.wem.2o19.04.006 sis, treatment, and functional management. Chest. 2016;150:966 971. lP MID : 27 3727 37) doi 1 0. 10 1 6 / j. chest. 20 16. 0 6. 006 : Luks AM, Swenson ER, BArtsch P Acute high-altitude sickness. Eur Respir Rev 2017:26. [PMID: 28143879] doi:10.1183/16000617.0096 2016 Common ICU Conditions Meier D, Collet TH, Locatelli I, et al. Does this patient have acute mountain Cavalcanti AB, Suzumura EA, Laranjeira LN, et al; Writing Group for the sickness?: the Rational Clinical Examination systematic review. JAMA. Alveolar Recruitment for Acute Respiratory Distress Syndrome Trial (ART) 2017;318:1810-1819. [PMID: 29t364491 doi:10.1001/jama.2077.76792 Investigators. Effect of lung recruitment and titrated positive end expira Nicholson TT, Sznajder Jl. Fitness to fly in patients with lung disease. Ann Am tory pressure (PEEP) vs low PEEP on mortality in patients with acute res Thorac Soc. 2014:111614-22. [PMID: 25393882] doi:10.1513/AnnalsATS. piratory distress syndrome: A randomized clinical trial. JAMA. 2017;318: 201406-234PS 1335 1345. [PMID: 28973363] doir10.1001/jama.2oU.74177

Luks AM, Swenson ER, BArtsch P Acute high-altitude sickness. Eur Respir Rev 2017:26. [PMID: 28143879] doi:10.1183/16000617.0096 2016 Common ICU Conditions Meier D, Collet TH, Locatelli I, et al. Does this patient have acute mountain Cavalcanti AB, Suzumura EA, Laranjeira LN, et al; Writing Group for the sickness?: the Rational Clinical Examination systematic review. JAMA. Alveolar Recruitment for Acute Respiratory Distress Syndrome Trial (ART) 2017;318:1810-1819. [PMID: 29t364491 doi:10.1001/jama.2077.76792 Investigators. Effect of lung recruitment and titrated positive end expira Nicholson TT, Sznajder Jl. Fitness to fly in patients with lung disease. Ann Am tory pressure (PEEP) vs low PEEP on mortality in patients with acute res Thorac Soc. 2014:111614-22. [PMID: 25393882] doi:10.1513/AnnalsATS. piratory distress syndrome: A randomized clinical trial. JAMA. 2017;318: 201406-234PS 1335 1345. [PMID: 28973363] doir10.1001/jama.2oU.74177 West JB. Physiological effects ofchronic hypoxia. N Engl J Med. 2017;376:1965- Fan E, Del Sorbo L, Goligher EC, et al; American Thoracic Society, European 1971. [PMID: 28514605] doi:10.1056/NEJMral612008 Society of Intensive Care Medicine, and Society of Critical Care Medicine' An official American Thoracic Society/European Society of Intensive Care Critical Care Medicine: ICU Utilization Medicine/Society of Critical Care Medicine clinical practice guideline: Hall KK, Lim A, Gale B. The use of rapid response teams to reduce failure to mechanical ventilation in adult patients with acute respiratory distress rescue events: A systematic review. J Patient saf. 2020;16:53-57. [PMID; syndrome. AmJ RespirCritCare Med. 2017;195:1253 1263. [PMID: 28459336] 328099941 doi:10.1097r PTS.0oo0000o00000748 doi:10.1164/rccm.201703-0548ST

West JB. Physiological effects ofchronic hypoxia. N Engl J Med. 2017;376:1965- Fan E, Del Sorbo L, Goligher EC, et al; American Thoracic Society, European 1971. [PMID: 28514605] doi:10.1056/NEJMral612008 Society of Intensive Care Medicine, and Society of Critical Care Medicine' An official American Thoracic Society/European Society of Intensive Care Critical Care Medicine: ICU Utilization Medicine/Society of Critical Care Medicine clinical practice guideline: Hall KK, Lim A, Gale B. The use of rapid response teams to reduce failure to mechanical ventilation in adult patients with acute respiratory distress rescue events: A systematic review. J Patient saf. 2020;16:53-57. [PMID; syndrome. AmJ RespirCritCare Med. 2017;195:1253 1263. [PMID: 28459336] 328099941 doi:10.1097r PTS.0oo0000o00000748 doi:10.1164/rccm.201703-0548ST Nates JL, Nunnally M, Kleinpell R, et al. ICU admission, discharge, and triage Global Initiative for Asthma. Global stratery for asthma management and pre- guidelines: A iramework to enhance clinical operations, development of vention, 2021. Accessed May 5, 2021. https://ginasthma.org/gina-reports/ institutional policies, and further research. Crit Care Med. 2016;44:1553 Global lnitiative for Chronic Obstructive Lung Disease. Global strategr for the 602. [PMID: 27428118) doi:10.1097/ccM.0000000000001856 diagnosis, management, and prevention of chronic obstructive pulmonary Zampieri FG, Salluh JIF, Azevedo LCP et al; ORCHESTRA Study Investigators disease: 2020 report. Accessed September 27, 2o2o' https;//goldcopd'org/ ICU staffing feature phenotypes and their relationship with patients' gold-reports/ 91

Bibliography I".e\,y MM, Evans LE, Rhodes A. The suwiving sepsis campaign bundle: 2018 Epstein Y, Yanovich R Heatstroke. N Engl J Med. 2019;380:2,+49-2459. [PMID: update [Editorial]. Intensive Care Med. 2018;44:925-92S. [PMID: 29675566] 312164001 doi:10.1056/NEJMral810762 doi:10.1007/s00134-018-5085-0 Heffetig FM, Kirk MA" McKay CA Jr. Hazardous chemical emergencies and poi- Moss M, Huang DT, Brower RG, et al; National Heart, Lung, and Blood Institute sonings. N Engl J Med. 2019;380:1638-1655. [PMID: 31018070] doi:10.1056/ PETAL Clinical Trials Network. Early neuromuscular blockade in the acute NEJMra1504690 respiratory distress syndrome. N Engl J Med. 2019;380:1997-2008. [PMID: Loverde D, Files DC, Krishnaswamy G. Angioedema. Crit Care Med. 2017; 311123831 doi:10.1056/NEJMoal901686 45:725-735. IPMID: 28291095] doi:10.1097/CCM.0000000000002281 Rhodes A, Evans LE, Alhazzani W et al. Surviving sepsis campaign: Modi S, Dharaiya D, Schultz L, et al. Neuroleptic malignant slmdrcme: compli- international guidelines for management of sepsis and septic shock: 2016. cations, outcomes, and mortality. Neurocrit Carc. 2O16;24:97 -103. [PMID: Crit Care Med. 2017;45:486-552. [PMID: 28098591] doi:10.1097/CCM. 262233361 doi;10.1007/s12028-015-0162-5 0000000000002255 Ng PCY, tong BJ, Davis WT, et al. Toxic alcohol diagnosis and management: an Singer M, Deutschman CS, Seymour CW, et a]. The third intemational consen- emergency medicine review. Intern Emerg Med. 2018;13:375-3$. [PMID: sus definitions for sepsis and septic shock (Sepsis-3). JAMA 2016;315:801- 29 477 lall doi:lO.1007 /slf39 - 018 - U99 - 9 10. [PMID: 269033381 doi:10.1001/jama.2016.0287 Rothberg DL, Makarewich CA. Fat embolism and fat embolism syndrome. J Singer P, Blaser AR, Berger MM, et al. ESPEN guideline on clinical nutrition in Am Acad Orthop Surg. 2019;27:e346-e355. [PMID: 30958807] doi:10.5435/ the intensive care unit. Clin Nutr. 2019;38:48-79. [PMID: 30348463] JAAOS-D 17 00s71 doi:10.1016 /j.cInu.2018.08.037 Shaker MS, Wallace DY Golden DBK, et al; Collaborators. Anaphylaxis-a 2020 Thompson Bl Chambers RC, Liu KD. Acute respiratory distress srar&ome. N practice panmeter update, systematic rel'iew, and Grading of Recommen- Engl J Med. 2017;377 :562- 57 2. IPMID: 287928731 doi:10.10S6/NEJMra16O807/ dations, Assessment, Development and Evaluation (GRADE) analysis. J Allergr Clin Immunol. 2020;145:1802-1123. [PMID: 32001253] Speclffc Cridcal Care Topics Vasquez DN, Plante L, Basualdo MN, et al. Obstetric disorders in the ICU. Semin Elmer J, Callaway CW. The brain after cardiac arrest. Semin Neurol. 2017;37:19- Respir Crit Care Med. 2017;38:218-234. [PMID: 28561253] doi:10.1055/s- 24. IPMID : 28147 4141 doi:10.1055/s-0036-1597833 0037-1600910

I".e\,y MM, Evans LE, Rhodes A. The suwiving sepsis campaign bundle: 2018 Epstein Y, Yanovich R Heatstroke. N Engl J Med. 2019;380:2,+49-2459. [PMID: update [Editorial]. Intensive Care Med. 2018;44:925-92S. [PMID: 29675566] 312164001 doi:10.1056/NEJMral810762 doi:10.1007/s00134-018-5085-0 Heffetig FM, Kirk MA" McKay CA Jr. Hazardous chemical emergencies and poi- Moss M, Huang DT, Brower RG, et al; National Heart, Lung, and Blood Institute sonings. N Engl J Med. 2019;380:1638-1655. [PMID: 31018070] doi:10.1056/ PETAL Clinical Trials Network. Early neuromuscular blockade in the acute NEJMra1504690 respiratory distress syndrome. N Engl J Med. 2019;380:1997-2008. [PMID: Loverde D, Files DC, Krishnaswamy G. Angioedema. Crit Care Med. 2017; 311123831 doi:10.1056/NEJMoal901686 45:725-735. IPMID: 28291095] doi:10.1097/CCM.0000000000002281 Rhodes A, Evans LE, Alhazzani W et al. Surviving sepsis campaign: Modi S, Dharaiya D, Schultz L, et al. Neuroleptic malignant slmdrcme: compli- international guidelines for management of sepsis and septic shock: 2016. cations, outcomes, and mortality. Neurocrit Carc. 2O16;24:97 -103. [PMID: Crit Care Med. 2017;45:486-552. [PMID: 28098591] doi:10.1097/CCM. 262233361 doi;10.1007/s12028-015-0162-5 0000000000002255 Ng PCY, tong BJ, Davis WT, et al. Toxic alcohol diagnosis and management: an Singer M, Deutschman CS, Seymour CW, et a]. The third intemational consen- emergency medicine review. Intern Emerg Med. 2018;13:375-3$. [PMID: sus definitions for sepsis and septic shock (Sepsis-3). JAMA 2016;315:801- 29 477 lall doi:lO.1007 /slf39 - 018 - U99 - 9 10. [PMID: 269033381 doi:10.1001/jama.2016.0287 Rothberg DL, Makarewich CA. Fat embolism and fat embolism syndrome. J Singer P, Blaser AR, Berger MM, et al. ESPEN guideline on clinical nutrition in Am Acad Orthop Surg. 2019;27:e346-e355. [PMID: 30958807] doi:10.5435/ the intensive care unit. Clin Nutr. 2019;38:48-79. [PMID: 30348463] JAAOS-D 17 00s71 doi:10.1016 /j.cInu.2018.08.037 Shaker MS, Wallace DY Golden DBK, et al; Collaborators. Anaphylaxis-a 2020 Thompson Bl Chambers RC, Liu KD. Acute respiratory distress srar&ome. N practice panmeter update, systematic rel'iew, and Grading of Recommen- Engl J Med. 2017;377 :562- 57 2. IPMID: 287928731 doi:10.10S6/NEJMra16O807/ dations, Assessment, Development and Evaluation (GRADE) analysis. J Allergr Clin Immunol. 2020;145:1802-1123. [PMID: 32001253] Speclffc Cridcal Care Topics Vasquez DN, Plante L, Basualdo MN, et al. Obstetric disorders in the ICU. Semin Elmer J, Callaway CW. The brain after cardiac arrest. Semin Neurol. 2017;37:19- Respir Crit Care Med. 2017;38:218-234. [PMID: 28561253] doi:10.1055/s- 24. IPMID : 28147 4141 doi:10.1055/s-0036-1597833 0037-1600910 92

ut Pulmonary and Critical Care Medicine 6' t- (l, Self-Assessment Test tr UI v! (l, vt vr This self-assessment test contains one-best-answer multiple-choice questions. please read these directions carefully (l, before answering the questions. Answers, critiques, and bibliographies immediately follow these multiple-choice t/t questions. The American College of Physicians (ACP) is accredited by the Accreditation Council for Continuing Medical Education (ACCME) to provide continuing medical education for physicians. The American College of Physicians designates MKSAP 19 Pulmonary and Critical Care Medicine for a maximum of 25.75 AMA PRA Category l CreditsTM. Physicians should claim only the credit commensurate with the extent of their participation in the activity. Successful completion of the CME activity, which includes participation in the evaluation component, enables the participant to earn up to 25.75 medical knowledge MOC points in the American Board of Internal Medicine's Maintenance of Certiflcation (MOC) program. It is the CME activity provider's responsibility to submit participant completion information to ACCME for the purpose of granting MOC credit.

Successful completion of the CME activity, which includes participation in the evaluation component, enables the participant to earn up to 25.75 medical knowledge MOC points in the American Board of Internal Medicine's Maintenance of Certiflcation (MOC) program. It is the CME activity provider's responsibility to submit participant completion information to ACCME for the purpose of granting MOC credit. Earn Credits or MOC Points Online To earn CME credits or to apply for MOC points, MKSAP users need to answer at least one of two questions correctly (earning a score of at least 50%) and click the Submit CME button. Each single MKSAP L9 self-assessment question qualifles for one quarter of a CME credit hour or ABIM MOC point. MKSAP 19 Subscribers can enter their self-assessment question answers and submit for CME/MOC in two ways: 1. Users of MKSAP 19 Complete who prefer to use their print books and a paper answer sheet to study and record their answers can use the printed answer sheet at the back of this book to record their answers. The corresponding online answer sheets, which are available on the MKSAP 19 Resource Page, may be used to transcribe answers onto the online answer sheets. Users may then submit their answers to qualify for CME credits or MOC points (see below for information on Opting in for MOC). Users who prefer to record their answers on a paper answer sheet should save their answer sheet for future use. Users who study with MKSAP 19 print can also submit their answers directly within MKSAP 19 Digital by accessing the self-assessment ques- tions dashboard and selecting the preferred subspecialty section to begin answering questions. 2. Users of MKSAP 19 Digital can enter their answers within the digital program by accessing the self-assessment questions dashboard and selecting the preferred subspecialty section to begin answering questions and clicking the Submit CME button once they qualiff for CME and are ready to submit. Learners should keep in mind theiryearly CME and MOC deadlines when determining the appropriate time to submit. Learners' CME/MOC submission progress will be shown on the MKSAP 19 Digital CME/MOC/CPD page.

2. Users of MKSAP 19 Digital can enter their answers within the digital program by accessing the self-assessment questions dashboard and selecting the preferred subspecialty section to begin answering questions and clicking the Submit CME button once they qualiff for CME and are ready to submit. Learners should keep in mind theiryearly CME and MOC deadlines when determining the appropriate time to submit. Learners' CME/MOC submission progress will be shown on the MKSAP 19 Digital CME/MOC/CPD page. Opting in for MOC MKSAP 19 users can opt in for simultaneous submission of CME and MOC points as they answer self-assessment questions. To opt in, users will be required to complete a form requesting their name, date of birth, and ABIM number. The MOC Opt-in Form will be presented upon the user's flrst CME submission and needs to be completed only once. 93

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Directions Each of the numbered items rs followed by lettered ansuzers. Se/ect t he OllE lettered la answer that is BES1 in each case. o, F (l, E tr Item I An B7-year-old woman was hospitalized 2 days ago fbr sep- Chest radiograph reveals a large right pneumothorax and no signs oftension. Smoking cessation counseling ancl an offer of vareni t UI (u la t sis related to pyelonephritis. Medical history is significant for hypertension and heart failure. She has responded to cline are planned at the time olclischarge. (u fluid resuscitation and antibiotic therapy but is intermit tt tently confused. She reports no pain. Attempts have been Which of the following is the most appropriate additional made not to interrupt her night time sleep. Nurses provide pneumothorax management? frequent orientation, and she has been provided with her (A) Catheter thoracostomy fbllowed by pleurodesis glasses and hearing aids. Medications are ceftriaxone, aceta- I (U) Needle aspiration minophen, carvedilol, hydrochlorothiazide, and lisinopril. I On physical eramination, vital signs are normal. Ox1,- (C) Observatior-r gen saturation is 92'l. breathing oxygen, 2 Lrmin by nasirl (D) Supplemental oxygen and observation cannula. She is awake and oriented. There are no local neurologic deficits.

Directions Each of the numbered items rs followed by lettered ansuzers. Se/ect t he OllE lettered la answer that is BES1 in each case. o, F (l, E tr Item I An B7-year-old woman was hospitalized 2 days ago fbr sep- Chest radiograph reveals a large right pneumothorax and no signs oftension. Smoking cessation counseling ancl an offer of vareni t UI (u la t sis related to pyelonephritis. Medical history is significant for hypertension and heart failure. She has responded to cline are planned at the time olclischarge. (u fluid resuscitation and antibiotic therapy but is intermit tt tently confused. She reports no pain. Attempts have been Which of the following is the most appropriate additional made not to interrupt her night time sleep. Nurses provide pneumothorax management? frequent orientation, and she has been provided with her (A) Catheter thoracostomy fbllowed by pleurodesis glasses and hearing aids. Medications are ceftriaxone, aceta- I (U) Needle aspiration minophen, carvedilol, hydrochlorothiazide, and lisinopril. I On physical eramination, vital signs are normal. Ox1,- (C) Observatior-r gen saturation is 92'l. breathing oxygen, 2 Lrmin by nasirl (D) Supplemental oxygen and observation cannula. She is awake and oriented. There are no local neurologic deficits. Which of the following is the most appropriate measure to Item 4 A 72-year-old man is evaluated in the emergency depart' ment fbr decreasing responsiveness alter he spent the day tr prevent delirium? at the zoo. The outside temperature was 38.9 'C (102.0 "F). (A) Early mobilization [{e also has hypertension. Medications are hydrochlorothi (B) Haloperidol azide and lisinopril. (C) Lorazepam On physical examination, tempe,rature is 40.5 'C (104.9 'I), blood pressure is 97154 mnr [-lg, pulse ratc is (D) Meiatonin I l7lmin, respiration rate is 22lmin, and oxygen saturation is 96')1, with the patient breathing ambient air. He is somno

Which of the following is the most appropriate measure to Item 4 A 72-year-old man is evaluated in the emergency depart' ment fbr decreasing responsiveness alter he spent the day tr prevent delirium? at the zoo. The outside temperature was 38.9 'C (102.0 "F). (A) Early mobilization [{e also has hypertension. Medications are hydrochlorothi (B) Haloperidol azide and lisinopril. (C) Lorazepam On physical examination, tempe,rature is 40.5 'C (104.9 'I), blood pressure is 97154 mnr [-lg, pulse ratc is (D) Meiatonin I l7lmin, respiration rate is 22lmin, and oxygen saturation is 96')1, with the patient breathing ambient air. He is somno Item 2 lent. His skin is flushed, warm. and dry. Other than tachy cardia, cardiac:rnd pulmonary examinations are normal. A 42 year-old man is evaluated at a follow up appointment. l.aboratory results are pending. He underwent polysomnography 6 weeks ago because of suspected obstructive sleep apnea. the study showed mod Which of the following is the most appropriate treatment? erate obstructive sleep apnea (apnea-hypopnea index 20) that was controlled with continuous positive airway pres- (A) Acetaminophen sure (CPAP). Although daytime alertness has improved (B) Dantrolene with CPAP, the apparatus is cumbersome to transport on (C) Evaporativecooling his frequent business trips. At his last visit, the physical (D) Immersion in ice water examination was normal except for a BI\41 of 34. The patient is enrolled in a supervised weight loss program and has started to exercise.

Item 2 lent. His skin is flushed, warm. and dry. Other than tachy cardia, cardiac:rnd pulmonary examinations are normal. A 42 year-old man is evaluated at a follow up appointment. l.aboratory results are pending. He underwent polysomnography 6 weeks ago because of suspected obstructive sleep apnea. the study showed mod Which of the following is the most appropriate treatment? erate obstructive sleep apnea (apnea-hypopnea index 20) that was controlled with continuous positive airway pres- (A) Acetaminophen sure (CPAP). Although daytime alertness has improved (B) Dantrolene with CPAP, the apparatus is cumbersome to transport on (C) Evaporativecooling his frequent business trips. At his last visit, the physical (D) Immersion in ice water examination was normal except for a BI\41 of 34. The patient is enrolled in a supervised weight loss program and has started to exercise. Which of the following is the most appropriate Item 5 A 67 year-old man is evaluated fbr progressive shortness tr of breatl'r and dry cough over the past ll months. [Ie has a treatment? 40 pack -year history of cigarette smoking. His only medi (A) Hypoglossal nerve stimulator cation is an albnterol inhaler. On physical examination, pulse rate is 9Olmin ancl (B) Maxillomandibularadvancementsurgery respiration rate is 24lmin. Oxygen saturation is 887, with (C) Oral appliance the patient breathing ambient air. Auscultation demon (D) Uvulopalatopharyngoplasty strates bibasilar crackles. Clubbing is present. Spirometry shor.t,s an FVC of 110'X, of predicted. an FEV, of 95'il, of predicted. an FEV'i FVC ratio of 0.68. ar.rd a

Which of the following is the most appropriate Item 5 A 67 year-old man is evaluated fbr progressive shortness tr of breatl'r and dry cough over the past ll months. [Ie has a treatment? 40 pack -year history of cigarette smoking. His only medi (A) Hypoglossal nerve stimulator cation is an albnterol inhaler. On physical examination, pulse rate is 9Olmin ancl (B) Maxillomandibularadvancementsurgery respiration rate is 24lmin. Oxygen saturation is 887, with (C) Oral appliance the patient breathing ambient air. Auscultation demon (D) Uvulopalatopharyngoplasty strates bibasilar crackles. Clubbing is present. Spirometry shor.t,s an FVC of 110'X, of predicted. an FEV, of 95'il, of predicted. an FEV'i FVC ratio of 0.68. ar.rd a tr Item 3 A 25-year-old man is evaluated in the emergency clepart- Dr.<:o of'36% of predicted. An echocardiogram shows nornral left ventricle ejcc tion lraction. Right ventricle systolic pressure is 66 mm llg. ment fbr worsening shortness of breath and right-side pleuritic chest pain. which developed t hour ago. He has Representative high-resolution CT chest images are an B pack year history of smoking cigarettes. His medical slrown (top ol next page). history is otherwise unremarkable, including the absence of lung disease. He is a professional scuba diver. Which of the following is the most likely diagnosis? On physical examination, blood presswe is 150/70 mm Hg, (A) Acute interstitiul pneumonia pulse rate is 105/min, and respiration rate is 30lmin. Oxy- (B) Combined pulmonary flbrosis and emphysema gen saturation is 92"/,, with the ilatient breathing ambient air. There are decreased breath sounds, reduced expansion. (C) Desquamativeinterstitialpneumonia and hyperresonance to percussion on the right side. (l)) Idiopathic pulmonary fibrosis

tr Item 3 A 25-year-old man is evaluated in the emergency clepart- Dr.<:o of'36% of predicted. An echocardiogram shows nornral left ventricle ejcc tion lraction. Right ventricle systolic pressure is 66 mm llg. ment fbr worsening shortness of breath and right-side pleuritic chest pain. which developed t hour ago. He has Representative high-resolution CT chest images are an B pack year history of smoking cigarettes. His medical slrown (top ol next page). history is otherwise unremarkable, including the absence of lung disease. He is a professional scuba diver. Which of the following is the most likely diagnosis? On physical examination, blood presswe is 150/70 mm Hg, (A) Acute interstitiul pneumonia pulse rate is 105/min, and respiration rate is 30lmin. Oxy- (B) Combined pulmonary flbrosis and emphysema gen saturation is 92"/,, with the ilatient breathing ambient air. There are decreased breath sounds, reduced expansion. (C) Desquamativeinterstitialpneumonia and hyperresonance to percussion on the right side. (l)) Idiopathic pulmonary fibrosis 95

Self-Assessment Test vt .D a D 6 UI (D UI UI (D .D gt i ITEM 5 Item 6 (C) CT guided lung biopsy A 36 year old woman is evaluated for a change in her (D) FluorodeoxyglucosePET asthma status. She has spirometry conflrmed asthma; she (E) No further follorn,-up has never required hospitalization. She is a nonsmoker and has allergic rhinitis. Her only medication is an albuterol metered dose inhaler as needed. She now requires albuterol Item 8 use three times weekly but never more than once per day. A 59-year old man is seen in a follow-up visit for a 6 month She demonstrates good inhaler technique. history of progressively worsening chronic cough produc On physical examination, vital signs are normal. Oxy tive of small amounts of thin clear sputum and dyspnea gen saturation is 9B%, with the patient breathing ambient on exertion. He has shortness of breath when he walks air. BMI is 24. She is not currently wheezing. The remainder quickly and when he walks uphill. He has a 45 pack year of the examination is normal. smoking history but quit 2 years ago. He has been using Spirometry today is normal. albuterol as needed since his diagnosis of COPD 3 months ago, but he remains symptomatic. Which of the following is the most appropriate management? On physical examination, oxygen saturation is 95'1, with the patient breathing ambient air. Scattered expira- (A) Beclomethasone dipropionatewith albuterol tory wheezing is heard. Cardiac examination is normal. (B) Methacholinechallengetesting Chest radiograph from 3 months ago shows flattened (C) Monlelukasl at bedtime diaphragm but no inflltrate. (D) No additional management Spirometry at the time of diagnosis showed reduced postbronchodilator FEV,/FVC ratio and FEV, of 69"/,, of predicted. Item 7 A 53 year old woman presents for follow-up evaluation of Which of the following is the most appropriate an incidentally found 4 mm solid lung nodule in the right pharmacologic treatment? lower lobe on abdominal CT scan. The CT scan showed no (A) Inhaled fluticasone propionate salmeterol other nodules, no lymphadenopathy, and unremarkable (B) Inhaled tiotropium bromide lung parenchyma. There are no old scans for comparison. She has no personal or family history of lung cancer. (C) Prednisone She is asymptomatic, a lifelong nonsmoker, and has (D) Roflumitast no signiflcant exposure history.

Item 6 (C) CT guided lung biopsy A 36 year old woman is evaluated for a change in her (D) FluorodeoxyglucosePET asthma status. She has spirometry conflrmed asthma; she (E) No further follorn,-up has never required hospitalization. She is a nonsmoker and has allergic rhinitis. Her only medication is an albuterol metered dose inhaler as needed. She now requires albuterol Item 8 use three times weekly but never more than once per day. A 59-year old man is seen in a follow-up visit for a 6 month She demonstrates good inhaler technique. history of progressively worsening chronic cough produc On physical examination, vital signs are normal. Oxy tive of small amounts of thin clear sputum and dyspnea gen saturation is 9B%, with the patient breathing ambient on exertion. He has shortness of breath when he walks air. BMI is 24. She is not currently wheezing. The remainder quickly and when he walks uphill. He has a 45 pack year of the examination is normal. smoking history but quit 2 years ago. He has been using Spirometry today is normal. albuterol as needed since his diagnosis of COPD 3 months ago, but he remains symptomatic. Which of the following is the most appropriate management? On physical examination, oxygen saturation is 95'1, with the patient breathing ambient air. Scattered expira- (A) Beclomethasone dipropionatewith albuterol tory wheezing is heard. Cardiac examination is normal. (B) Methacholinechallengetesting Chest radiograph from 3 months ago shows flattened (C) Monlelukasl at bedtime diaphragm but no inflltrate. (D) No additional management Spirometry at the time of diagnosis showed reduced postbronchodilator FEV,/FVC ratio and FEV, of 69"/,, of predicted. Item 7 A 53 year old woman presents for follow-up evaluation of Which of the following is the most appropriate an incidentally found 4 mm solid lung nodule in the right pharmacologic treatment? lower lobe on abdominal CT scan. The CT scan showed no (A) Inhaled fluticasone propionate salmeterol other nodules, no lymphadenopathy, and unremarkable (B) Inhaled tiotropium bromide lung parenchyma. There are no old scans for comparison. She has no personal or family history of lung cancer. (C) Prednisone She is asymptomatic, a lifelong nonsmoker, and has (D) Roflumitast no signiflcant exposure history. Which ofthe following is the most appropriate management? (A) Bronchoscopy with lung biopsy Item 9 r\ :15 vear old nran is evaluated in lhe emergency clcplrt tr rrent .1 horirs al'tcr bcing rescued fionr his bnrning honrc (B) CT of'chest in 12 months br'{irefightcrs. lle initiall! relirserl transportation to thc

Which ofthe following is the most appropriate management? (A) Bronchoscopy with lung biopsy Item 9 r\ :15 vear old nran is evaluated in lhe emergency clcplrt tr rrent .1 horirs al'tcr bcing rescued fionr his bnrning honrc (B) CT of'chest in 12 months br'{irefightcrs. lle initiall! relirserl transportation to thc 96

I t Self-Assessment Test vt t I tr CONT, hospital but now desires an evaluation. He reports tracheal irritation with breathir-rg, sore throat, and a change in his voice. Arterial blood ges studies (at time of discharge): pH Pco, 7.42 44mm Hg (5.8 kPa) 6'

t I tr CONT, hospital but now desires an evaluation. He reports tracheal irritation with breathir-rg, sore throat, and a change in his voice. Arterial blood ges studies (at time of discharge): pH Pco, 7.42 44mm Hg (5.8 kPa) 6' (l, On physical examination, he is alert and in moder Po, 55 mm Hg (7.3 kPa) E vt L ate pain. Temperature is 37..5 'C (99.5 "F), blood pressure vt o vt is I44l9O mm t{g, pulse rate is 100/min, and respiration Which of the following is the most appropriate additional r^ rate is 26lmin. Oxygen saturation is 967, with the patient treatment? L breathing ambient air. He has dysphonia. There is no soot (A) Aminophylline (u in the nares or the oral pharynx or burns on his face, r ; (B) Home oxygen neck, or thorax. Nonobstructing edema of the oropharynx is noted. Cardiac examination reveals a regular rhythm. (C) Noninvasive positive pressure ventilation , (D) Stop current inhalers; start inhaled fluticasone Chest is clear to auscultation: there is no stridor. :

(l, On physical examination, he is alert and in moder Po, 55 mm Hg (7.3 kPa) E vt L ate pain. Temperature is 37..5 'C (99.5 "F), blood pressure vt o vt is I44l9O mm t{g, pulse rate is 100/min, and respiration Which of the following is the most appropriate additional r^ rate is 26lmin. Oxygen saturation is 967, with the patient treatment? L breathing ambient air. He has dysphonia. There is no soot (A) Aminophylline (u in the nares or the oral pharynx or burns on his face, r ; (B) Home oxygen neck, or thorax. Nonobstructing edema of the oropharynx is noted. Cardiac examination reveals a regular rhythm. (C) Noninvasive positive pressure ventilation , (D) Stop current inhalers; start inhaled fluticasone Chest is clear to auscultation: there is no stridor. : Arterial blood gas studies: pll 7.45 Pr;o, Po, 35 mm Hg (a.7 kPa) 95 mm He (12.6 kPa) Item 12 A 74-year old man is evaluated in the ICU fbr sep tr sis and hypotension. A central venous catheter has just A chest radiograph shows no inflltrates. been inserted into the left internal jugular vein under ultrasound visualization to start vasopressor therapy. As Which of the following is the most appropriate the catheter line is being secured, the patient suddenly management? becomes more hypotensive. Medications are propofol, (A) Bronchoscopy piperacillin tazobactam, and vancomycin. 'l'emperature is 37.8 'C (100.0 'F), blood pressure is (B) Methylprednisolone 74155 mm Hg, pulse rate is 118/min, and respiration rate (C) Nebulizedepinephrine is 18/min on mechanical ventilation. Oxygen saturation is (D) Noninvasive positive pressure ventilation 91o1, on Fro, of 1.00. Breath sounds are diminished bilater ally. Heart sounds are diminished.

Arterial blood gas studies: pll 7.45 Pr;o, Po, 35 mm Hg (a.7 kPa) 95 mm He (12.6 kPa) Item 12 A 74-year old man is evaluated in the ICU fbr sep tr sis and hypotension. A central venous catheter has just A chest radiograph shows no inflltrates. been inserted into the left internal jugular vein under ultrasound visualization to start vasopressor therapy. As Which of the following is the most appropriate the catheter line is being secured, the patient suddenly management? becomes more hypotensive. Medications are propofol, (A) Bronchoscopy piperacillin tazobactam, and vancomycin. 'l'emperature is 37.8 'C (100.0 'F), blood pressure is (B) Methylprednisolone 74155 mm Hg, pulse rate is 118/min, and respiration rate (C) Nebulizedepinephrine is 18/min on mechanical ventilation. Oxygen saturation is (D) Noninvasive positive pressure ventilation 91o1, on Fro, of 1.00. Breath sounds are diminished bilater ally. Heart sounds are diminished. tr Item 10 A 42-year old man is evaluated for fatigue, dyspnea, and Which of the following is the most appropriate next management step? lightheadedness. He was diagnosed with a provoked pul- monary embolism 5 months ago and has been taking apix (A) Chest C'l aban since then. Initially, his dyspnea and tachycardia (B) Chestultrasonography improved, but over the past 2 months, he has had progres (C) Needlethoracostomy sive exertional dyspnea. (D) Removal of central venous catheter On physical examination, vital signs are normal. BMI is 28. Cardiopulmonary examination is normal. An echocardiogram reveals right atrial enlargement and right ventricular hypertrophy and an elevated mean Item 13 pulmonary artery pressure. A 3S-year-old woman is evaluated for a cough and wheez- ing occurring several times during the week, unrelated to Which of the following is the most appropriate diagnostic exercise. She has a history of asthma that was previously test? well controlled with a budesonide inhaler. She is also tak- ing albuterol flve times weekly with good response. Her (A) CTangiographyofthe chest symptoms have woken her once in the past month. She (B) D dimer assay reports no additional symptoms and no environmental (C) Rigtrt heart catheterization and pulmonary angio- triggers. She is a nonsmoker. Inhaler technique is good. graphy On physical examination, vital signs are normal. Oxy- gen saturation is 96% with the patient breathing ambient (D) Ventilation/perfusion scan air. Expiratory wheezing is noted.

tr Item 10 A 42-year old man is evaluated for fatigue, dyspnea, and Which of the following is the most appropriate next management step? lightheadedness. He was diagnosed with a provoked pul- monary embolism 5 months ago and has been taking apix (A) Chest C'l aban since then. Initially, his dyspnea and tachycardia (B) Chestultrasonography improved, but over the past 2 months, he has had progres (C) Needlethoracostomy sive exertional dyspnea. (D) Removal of central venous catheter On physical examination, vital signs are normal. BMI is 28. Cardiopulmonary examination is normal. An echocardiogram reveals right atrial enlargement and right ventricular hypertrophy and an elevated mean Item 13 pulmonary artery pressure. A 3S-year-old woman is evaluated for a cough and wheez- ing occurring several times during the week, unrelated to Which of the following is the most appropriate diagnostic exercise. She has a history of asthma that was previously test? well controlled with a budesonide inhaler. She is also tak- ing albuterol flve times weekly with good response. Her (A) CTangiographyofthe chest symptoms have woken her once in the past month. She (B) D dimer assay reports no additional symptoms and no environmental (C) Rigtrt heart catheterization and pulmonary angio- triggers. She is a nonsmoker. Inhaler technique is good. graphy On physical examination, vital signs are normal. Oxy- gen saturation is 96% with the patient breathing ambient (D) Ventilation/perfusion scan air. Expiratory wheezing is noted. tr Item 11 A S9-year-old woman was hospitalized for a first COPD Which of the following treatments should be started? (A) Add formoterol exacerbation 5 days ago and is now preparing for discharge. (B) Azithromycin She quit smoking 5 years ago. Immunizations are up to date. (C) Prednisone Medications are daily tiotropium bromide and albuterol inhalers as needed. Prednisone is to be discontinued today. (D) Tiotropium On physical examination, vital signs are normal. Oxy- gen saturation at rest is 87'7, with the patient breathing ambient air. Breath sounds are distant, without wheezing. Cardiovascular examination is normal. Item 14 A S7-year-old woman is evaluated at a fbllow 'up visit after tr Complete blood count is normal. discharge trom the hospital for a COPD exacerbation. This

tr Item 11 A S9-year-old woman was hospitalized for a first COPD Which of the following treatments should be started? (A) Add formoterol exacerbation 5 days ago and is now preparing for discharge. (B) Azithromycin She quit smoking 5 years ago. Immunizations are up to date. (C) Prednisone Medications are daily tiotropium bromide and albuterol inhalers as needed. Prednisone is to be discontinued today. (D) Tiotropium On physical examination, vital signs are normal. Oxy- gen saturation at rest is 87'7, with the patient breathing ambient air. Breath sounds are distant, without wheezing. Cardiovascular examination is normal. Item 14 A S7-year-old woman is evaluated at a fbllow 'up visit after tr Complete blood count is normal. discharge trom the hospital for a COPD exacerbation. This 97

Self-Assessment Test l/! (D gt Ut tr c0Nl was her third hospitalization for a COPD exacerbation in the past 6 months. She no longer smokes cigarettes. Medications are fluticasone-umeclidinium-vilanterol and Chest radiograph reveals bilateral symmetric hilar prominence with clear lung flelds. Interferon-yrelease assay is normal. o UI la albuterol inhalers. She has been adherent with her med- ication, has excellent inhaler technique. and continues to Which of the following is the most appropriate .D use home oxygen. Between exacerbations she has a cough management? productive o{' thin, colorless sputum. .D On physical examination. vital signs are normal. Oxy- (A) Bronchoscopicbiopsy UI gen saturation is 93'l. breathing oxygen, 2 Llmin by nasal (B) Methotrexate cannula. Scattered expiratory wheezing is heard. Cardiac (C) Prednisone examination is normal. (D) Observation Spirometry shor.r.s postbronchodilator reduced FEVr/ FVC ratio and an FEV, of 45'X, of predicted. In{luenza, COVID-19, and pneumococcal pneumonia Item 17 vaccinations are brought up to date. The patient is enrolled A 40-year old man is evaluated 10 days after an emer in a pulmonary rehabilitation program. a,,-Antitrypsin gency department visit for a cough, chest tightness, level is normal. wheezing, and shortness of breath. He was treated with nebulized albuterol and sent home with a S-day course Which of the following additional long-term treatments is of prednisone and an albuterol metered-dose inhaler. most appropriate? Since completing the prednisone, he has felt well, with (A) cr, Antitrypsin augmentation therapy no further symptoms and no need to use the albuterol. He (B) Azithromycin reports a similar episode requiring an emergency depart- (C) Metoprolol ment visit l year ago. On physical examination, vital signs are normal. Oxy- (D) Oral N acetylcysteine gen saturation is 97% with the patient breathing ambient air. Cardiopulmonary examination is normal. Spirometry is normal.

gt Ut tr c0Nl was her third hospitalization for a COPD exacerbation in the past 6 months. She no longer smokes cigarettes. Medications are fluticasone-umeclidinium-vilanterol and Chest radiograph reveals bilateral symmetric hilar prominence with clear lung flelds. Interferon-yrelease assay is normal. o UI la albuterol inhalers. She has been adherent with her med- ication, has excellent inhaler technique. and continues to Which of the following is the most appropriate .D use home oxygen. Between exacerbations she has a cough management? productive o{' thin, colorless sputum. .D On physical examination. vital signs are normal. Oxy- (A) Bronchoscopicbiopsy UI gen saturation is 93'l. breathing oxygen, 2 Llmin by nasal (B) Methotrexate cannula. Scattered expiratory wheezing is heard. Cardiac (C) Prednisone examination is normal. (D) Observation Spirometry shor.r.s postbronchodilator reduced FEVr/ FVC ratio and an FEV, of 45'X, of predicted. In{luenza, COVID-19, and pneumococcal pneumonia Item 17 vaccinations are brought up to date. The patient is enrolled A 40-year old man is evaluated 10 days after an emer in a pulmonary rehabilitation program. a,,-Antitrypsin gency department visit for a cough, chest tightness, level is normal. wheezing, and shortness of breath. He was treated with nebulized albuterol and sent home with a S-day course Which of the following additional long-term treatments is of prednisone and an albuterol metered-dose inhaler. most appropriate? Since completing the prednisone, he has felt well, with (A) cr, Antitrypsin augmentation therapy no further symptoms and no need to use the albuterol. He (B) Azithromycin reports a similar episode requiring an emergency depart- (C) Metoprolol ment visit l year ago. On physical examination, vital signs are normal. Oxy- (D) Oral N acetylcysteine gen saturation is 97% with the patient breathing ambient air. Cardiopulmonary examination is normal. Spirometry is normal. tr Item 15 A 63 year old man is evaluated for dyspnea. The patient Which of the following is the most appropriate has newly diagnosed stage IV lung adenocarcinoma with a management? right malignant pleural effusion. A thoracentesis removed (A) Budesonide salmeterol 1200 mL of bloody fluid 5 days ago with relief of dysp- nea. Follow up chest radiograph documented incomplete (B) Fluticasone expansion of the right lung, with air replacing the removed (C) Measurement of exhaled nitric oxide pleural fluid. He has returned to the emergency depart- (D) Methacholinechallengetesting ment today with increasing dyspnea. On physical examination, vital signs are normal. Res piration rate is l8/min. Oxygen saturation is 93% with the patient breathing ambient air. Lung examination is consistent with a large right pleural effusion. Item 18 A 59 year-old woman is evaluated 5 days after her admis- tr sion to the hospital for septic shock r.t ith no obvious source Repeat chest radiograph shows a large right sided of infection. She is neutropenic. She has large B-cell lym- pleural effusion with loculations. phoma and received her last course of chemotherapy (rituximab, cyclophosphamide, doxorubicin, vincristine, Which of the following is the most appropriate and prednisone) 5 days before admission. Piperacillin management? tazobactam, gentamicin, and vancomycin were initiated. (A) Chemicalpleurodesis Gentamicin and vancomycin were discontinued 2 days ago (B) lndwelling pleural catheter fbllowing conlirmation of negative blood cultures. She is clinically improved and has been afebrile for 24 hours. (C) Repeatthoracentesis On physical examination, temperature is 36.9 'C (D) Surgical decortication (98.4 'F); the remainder of the vital signs and physical examination findings are normal. Laboratory studies show a leukocyte count of Item 16 1500/pL (1.5 x 10e/1.); absolute neutrophil count is 100/pL (0.1 x to'q/L). A 31-year-old man is evaluated following an abnormal flnding on a chest radiograph obtained as a part of pre employment screening. He is a lifelong nonsmoker with no Which of the following is the most appropriate treatment? history of dust exposure. His medical history is unremark- (A) Change to imipenem cilastatin able, and he has no known respiratory or constitutional symptoms. (B) Discontinuepiperacillin tazobactam The vital signs and physical examination are normal. (C) No change in treatment Spirometry is normal. (D) Startvoriconazole

tr Item 15 A 63 year old man is evaluated for dyspnea. The patient Which of the following is the most appropriate has newly diagnosed stage IV lung adenocarcinoma with a management? right malignant pleural effusion. A thoracentesis removed (A) Budesonide salmeterol 1200 mL of bloody fluid 5 days ago with relief of dysp- nea. Follow up chest radiograph documented incomplete (B) Fluticasone expansion of the right lung, with air replacing the removed (C) Measurement of exhaled nitric oxide pleural fluid. He has returned to the emergency depart- (D) Methacholinechallengetesting ment today with increasing dyspnea. On physical examination, vital signs are normal. Res piration rate is l8/min. Oxygen saturation is 93% with the patient breathing ambient air. Lung examination is consistent with a large right pleural effusion. Item 18 A 59 year-old woman is evaluated 5 days after her admis- tr sion to the hospital for septic shock r.t ith no obvious source Repeat chest radiograph shows a large right sided of infection. She is neutropenic. She has large B-cell lym- pleural effusion with loculations. phoma and received her last course of chemotherapy (rituximab, cyclophosphamide, doxorubicin, vincristine, Which of the following is the most appropriate and prednisone) 5 days before admission. Piperacillin management? tazobactam, gentamicin, and vancomycin were initiated. (A) Chemicalpleurodesis Gentamicin and vancomycin were discontinued 2 days ago (B) lndwelling pleural catheter fbllowing conlirmation of negative blood cultures. She is clinically improved and has been afebrile for 24 hours. (C) Repeatthoracentesis On physical examination, temperature is 36.9 'C (D) Surgical decortication (98.4 'F); the remainder of the vital signs and physical examination findings are normal. Laboratory studies show a leukocyte count of Item 16 1500/pL (1.5 x 10e/1.); absolute neutrophil count is 100/pL (0.1 x to'q/L). A 31-year-old man is evaluated following an abnormal flnding on a chest radiograph obtained as a part of pre employment screening. He is a lifelong nonsmoker with no Which of the following is the most appropriate treatment? history of dust exposure. His medical history is unremark- (A) Change to imipenem cilastatin able, and he has no known respiratory or constitutional symptoms. (B) Discontinuepiperacillin tazobactam The vital signs and physical examination are normal. (C) No change in treatment Spirometry is normal. (D) Startvoriconazole 98

Self-Assessment Test UI o, tr Item 19 A 49-year-old man is transferred liom a psychiatric hos her chest. Estimated central venous pressure is normal Other than tachycardia, cardiac examination is normal There are diffuse lung crackles. q, pital to the emergency department because of a change E in vital signs and encephalopathy. He has schizophrenia ta Arterial blood gas studies: U! and depression. He was hospitalized 3 days ago for acute pll 7.3 o ut ra psychosis and attempted suicide. In the psychiatric hos- P{to, 50 mm Hg (6.6 kPa) pital, he was treated with risperidone and fluoxetine. He Po, 66 mm Hg (B.B kPa) (u subsequently developed nausea and vomiting and was r/t Chest radiograph is shown. prescribed promethazine. On physical examination, temperature is 39.5 'C (103.1 'F). blood pressure is 173/112 mm Hg, pulse rate is 132i min, respiration rate is 26lmilt, and oxygen saturation is 99'1, with the patient breathing ambient air. He is dia- phoretic and tachypneic, with clear lungs. He has tachy cardia without murmur, gallops, or rubs. Muscles are rigid. Deep tendon reflexes are normal. Promethazine is discontinued.

UI o, tr Item 19 A 49-year-old man is transferred liom a psychiatric hos her chest. Estimated central venous pressure is normal Other than tachycardia, cardiac examination is normal There are diffuse lung crackles. q, pital to the emergency department because of a change E in vital signs and encephalopathy. He has schizophrenia ta Arterial blood gas studies: U! and depression. He was hospitalized 3 days ago for acute pll 7.3 o ut ra psychosis and attempted suicide. In the psychiatric hos- P{to, 50 mm Hg (6.6 kPa) pital, he was treated with risperidone and fluoxetine. He Po, 66 mm Hg (B.B kPa) (u subsequently developed nausea and vomiting and was r/t Chest radiograph is shown. prescribed promethazine. On physical examination, temperature is 39.5 'C (103.1 'F). blood pressure is 173/112 mm Hg, pulse rate is 132i min, respiration rate is 26lmilt, and oxygen saturation is 99'1, with the patient breathing ambient air. He is dia- phoretic and tachypneic, with clear lungs. He has tachy cardia without murmur, gallops, or rubs. Muscles are rigid. Deep tendon reflexes are normal. Promethazine is discontinued. Which of the following is the most appropriate initial treatment? (A) Discontinuefluoxetine (B) Discontinuerisperidone (C) Startcyproheptadine (D) Start dantrolene

UI o, tr Item 19 A 49-year-old man is transferred liom a psychiatric hos her chest. Estimated central venous pressure is normal Other than tachycardia, cardiac examination is normal There are diffuse lung crackles. q, pital to the emergency department because of a change E in vital signs and encephalopathy. He has schizophrenia ta Arterial blood gas studies: U! and depression. He was hospitalized 3 days ago for acute pll 7.3 o ut ra psychosis and attempted suicide. In the psychiatric hos- P{to, 50 mm Hg (6.6 kPa) pital, he was treated with risperidone and fluoxetine. He Po, 66 mm Hg (B.B kPa) (u subsequently developed nausea and vomiting and was r/t Chest radiograph is shown. prescribed promethazine. On physical examination, temperature is 39.5 'C (103.1 'F). blood pressure is 173/112 mm Hg, pulse rate is 132i min, respiration rate is 26lmilt, and oxygen saturation is 99'1, with the patient breathing ambient air. He is dia- phoretic and tachypneic, with clear lungs. He has tachy cardia without murmur, gallops, or rubs. Muscles are rigid. Deep tendon reflexes are normal. Promethazine is discontinued. Which of the following is the most appropriate initial treatment? (A) Discontinuefluoxetine (B) Discontinuerisperidone (C) Startcyproheptadine (D) Start dantrolene Item 20 A 38 year old man is evaluated for shortness ofbreath and a dry cough for the past 3 months. He has a 20-pack-year smoking history and continues to smoke. On physical examination, vital signs are normal. Oxy gen saturation is 92% with the patient breathing ambient air. Auscultation ofthe Iungs reveals coarse bibasilar inspi- ratory crackles. The cardiac examination and remainder of the physical examination are normal. Chest radiograph demonstrates bilateral reticular inflltrates. High-resolution chest CT demonstrates patchy ground-glass inflltrates with lower lobe predominance. Ilemoglobin has remained stable. Echocardiogram Pulmonary function testing shows an FVC of 65% of pre- reveals a normal ejection fiaction and valvular function. dicted, an FEV,/FVC ratio of 0.81, and a DLCo of 56% of FICG shows only sinus tachycardia. predicted. Which of the following is the most likely diagnosis? Which of the following is the most appropriate treatment? (A) Acute respiratory distress syndrome (B) Diftuse alveolar hemorrhage (A) Glucocorticoids (C) Pulmonary edema (B) Methotrexate (D) Pulmonary embolism (C) Pirfenidone (D) Smoking cessation Item 22 A 28 year-old woman is evaluated for sleepiness and dif-

Item 20 A 38 year old man is evaluated for shortness ofbreath and a dry cough for the past 3 months. He has a 20-pack-year smoking history and continues to smoke. On physical examination, vital signs are normal. Oxy gen saturation is 92% with the patient breathing ambient air. Auscultation ofthe Iungs reveals coarse bibasilar inspi- ratory crackles. The cardiac examination and remainder of the physical examination are normal. Chest radiograph demonstrates bilateral reticular inflltrates. High-resolution chest CT demonstrates patchy ground-glass inflltrates with lower lobe predominance. Ilemoglobin has remained stable. Echocardiogram Pulmonary function testing shows an FVC of 65% of pre- reveals a normal ejection fiaction and valvular function. dicted, an FEV,/FVC ratio of 0.81, and a DLCo of 56% of FICG shows only sinus tachycardia. predicted. Which of the following is the most likely diagnosis? Which of the following is the most appropriate treatment? (A) Acute respiratory distress syndrome (B) Diftuse alveolar hemorrhage (A) Glucocorticoids (C) Pulmonary edema (B) Methotrexate (D) Pulmonary embolism (C) Pirfenidone (D) Smoking cessation Item 22 A 28 year-old woman is evaluated for sleepiness and dif- tr Item 21 A l)6 year old woman is evaluated fbr respiratory fail flculty staying awake over the past 6 months. She works as a hospital respiratory therapist. Half of her shifts are ure requiring invasive mechanical ventilation following a from 7:00 pu to 7:00 eu. The sleepiness subsides by the motor vehicle accident. time she drives home, and she then has difficulty falling On physical examination, temperature is 38.0 'C asleep during the day. Her sleepiness has slowed her cog- (100.4 "F), biood pressure is 100/65 mm Hg, pulse rate is nitive processing during working hours and has resulted 100/min, and respiration rate is 26lmin. Oxygen saturation in depressed mood. is 90'1, with an Fro, of 0.50 and positive end-expiratory On physical examination, blood pressure is 118/68 mm pressure of 12 cm HrO. There are multiple contusions on Hg and pulse rate is 76lmin. BMI is 24.

tr Item 21 A l)6 year old woman is evaluated fbr respiratory fail flculty staying awake over the past 6 months. She works as a hospital respiratory therapist. Half of her shifts are ure requiring invasive mechanical ventilation following a from 7:00 pu to 7:00 eu. The sleepiness subsides by the motor vehicle accident. time she drives home, and she then has difficulty falling On physical examination, temperature is 38.0 'C asleep during the day. Her sleepiness has slowed her cog- (100.4 "F), biood pressure is 100/65 mm Hg, pulse rate is nitive processing during working hours and has resulted 100/min, and respiration rate is 26lmin. Oxygen saturation in depressed mood. is 90'1, with an Fro, of 0.50 and positive end-expiratory On physical examination, blood pressure is 118/68 mm pressure of 12 cm HrO. There are multiple contusions on Hg and pulse rate is 76lmin. BMI is 24. 99

Self-Assessment Test t/t .D Which of the following is the most appropriate symptoms started after she mopped up a spill in the D la management? cleaning supplies cabinet. Medical history is otheru'ise Ut (D unremarkable. (a (A) Education and counseling Ut On physical examination, respiration rate is 20:min. (B) Home sleep apnea testing Oxygen saturation is 98'1, with the patient breathing ambi- .D (C) Modaflnil ent air. There is diffuse expiratory wheezing over both lung (D) Zolpidem lields. .D Spirometry reveals an FVC of 88'1, of predicted. an Ut FEV, of 55'7, of predicted, and an p51t,,FVC ratio ol 0.6.

t/t .D Which of the following is the most appropriate symptoms started after she mopped up a spill in the D la management? cleaning supplies cabinet. Medical history is otheru'ise Ut (D unremarkable. (a (A) Education and counseling Ut On physical examination, respiration rate is 20:min. (B) Home sleep apnea testing Oxygen saturation is 98'1, with the patient breathing ambi- .D (C) Modaflnil ent air. There is diffuse expiratory wheezing over both lung (D) Zolpidem lields. .D Spirometry reveals an FVC of 88'1, of predicted. an Ut FEV, of 55'7, of predicted, and an p51t,,FVC ratio ol 0.6. tr Item 23 A 77-year-old man is evaluated in the hospital for shortness Postbronchodilator testing reveals signiflcant bronchodi- lator responsiveness. Chest radiograph is normal. of breath, dry cough. pleuritic chest pain, and uninten tional 9-kg (20 lb) weight loss over the past 6 months. On physical examination, the patient appears chron- Which of the following is the most appropriate next ically ill. Vital signs are normal. BMI is 19. There are diagnostic step? decreased breath sounds at the right base. (A) Allergy testing Chest radiograph demonstrates an apparent pleural (B) Bronchoscopy effusion on the right side, but CT scan reveals a nodular pleura-based mass on the right side. (C) Methacholine challenge test (D) Review Safety Data Sheet Which of the following is the most likely occupational exposure? Item 26 (A) Asbestos A 66 year-old man is evaluated for a 7 month history of (B) Coal gradually progressive shortness of breath and dry cough. (C) Cobalt Medical history is otherwise unremarkable, and he takes (D) silica no medications. On physical examination, vital signs are normal. Oxy- gen saturation is 93% with the patient breathing ambi- Item 24 ent air. Auscultation reveals flne end-inspiratory bibasilar A SO-year-old man is referred for poorly controlled crackles. Clubbing is present. There are no rashes or edema. asthma. Triggers include exercise and exposure to dust, Cardiac examination is unremarkable. pollen, and fumes. He has allergic rhinitis. He has been Chest radiograph reveals small lung volumes and treated with several courses of glucocorticoids, but symp- bibasilar reticular inflltrates without lymphadenopathy. toms recurred after he stopped treatment despite regular Spirometry reveals an FEV,/FVC ratio of 0.87, an FVC of use of his fluticasone salmeterol and tiotropium inhal- 62'X, ofpredicted, and a DLCo of48% ofpredicted. ers. His only other medication is albuterol. He has good inhaler technique. Which of the following is the most appropriate diagnostic On physical examination, vital signs are normal. test to perform next? BMI is 23. Pulmonary examination reveals few expiratory (A) Bronchoscopic lung biopsy wheezes. The remainder of the examination is unremark- (B) Cardiopulmonary exercise test able. Laboratory studies reveal a normal total IgE level and (C) Chest CT angiography complete blood count. (D) High-resolution chest CT Chest radiograph is normal. Spirometry demonstrates (E) Transthoracicechocardiography moderate airflow obstruction that improves with bron- chodilators.

tr Item 23 A 77-year-old man is evaluated in the hospital for shortness Postbronchodilator testing reveals signiflcant bronchodi- lator responsiveness. Chest radiograph is normal. of breath, dry cough. pleuritic chest pain, and uninten tional 9-kg (20 lb) weight loss over the past 6 months. On physical examination, the patient appears chron- Which of the following is the most appropriate next ically ill. Vital signs are normal. BMI is 19. There are diagnostic step? decreased breath sounds at the right base. (A) Allergy testing Chest radiograph demonstrates an apparent pleural (B) Bronchoscopy effusion on the right side, but CT scan reveals a nodular pleura-based mass on the right side. (C) Methacholine challenge test (D) Review Safety Data Sheet Which of the following is the most likely occupational exposure? Item 26 (A) Asbestos A 66 year-old man is evaluated for a 7 month history of (B) Coal gradually progressive shortness of breath and dry cough. (C) Cobalt Medical history is otherwise unremarkable, and he takes (D) silica no medications. On physical examination, vital signs are normal. Oxy- gen saturation is 93% with the patient breathing ambi- Item 24 ent air. Auscultation reveals flne end-inspiratory bibasilar A SO-year-old man is referred for poorly controlled crackles. Clubbing is present. There are no rashes or edema. asthma. Triggers include exercise and exposure to dust, Cardiac examination is unremarkable. pollen, and fumes. He has allergic rhinitis. He has been Chest radiograph reveals small lung volumes and treated with several courses of glucocorticoids, but symp- bibasilar reticular inflltrates without lymphadenopathy. toms recurred after he stopped treatment despite regular Spirometry reveals an FEV,/FVC ratio of 0.87, an FVC of use of his fluticasone salmeterol and tiotropium inhal- 62'X, ofpredicted, and a DLCo of48% ofpredicted. ers. His only other medication is albuterol. He has good inhaler technique. Which of the following is the most appropriate diagnostic On physical examination, vital signs are normal. test to perform next? BMI is 23. Pulmonary examination reveals few expiratory (A) Bronchoscopic lung biopsy wheezes. The remainder of the examination is unremark- (B) Cardiopulmonary exercise test able. Laboratory studies reveal a normal total IgE level and (C) Chest CT angiography complete blood count. (D) High-resolution chest CT Chest radiograph is normal. Spirometry demonstrates (E) Transthoracicechocardiography moderate airflow obstruction that improves with bron- chodilators. Which of the following is the most appropriate diagnostic test to perform next? Item 27 A 24 year old woman is evaluated in the emergency tr department for acute onset ofdyspnea and pleuritic chest (A) Absolute blood eosinophil count pain. She is 10 weeks pregnant. She is otherwise well. and (B) cr,-Antitrypsin level her only medication is folic acid. (C) Aspergillus-specific IgE level On physical examination. temperature is 37.7 "C (99.9 'F). blood pressure is 140,'78 mm Hg, pulse rate is (D) Measurement of common allergen-speciflc IgE levels 90/min, respiration rate is 24rmin, and oxygen saturation is 95'){, with the patient breathing ambient air. Cardiopul monary examination is normal. There is no evidence of tr Item 25 A 46 year old woman is evaluated for cough, shortness deep venous thrombosis. A chest radiograph is normal. A ventilationrperfusion of breath, wheezing, and chest tightness of 3 weeks' lung scan is interpreted as high probability for pulmo duration. The patient is a janitor in a hospital, and her nary embolism.

Which of the following is the most appropriate diagnostic test to perform next? Item 27 A 24 year old woman is evaluated in the emergency tr department for acute onset ofdyspnea and pleuritic chest (A) Absolute blood eosinophil count pain. She is 10 weeks pregnant. She is otherwise well. and (B) cr,-Antitrypsin level her only medication is folic acid. (C) Aspergillus-specific IgE level On physical examination. temperature is 37.7 "C (99.9 'F). blood pressure is 140,'78 mm Hg, pulse rate is (D) Measurement of common allergen-speciflc IgE levels 90/min, respiration rate is 24rmin, and oxygen saturation is 95'){, with the patient breathing ambient air. Cardiopul monary examination is normal. There is no evidence of tr Item 25 A 46 year old woman is evaluated for cough, shortness deep venous thrombosis. A chest radiograph is normal. A ventilationrperfusion of breath, wheezing, and chest tightness of 3 weeks' lung scan is interpreted as high probability for pulmo duration. The patient is a janitor in a hospital, and her nary embolism. 100 t

Self-Assessment Test UI €, B CONI Which of the following is the most appropriate treatment? Item 30 A 69-year-old man is evaluated for shortness of breath (u (A) Dabigatran and a dry cough progressing over the past 7 months. His tl (B) Fondaparinux medical history is otherwise unremarkable, and he does vt (l, (C) Low-molecular-weight heparin not take any medications. t! t On physical examination, respiration rate is 25/min. (D) Rivaroxaban Oxygen saturation is 94'k with the patient breathing (Fl) Unfractionated heparin followed by warfarin ambient air. Auscultation of the lungs reveals Velcro-like o vt crackles at both Iung bases. Cardiac examination is normal. Laboratory test results, including serologic tests for

UI €, B CONI Which of the following is the most appropriate treatment? Item 30 A 69-year-old man is evaluated for shortness of breath (u (A) Dabigatran and a dry cough progressing over the past 7 months. His tl (B) Fondaparinux medical history is otherwise unremarkable, and he does vt (l, (C) Low-molecular-weight heparin not take any medications. t! t On physical examination, respiration rate is 25/min. (D) Rivaroxaban Oxygen saturation is 94'k with the patient breathing (Fl) Unfractionated heparin followed by warfarin ambient air. Auscultation of the lungs reveals Velcro-like o vt crackles at both Iung bases. Cardiac examination is normal. Laboratory test results, including serologic tests for tr Item 28 A 77-year-c:ld man is evaluated fbr acute agitation with connective tissue disease, are negative. Pulmonary function testing reveals a restrictive pat tern and aDrco of 42% of predicted. worsening of oxygenation, hypotension. and tachycar dia over the last 30 minutes. FIe was hospitalized 2 days Chest radiograph reveals reticular inflltrates in the ago with pneumonia and hypoxemic respiratory failure lower lung zones. High-resolution chest CT scan flndings requiring mechanical ventilation. Medical history is also are consistent with a usual interstitial pneumonia pattern. significant for COPD and heart failure. N4edications are cefotaxime, levofloxacin, propofbl, furosemide, albuterol, Which of the following is the most appropriate treatment? and low-molecular-r,veight heparin. (A) N-acetylcysteine On physical examination. temperature is 37.8 'C (B) Pirfenidone (100.0 "F), biood pressure is 102155 mm Hg, pulse rate is 122lmin, and respiration rate is 30/min. Oxygen sat- (C) Prednisone, N-acetylcysteine, and azathioprine uration is B7'1, with a tidal volume of 42O mL, a posi (D) Warfarin tive end-expiratory pressure of B cm HrO, and Fto, of 0.50. Trachea is midline. Pulmonary examination reveals decreased breath sounds bilaterally. Ihe jugular vein is diflicult to visualize; an S., is present. Item 31 A 50 year-old woman was admitted to the ICU 24 hours tr ago for management of acute respiratory distress syn- Which of the following is the most appropriate drome due to pneumonia. She is on a mechanical ven- management? tilator. She is receiving vasopressors for hypotension. (A) Bedside thoracicultrasonography Medications are norepinephrine, fentanyl drip, and propofbl drip. (Il) CT of the chest On physical examination, vital signs are stable. Oxy- (C) Inlusion of cisatracurium gen saturation is 90%, with an Fto, of 0.60, and positive (D) Needlethoracostomy end-expiratory pressure is 12 cm HrO. the patient is deeply sedated and unresponsive to physical stimulation.

tr Item 28 A 77-year-c:ld man is evaluated fbr acute agitation with connective tissue disease, are negative. Pulmonary function testing reveals a restrictive pat tern and aDrco of 42% of predicted. worsening of oxygenation, hypotension. and tachycar dia over the last 30 minutes. FIe was hospitalized 2 days Chest radiograph reveals reticular inflltrates in the ago with pneumonia and hypoxemic respiratory failure lower lung zones. High-resolution chest CT scan flndings requiring mechanical ventilation. Medical history is also are consistent with a usual interstitial pneumonia pattern. significant for COPD and heart failure. N4edications are cefotaxime, levofloxacin, propofbl, furosemide, albuterol, Which of the following is the most appropriate treatment? and low-molecular-r,veight heparin. (A) N-acetylcysteine On physical examination. temperature is 37.8 'C (B) Pirfenidone (100.0 "F), biood pressure is 102155 mm Hg, pulse rate is 122lmin, and respiration rate is 30/min. Oxygen sat- (C) Prednisone, N-acetylcysteine, and azathioprine uration is B7'1, with a tidal volume of 42O mL, a posi (D) Warfarin tive end-expiratory pressure of B cm HrO, and Fto, of 0.50. Trachea is midline. Pulmonary examination reveals decreased breath sounds bilaterally. Ihe jugular vein is diflicult to visualize; an S., is present. Item 31 A 50 year-old woman was admitted to the ICU 24 hours tr ago for management of acute respiratory distress syn- Which of the following is the most appropriate drome due to pneumonia. She is on a mechanical ven- management? tilator. She is receiving vasopressors for hypotension. (A) Bedside thoracicultrasonography Medications are norepinephrine, fentanyl drip, and propofbl drip. (Il) CT of the chest On physical examination, vital signs are stable. Oxy- (C) Inlusion of cisatracurium gen saturation is 90%, with an Fto, of 0.60, and positive (D) Needlethoracostomy end-expiratory pressure is 12 cm HrO. the patient is deeply sedated and unresponsive to physical stimulation. tr Item 29 A 62-year-old woman is evalualed in the emergency Which of the following is the most appropriate management? department for fatigue, headaches, confusion, and weak- (A) Downward titration of sedation medication ness that have progressed over the past 6 weeks. She has (B) Electroencephalography an 11.3 kg (25 lb) unintentional weight loss over the past month. She has an B5-pack-year history of smoking and (C) Head CT quit smoking 3 months ago. (D) Hold sedation and analgesia On physical examination, blood pressure is 125/75 mm I-lg, pulse rate is 92lmin, respiration rate is 21lmin, and oxygen saturation is B9'/n with the patient breathing ambi- ent air. BMI is 17. An expiratory wheeze is noted on the left Item 32 A 45-year-old woman is evaluated for increasing short- tr side. The remainder of the examination is normal. ness of breath and fatigue for the past 6 weeks and Laboratory er.aluation reveals a serum sodium level of weight loss of 4.5 kg (to tU) over the past 2 months. She 123 mEq/L (123 mmol'L). has no other symptoms. She has a history of rheumatoid CT scan of the chest shows a 4-cm mediastinal mass arthritis. Her only medications are methotrexate and compressing the left upper iobe bronchus with associated fblic acid. bulky mediastinal lymphadenopathy. On physical examination, vital signs are normal. Typ- ical chronic changes of rheumatoid arthritis are present in Which of the following is the most likely diagnosis? her hands, wrists, and feet in the absence of active syno- (A) Adenocarcinoma of lung vitis. Chest findings are consistent with bilateral pleural eflusions. (B) Fibrosingmediastinitis Complete blood count is normal. Serum lactate dehy- (C) Large cell lung cancer drogenase level is 200 UlL, and total serum protein level is (D) Small cell lung cancer 6 s/dl (60 s/L).

tr Item 29 A 62-year-old woman is evalualed in the emergency Which of the following is the most appropriate management? department for fatigue, headaches, confusion, and weak- (A) Downward titration of sedation medication ness that have progressed over the past 6 weeks. She has (B) Electroencephalography an 11.3 kg (25 lb) unintentional weight loss over the past month. She has an B5-pack-year history of smoking and (C) Head CT quit smoking 3 months ago. (D) Hold sedation and analgesia On physical examination, blood pressure is 125/75 mm I-lg, pulse rate is 92lmin, respiration rate is 21lmin, and oxygen saturation is B9'/n with the patient breathing ambi- ent air. BMI is 17. An expiratory wheeze is noted on the left Item 32 A 45-year-old woman is evaluated for increasing short- tr side. The remainder of the examination is normal. ness of breath and fatigue for the past 6 weeks and Laboratory er.aluation reveals a serum sodium level of weight loss of 4.5 kg (to tU) over the past 2 months. She 123 mEq/L (123 mmol'L). has no other symptoms. She has a history of rheumatoid CT scan of the chest shows a 4-cm mediastinal mass arthritis. Her only medications are methotrexate and compressing the left upper iobe bronchus with associated fblic acid. bulky mediastinal lymphadenopathy. On physical examination, vital signs are normal. Typ- ical chronic changes of rheumatoid arthritis are present in Which of the following is the most likely diagnosis? her hands, wrists, and feet in the absence of active syno- (A) Adenocarcinoma of lung vitis. Chest findings are consistent with bilateral pleural eflusions. (B) Fibrosingmediastinitis Complete blood count is normal. Serum lactate dehy- (C) Large cell lung cancer drogenase level is 200 UlL, and total serum protein level is (D) Small cell lung cancer 6 s/dl (60 s/L). 101

Self-Assessment Test v! .D UI vt (D tr Leukocytes I CONT, Pleural fluid studies: pl 600 pl- (0.6 x 10" l-) (70 ll.rnphocl tcs) 7.1 Item 34 A iJ7 \'car old u'oman is cvaluittccl itt the entergencl' tr dcplrtnrent for headache. clyspneir. ancl cougl-t. Tn'o davs tt UI (llucose 100 rng, cll (5.5 mnrol l-) lgo shc traveled frotrr her honre irt :100 meters (98-l feet) L.actate 85 U,'1. abovc serr level to a mountair-r ski resort u'here the slopes .D clcl.rydrogenase rrre as high as 391.4 nletcrs (t2.811 feet). She developecl { Total protein 4.1 grn dt- (11 g l.) the heaclache 1'esterdal'. and todirl it is \\.orse and she has .D Totalcholesterol 120 mg dL (:1.1 nrmol I-) gr shortness ot breath ancl a cougl.r. Trigllrcerides 1.10 nrg dL (1.58 rnrnol l-) On ph1'sical examinrrtiolr. temperatllre is 38.0 -C Chest radiograph demonstrutcs bilaterill pleural ellir (10o. I 'F). blood pressurc is l2l 72 lnm Hg. pulse rate is sions and bulkl' mediastinal 11'n.rphldenopathr..'[horacen I l5 nrin. and respiratir)n ratc is 2B r.nin. Or1'gen saturation tcsis is perfbrmed. ancl 1100 ml. ot milkl'ftuid is drainecl. is 8l ' rr ith the patient bre:ithing ambient irir. Inspiratorl' crircklcs are present bilatcralll . Which of the following is the most likely diagnosis? (.hest radiograph dcmonstr-atcs pntcl.tl alveolar infil I r-:) I ('s- (A) Cholesterol efiusion Iligh flow supplerne ntrl o\\l1clr b1' nasal cannultt is (i3) Chylothorax init iiited. (C) t.lmpyema ([)) Rheumatoid effusion Which of the following is the most appropriate additional treatment? (.\),\cctazol:rmide. oralll Item 33 (B) (.cliriarone. intravcnouslv A 66 year old man is evaluated for gradually progressive dyspnea and dry cough over the past 6 months. He has a ((.) I)escent to a lo.,r'er altitude 30 pack year history of smoking; he stopped 10 years ago. (l)) I)eramethasone. orallr' Medical history is otherwise unremarkable. (E) [rurosemide. intravcnouslv On physical examination, respiration rate is 22lmin. Oxygen saturation is 93'7, with the patient breathing ambient air. Auscultation of the lungs reveals flne end- inspiratory Velcro like crackles at both lung bases. Club- bing is present. Item 35 .-\n ti I 1'ear old mirn liring in ir nursing home is evaluated tr in the enrergencl clcpartnrcnt for receut onset of unre Spirometry shows an FVC of 55'7, of predicted. an slronsile ness and fever. IIe hirs .\lzhcinrer dementi:r. FEVr/FVC ratio of 0.91, and a Dt.rrr of 42'l, of predicted. On pl'r1'sical eraminiilior.r. tenrperature is il9.;l '(- A high-resolution CT scan of the chest is shown. (102.7'F). blood pressurc is il|.50 rnm Hg. pr.rlse rate is 106 nrin. and respiration rate is lB n1in. Or1'gen saturation is 95", u ith the patient breathing anrbient irir. The pxticnt is responsive onll to ph1 sicril stinruli. Cirrdiopulrno nilrv c\:lmination reveals normll heart :rnd lung souncls. Abdomir-ral examination is norrn:rl. A 6 x 6 cm necrotic sacrll decnbitus r'r'our-rd is present. Lirboratorl' data are pending. Bloocl cultures are ol)triued.

pl 600 pl- (0.6 x 10" l-) (70 ll.rnphocl tcs) 7.1 Item 34 A iJ7 \'car old u'oman is cvaluittccl itt the entergencl' tr dcplrtnrent for headache. clyspneir. ancl cougl-t. Tn'o davs tt UI (llucose 100 rng, cll (5.5 mnrol l-) lgo shc traveled frotrr her honre irt :100 meters (98-l feet) L.actate 85 U,'1. abovc serr level to a mountair-r ski resort u'here the slopes .D clcl.rydrogenase rrre as high as 391.4 nletcrs (t2.811 feet). She developecl { Total protein 4.1 grn dt- (11 g l.) the heaclache 1'esterdal'. and todirl it is \\.orse and she has .D Totalcholesterol 120 mg dL (:1.1 nrmol I-) gr shortness ot breath ancl a cougl.r. Trigllrcerides 1.10 nrg dL (1.58 rnrnol l-) On ph1'sical examinrrtiolr. temperatllre is 38.0 -C Chest radiograph demonstrutcs bilaterill pleural ellir (10o. I 'F). blood pressurc is l2l 72 lnm Hg. pulse rate is sions and bulkl' mediastinal 11'n.rphldenopathr..'[horacen I l5 nrin. and respiratir)n ratc is 2B r.nin. Or1'gen saturation tcsis is perfbrmed. ancl 1100 ml. ot milkl'ftuid is drainecl. is 8l ' rr ith the patient bre:ithing ambient irir. Inspiratorl' crircklcs are present bilatcralll . Which of the following is the most likely diagnosis? (.hest radiograph dcmonstr-atcs pntcl.tl alveolar infil I r-:) I ('s- (A) Cholesterol efiusion Iligh flow supplerne ntrl o\\l1clr b1' nasal cannultt is (i3) Chylothorax init iiited. (C) t.lmpyema ([)) Rheumatoid effusion Which of the following is the most appropriate additional treatment? (.\),\cctazol:rmide. oralll Item 33 (B) (.cliriarone. intravcnouslv A 66 year old man is evaluated for gradually progressive dyspnea and dry cough over the past 6 months. He has a ((.) I)escent to a lo.,r'er altitude 30 pack year history of smoking; he stopped 10 years ago. (l)) I)eramethasone. orallr' Medical history is otherwise unremarkable. (E) [rurosemide. intravcnouslv On physical examination, respiration rate is 22lmin. Oxygen saturation is 93'7, with the patient breathing ambient air. Auscultation of the lungs reveals flne end- inspiratory Velcro like crackles at both lung bases. Club- bing is present. Item 35 .-\n ti I 1'ear old mirn liring in ir nursing home is evaluated tr in the enrergencl clcpartnrcnt for receut onset of unre Spirometry shows an FVC of 55'7, of predicted. an slronsile ness and fever. IIe hirs .\lzhcinrer dementi:r. FEVr/FVC ratio of 0.91, and a Dt.rrr of 42'l, of predicted. On pl'r1'sical eraminiilior.r. tenrperature is il9.;l '(- A high-resolution CT scan of the chest is shown. (102.7'F). blood pressurc is il|.50 rnm Hg. pr.rlse rate is 106 nrin. and respiration rate is lB n1in. Or1'gen saturation is 95", u ith the patient breathing anrbient irir. The pxticnt is responsive onll to ph1 sicril stinruli. Cirrdiopulrno nilrv c\:lmination reveals normll heart :rnd lung souncls. Abdomir-ral examination is norrn:rl. A 6 x 6 cm necrotic sacrll decnbitus r'r'our-rd is present. Lirboratorl' data are pending. Bloocl cultures are ol)triued. Which of the following is the most appropriate resuscitative treatment? (.\) 5 alburnin solution (B) l;r tnrEtl bic;rrbonrrtc in 5' drrlrosr ((-) I Ildroxl'eth1,l starch (l)) I.actated Ringer solutior.r

Which of the following is the most appropriate resuscitative treatment? (.\) 5 alburnin solution (B) l;r tnrEtl bic;rrbonrrtc in 5' drrlrosr ((-) I Ildroxl'eth1,l starch (l)) I.actated Ringer solutior.r Item 36 A 63 year-old woman is evaluated at a follor,r'-up visit for Which of the following is the most likely diagnosis? a solitary pulmonary nodule. Six months ago CT angio (A) Cryptogenicorganizing pneumonia graphy (CTA) was performed to evaluate a possible pulmo- (B) Idiopathic pulmonary flbrosis nary embolism. The CTA u,as negati\re but demonstrated an B mm ground-glass (subsolid) nodule in the left upper (C) Nonspeciflcinterstitial pneumonia lobe. The patient has a 21 pack year history of cigarette (D) Respiratorybronchiolitis associated interstitial lung smoking but stopped 6 months ago. Medical history is oth disease erwise unremarkable, and she takes no medications. 102

Self-Assessment Test UI On physical examination, vital signs and other exam- o, I l0i min. and respiration rate is 24lnrir.r. Oxygen saturation F ination findings are normal. is BB',1, lvith the patient breathing ambie'nt air. '[herc are A repeat chest CT scan 6 months after the initial scan q, coarse rhonchi and decreased breath sour.rds and dullness E shows no change in the size or characteristics of the nodule. to percussion over the left lower l.ralf ot tl.re chest. Ut CT scan of'the cl-rest shows lefi lower lobe consolida tt (l, vt Which of the following is the most appropriate tion and locul:rted left pleural eflusion. A thoracentesis is t management? peribrmed. (A) Chest CT every 2 years for 5 years o vt Which of the following pleural fluid tests is most (B) Chest CT in 12 months appropriate in directing therapy? (C) FluorodeoxyglucosePET (A) Lactatedehyclrogenase (D) Surgical resection (B) plt (C) Procalcitonin Item 37 (l)) '1'otal protcill A 57-year-old woman is evaluated for a 4-month history of progressive exertional dyspnea and occasional chest pain and palpitations. She has limited cutaneous systemic scle- Item 40 rosis with Raynaud phenomenon and gastroesophageal A 27 year-old woman is evaluated for a cough and chest reflux disease. Medications are omeprazole and diltiazem. tightness that occur during and after exercise. She has been On physical examination, blood pressure is lO7l74 mm training for her first marathon, but she has been unable to Hg and pulse rate is 90/min. Oxygen saturation is nor increase her training intensity because of these symptoms. mal at rest. Characteristic skin findings of limited cutane- She denies cough or chest tightness at any other time. She ous systemic sclerosis are present. New cardiac flndings reports no stridor, throat tightness, or noisy inspiration include jugular venous distention, persistent splitting of during the episodes. 1 Sr, and 2/6 systolic murmur at the left lower sternal border On physical examination, vital signs and pulmonary that increases with inspiration. Lungs are clear. examination are normal. ECG shows a heart rate of 95/min and is otherwise Baseline spirometry is normal. Exercise testing demon : normal. Chest radiograph is normal. Echocardiography strates a signiflcant decrease in FEV, from baseline. performed 12 months ago was normal. I Which of the following inhaled medications is the most Which of the following is the most appropriate diagnostic appropriate next step in treatment? test? (A) Salmeterol daily (A) CTangiographyofthechest (B) Budesonide twice daily t (B) Echocardiography (C) Budesonide-formoterolbefore exercise (C) Exercise stress test (D) Ipratropium belore exercise (D) Pulmonary function testing

UI On physical examination, vital signs and other exam- o, I l0i min. and respiration rate is 24lnrir.r. Oxygen saturation F ination findings are normal. is BB',1, lvith the patient breathing ambie'nt air. '[herc are A repeat chest CT scan 6 months after the initial scan q, coarse rhonchi and decreased breath sour.rds and dullness E shows no change in the size or characteristics of the nodule. to percussion over the left lower l.ralf ot tl.re chest. Ut CT scan of'the cl-rest shows lefi lower lobe consolida tt (l, vt Which of the following is the most appropriate tion and locul:rted left pleural eflusion. A thoracentesis is t management? peribrmed. (A) Chest CT every 2 years for 5 years o vt Which of the following pleural fluid tests is most (B) Chest CT in 12 months appropriate in directing therapy? (C) FluorodeoxyglucosePET (A) Lactatedehyclrogenase (D) Surgical resection (B) plt (C) Procalcitonin Item 37 (l)) '1'otal protcill A 57-year-old woman is evaluated for a 4-month history of progressive exertional dyspnea and occasional chest pain and palpitations. She has limited cutaneous systemic scle- Item 40 rosis with Raynaud phenomenon and gastroesophageal A 27 year-old woman is evaluated for a cough and chest reflux disease. Medications are omeprazole and diltiazem. tightness that occur during and after exercise. She has been On physical examination, blood pressure is lO7l74 mm training for her first marathon, but she has been unable to Hg and pulse rate is 90/min. Oxygen saturation is nor increase her training intensity because of these symptoms. mal at rest. Characteristic skin findings of limited cutane- She denies cough or chest tightness at any other time. She ous systemic sclerosis are present. New cardiac flndings reports no stridor, throat tightness, or noisy inspiration include jugular venous distention, persistent splitting of during the episodes. 1 Sr, and 2/6 systolic murmur at the left lower sternal border On physical examination, vital signs and pulmonary that increases with inspiration. Lungs are clear. examination are normal. ECG shows a heart rate of 95/min and is otherwise Baseline spirometry is normal. Exercise testing demon : normal. Chest radiograph is normal. Echocardiography strates a signiflcant decrease in FEV, from baseline. performed 12 months ago was normal. I Which of the following inhaled medications is the most Which of the following is the most appropriate diagnostic appropriate next step in treatment? test? (A) Salmeterol daily (A) CTangiographyofthechest (B) Budesonide twice daily t (B) Echocardiography (C) Budesonide-formoterolbefore exercise (C) Exercise stress test (D) Ipratropium belore exercise (D) Pulmonary function testing Item 41 Item 38 A 27 year-old w,ornu.t is evalu:rted in the emergency A S2-year old man is evaluated following a diagnosis of clcpxrtment fbr tlifficulty breathing fbllowing a horncl severe obstructive sleep apnea 8 weeks ago. He was pre- sting to the leg. scribed auto adjusting positive airway pressure therapy. On physical examination, blood pressure is 86r 54 mtn He uses a nasal mask with heated humidification. He still llg, pulse rate is lll0/min. and respiration rate is 20/nlin. feels drowsy during the day. I.ixpirirtory wheezing is notecl. Hcr lips are swollen. Urti clrial skin lesions are present. Which of the following is the most appropriate SIre is aclministered 1 L of irrtravenous 0.9'x, saline, management? ncbr,rl ized albuterol. and intrtrtnuscular epinephrinc. Vital signs norm;rlize, irncl dyspnea improves. Forty fivc tnin (A) Assess adherence Lltes later, systolic blood pressure is 90 mm Hg, pulse rlte (B) Bilevel positive airway pressure ventilation is l28imin. ar-rd wheezir.rg has returncd. : (C) Eszopiclone (D) Modaflnil Which of the following is the most appropriate treatment? i (A) t)ipl-renhydratrrinc 1

Item 41 Item 38 A 27 year-old w,ornu.t is evalu:rted in the emergency A S2-year old man is evaluated following a diagnosis of clcpxrtment fbr tlifficulty breathing fbllowing a horncl severe obstructive sleep apnea 8 weeks ago. He was pre- sting to the leg. scribed auto adjusting positive airway pressure therapy. On physical examination, blood pressure is 86r 54 mtn He uses a nasal mask with heated humidification. He still llg, pulse rate is lll0/min. and respiration rate is 20/nlin. feels drowsy during the day. I.ixpirirtory wheezing is notecl. Hcr lips are swollen. Urti clrial skin lesions are present. Which of the following is the most appropriate SIre is aclministered 1 L of irrtravenous 0.9'x, saline, management? ncbr,rl ized albuterol. and intrtrtnuscular epinephrinc. Vital signs norm;rlize, irncl dyspnea improves. Forty fivc tnin (A) Assess adherence Lltes later, systolic blood pressure is 90 mm Hg, pulse rlte (B) Bilevel positive airway pressure ventilation is l28imin. ar-rd wheezir.rg has returncd. : (C) Eszopiclone (D) Modaflnil Which of the following is the most appropriate treatment? i (A) t)ipl-renhydratrrinc 1 tr Item 39 An 81 year old man is evalulted in the htlspital fbr pneu- (B) I'.pinephrine ((l) FanTotidinc monia. : On physical exantiuation. temperattlrc is llU.0 'C (l)) N,{ethylpredttisoloue (i00.4'f'). blood pressure is 119'65 mm Hg. pttlse r:rte is (fl) Norepinephrine 103

Self-Assessment Test tt .D On physical examination, vital signs are normal. D lr! t^ tr Item 42 A 32-year old man is evaluatecl in the emergency clepart Oxygen saturation is 93% with the patient breathing ambient air. There are diminished breath sounds. .D ment after being lound unresponsive at home. Methaclone U) A 6 minute walk test shows a minimum oxygen sat UI and lorazepam pill bottles were lbund nearby. At the uration of 90% with the patient breathing ambient air. (D scene. respiratory rate was 6/'min. fle was adn-rinisterecl Spirometry shows an FEV, of 35% of predicted and a Dlco supplemental oxygen and intranasal naloxone. fblk:lwed { .D by intravenous naloxone. Food four,d in his ntouth was of42% ofpredicted. Chest imaging shows upper-lobe predominant UI cleared. emphysema. In the emergency department, intravenous naloxone is repeated. Temperature is 37.2'C (99.0'F), blood pressure is 120/68 mm Hg, pulse rate is B0itnin, respiratory rate is Which of the following is the most appropriate treatment? 10/min, and oxygen saturation is 90'1, breathing oxygen. (A) Long-term azithromycintherapy 5 L/min by nasal cannula. 'll,e patient is unrespottsit'e. (B) Lung volume reduction surgery Pupillary miosis is present but responsive to light. The fingerstick blood glucose level is 88 mgicll. (C) Roflumilast (4.9 mmoli L). (D) Supplementaloxygen Portable chest radiograph shows a right lower lclbe infiltrate. Item 45 Which of the following is the most appropriate A 4B-year-old nran is evaluated in the emergency depart- EX treatment? nlent fbr an acllte uryocardial infarction. Medical history (A) Endotracheal intubation is significant tirr hyperlipiden.ria. His only meclicati<tn is atorvastatin. (B) Flumazenil On physical exat.nination, pulse rate is 56/n.rir-r. Other (C) Intravenous naloxone infusion vital signs are normal. Oxygen saturation is 96'){, with the (D) Oxygen by nonrebreather mask patient breathing arnbierrt air. Cardiac examination reveals an S,,. Lungs are clear. lhe initial serum troponin I level is elevatecl. An ECC Item 43 shows S'l'-segnrent elevations in leads ll, lll. and aVF. A A 23-year-old man is evaluated for cough, rhinorrhea, and chest radbgrirph is nonnal. wheezing of 3 weeks' duration. He has no fevers, chills, or chest pain and no history of asthma or allergies. He is a Which of the following is the most appropriate oxygen pastry chef and notes that his symptoms improve on non- management? working weekends. t (A) Oxygen by nonrebreather mask On physical examination, vital signs are normal. Oxy- gen saturation is 94% with the patient breathing ambient (ts) Ox),gen by Venturi mask air. Expiratory wheezing is noted. (C) Oxygen. 3 l.inTin by rrasal cilnnula Laboratory studies show a normal Aspergillus-speciflc (D) No additional oxygen managenreut i IgE level. Spirometry reveals moderate airflow obstruction that i

tt .D On physical examination, vital signs are normal. D lr! t^ tr Item 42 A 32-year old man is evaluatecl in the emergency clepart Oxygen saturation is 93% with the patient breathing ambient air. There are diminished breath sounds. .D ment after being lound unresponsive at home. Methaclone U) A 6 minute walk test shows a minimum oxygen sat UI and lorazepam pill bottles were lbund nearby. At the uration of 90% with the patient breathing ambient air. (D scene. respiratory rate was 6/'min. fle was adn-rinisterecl Spirometry shows an FEV, of 35% of predicted and a Dlco supplemental oxygen and intranasal naloxone. fblk:lwed { .D by intravenous naloxone. Food four,d in his ntouth was of42% ofpredicted. Chest imaging shows upper-lobe predominant UI cleared. emphysema. In the emergency department, intravenous naloxone is repeated. Temperature is 37.2'C (99.0'F), blood pressure is 120/68 mm Hg, pulse rate is B0itnin, respiratory rate is Which of the following is the most appropriate treatment? 10/min, and oxygen saturation is 90'1, breathing oxygen. (A) Long-term azithromycintherapy 5 L/min by nasal cannula. 'll,e patient is unrespottsit'e. (B) Lung volume reduction surgery Pupillary miosis is present but responsive to light. The fingerstick blood glucose level is 88 mgicll. (C) Roflumilast (4.9 mmoli L). (D) Supplementaloxygen Portable chest radiograph shows a right lower lclbe infiltrate. Item 45 Which of the following is the most appropriate A 4B-year-old nran is evaluated in the emergency depart- EX treatment? nlent fbr an acllte uryocardial infarction. Medical history (A) Endotracheal intubation is significant tirr hyperlipiden.ria. His only meclicati<tn is atorvastatin. (B) Flumazenil On physical exat.nination, pulse rate is 56/n.rir-r. Other (C) Intravenous naloxone infusion vital signs are normal. Oxygen saturation is 96'){, with the (D) Oxygen by nonrebreather mask patient breathing arnbierrt air. Cardiac examination reveals an S,,. Lungs are clear. lhe initial serum troponin I level is elevatecl. An ECC Item 43 shows S'l'-segnrent elevations in leads ll, lll. and aVF. A A 23-year-old man is evaluated for cough, rhinorrhea, and chest radbgrirph is nonnal. wheezing of 3 weeks' duration. He has no fevers, chills, or chest pain and no history of asthma or allergies. He is a Which of the following is the most appropriate oxygen pastry chef and notes that his symptoms improve on non- management? working weekends. t (A) Oxygen by nonrebreather mask On physical examination, vital signs are normal. Oxy- gen saturation is 94% with the patient breathing ambient (ts) Ox),gen by Venturi mask air. Expiratory wheezing is noted. (C) Oxygen. 3 l.inTin by rrasal cilnnula Laboratory studies show a normal Aspergillus-speciflc (D) No additional oxygen managenreut i IgE level. Spirometry reveals moderate airflow obstruction that i improves after inhaled albuterol. Chest radiograph is normal. Item 46 A 52-year-old man is evaluated after hospital discharge tr fbr total krree arthroplasty. In the recovery room lbllowing Which of the following is the most likely diagnosis? the procedure, he was reintubated because of hypoxemia. (A) Acute bronchitis which was then comlrletely resolved. The postintubaticln chest radiograph was normal. Hypoxernia did not return (B) Acutehypersensitivitypneumonitis following extubation 24 hours l:rter, ancl clxygenation was (C) Allergicbronchopulmonaryaspergillosis nornral at discharge on hospital day,1. He also has hyper i (D) Occupationalasthma tension. Medications are lisinopril irnd short-term apixaban ftlr postarthroplastv venous tl'rroniboembolisn.r prophylaxis. On physicalexaminatior.r. vital signs are normal. BMI is Item 44 31. Neck circumference is 42 cm (t0.5 in). I{e has a lolr,-lying A 62 year-old man is evaluated in follow up examination soft palate. [-ung and heart examiniitions are normal. l for COPD. Despite smoking cessation, adherence to his medical regimen, good inhaler technique, and participation Which of the following is the most likely cause of the in pulmonary rehabilitation, he continues to experience hypoxemia? breathlessness with mild exertion and has diminished qual- (A) Aspiration pneurnoniu ity of life. He has a minimal dry cough, and he has never required treatment for an acute exacerbation of COPD. (B) Obstructive sleep apnea : Medications are fluticasone-umeclidinium vilanterol and (C) Pulmonary edenta albuterol inhalers as needed. Immunizations are up to date. (D) Puhnor-rary embolism

improves after inhaled albuterol. Chest radiograph is normal. Item 46 A 52-year-old man is evaluated after hospital discharge tr fbr total krree arthroplasty. In the recovery room lbllowing Which of the following is the most likely diagnosis? the procedure, he was reintubated because of hypoxemia. (A) Acute bronchitis which was then comlrletely resolved. The postintubaticln chest radiograph was normal. Hypoxernia did not return (B) Acutehypersensitivitypneumonitis following extubation 24 hours l:rter, ancl clxygenation was (C) Allergicbronchopulmonaryaspergillosis nornral at discharge on hospital day,1. He also has hyper i (D) Occupationalasthma tension. Medications are lisinopril irnd short-term apixaban ftlr postarthroplastv venous tl'rroniboembolisn.r prophylaxis. On physicalexaminatior.r. vital signs are normal. BMI is Item 44 31. Neck circumference is 42 cm (t0.5 in). I{e has a lolr,-lying A 62 year-old man is evaluated in follow up examination soft palate. [-ung and heart examiniitions are normal. l for COPD. Despite smoking cessation, adherence to his medical regimen, good inhaler technique, and participation Which of the following is the most likely cause of the in pulmonary rehabilitation, he continues to experience hypoxemia? breathlessness with mild exertion and has diminished qual- (A) Aspiration pneurnoniu ity of life. He has a minimal dry cough, and he has never required treatment for an acute exacerbation of COPD. (B) Obstructive sleep apnea : Medications are fluticasone-umeclidinium vilanterol and (C) Pulmonary edenta albuterol inhalers as needed. Immunizations are up to date. (D) Puhnor-rary embolism 104

5elf-Assessment Test .A tr Item 47 A 66-year-old man who is undergoing annual low-dose CT Lung sounds are distant. A healing surgical wound is pres, ent. The remainder of the examination is unremarkable. G'

tr Item 47 A 66-year-old man who is undergoing annual low-dose CT Lung sounds are distant. A healing surgical wound is pres, ent. The remainder of the examination is unremarkable. G' (l, for lung cancer screening is evaluated following the dis, Laboratory studies: tr covery of a solitary 1.5-cm lung nodule in the right upper Bicarbonate vt 33 mEq/L (SS mmol/L) tt (l, lobe. There is no lymphadenopathy or effusion seen on Arterial blood gases: UI ta the CT scan. He has a chronic cough and a 90-pack,year pH 7.2s smoking history. His medical history is otherwise unre- Pco, 78 mm Hg (tO.+ t<pa) markable, and he takes no medications. Po, 66 mm Hg (8.8 kPa) = t (t, On physical examination, vital signs and the remain, der of the physical examination are normal. Pulmonary function tests performed 1 month ago Laboratory studies, including liver chemistry tests and demonstrated a restrictive pattern. measurement of sodium and calcium levels, are normal. Chest radiograph shows small lung fields.

(l, for lung cancer screening is evaluated following the dis, Laboratory studies: tr covery of a solitary 1.5-cm lung nodule in the right upper Bicarbonate vt 33 mEq/L (SS mmol/L) tt (l, lobe. There is no lymphadenopathy or effusion seen on Arterial blood gases: UI ta the CT scan. He has a chronic cough and a 90-pack,year pH 7.2s smoking history. His medical history is otherwise unre- Pco, 78 mm Hg (tO.+ t<pa) markable, and he takes no medications. Po, 66 mm Hg (8.8 kPa) = t (t, On physical examination, vital signs and the remain, der of the physical examination are normal. Pulmonary function tests performed 1 month ago Laboratory studies, including liver chemistry tests and demonstrated a restrictive pattern. measurement of sodium and calcium levels, are normal. Chest radiograph shows small lung fields. Which of the followturg is the most appropriate test to Which of the following is the most appropriate treatment? perform next? (A) Acetazolamide (A) Endobronchial ultrasonography (B) Bilevel positive airway pressure (B) High-resolution CT (C) Continuous positive airway pressure (C) IntegratedPET/CT (D) Intubation and mechanical ventilation (D) Sputum cytology Item 50 E tr Item 48 A 29-year-old woman was hospitalized 24 hours ago with A S8-year-old man hospitalized 5 days ago for a COPD exac- erbation is now evaluated for discharge. He required bilevel positive airway pressure for 1 day because ofacute hyper- hypoxemic respiratory failure due to influenza pneumonia. capnic and hypoxic respiratory failure. He was treated with She was intubated and placed on mechanical ventilation. prednisone and levofloxacin. This is his second hospital- Treatment includes lactated Ringer solution, intravenous ization for a COPD exacerbation in the past 6 months and peramivir, propofol, fentanyl, and norepinephrine. the fourth course of prednisone for his COPD in that time. On physical examination, temperature is 38.1 "C Before hospitalization, his baseline function was limit- (100.6 "F), blood pressure is 109/59 mm Hg, pulse rate is ing dyspnea after walking a few minutes. Medications are 90/min, and respiration rate is 24lmin. The arterial Po, inhaled fluticasone furoate-umeclidinium-vilanterol. is 60 mm Hg on Flo, of 0.65, and positive end-expiratory On physical examination, oxygen saturation is 96% pressure is 10 cm HrO. Tidal volume is 6 ml/kg ideal body with the patient breathing ambient air. BMI is 29. He weight, and plateau pressure is 27 cm HrO. The patient is coughs frequently during examination, and faint expira- sedated but wakes to touch and is calm. Pulmonary rhon- tory wheezing is present in the upper lobes of the lungs. chi are present bilaterally. Cardiac examination is normal. Chest radiograph shows bilateral opacities. Echocar, diogram reveals normal cardiac function and chamber size. Arterial blood gas studies (at time of discharge): pH 7.39 Which of the following is the most appropriate Pco, 43 mm Hg (S.z t<Pa) intervention to improve oxygenation? Po, 75 mm Hg (10.0 kPa)

Which of the followturg is the most appropriate test to Which of the following is the most appropriate treatment? perform next? (A) Acetazolamide (A) Endobronchial ultrasonography (B) Bilevel positive airway pressure (B) High-resolution CT (C) Continuous positive airway pressure (C) IntegratedPET/CT (D) Intubation and mechanical ventilation (D) Sputum cytology Item 50 E tr Item 48 A 29-year-old woman was hospitalized 24 hours ago with A S8-year-old man hospitalized 5 days ago for a COPD exac- erbation is now evaluated for discharge. He required bilevel positive airway pressure for 1 day because ofacute hyper- hypoxemic respiratory failure due to influenza pneumonia. capnic and hypoxic respiratory failure. He was treated with She was intubated and placed on mechanical ventilation. prednisone and levofloxacin. This is his second hospital- Treatment includes lactated Ringer solution, intravenous ization for a COPD exacerbation in the past 6 months and peramivir, propofol, fentanyl, and norepinephrine. the fourth course of prednisone for his COPD in that time. On physical examination, temperature is 38.1 "C Before hospitalization, his baseline function was limit- (100.6 "F), blood pressure is 109/59 mm Hg, pulse rate is ing dyspnea after walking a few minutes. Medications are 90/min, and respiration rate is 24lmin. The arterial Po, inhaled fluticasone furoate-umeclidinium-vilanterol. is 60 mm Hg on Flo, of 0.65, and positive end-expiratory On physical examination, oxygen saturation is 96% pressure is 10 cm HrO. Tidal volume is 6 ml/kg ideal body with the patient breathing ambient air. BMI is 29. He weight, and plateau pressure is 27 cm HrO. The patient is coughs frequently during examination, and faint expira- sedated but wakes to touch and is calm. Pulmonary rhon- tory wheezing is present in the upper lobes of the lungs. chi are present bilaterally. Cardiac examination is normal. Chest radiograph shows bilateral opacities. Echocar, diogram reveals normal cardiac function and chamber size. Arterial blood gas studies (at time of discharge): pH 7.39 Which of the following is the most appropriate Pco, 43 mm Hg (S.z t<Pa) intervention to improve oxygenation? Po, 75 mm Hg (10.0 kPa) (A) Increaselevelofsedation Prehospitalization spirometry showed a postbron- chodilator reduced FEVI/FVC ratio and an FEV, of 42"tr of (B) Perform recruitment maneuver predicted. (C) Prone positioning Inhaler technique is reviewed. He is enrolled in a (D) Stan diuretics supervised pulmonary rehabilitation program. Immuniza- tions are up to date.

(A) Increaselevelofsedation Prehospitalization spirometry showed a postbron- chodilator reduced FEVI/FVC ratio and an FEV, of 42"tr of (B) Perform recruitment maneuver predicted. (C) Prone positioning Inhaler technique is reviewed. He is enrolled in a (D) Stan diuretics supervised pulmonary rehabilitation program. Immuniza- tions are up to date. tr Item 49 A S5-year-old woman is hospitalized for increased day- Which of the following is the most appropriate additional treatment? time sleepiness that has progressed since discharge from (A) Nocturnal noninvasive bilevel positive airway pres- the hospital 2 days ago. She had right knee arthroplasty sure ventilation for osteoarthritis-related severe knee pain. She has a (B) Roflumilast history of obesity, hypertension, and type 2 diabetes mel- litus. Medications are lisinopril, metformin, and liraglu- (C) Supplementaloxygen tide. In addition, she was discharged on oxycodone and (D) No additional treatment enoxaparin. On physical examination, respiration rate is l2lmin; the remainder of the vital signs are normal. BMI is 44. Oxy- gen saturation is 94% breathing oxygen, 5 L/min by nasal Item 51 A S5*year-old man is evaluated for a 2-month history of tr cannula. She is sleepy but easily aroused and cooperative. shoulder pain and progressive weakness in his right hand. 105

Self-Assessment Test l T o 'fhe pain radiates to his scapula. He has no shortness of (C) Obtain arterial blood gases Al Ut lll breath or cough. He has a l)0 pack-year smoking history (D) Obtain CT angiograPhY UI C0NT rn6 quit smoking 15 years ago. I{is only medication is ibu" TD Ut prof'en tbr pain. UI (D On physical examination, vital signs are normal' Pto sis and miosis of the right eye are observed. He has mild Item 53 A77 year-o\d man is evaluated in the emergency depart- tr atrophy of the right hand muscles and decreased grip ment following two episodes of melena. He reports no .D t^ strength in his right hand. Lungs are clear to auscultation. dyspnea or lightheadedness and no hematemesis. Medical Complete blood count and metabolic proflle are history is signiflcant for cirrhosis secondary to hepatitis C normal. virus, which has previously been well compensated. IIe Chest radiograph is shown. also has grade 1 esophageal varices but no history of gas trointestinal bleeding. His only medication is propranolol. On physicat examination, the patient is alert and ori ented. Temperature is normal, blood pressure is 85/45 mm FIg, pulse rate is 76lmin, and respiration rate is 18/min. Oxygen saturation is 97'7, with the patient breathing ambi :

(D On physical examination, vital signs are normal' Pto sis and miosis of the right eye are observed. He has mild Item 53 A77 year-o\d man is evaluated in the emergency depart- tr atrophy of the right hand muscles and decreased grip ment following two episodes of melena. He reports no .D t^ strength in his right hand. Lungs are clear to auscultation. dyspnea or lightheadedness and no hematemesis. Medical Complete blood count and metabolic proflle are history is signiflcant for cirrhosis secondary to hepatitis C normal. virus, which has previously been well compensated. IIe Chest radiograph is shown. also has grade 1 esophageal varices but no history of gas trointestinal bleeding. His only medication is propranolol. On physicat examination, the patient is alert and ori ented. Temperature is normal, blood pressure is 85/45 mm FIg, pulse rate is 76lmin, and respiration rate is 18/min. Oxygen saturation is 97'7, with the patient breathing ambi : ent air. lcterus is present. Extremities are cool to touch. The abdomen is unremarkable. Hemoglobin is 6.5 g/dl (OS glL). i : Two peripheral intravenous lines are inserted, and fluid resuscitation with 0.9'7, saline is initiated. r

ent air. lcterus is present. Extremities are cool to touch. The abdomen is unremarkable. Hemoglobin is 6.5 g/dl (OS glL). i : Two peripheral intravenous lines are inserted, and fluid resuscitation with 0.9'7, saline is initiated. r Which of the following is the most appropriate additional : treatment? : (A) Esophageal balloon tamponade ? l (B) Norepinephrine (C) Packed red blood cell transfusion (D) Transjugular intrahepatic portosystemic shunt

(A) Esophageal balloon tamponade ? l (B) Norepinephrine (C) Packed red blood cell transfusion (D) Transjugular intrahepatic portosystemic shunt Item 54 A 29-year old man is evaluated in the emergency depart tr rnent after transport by emergency medical services. He was found sitting on his garage floor, lethargic, with an Which of the following is the most appropriate next step in empty container of automotive coolant nearby. management? On physical examination, temperature is 37.4 "C (99.3'F), (A) Bronchoscopy wilh biopsy blood pressure is 108/58 mm Hg, pulse rate is 118/min. respiration rate is 26lmin, and oxygen saturation is 99'X, (B) CI'ofchest with the patient breathing ambient air. He arouses briefly (C) CT-guided biopsy to loud voice but is not interactive. (t)) Referral for surgical resection Laboratory studies: Creatinine 1.3 mg/dl (114.9 pmouL) Normal tr Item 52 A l)6 year oldlvoman is hospitalized with community acquired Glucose Sodium Potassium 138 mEqi L (t3B mmoltl,) 4.8 mEqi L (+.s mmolrL) pneumonia. She has a l-ristory of systemic lupus erl.thematosus Chtoride 104 mEqlL (t0+ mmoli L) and Raynaud phenomenon. which have been clinically stable Bicarbonate 12 mEqi L (t2 mmoirL) with nif'edipine and hydroxychloroquine. Levofloxacin was l.actate Normal initiated 2 hours ago in the emergency department. Calculated osmolal gap tslevated On physical examinatbn, temperature is 37.8 "C (100.0 "F); Arterial blood gas studies the remainder of the vital signs are nomal. Oxygen saturation pH 7.25 by finger pulse oximetry was initially 92'1, but has decreased to Pco, 28 mm Hg (3.7 kPa) B4',{, despite the addition of supplemental oxygen at 3 Li min Prt, 98 mm Hg (13.0 kPa) by nasal cannula. Pulmonary exanrination reveals scattered coarse rhonchi and crackles in the right lower lobe. Cardiac exanlination is normal- Extrenrities are cool. Which of the following is the most appropriate treatment? (A) Ethar-rol Which ofthe following is the most appropriate management? (B) Fomepizole (A) Change to Fto, of 0.50 by large resenroir oxygen mask (C) Fomepizole and hemodialysis (B) Change to earlobe pulse oximetry probe (D) Lorazepam

Item 54 A 29-year old man is evaluated in the emergency depart tr rnent after transport by emergency medical services. He was found sitting on his garage floor, lethargic, with an Which of the following is the most appropriate next step in empty container of automotive coolant nearby. management? On physical examination, temperature is 37.4 "C (99.3'F), (A) Bronchoscopy wilh biopsy blood pressure is 108/58 mm Hg, pulse rate is 118/min. respiration rate is 26lmin, and oxygen saturation is 99'X, (B) CI'ofchest with the patient breathing ambient air. He arouses briefly (C) CT-guided biopsy to loud voice but is not interactive. (t)) Referral for surgical resection Laboratory studies: Creatinine 1.3 mg/dl (114.9 pmouL) Normal tr Item 52 A l)6 year oldlvoman is hospitalized with community acquired Glucose Sodium Potassium 138 mEqi L (t3B mmoltl,) 4.8 mEqi L (+.s mmolrL) pneumonia. She has a l-ristory of systemic lupus erl.thematosus Chtoride 104 mEqlL (t0+ mmoli L) and Raynaud phenomenon. which have been clinically stable Bicarbonate 12 mEqi L (t2 mmoirL) with nif'edipine and hydroxychloroquine. Levofloxacin was l.actate Normal initiated 2 hours ago in the emergency department. Calculated osmolal gap tslevated On physical examinatbn, temperature is 37.8 "C (100.0 "F); Arterial blood gas studies the remainder of the vital signs are nomal. Oxygen saturation pH 7.25 by finger pulse oximetry was initially 92'1, but has decreased to Pco, 28 mm Hg (3.7 kPa) B4',{, despite the addition of supplemental oxygen at 3 Li min Prt, 98 mm Hg (13.0 kPa) by nasal cannula. Pulmonary exanrination reveals scattered coarse rhonchi and crackles in the right lower lobe. Cardiac exanlination is normal- Extrenrities are cool. Which of the following is the most appropriate treatment? (A) Ethar-rol Which ofthe following is the most appropriate management? (B) Fomepizole (A) Change to Fto, of 0.50 by large resenroir oxygen mask (C) Fomepizole and hemodialysis (B) Change to earlobe pulse oximetry probe (D) Lorazepam 106

f t t Self-Assessment Test ra (u I i tr Item 55 A 4S-year old woman is evaluated in the emergency Which of the following is the most appropriate additional management? q, department 2 days after elective laparoscopic cholecys' (A) Cosyr-rtropin stimulation test E tn tectomy. She is flebrile, has emesis, and reports abdominal (B) lntravenous hydrocortisone tt (l, pain and fullness. t i (C) Intravenous immune globulin vt t On physical examination, temperature is 38.4 "C (101.1 "F), blood pressure is 110/50 mm Hg, pulse rate is 115/min, respira (D) Procnlcitonin measurement t (l, tion rate is 28/min, and oxygen saturation is 94'7, with the vt patient breathing ambient air. Abdominal examination I

ra (u I i tr Item 55 A 4S-year old woman is evaluated in the emergency Which of the following is the most appropriate additional management? q, department 2 days after elective laparoscopic cholecys' (A) Cosyr-rtropin stimulation test E tn tectomy. She is flebrile, has emesis, and reports abdominal (B) lntravenous hydrocortisone tt (l, pain and fullness. t i (C) Intravenous immune globulin vt t On physical examination, temperature is 38.4 "C (101.1 "F), blood pressure is 110/50 mm Hg, pulse rate is 115/min, respira (D) Procnlcitonin measurement t (l, tion rate is 28/min, and oxygen saturation is 94'7, with the vt patient breathing ambient air. Abdominal examination I I Item 58 I reveals right upper quadrant tenderness and diminished l I and inlrequent bowel sounds. There are decreased breath A 2S-year-old man is seen in follow-up examination for I sounds in the right lung base. t he patient is confused. Lap asthma diagnosed 2 months ago. He reports that his symp- I I aroscopy wounds are intact, with no drainage or erythema. toms are now well controlled without use of his rescue I inhaler, and results of the Asthma Control Test conflrm t Which of the following is the best venue of care for this well-controlled asthma. During the visit, he describes feel- I

I Item 58 I reveals right upper quadrant tenderness and diminished l I and inlrequent bowel sounds. There are decreased breath A 2S-year-old man is seen in follow-up examination for I sounds in the right lung base. t he patient is confused. Lap asthma diagnosed 2 months ago. He reports that his symp- I I aroscopy wounds are intact, with no drainage or erythema. toms are now well controlled without use of his rescue I inhaler, and results of the Asthma Control Test conflrm t Which of the following is the best venue of care for this well-controlled asthma. During the visit, he describes feel- I patient? ing down on many days, with difflculty falling asleep and t early morning awakening. Depression screening with the I I (A) Emergency department obsenration unit Patient Health Questionnaire-2 is positive. Medications are (B) General medical ward beclomethasone, montelukast, and albuterol. i I (C) ICU On physical examination, vital signs and pulmonary (D) Outpatient examination are normal. t I

I (A) Emergency department obsenration unit Patient Health Questionnaire-2 is positive. Medications are (B) General medical ward beclomethasone, montelukast, and albuterol. i I (C) ICU On physical examination, vital signs and pulmonary (D) Outpatient examination are normal. t I I Which of the following is the most appropriate treatment? Item 56 (A) Begin escitalopram I A 23-year-old woman is evaluated for chronic cough. She (B) Begin salmeterol reports several episodes of chronic bronchitis as a child t (C) Stop beclomethasone; begin budesonide-formoterol and persistent cough productive ofthick purulent sputum since childhood. She also has chronic nasal congestion and (D) Stop montelukast t chronic diarrhea. Medications are albuterol and glucocor- ticoid inhalers and benzonatate as needed. On physical examination, vital signs are normal; oxy- gen saturation is 96% with the patient breathing ambient Item 59 A 29-year old man is evaluated in the hospital for hem tr air. BMI is 18. Lung examination reveals bilateral diffuse orrhagic shock. He has osteogenesis imperf'ecta and r,lras crackles. The remainder of the examination is normal. admitted for a right hip fiacture repair 2 days ago. He was Complete blood count and immunoglobulin levels are placed on low-molecular-weight heparin postoperatively. normal. Blood pressure is 84144 mm Hg, pulse rate is 132/min, Chest CT scan shows bilateral upper-lobe-predominant and respiration rate is 31/min. Oxygen saturation is 91'2, bronchiectasis with luminal fl lling. using a nonrebreather mask. Cardiac examination reveals Spirometry shows an FEV, of 68% of predicted. tachycardia but no murmurs or gallops. He has copious amounts of blood coming from his nose, and there is swell- Which of the following is the most likely diagnosis? ing, bruising, and oozing at the surgical site. Ile has an 1B-gauge peripheral intravenous catheter in (A) Allergic bronchopulmonary aspergillosis his left forearm. (B) a, Antitrypsin deficiency (C) Cystic flbrosis Which of the following is the most appropriate form of (D) IgA deflciency additional intravenous access in this patient? (A) Peripherally inserted central venous catheter (B) ts Gauge peripheral catheterinthe right arm tr Item 57 A 45 year old woman is evaluated in the ICU for septic shock (C) Intraosseous needle in the right humerus (D) I'riple-lumen catheter in the left femoral vein secondary to a necrotic diabetic fbot infection. She has not responded to initial resuscitation with 30 ml/kg Ringer lac tate infusion and vasopressor therapy. Medications are low molecular-weight heparin, insulin glargine, norepinephrine. vasopressin, metronidazole, ceftriaxone, and vancomycin. Item 60 A 55 year-old man is evaluated in the emergency depart tr On physical examination, temperature is 38.6 'C (101.5 "F), ment for abdominal pain and flever of 12 hours' duration. bloodpressure is 78146 mm Hg, pulse rate is 102/min, and respi On physical examination, temperature is 38.3 "C ration rate is 16/min. Oxygen saturation is 95'lo with the patient (100.9'F), blood pressure is 90/60 mm tlg, pulse rate is breathing :rmbient air. A 4-cm diameter. recently debrided 110/min, and respiration rate is 26lmin. Oxyge n saturation ulceris present overthe dorsal metacarpophalangeal jointofthe is 95'7, with the patient breathing ambient air. lhe patient great toe, extending to bone. is confused. Scleral icterus is noted. There is tenderness to

I Which of the following is the most appropriate treatment? Item 56 (A) Begin escitalopram I A 23-year-old woman is evaluated for chronic cough. She (B) Begin salmeterol reports several episodes of chronic bronchitis as a child t (C) Stop beclomethasone; begin budesonide-formoterol and persistent cough productive ofthick purulent sputum since childhood. She also has chronic nasal congestion and (D) Stop montelukast t chronic diarrhea. Medications are albuterol and glucocor- ticoid inhalers and benzonatate as needed. On physical examination, vital signs are normal; oxy- gen saturation is 96% with the patient breathing ambient Item 59 A 29-year old man is evaluated in the hospital for hem tr air. BMI is 18. Lung examination reveals bilateral diffuse orrhagic shock. He has osteogenesis imperf'ecta and r,lras crackles. The remainder of the examination is normal. admitted for a right hip fiacture repair 2 days ago. He was Complete blood count and immunoglobulin levels are placed on low-molecular-weight heparin postoperatively. normal. Blood pressure is 84144 mm Hg, pulse rate is 132/min, Chest CT scan shows bilateral upper-lobe-predominant and respiration rate is 31/min. Oxygen saturation is 91'2, bronchiectasis with luminal fl lling. using a nonrebreather mask. Cardiac examination reveals Spirometry shows an FEV, of 68% of predicted. tachycardia but no murmurs or gallops. He has copious amounts of blood coming from his nose, and there is swell- Which of the following is the most likely diagnosis? ing, bruising, and oozing at the surgical site. Ile has an 1B-gauge peripheral intravenous catheter in (A) Allergic bronchopulmonary aspergillosis his left forearm. (B) a, Antitrypsin deficiency (C) Cystic flbrosis Which of the following is the most appropriate form of (D) IgA deflciency additional intravenous access in this patient? (A) Peripherally inserted central venous catheter (B) ts Gauge peripheral catheterinthe right arm tr Item 57 A 45 year old woman is evaluated in the ICU for septic shock (C) Intraosseous needle in the right humerus (D) I'riple-lumen catheter in the left femoral vein secondary to a necrotic diabetic fbot infection. She has not responded to initial resuscitation with 30 ml/kg Ringer lac tate infusion and vasopressor therapy. Medications are low molecular-weight heparin, insulin glargine, norepinephrine. vasopressin, metronidazole, ceftriaxone, and vancomycin. Item 60 A 55 year-old man is evaluated in the emergency depart tr On physical examination, temperature is 38.6 'C (101.5 "F), ment for abdominal pain and flever of 12 hours' duration. bloodpressure is 78146 mm Hg, pulse rate is 102/min, and respi On physical examination, temperature is 38.3 "C ration rate is 16/min. Oxygen saturation is 95'lo with the patient (100.9'F), blood pressure is 90/60 mm tlg, pulse rate is breathing :rmbient air. A 4-cm diameter. recently debrided 110/min, and respiration rate is 26lmin. Oxyge n saturation ulceris present overthe dorsal metacarpophalangeal jointofthe is 95'7, with the patient breathing ambient air. lhe patient great toe, extending to bone. is confused. Scleral icterus is noted. There is tenderness to 107

Self-Assessment Test t,l (D + UI UI (D tr CONT palpation in the right upper quadrant. The remainder of the examination is unremarkable. (C) Overnight oximetry (D) Polysomnography Ut laboratory studies: Leukocy.te count Ut 22,000/pL (22 x 10e, L) (D Alanine aminotransaminase 44B U1L Bilirubin 'fotal Item 63 A 64 year-old woman has been hospitalized for 4 days for tr .D 5.0 mgi dL (8S.S pmol'L) a first COPD exacerbaticin and is nou, being discharged. t Direct 4.0 mgi dL (68.4 pmolrl) Before hospitalization she had mild symptoms such as Creatinine 2.0 mgldl (U6.8 Umol/L) breathlessness when hurrying on level ground or Lipase 56 U/1. up a slight hill. She stopped smoking 7 years ago."t,alking Immu- Ultrasound ot' the right upper quadrant reveals a nizations are up to date. Medications are a fluticasone normal-appearing liver and gallbladderr the bile duct is furoate umeclidinium-vilanterol inhaler and an additional dilated. day ofprednisone. Today, vital signs are normal. Breath sounds are distant without rn,heezing. Cardiovascular examination is normal. Which of the following is the most likely diagnosis? A review of the admission chest radiograph shorts (A) Acute cholangitis homogeneous emphysema without other findings. Today. (B) Acutecholccystitis results of laboratory evaluation are normal. Spirometry (C) Pancreatitis shows a FEVr/FVC ratio of 0.6 and an FEV, 12"/. ot'pre- dicted. A 6-minute walk test shor.ts a minimum oxygen (D) Pyogenic liver abscess saturation of 89'2, with the patient breathing ambient air.

t,l (D + UI UI (D tr CONT palpation in the right upper quadrant. The remainder of the examination is unremarkable. (C) Overnight oximetry (D) Polysomnography Ut laboratory studies: Leukocy.te count Ut 22,000/pL (22 x 10e, L) (D Alanine aminotransaminase 44B U1L Bilirubin 'fotal Item 63 A 64 year-old woman has been hospitalized for 4 days for tr .D 5.0 mgi dL (8S.S pmol'L) a first COPD exacerbaticin and is nou, being discharged. t Direct 4.0 mgi dL (68.4 pmolrl) Before hospitalization she had mild symptoms such as Creatinine 2.0 mgldl (U6.8 Umol/L) breathlessness when hurrying on level ground or Lipase 56 U/1. up a slight hill. She stopped smoking 7 years ago."t,alking Immu- Ultrasound ot' the right upper quadrant reveals a nizations are up to date. Medications are a fluticasone normal-appearing liver and gallbladderr the bile duct is furoate umeclidinium-vilanterol inhaler and an additional dilated. day ofprednisone. Today, vital signs are normal. Breath sounds are distant without rn,heezing. Cardiovascular examination is normal. Which of the following is the most likely diagnosis? A review of the admission chest radiograph shorts (A) Acute cholangitis homogeneous emphysema without other findings. Today. (B) Acutecholccystitis results of laboratory evaluation are normal. Spirometry (C) Pancreatitis shows a FEVr/FVC ratio of 0.6 and an FEV, 12"/. ot'pre- dicted. A 6-minute walk test shor.ts a minimum oxygen (D) Pyogenic liver abscess saturation of 89'2, with the patient breathing ambient air. tr Item 61 A 2S-year-old woman is evaluated in the ernergency deparl- Which of the following is the most appropriate additional treatment? ment for severe agitation. The patient is uncooperative. A (A) a,-Antitrypsin augmentation therapy friend reports that the patient had been snorting cocaine. (B) t.ung volume reduction surgery Paroxetine and tramadol are found in the patient's backpack. (C) Pulmonaryrehabilitation On physical examination, temperature is 39.4 'C (102.9 "F), blood pressure is 164182 mm Hg, pulse rate is (D) Supplemental home oxygen 112lmin, respiration rate is 22imin. and oxygen satura- tion is 9B'7, with the patient breathing ambient air. She is diaphoretic and tremulous. Myoclonus and hyperreflexia Item 64 are present. A 61-year-old woman is evaluated in the emergency department for a COPD exacerbation characterized by Which ofthe following is the most appropriate treatment? increased dyspnea and increased purulent sputum pro- (A) Acetaminophen duction. Home medications are mometasone furoate- formoterol, tiotropium bromide, and albuterol inhalers. (B) Fentanyl On physical examination, temperature is 37.2 'C (C) Lorazepanr (99.0 'F), blood pressure is 135i82 mm Hg, pulse rate is (D) Propranolol 112/min, respiration rate is 2llmin, and oxygen saturation is 94% breathing oxygen, 5 L/min by nasal cannula. Pulmo- nary examination reveals diffuse expiratory wheezing but Item 62 no use of accessory muscles. The remainder of the physical A 72-year-old man is evaluated for daytime sleepiness. His examination is noncontributory. wife notes that he snores. He sleeps 8 hours each night. On Arterial blood gas studies: most days of the week, he feels sleepy and will nap for 45 min- pH 7.36 utes. Medical history is sigfficant for atrial flbrillation and Pco, 43 mm Hg (s.z tPa) heart failure. Medications are valsartan-sacubitril, metopro- Po, 65 mm Hg (8.6 kPa) lol, furosemide, spironolactone, empagliflozin, and apixaban. On physical examination, vital signs are normal. BMI Chest radiograph shows hyperinflation and flattened is 27. Low-lying soft palate, irregularly irregular cardiac diaphragm but no inflltrate. rhythm, normal central venous pressure, clear lung flelds, Nebulized albuterol and oral azithromycin are initiated. and chronic venous stasis are present. Transthoracic echocardiogram obtained 1 year ago Which of the following is the most appropriate additional showed left ventricular enlargement and left ventricular management? ejection fraction of 40"/.. (A) High-flow nasal cannula (B) Noninvasive bilevel positive airway pressure Which of the following is the most appropriate test? ventilation (A) Actigraphy (C) Prednisone (B) Home sleep apnea testing (D) Sputum culture

tr Item 61 A 2S-year-old woman is evaluated in the ernergency deparl- Which of the following is the most appropriate additional treatment? ment for severe agitation. The patient is uncooperative. A (A) a,-Antitrypsin augmentation therapy friend reports that the patient had been snorting cocaine. (B) t.ung volume reduction surgery Paroxetine and tramadol are found in the patient's backpack. (C) Pulmonaryrehabilitation On physical examination, temperature is 39.4 'C (102.9 "F), blood pressure is 164182 mm Hg, pulse rate is (D) Supplemental home oxygen 112lmin, respiration rate is 22imin. and oxygen satura- tion is 9B'7, with the patient breathing ambient air. She is diaphoretic and tremulous. Myoclonus and hyperreflexia Item 64 are present. A 61-year-old woman is evaluated in the emergency department for a COPD exacerbation characterized by Which ofthe following is the most appropriate treatment? increased dyspnea and increased purulent sputum pro- (A) Acetaminophen duction. Home medications are mometasone furoate- formoterol, tiotropium bromide, and albuterol inhalers. (B) Fentanyl On physical examination, temperature is 37.2 'C (C) Lorazepanr (99.0 'F), blood pressure is 135i82 mm Hg, pulse rate is (D) Propranolol 112/min, respiration rate is 2llmin, and oxygen saturation is 94% breathing oxygen, 5 L/min by nasal cannula. Pulmo- nary examination reveals diffuse expiratory wheezing but Item 62 no use of accessory muscles. The remainder of the physical A 72-year-old man is evaluated for daytime sleepiness. His examination is noncontributory. wife notes that he snores. He sleeps 8 hours each night. On Arterial blood gas studies: most days of the week, he feels sleepy and will nap for 45 min- pH 7.36 utes. Medical history is sigfficant for atrial flbrillation and Pco, 43 mm Hg (s.z tPa) heart failure. Medications are valsartan-sacubitril, metopro- Po, 65 mm Hg (8.6 kPa) lol, furosemide, spironolactone, empagliflozin, and apixaban. On physical examination, vital signs are normal. BMI Chest radiograph shows hyperinflation and flattened is 27. Low-lying soft palate, irregularly irregular cardiac diaphragm but no inflltrate. rhythm, normal central venous pressure, clear lung flelds, Nebulized albuterol and oral azithromycin are initiated. and chronic venous stasis are present. Transthoracic echocardiogram obtained 1 year ago Which of the following is the most appropriate additional showed left ventricular enlargement and left ventricular management? ejection fraction of 40"/.. (A) High-flow nasal cannula (B) Noninvasive bilevel positive airway pressure Which of the following is the most appropriate test? ventilation (A) Actigraphy (C) Prednisone (B) Home sleep apnea testing (D) Sputum culture 108

Self.Assessment Test tr Item 55 A ,l8-year old rnan is erraluated in the hospital fbr acute On physical exirrninatior.r, tempcritture is llB.0 "C (100.,1 'F). blood pressure is 1S0/9.5 rnm IIg. pulse rate is UI c,

tr Item 55 A ,l8-year old rnan is erraluated in the hospital fbr acute On physical exirrninatior.r, tempcritture is llB.0 "C (100.,1 'F). blood pressure is 1S0/9.5 rnm IIg. pulse rate is UI c, onset of'hyperpyrexia and muscle rigiclity. IJe was hospi 100 mi11. ancl respiration rate is 30i ntilt. Orygen saturxtion (l, talized l2 hours ago tbr upper gastrointestinal bleeding. is li6')1, breathing oxlrger.r. 2 I_r,min tty nasal car.urula. Bilat E UI Within the last hour he unclerwent upper endosc<tpy using t'r'ul wheczes llre l)rcscltl. vt q, rapicl sequcnce intubation with succinylcholine anci eto_ vl Afterial blood gas studies: ta nridate. Soon after completion of the procedure, he clevel oped f'ever, tachypnea, and tacl.rycardia. I 1rl 7.22 g Pto, 75 rnm Hg (10.0 kpa) o ta On physical exanrination, temperature is 40.6 .C I)o, (105.1 "F), blood pressure is ll2i6B mm Hg, pulse rate 66 rnrn IIg (8.8 kpa) is l30lrnin, respiration rate is 26lnlin. and oxygen saturation Chest ra(liograph shows no iltfiltrates. is 99'X, breathing oxygen, )l.lmin by nasal cannula. He has generalized muscle rigidity and cannot open his mouth. Which of the following is the most appropriate treatment? Neurologic examination is otherwise normal. (A) llilevel positive airw.ay pressure Cooling measures are implemented. (li) (.ontinr.rous posilive lirrnal prcssur(' ((.) Iligh flor,t, nasal cannula Which of the following is the most appropriate pharmacologic treatment? ([)) Intr-rbation and ntechanica] ventilation (A) Acetarninophen (B) Cyprriheptadine (C) Dantrolene Item 68 An u4 year old ntan is evaluated in the ernergency depart nrent fbr presuntecl sepsis. He lives in a nursing honte. ancl tr (D) Diltiazenr nurses noted that he rvas lebrile irnd lethargic. Me'dical history and medications are not intnrecliately available. Item 65 On physical exantination. tenlpcrature is ll9.u '(l (102.7 '1.). blood pressure is 88/50 mnt Hg, pulse rate is A 70 year-old man is evaluated with overnight polysom- l16i min. anct respiration rate is 26lmirr. Oxygen saturation is nography because of fatigue, nocturnal awakenings, and c)s'L breathing oxygen, 3 I-rmin by nasirl cannula. The putient nocturnal dyspnea. He has heart failure with reduced ejec- is confusecl but responds to l,oice cor-nrnands. Cardiopul tion fraction and atrial flbrillation. Medications are metopro- nronary exalrination reveals tachycardia and nonnal heart lo1, valsartan-sacubitril, spironolactone, and rivaroxaban. sounds. I{hortchi are auscullated over the left lower lobe. Polysomnogram tracing from the respiratory flow Crystalloicl f luid rc'suscitation is initiated witl-r a target channel is shown. An upward deflection indicates inspira- of ll0 rrl./kt{. tion and a downward deflection indicates exhalation. Complete blo<ld count, metabolic panel, iactate. ancl coirgulation studies are pending. Blood cultures are obtained.

onset of'hyperpyrexia and muscle rigiclity. IJe was hospi 100 mi11. ancl respiration rate is 30i ntilt. Orygen saturxtion (l, talized l2 hours ago tbr upper gastrointestinal bleeding. is li6')1, breathing oxlrger.r. 2 I_r,min tty nasal car.urula. Bilat E UI Within the last hour he unclerwent upper endosc<tpy using t'r'ul wheczes llre l)rcscltl. vt q, rapicl sequcnce intubation with succinylcholine anci eto_ vl Afterial blood gas studies: ta nridate. Soon after completion of the procedure, he clevel oped f'ever, tachypnea, and tacl.rycardia. I 1rl 7.22 g Pto, 75 rnm Hg (10.0 kpa) o ta On physical exanrination, temperature is 40.6 .C I)o, (105.1 "F), blood pressure is ll2i6B mm Hg, pulse rate 66 rnrn IIg (8.8 kpa) is l30lrnin, respiration rate is 26lnlin. and oxygen saturation Chest ra(liograph shows no iltfiltrates. is 99'X, breathing oxygen, )l.lmin by nasal cannula. He has generalized muscle rigidity and cannot open his mouth. Which of the following is the most appropriate treatment? Neurologic examination is otherwise normal. (A) llilevel positive airw.ay pressure Cooling measures are implemented. (li) (.ontinr.rous posilive lirrnal prcssur(' ((.) Iligh flor,t, nasal cannula Which of the following is the most appropriate pharmacologic treatment? ([)) Intr-rbation and ntechanica] ventilation (A) Acetarninophen (B) Cyprriheptadine (C) Dantrolene Item 68 An u4 year old ntan is evaluated in the ernergency depart nrent fbr presuntecl sepsis. He lives in a nursing honte. ancl tr (D) Diltiazenr nurses noted that he rvas lebrile irnd lethargic. Me'dical history and medications are not intnrecliately available. Item 65 On physical exantination. tenlpcrature is ll9.u '(l (102.7 '1.). blood pressure is 88/50 mnt Hg, pulse rate is A 70 year-old man is evaluated with overnight polysom- l16i min. anct respiration rate is 26lmirr. Oxygen saturation is nography because of fatigue, nocturnal awakenings, and c)s'L breathing oxygen, 3 I-rmin by nasirl cannula. The putient nocturnal dyspnea. He has heart failure with reduced ejec- is confusecl but responds to l,oice cor-nrnands. Cardiopul tion fraction and atrial flbrillation. Medications are metopro- nronary exalrination reveals tachycardia and nonnal heart lo1, valsartan-sacubitril, spironolactone, and rivaroxaban. sounds. I{hortchi are auscullated over the left lower lobe. Polysomnogram tracing from the respiratory flow Crystalloicl f luid rc'suscitation is initiated witl-r a target channel is shown. An upward deflection indicates inspira- of ll0 rrl./kt{. tion and a downward deflection indicates exhalation. Complete blo<ld count, metabolic panel, iactate. ancl coirgulation studies are pending. Blood cultures are obtained. Which of the tbllowing is the most appropriate immediate next marlagement step? (;\) i\ntibiotics (ll) (lhest radiographl, ((l) hrtubation On physical examination, vital signs are normal. Oxy- (l)) Norepinephrine gen saturation is 97o/" with the patient breathing ambient air. BMI is 23.5. Neck circumference is 39.4 cm (15.5 in). Heart rhythm is irregularly irregular. Lungs are clear. Item 69 A 63-year old woman is evaluated during a routine visit. Which of the following is the most likely diagnosis? She has a 37-pack-year history of cigarette smoking and quit smoking at age 55 years. She has COPD but reports (A) Central sleep apnea no symptoms concerning for lung cancer. Medications are (B) Obstructive sleep apnea tiotropium inhaler and albuterol inhaler. (C) Sleep relatedhypoventilation (D) Treatment-emergent central sleep apnea Which of the following is the most appropriate lung cancer screening test? (A) Chestradiography Item 67 (B) FluorodeoxyglucosePET A 65-year old woman is evaluated in the ernergency (C) Low-dose chest CT department lbr an acute exacerbation of COPD. Medica tions are budesonide'fbrmoterol inhaier antt albuterol- (D) Sputum cytology ipratropium. (E) No screening

Which of the tbllowing is the most appropriate immediate next marlagement step? (;\) i\ntibiotics (ll) (lhest radiographl, ((l) hrtubation On physical examination, vital signs are normal. Oxy- (l)) Norepinephrine gen saturation is 97o/" with the patient breathing ambient air. BMI is 23.5. Neck circumference is 39.4 cm (15.5 in). Heart rhythm is irregularly irregular. Lungs are clear. Item 69 A 63-year old woman is evaluated during a routine visit. Which of the following is the most likely diagnosis? She has a 37-pack-year history of cigarette smoking and quit smoking at age 55 years. She has COPD but reports (A) Central sleep apnea no symptoms concerning for lung cancer. Medications are (B) Obstructive sleep apnea tiotropium inhaler and albuterol inhaler. (C) Sleep relatedhypoventilation (D) Treatment-emergent central sleep apnea Which of the following is the most appropriate lung cancer screening test? (A) Chestradiography Item 67 (B) FluorodeoxyglucosePET A 65-year old woman is evaluated in the ernergency (C) Low-dose chest CT department lbr an acute exacerbation of COPD. Medica tions are budesonide'fbrmoterol inhaier antt albuterol- (D) Sputum cytology ipratropium. (E) No screening 109

Self-Assessment Test t/t lD Which of the following is the most appropriate diagnostic D UI UI tr Item 70 A 55 year old man is evaluated in the hospital for fever. test for evaluation ofthe pleural effusion? (A) Bedside thoracic ultrasonographl' (D UI dry cough. and shortness of breath of 3 days' duration' UI He has advanced squamolls cell lung cancer, for which he (B) Chest CT with contrast = lD recently started treatment with pembroluzimab. The patient (C) Lateral decubitus film received tltoracic radiation to the right hilum 2 months ago' (D) Thoracic MRI oC .D On physical examination. temperature is 37.8 (,t (100.0'F). blood pressure is 110/70 mm Hg. pulse rate is 102r'min. and respiration rate is 22i min. Oxygen satura- tion is 92'./, with the patient breathing ambient air. BMI is 17. Crackles are present in the right infrascapular region. Item 72 A 54 year old man is evaluated in the emergency depart' tr Cardiovascular examination is normal. ment for shock. He is confused and inattentive. Medical C'l' scan of the chest is shown. records indicate that he has hypertension, hyperlipidemia. and diabetes. Medications are atorvastatin, metformin, valsartan, and hydr<lchlorothiazide. On physical examination, the patient is awake but disoriented. Blood pressure is 82/54 mm Hg, pulse rate is 118/min, and respiration rate is 26lmin. Oxygen satttra tion is B9'X, with the patient breathing ambient air. Skin is cool and clammy. Ihere is jugular venous distention to the angle of the jaw. tleart sounds are distant but without murmur, rubs. or gallops. Diffuse pulmonary crackles are present. I t ECG shows sinus tachycardia (rate 118/min). Resuscitation eflorts are initiatecl. Portable chest radi - * ography and laboratory studies have been ordered.

t/t lD Which of the following is the most appropriate diagnostic D UI UI tr Item 70 A 55 year old man is evaluated in the hospital for fever. test for evaluation ofthe pleural effusion? (A) Bedside thoracic ultrasonographl' (D UI dry cough. and shortness of breath of 3 days' duration' UI He has advanced squamolls cell lung cancer, for which he (B) Chest CT with contrast = lD recently started treatment with pembroluzimab. The patient (C) Lateral decubitus film received tltoracic radiation to the right hilum 2 months ago' (D) Thoracic MRI oC .D On physical examination. temperature is 37.8 (,t (100.0'F). blood pressure is 110/70 mm Hg. pulse rate is 102r'min. and respiration rate is 22i min. Oxygen satura- tion is 92'./, with the patient breathing ambient air. BMI is 17. Crackles are present in the right infrascapular region. Item 72 A 54 year old man is evaluated in the emergency depart' tr Cardiovascular examination is normal. ment for shock. He is confused and inattentive. Medical C'l' scan of the chest is shown. records indicate that he has hypertension, hyperlipidemia. and diabetes. Medications are atorvastatin, metformin, valsartan, and hydr<lchlorothiazide. On physical examination, the patient is awake but disoriented. Blood pressure is 82/54 mm Hg, pulse rate is 118/min, and respiration rate is 26lmin. Oxygen satttra tion is B9'X, with the patient breathing ambient air. Skin is cool and clammy. Ihere is jugular venous distention to the angle of the jaw. tleart sounds are distant but without murmur, rubs. or gallops. Diffuse pulmonary crackles are present. I t ECG shows sinus tachycardia (rate 118/min). Resuscitation eflorts are initiatecl. Portable chest radi - * ography and laboratory studies have been ordered. I= Which of the following is the most appropriate additional a' test? (A) CTangiography (B) Pulmonary arterycatheterization (C) Transesophageal echocardiography (D) Transthoracic echocardiography

I= Which of the following is the most appropriate additional a' test? (A) CTangiography (B) Pulmonary arterycatheterization (C) Transesophageal echocardiography (D) Transthoracic echocardiography Bronchoscopy is unremarkable; bronchoalveolar lavage fluid cultures are negative. Item 73 A 34-year-old woman with fistulizing Crohn disease is tr evaluated in the ICU 10 days after she was admitted with surgical complications. She has been unable to be weaned Which of the following is the most likely diagnosis? from mechanical ventilation. Tube leedings were initiated (A) Hospitrl'acquired pncurnorria 48 hours after ICU admission but have not advanced above (B) I{ypersensitivity pnc'umonitis 50'X, ofher nutritional goal because ofrecurrent abdominal distention and emesis. She has lost 1.8 kg (4 lb) over the (C) Pulmonary edema last week. The ileostomy bag contains gas and liquid feces. (D) Radiationpneumonitis Medications are low molecular weight heparin, metoclo pramide, fentanyl, piperacillin-tazobactam, mesalamine, and oral budesonide. tr Item 71 A 45 year old woman is evaluated in the ICU for community On physical examination, vital signs are normal. BMI is 20. She is intubated. on mechanical ventilation. and a naso- acquired pneumonia and septic shock. Appropriate resus- gastric f,eeding tr"rbe is in place. She has a healing abdominal citatior-r eflbrts are under way. surgical wound and an ileostomy. Borvel sounds are present, On physical examination, temperature is 39.2 'C and the abdomen is distended. (102.6 "1.'). blood pressure is 92i50 mm Hg, pulse rate is Abdominal radiograph reveals gas throughout the 120.,min, ancl respiration r:rte is 25rmin. Oxygen saturation small bowel and no evidence of obstruction. is 85'X, on bilevel positive airway pressure, and Fro, is 0.60. Auscultation ofthe lungs reveals decreased breath sounds Which of the foltowing is the most appropriate over thc lelt lung base. management? Chest radiograph reveals scattered infiltrates in the lower lungs with dense consolidation in the lefl lower lobe (A) Add megestrol acetate and a small left pleural eflusion. (B) Addmethylnaltrexone

Bronchoscopy is unremarkable; bronchoalveolar lavage fluid cultures are negative. Item 73 A 34-year-old woman with fistulizing Crohn disease is tr evaluated in the ICU 10 days after she was admitted with surgical complications. She has been unable to be weaned Which of the following is the most likely diagnosis? from mechanical ventilation. Tube leedings were initiated (A) Hospitrl'acquired pncurnorria 48 hours after ICU admission but have not advanced above (B) I{ypersensitivity pnc'umonitis 50'X, ofher nutritional goal because ofrecurrent abdominal distention and emesis. She has lost 1.8 kg (4 lb) over the (C) Pulmonary edema last week. The ileostomy bag contains gas and liquid feces. (D) Radiationpneumonitis Medications are low molecular weight heparin, metoclo pramide, fentanyl, piperacillin-tazobactam, mesalamine, and oral budesonide. tr Item 71 A 45 year old woman is evaluated in the ICU for community On physical examination, vital signs are normal. BMI is 20. She is intubated. on mechanical ventilation. and a naso- acquired pneumonia and septic shock. Appropriate resus- gastric f,eeding tr"rbe is in place. She has a healing abdominal citatior-r eflbrts are under way. surgical wound and an ileostomy. Borvel sounds are present, On physical examination, temperature is 39.2 'C and the abdomen is distended. (102.6 "1.'). blood pressure is 92i50 mm Hg, pulse rate is Abdominal radiograph reveals gas throughout the 120.,min, ancl respiration r:rte is 25rmin. Oxygen saturation small bowel and no evidence of obstruction. is 85'X, on bilevel positive airway pressure, and Fro, is 0.60. Auscultation ofthe lungs reveals decreased breath sounds Which of the foltowing is the most appropriate over thc lelt lung base. management? Chest radiograph reveals scattered infiltrates in the lower lungs with dense consolidation in the lefl lower lobe (A) Add megestrol acetate and a small left pleural eflusion. (B) Addmethylnaltrexone 110

I Self-Assessment Test r^ tr CONT. (C) Increase fiber in the enteral diet (D) Stop enteral nutrition; start parenteral nutrition pneumonia that progressed to acute respiratory distress syndrome requiring intubation and mechanical ventiia tion. Since intubation. daily routine laboratory evalua €,

r^ tr CONT. (C) Increase fiber in the enteral diet (D) Stop enteral nutrition; start parenteral nutrition pneumonia that progressed to acute respiratory distress syndrome requiring intubation and mechanical ventiia tion. Since intubation. daily routine laboratory evalua €, €, tion has detected a slow decline in hemoglobin level from t^ Item 74 12.5 gidl (tZS gil) to the current level o19.0 g/dl (90 gll). t (l, 'lhere is no evidence of bleeding. Medications are propofol v! (,t A 44 year old woman is evaluated for daytime sleepi- ness of 1 year's duration. She sleeps 8 to 9 hours nightly. infusion, fentanyl infusions, and celbtaxime and levofloxacin. She naps during the day. She has chronic musculoskeletal Laboratory studies document normal platelet and leu (l, kocyte counts. The reticulocyte count is elevated. and the rr't back pain and depression. Medications are venlafaxine and sustained release oxycodone. peripheral blood smear, other than documenting reticulo On physical examination, respiration rate is l2lmin; cytosis, is normal. The direct antigl<lbulin test is negative. the remainder of the vital signs are normal. She has antal- and there is no labrtratory evidence of hemolysis. gic gait and limited trunk flexion due to pain. Oropharyn- geal airway is patent. Nasal, lung, and heart examinations Which of the following is the most appropriate are normal. There is no peripheral edema. management? Polysomnography documents central sleep apnea (A) Discontinue routine blood testing without obstructive sleep apnea. (B) Erythropoietin adn.rinistration (C) Iron studies Which of the following is the most appropriate treatment? (D) Transfusion (A) Adaptive servo ventilation (B) Continuous positive airway pressure (C) Modaflnil (D) Pain rehabilitation program Item 77 A 28 year old woman is evaluated in the emergency depart tr ment lor severe headache and blurred vision of 8 hours' duration. She is 35 weeks pregnant. She has no history ol Item 75 hypertension. Her only medication is a multivitamin. A 64 year old man is treated in the emergency department On physical examination, blood pressure is 200, for a COPD exacerbation characterized by worsened dysp 110 mm Hg, pulse rate is 90/min, and respiration rate is nea, cough, and increased purulent sputum. Home medi- 20/min. Oxygen saturation is 96'1, with the patient breath cations are inhaled fluticasone-vilanterol and tiotropium. ing ambient air. No focal neurc.rlogic deficits are notecl. On physical examination, temperature is 36.9 "C l.aboratory studies reveal a hemoglobin level of 12 g,rdl (98.4 'F), blood pressure is 129l7l mm Hg, pulse rate is (120 g/t.), a platelet coLrnt ofl20,000lpl (120 x l0e1L), and

€, tion has detected a slow decline in hemoglobin level from t^ Item 74 12.5 gidl (tZS gil) to the current level o19.0 g/dl (90 gll). t (l, 'lhere is no evidence of bleeding. Medications are propofol v! (,t A 44 year old woman is evaluated for daytime sleepi- ness of 1 year's duration. She sleeps 8 to 9 hours nightly. infusion, fentanyl infusions, and celbtaxime and levofloxacin. She naps during the day. She has chronic musculoskeletal Laboratory studies document normal platelet and leu (l, kocyte counts. The reticulocyte count is elevated. and the rr't back pain and depression. Medications are venlafaxine and sustained release oxycodone. peripheral blood smear, other than documenting reticulo On physical examination, respiration rate is l2lmin; cytosis, is normal. The direct antigl<lbulin test is negative. the remainder of the vital signs are normal. She has antal- and there is no labrtratory evidence of hemolysis. gic gait and limited trunk flexion due to pain. Oropharyn- geal airway is patent. Nasal, lung, and heart examinations Which of the following is the most appropriate are normal. There is no peripheral edema. management? Polysomnography documents central sleep apnea (A) Discontinue routine blood testing without obstructive sleep apnea. (B) Erythropoietin adn.rinistration (C) Iron studies Which of the following is the most appropriate treatment? (D) Transfusion (A) Adaptive servo ventilation (B) Continuous positive airway pressure (C) Modaflnil (D) Pain rehabilitation program Item 77 A 28 year old woman is evaluated in the emergency depart tr ment lor severe headache and blurred vision of 8 hours' duration. She is 35 weeks pregnant. She has no history ol Item 75 hypertension. Her only medication is a multivitamin. A 64 year old man is treated in the emergency department On physical examination, blood pressure is 200, for a COPD exacerbation characterized by worsened dysp 110 mm Hg, pulse rate is 90/min, and respiration rate is nea, cough, and increased purulent sputum. Home medi- 20/min. Oxygen saturation is 96'1, with the patient breath cations are inhaled fluticasone-vilanterol and tiotropium. ing ambient air. No focal neurc.rlogic deficits are notecl. On physical examination, temperature is 36.9 "C l.aboratory studies reveal a hemoglobin level of 12 g,rdl (98.4 'F), blood pressure is 129l7l mm Hg, pulse rate is (120 g/t.), a platelet coLrnt ofl20,000lpl (120 x l0e1L), and 96/min, respiration rate is l8/min, and oxygen satura- a urine protein-creatinine ratio of 600 mgr'g. Aminotrans tion is 92'1, breathing oxygen, 2 Llmin by nasal cannula. terase levels are normal. Lung examination reveals expiratory wheezing and mildly Blood pressure is reduced to 180il00 mm Hg with labored respirations. The remainder of the physical exam- intravenous labetalol. ination is normal. Which of the following is the most appropriate next step in Arterial blood qas studies: management? pH 7.39 Pco, 41 mm Hg (5.4 kPa) (A) Delivery Po, 61 mm Hc (8.1 kPa) (B) Intravenousbetamethasone Chest radiograph shows a flattened diaphragm but no (C) lntravenous enalapril inflltrates or pleural effusions. (D) Intravenous sodium nitroprusside Treatment is initiated with prednisone and nebulized albuterol-ipratropium.

96/min, respiration rate is l8/min, and oxygen satura- a urine protein-creatinine ratio of 600 mgr'g. Aminotrans tion is 92'1, breathing oxygen, 2 Llmin by nasal cannula. terase levels are normal. Lung examination reveals expiratory wheezing and mildly Blood pressure is reduced to 180il00 mm Hg with labored respirations. The remainder of the physical exam- intravenous labetalol. ination is normal. Which of the following is the most appropriate next step in Arterial blood qas studies: management? pH 7.39 Pco, 41 mm Hg (5.4 kPa) (A) Delivery Po, 61 mm Hc (8.1 kPa) (B) Intravenousbetamethasone Chest radiograph shows a flattened diaphragm but no (C) lntravenous enalapril inflltrates or pleural effusions. (D) Intravenous sodium nitroprusside Treatment is initiated with prednisone and nebulized albuterol-ipratropium. Which of the following is the most appropriate additional treatment? Item 78 A 57 year-old woman is evaluated for progressive dyspnea tr of l year's duration. She has otherwise been well and takes (A) Intravenous theophylline no medications. (B) Intravenous piperacillin-tazobactam On physical examination, blood pressure is l21i B2 mm Hg. Oxygen saturation is 94'7, '*'ith the patient breathing (C) Noninvasive bilevel positive airway pressure irmbient air. There is a grade 2/6 systolic murmur at the ventilation left lower sternal border that increases with inspiration (D) Oral azithromycin and persistent splitting of Sr. Central venQus pressure is elevated. There is a prominent venous o wave. ECG shows right atrial enlargement. Chest radiograph

Which of the following is the most appropriate additional treatment? Item 78 A 57 year-old woman is evaluated for progressive dyspnea tr of l year's duration. She has otherwise been well and takes (A) Intravenous theophylline no medications. (B) Intravenous piperacillin-tazobactam On physical examination, blood pressure is l21i B2 mm Hg. Oxygen saturation is 94'7, '*'ith the patient breathing (C) Noninvasive bilevel positive airway pressure irmbient air. There is a grade 2/6 systolic murmur at the ventilation left lower sternal border that increases with inspiration (D) Oral azithromycin and persistent splitting of Sr. Central venQus pressure is elevated. There is a prominent venous o wave. ECG shows right atrial enlargement. Chest radiograph tr Item 76 A 55 year- old woman is evaluated for progressive anemia shows prorninence of the pulmonary artery. Echocardio gram reveals a right ventricular systolic pressure of 64 mm Hg and an estimated right atrial pressure of 15 mm Hg. during her l2-day hospital stay. She was hospitalized for 111

Self-Assessment Test vt .D ffl t-el't vetttriculitr firnction is tltirmal. Pulm.nar1' Iuncti.tt Which of the following is the most appropriate D vr Ll t".ts shtxt dee rcitsecl I)t.cct but are othenvise nornral. \'e n management? tr (D C0NT 1i111io,.,r1lerfusion scan is ktw prollrrbility ftrr pr-rlnlonitn' (A) Begin omeprazole UI cmbolisnr. UI (B) Discontinue fluticasone salmeterol; begin fluticasone (D 2s0 pg Which of the following is the most appropriate management? (C) Increase fluticasone-salmeterol strength to 500/50 pg CD tt (D) Perform upper endoscopy (A) Coronary angir.rgraphy (B) Right heart cathetcrizaliotr ((l) Start nif'edipine Item 81 (D) Start silclenafil A 67 yeirr-old wolran is evaluated fbr a 6-month history of' EI dull right chest pain, persistent cough, and d1'spnea orl exer t tion. During this time sl.re krst 9.1 kg (20 lb) and had night

vt .D ffl t-el't vetttriculitr firnction is tltirmal. Pulm.nar1' Iuncti.tt Which of the following is the most appropriate D vr Ll t".ts shtxt dee rcitsecl I)t.cct but are othenvise nornral. \'e n management? tr (D C0NT 1i111io,.,r1lerfusion scan is ktw prollrrbility ftrr pr-rlnlonitn' (A) Begin omeprazole UI cmbolisnr. UI (B) Discontinue fluticasone salmeterol; begin fluticasone (D 2s0 pg Which of the following is the most appropriate management? (C) Increase fluticasone-salmeterol strength to 500/50 pg CD tt (D) Perform upper endoscopy (A) Coronary angir.rgraphy (B) Right heart cathetcrizaliotr ((l) Start nif'edipine Item 81 (D) Start silclenafil A 67 yeirr-old wolran is evaluated fbr a 6-month history of' EI dull right chest pain, persistent cough, and d1'spnea orl exer t tion. During this time sl.re krst 9.1 kg (20 lb) and had night tr Item 79 A 22 ycar old nran is evaluatecl iu the etrcrgencl- clepart s\,\'eats. SI.re is a retired ship refitter. She has a 2S-pack-year snroking history and quit smoking 20 years ago. On pl'rysicalexamination. vital signs are normal. There ment (tit)) after being puilecl fi-oln a partialll' frozcn lirke. tmmersion tinre is estimatecl to be 2 hours. He rvas ft.rutrcl are climinished breath sounds and dullness to percussiotr bv emcrgency n-redicll sen,ices and'uvas unrespot1sitre antl ovcr the right lor,ver hemithorax. Cardiac examination is pulselcss. He u'as inlubatecl. ancl aclvanced life support normal. u,as initiatecl. On arrival at the Et). pulse had rcturne(l Chest radkigraph clemonstrates a large pleural effusion ar-rd caruliopulnronar\ resuscitation lvas stolrped. Mechar-t on the right side as well as pleural plaques. Chest CT scau icirl venlil:rtion w:ls initiatecl. and itrtravenous fluids'"verc slror,vs b;rsilar fibrosis and moderate to large right sided pleu- aclministered. Wet clothes were removed. ralcfiirsion with associated pleural thickening and nodularity. On ph1,'sical exarnination. blood pressure is 92'60 nrnl Thoracentcsis f,ields 1200 mL of serosanguinous fluid: I tg. Temperature by an esophageal probe is 27.6 "C. (8i.7 'lr). chemical analysis is compatible with an exudative eflusion. There arc r-ro signs of traumar. hrterferon lrelerse assay is negative. Cytology {indings are n(jq,tiVe for nrllignlncl . I-aboratory studies: Clucose BB mgidl- (.1.9 mrnol,L) Which of the following is the most appropriate diagnostic Potassium 5..l rnliq'l- (5.'1 mmol l.) test to perform next? Arterial bloocl gas stutlies: pH 7.28 (A) Closed pleural biopsy Pco, 36 mm Hg (1.8 kPa) (B) Fluorodeoxyglucose PET Po, 110 mm rtg (14.6 klra) (C) Repeatthoracentesis (D) Thoracoscol.lic pleural biopsy Which of the following is the most appropriate warming technique? (A) Aclive inlcrnll rt,narnrirrg Item 82 (R) Clrutiopulnronarl hypuss narnring A 67-year old man is evaluated before airline travel. He is (C) llernodial)'sis planning a trip to Hawaii next month. He has COPD and (l)) Passive rewarmirrg becomes dyspneic when walking short distances on level ground. Results of his last pulmonary function test indi cated an FEV, of 40% of predicted. He has not yet required Item 8O oxygen supplementation. Medications are tiotropium, sal- meterol, and fluticasone and albuterol inhalers. A 54 year-old man is evaluated during a follow-up visit On physical examination, respiration rate is 16/min. for asthma. He has a 5-year history of persistent asthma. Auscultation of the lungs reveals a prolonged expiratory He has had one exacerbation within the last year, which phase with no wheezes. was treated with glucocorticoids. He reports no wheez- ing but notes an intermittent nonproductive cough. His Asthma Control Test score is 24, indicating well Which of the following is the most appropriate next step? controlled asthma. He reports adherence to his mainte- (A) High-altitude simulation test nance inhaler and demonstrates good inhaler technique. (B) Recommend against air travel He describes symptoms of epigastric burning following (C) Resting pulse oximetry meals. He has no other gastrointestinal symptoms. He does not smoke, and he exercises daily without limita- (D) No further testing needed tion. Medications are fluticasone-salmeterol 100/50 pg and an albuterol inhaler. On physical examination, vital signs are normal, and no wheezing is noted. Spirometry is normal. Fractional exhaled nitric oxide level is normal. Item 83 A 132 year-old \ /oman is evaluated in the hospital for ir ll n,eek history of'progressive shortness of breath, arthralgia, tr 112

Self-Assessment Test Ut lll and fatigue. lJcr only medication is pantoprazole fbr gas- Et troesophageal rr.llux disease. Meciical histitry is significant A reduction in which of the folloll,ing outcomes is most FG' likely with this preventive strateg5/? CoNL 6. RaYnaud phenomenon treated l,r'ith colcl avoiclance. She o, works in an accounting firrl and has no unusual environrnen (A) Gastroirrtestinal bleeciing E UI tal erposures. (B) Flospital sta1, vt q, On physical examination. blood pressure is 140,90 ntm (C) ICU stay UI Ut Hg, pulse rate is g8lmin, lnd respiration rate is 24lr.nin. (D) Mortrrlity Oxygen saturation is 90')1, breathing oxygen, 2 I_ nrin by +q, nasal cannula. Auscultation reveals crackles at both lung tt bases. She has pully appearing fir.rgers. The remaincler of' Item 85 the examination is normal. A 34 year old man is evaluated at a routine follow-up Laboratory studies: examination. He has a history of spirometry confirmed llemoglobin ll grdl (t t o git.) asthma. He reports feeling well and denies sinus symp C reactive protein .1 mgldl_ (,10 mg,'l.) toms, gastroesophageal reflux disease, and tobacco use. He Antinuclear ar.rtibocll' Positive demonstrates excellent inhaler technique. Medications are Antitopoisomerase I (anti Scl 70) l)ositive inhaled budesonide and albuterol. antibocly On physical examination, vital signs are normal, and the remainder of the examination is unremarkable. Chest radiograph shou,s bilateralll, increased nrark- ings urith a b:rsilar preciontinance witl.rout lyrnphaclenop athy. Which of the following is the most appropriate next step in Chest CT is shou,n. evaluation? (A) Administer the Asthma Control Test (B) Measure fractional exhaled nitric oxide (C) Obtain chest radiograph (D) Perform 6-minute walk test

Ut lll and fatigue. lJcr only medication is pantoprazole fbr gas- Et troesophageal rr.llux disease. Meciical histitry is significant A reduction in which of the folloll,ing outcomes is most FG' likely with this preventive strateg5/? CoNL 6. RaYnaud phenomenon treated l,r'ith colcl avoiclance. She o, works in an accounting firrl and has no unusual environrnen (A) Gastroirrtestinal bleeciing E UI tal erposures. (B) Flospital sta1, vt q, On physical examination. blood pressure is 140,90 ntm (C) ICU stay UI Ut Hg, pulse rate is g8lmin, lnd respiration rate is 24lr.nin. (D) Mortrrlity Oxygen saturation is 90')1, breathing oxygen, 2 I_ nrin by +q, nasal cannula. Auscultation reveals crackles at both lung tt bases. She has pully appearing fir.rgers. The remaincler of' Item 85 the examination is normal. A 34 year old man is evaluated at a routine follow-up Laboratory studies: examination. He has a history of spirometry confirmed llemoglobin ll grdl (t t o git.) asthma. He reports feeling well and denies sinus symp C reactive protein .1 mgldl_ (,10 mg,'l.) toms, gastroesophageal reflux disease, and tobacco use. He Antinuclear ar.rtibocll' Positive demonstrates excellent inhaler technique. Medications are Antitopoisomerase I (anti Scl 70) l)ositive inhaled budesonide and albuterol. antibocly On physical examination, vital signs are normal, and the remainder of the examination is unremarkable. Chest radiograph shou,s bilateralll, increased nrark- ings urith a b:rsilar preciontinance witl.rout lyrnphaclenop athy. Which of the following is the most appropriate next step in Chest CT is shou,n. evaluation? (A) Administer the Asthma Control Test (B) Measure fractional exhaled nitric oxide (C) Obtain chest radiograph (D) Perform 6-minute walk test Item 86 A 66 year old woman is evaluated in the ICLI for nran tr I IU I xgement of acute hvpoxic respirator), failure due to '"'iral pneunronia. She l.ras no othcr meclicirl problenrs and takes , no medications. On physical erantin:rtion, the patient is calnr. alert, and interactive. Tenlpcrature is :17.6 'C (99.7'F). bkx.rd pressure is 140r90 mm Hg, pulse rate is 100, rnin, and respiration rate is 32rnrin. Oxygen saturation is B9'x, breathing oxygen, :l L'min bv nasal cannula. l-ung e.xamination reveals bilat eral rhonchi and tach),pnea. Cardiac examination is nornral. On arterial bkxrd gas analysis \,vith the patiellt breath Which of the following is the most likely diagnosis? ing ambient air, pl I is 7.40, [t:o, is i]7 rnrn Hg (.1.9 kPa). iurd Po, is 5U rnm Hg (7.7 kPa). (A) Connective tissue discase -associated intcrstitial lLlng Chest radiograph shor,vs l.lilateral opacities. discase Therapy is initiated. (B) I I-r-persensitivit!' pneunronitis (C) Idiopathic pulmonary fibrosis Which of the following is the most appropriate additional (D) Srrcoidosis management of the patient's hypoxemia? (A) Intubation ancl t.nechat.rical.,'entilatior.r (B) No change in currellt rxanagenrellt tr Item A 84 66 year olcl u,oman is evaluated fbr stress ulcer (C) Noninvasive positive pressure vet.rtilation (l)) Oxl,gen by high flou'hurridifiecl nas:rl catrnula prophl'laxis. She has been in the ICU on nrechanical ven tilation fbr 72 hours fbr respiratory f trilure due to c<lr.nmu nity acquired pnc-umonia. She has required vasopressors and glucocorticoids to mirintain [.rer blood pressLlre. Item 87 She has acute kidney injury. Medications are ceftaro A 62-year old man is evaiuated during a follow-up visit line. levofloxacin, norepinephrir.re, dexamethasone, and for COPD. He continues to smoke one pack daily and has a lo."v molecular rveight heparin. She is receiving enleral 40-pack-year history. He can walk rapidly on a level sur- nutrition through a feeding tube. face but has breathlessness walking up a slight hill. He has The decision is made to initiate stress ulcer prophy not been hospitalized or seen urgently for an exacerbation. laxis with an oral proton pump inhibitor. Medications are salmeterol and tiotropium.

Item 86 A 66 year old woman is evaluated in the ICLI for nran tr I IU I xgement of acute hvpoxic respirator), failure due to '"'iral pneunronia. She l.ras no othcr meclicirl problenrs and takes , no medications. On physical erantin:rtion, the patient is calnr. alert, and interactive. Tenlpcrature is :17.6 'C (99.7'F). bkx.rd pressure is 140r90 mm Hg, pulse rate is 100, rnin, and respiration rate is 32rnrin. Oxygen saturation is B9'x, breathing oxygen, :l L'min bv nasal cannula. l-ung e.xamination reveals bilat eral rhonchi and tach),pnea. Cardiac examination is nornral. On arterial bkxrd gas analysis \,vith the patiellt breath Which of the following is the most likely diagnosis? ing ambient air, pl I is 7.40, [t:o, is i]7 rnrn Hg (.1.9 kPa). iurd Po, is 5U rnm Hg (7.7 kPa). (A) Connective tissue discase -associated intcrstitial lLlng Chest radiograph shor,vs l.lilateral opacities. discase Therapy is initiated. (B) I I-r-persensitivit!' pneunronitis (C) Idiopathic pulmonary fibrosis Which of the following is the most appropriate additional (D) Srrcoidosis management of the patient's hypoxemia? (A) Intubation ancl t.nechat.rical.,'entilatior.r (B) No change in currellt rxanagenrellt tr Item A 84 66 year olcl u,oman is evaluated fbr stress ulcer (C) Noninvasive positive pressure vet.rtilation (l)) Oxl,gen by high flou'hurridifiecl nas:rl catrnula prophl'laxis. She has been in the ICU on nrechanical ven tilation fbr 72 hours fbr respiratory f trilure due to c<lr.nmu nity acquired pnc-umonia. She has required vasopressors and glucocorticoids to mirintain [.rer blood pressLlre. Item 87 She has acute kidney injury. Medications are ceftaro A 62-year old man is evaiuated during a follow-up visit line. levofloxacin, norepinephrir.re, dexamethasone, and for COPD. He continues to smoke one pack daily and has a lo."v molecular rveight heparin. She is receiving enleral 40-pack-year history. He can walk rapidly on a level sur- nutrition through a feeding tube. face but has breathlessness walking up a slight hill. He has The decision is made to initiate stress ulcer prophy not been hospitalized or seen urgently for an exacerbation. laxis with an oral proton pump inhibitor. Medications are salmeterol and tiotropium. 113

Self-Assessment Test lrr o listed ingredients ol the hand sanitizer are ethanol and On physical examination, vital signs are normal. Oxy- gen saturation is 92% with the patient breathing ambient isopropyl alcohol. The patient has a history of chronic ut U) (D air. Faint expiratory wheezing is present. alcoholism. UI UI Spirometry shows an FEVI/FVC ratio of 0.58, and FEV, On physical examination, temperature is normal' is 62% ofpredicted. blood pressure is 112i68 mm Hg. pulse rate is 941min, o respiration rate is 14/min, and oxygen saturation is 96'1, Which of the following is the most appropriate additional breathing oxygen, '2 Llmin by nasal cannula. I-le arouses .D t, therapy? to painful stimuli. His speech is slurred. and he shows psy- chomotor slowing. Neurologic examination is otherwise (A) Chronic azithromycin therapy normal. (B) Prednisone The calculated anion gap is normal; the osmolal gap (C) Pulmonaryrehabilitation is elevated. (D) Smoking cessation Which of the following is the most appropriate management? Item 88 (A) Ethanol A 54 year old man is evaluated for a 2-year history of (B) Flumazenil chronic productive cough. He has intermittent wheezing, (C) Fomepizole shortness of breath with exertion, and nasal congestion. On physical examination, vital signs are normal. (D) Hemodialysis Bibasilar crackles are present. Cardiac examination is (E) Supportive care normal. CT scan of the chest shows cylindrical bronchiectasis of bilateral lower lobes.

lrr o listed ingredients ol the hand sanitizer are ethanol and On physical examination, vital signs are normal. Oxy- gen saturation is 92% with the patient breathing ambient isopropyl alcohol. The patient has a history of chronic ut U) (D air. Faint expiratory wheezing is present. alcoholism. UI UI Spirometry shows an FEVI/FVC ratio of 0.58, and FEV, On physical examination, temperature is normal' is 62% ofpredicted. blood pressure is 112i68 mm Hg. pulse rate is 941min, o respiration rate is 14/min, and oxygen saturation is 96'1, Which of the following is the most appropriate additional breathing oxygen, '2 Llmin by nasal cannula. I-le arouses .D t, therapy? to painful stimuli. His speech is slurred. and he shows psy- chomotor slowing. Neurologic examination is otherwise (A) Chronic azithromycin therapy normal. (B) Prednisone The calculated anion gap is normal; the osmolal gap (C) Pulmonaryrehabilitation is elevated. (D) Smoking cessation Which of the following is the most appropriate management? Item 88 (A) Ethanol A 54 year old man is evaluated for a 2-year history of (B) Flumazenil chronic productive cough. He has intermittent wheezing, (C) Fomepizole shortness of breath with exertion, and nasal congestion. On physical examination, vital signs are normal. (D) Hemodialysis Bibasilar crackles are present. Cardiac examination is (E) Supportive care normal. CT scan of the chest shows cylindrical bronchiectasis of bilateral lower lobes. Which of the following is the most appropriate diagnostic Item 91 A 63 year old woman is evaluated for increasing shortness tr of breath for the past 2 months. She has ischemic cardio- test to perform next? myopathy and a history of breast cancer treated with sur (A) Bronchoscopy with bronchoalveolar lavage gery and irradiation 9 years ago. When she was between 20 and 30 years of age, she worked installing brakes on (B) Immunoglobulinmeasurement automobiles. She is on guideline-directed medical therapy (C) Measurement of IgG response to pneumococcal for heart flailure. immunization On physical examination. vital signs normal. Cardiac (D) Nasal ciliary biopsy examination reveals an S,, mitral regurgitation, hepatomeg- aly. possible ascites. and peripheral eclema. There is dullness to percussion and absent breath sounds at the left base. Item 89 Chest radiograph shows a moderate Ieft sided pleural A 22-year old man is evaluated for a 6-week history of effusion but is otherwise normal. shortness ofbreath and cough. He is otherwise healthy and A thoracentesis removes 600 ml. of bloody fluid. 'lhe takes no medications. He works from home as a software pleural fluid lactate dehydrogenase (t.DH) level is 208 Ui L, developer. Two months ago, he acquired a pet parakeet. and the total protein level is 4.4 glL. Simultaneous serum On physical examination, other than a respiratory LDH level is 279 UlL, and total protein level is 7.6 UlL. rate of 25/min, vital signs are normal. Oxygen saturation is Pleural fluid cytology is pending. 93% with the patient breathing ambient air. Auscultation demonstrates inspiratory crackles over both lung flelds. Which of the following is the most likely diagnosis? The remainder of the physical examination is normal. (A) Benign asbestos pleural effusion Chest CT shows micronodular opacities in the mid- to upper-lung zones. (B) Heart lailure (C) Hepatichydrothorax Which of the following is the most appropriate (D) Malignant pleural effusion management? (A) Lung transplant (B) Nintedanib (C) Parakeet removal Item 92 A 54 year-old man is evaluated for nutritional supple- tr mentation. He was admitted to the ICU 3 days ago fbr (D) Surgical lung biopsy sepsis related to an empyema associated with community- acquired pneumonia. He was unable to maintain his nutritional needs before admission. and this has con- tr Item 90 A 34 year-old man is evaluated in the emergency depart tinued during hospitalization. He has lost an unknown quantity of weight. A decision is made to begin enteral ment after being found unresponsive in a homeless shelter f'eedings. IIis nutritional requirements are calculated to be with two empty bottles ol hand sanitizer. The pertinent 1460 calories daily.

Which of the following is the most appropriate diagnostic Item 91 A 63 year old woman is evaluated for increasing shortness tr of breath for the past 2 months. She has ischemic cardio- test to perform next? myopathy and a history of breast cancer treated with sur (A) Bronchoscopy with bronchoalveolar lavage gery and irradiation 9 years ago. When she was between 20 and 30 years of age, she worked installing brakes on (B) Immunoglobulinmeasurement automobiles. She is on guideline-directed medical therapy (C) Measurement of IgG response to pneumococcal for heart flailure. immunization On physical examination. vital signs normal. Cardiac (D) Nasal ciliary biopsy examination reveals an S,, mitral regurgitation, hepatomeg- aly. possible ascites. and peripheral eclema. There is dullness to percussion and absent breath sounds at the left base. Item 89 Chest radiograph shows a moderate Ieft sided pleural A 22-year old man is evaluated for a 6-week history of effusion but is otherwise normal. shortness ofbreath and cough. He is otherwise healthy and A thoracentesis removes 600 ml. of bloody fluid. 'lhe takes no medications. He works from home as a software pleural fluid lactate dehydrogenase (t.DH) level is 208 Ui L, developer. Two months ago, he acquired a pet parakeet. and the total protein level is 4.4 glL. Simultaneous serum On physical examination, other than a respiratory LDH level is 279 UlL, and total protein level is 7.6 UlL. rate of 25/min, vital signs are normal. Oxygen saturation is Pleural fluid cytology is pending. 93% with the patient breathing ambient air. Auscultation demonstrates inspiratory crackles over both lung flelds. Which of the following is the most likely diagnosis? The remainder of the physical examination is normal. (A) Benign asbestos pleural effusion Chest CT shows micronodular opacities in the mid- to upper-lung zones. (B) Heart lailure (C) Hepatichydrothorax Which of the following is the most appropriate (D) Malignant pleural effusion management? (A) Lung transplant (B) Nintedanib (C) Parakeet removal Item 92 A 54 year-old man is evaluated for nutritional supple- tr mentation. He was admitted to the ICU 3 days ago fbr (D) Surgical lung biopsy sepsis related to an empyema associated with community- acquired pneumonia. He was unable to maintain his nutritional needs before admission. and this has con- tr Item 90 A 34 year-old man is evaluated in the emergency depart tinued during hospitalization. He has lost an unknown quantity of weight. A decision is made to begin enteral ment after being found unresponsive in a homeless shelter f'eedings. IIis nutritional requirements are calculated to be with two empty bottles ol hand sanitizer. The pertinent 1460 calories daily. 114

Self-Assessment Test vt 6' tr CONI Which of the following is the most appropriate enteral feeding stratery for this patient? On physical examination, the patient is alert and cooperative. Blood pressure is 150/90 mm Hg, pulse rate is 100/min, and respiration rate is 26lmin. Oxygen saturation (1, (A) 1460 calories daily starting on day 1 is 93% with the patient breathing ambient air. Cardiopul vt (B) ZOOO calories daily starting on day 1 monary examination is normal. Neurologic examination UI (u (C) Incremental increase to1460 calories daily over vt shows moderate weakness of her feet, legs, hands, and UI 3 to 7 days arms. Di{Iuse areflexia is present but sensation is normal. (D) Incremental increase to 2000 calories daily over Arterial blood gas studies: o vt 3 to 7 days pH 7.34 Pco, 49 mm HC (6.5 kPa)

vt 6' tr CONI Which of the following is the most appropriate enteral feeding stratery for this patient? On physical examination, the patient is alert and cooperative. Blood pressure is 150/90 mm Hg, pulse rate is 100/min, and respiration rate is 26lmin. Oxygen saturation (1, (A) 1460 calories daily starting on day 1 is 93% with the patient breathing ambient air. Cardiopul vt (B) ZOOO calories daily starting on day 1 monary examination is normal. Neurologic examination UI (u (C) Incremental increase to1460 calories daily over vt shows moderate weakness of her feet, legs, hands, and UI 3 to 7 days arms. Di{Iuse areflexia is present but sensation is normal. (D) Incremental increase to 2000 calories daily over Arterial blood gas studies: o vt 3 to 7 days pH 7.34 Pco, 49 mm HC (6.5 kPa) Item 93 Po, B0 mm HC (10.6 kPa) Alveolar-arterialoxygengradient Normal A 24-year-old woman is evaluated for intermittent cough, Chest radiograph is normal. wheezing, and chest tightness of 1 month's duration. She There is a 22% decrement in forced vital capacity while reports worsening symptoms with exercise and with cat supine compared with the upright position. Maximal inspi- exposure. On physical examination, vital signs are normal. She has ratory pressure and maximal expiratory pressure are both less than 50% ofpredicted. end expiratory wheezing. Cardiac examination is normal. On spirometry, FEV, is 75% of predicted and improves signiflcantly following inhaled albuterol. Which of the following is the most likely cause of this patient's respiratory failure? Which of the following tests will help predict this patient's (A) Decreased ventilatory drive responsiveness to inhaled glucocorticoids? (B) Hypoxemic respiratory failure (A) Bronchial challenge testing (C) Neuromuscularweakness (B) Diflusing capacity for carbon monoxide (D) Pulmonary embolism (C) Fractional exhaled nitric oxide (D) Pulse oximetry Item 96 An B4-year old man is evaluated 3 days after he was admit tr ted to the ICU with a right lower lobe inflltrate and presumed tr Item 94 A 44-year-old woman is evaluated 1 day after right mas- sepsis. On the day of admission, the patient vomited, aspi- rated, and developed respiratory distress. In the emergency tectomy for breast cancer. Desaturations throughout the department, temperature was 38.3'C (100.9'F) ; tachypnea, night necessitated oxygen initiation. Medications are an tachycardia, hlpoxemia, and hypotension were also present. oral opioid and subcutaneous enoxaparin. Chest radiograph on admission showed an inflltrate in the On physical examination, temperature is 37.8 "C right lower lobe. lntravenous fluids, supplemental oxygen by (100.0'F), blood pressure is 140/60 mm Hg, pulse rate is nasal cannula, and broad-spectrum antibiotics were given. 90/min, and respiration rate is 28lmin. Oxygen saturation Over the nexl24 hours, the patient improved rapidly. is 93'l" breathing oxygen, 6 L/min by nasal cannula. The On today's physical examination, temperature is 37.1 "C patient has shallow breathing with splinting. Lung examina- (98.8 'F), blood pressure is 138/80 mm Hg, pulse rate is tion reveals diminished breath sounds at the right lung base, 66lmin, and respiration rate is 16lmin. Oxygen saturation is dullness on percussion, egophony in the right lower lobe, 95'7, with the patient breathing ambient air. and rhonchi. The remainder of the examination is normal. The patient's leukocyte count is 6,000/pL (O x fOg/L) Chest radiograph shows plate like opacities in the with a normal differential. lung bases consistent with atelectasis. Sputum and blood cultures are negative.

Item 93 Po, B0 mm HC (10.6 kPa) Alveolar-arterialoxygengradient Normal A 24-year-old woman is evaluated for intermittent cough, Chest radiograph is normal. wheezing, and chest tightness of 1 month's duration. She There is a 22% decrement in forced vital capacity while reports worsening symptoms with exercise and with cat supine compared with the upright position. Maximal inspi- exposure. On physical examination, vital signs are normal. She has ratory pressure and maximal expiratory pressure are both less than 50% ofpredicted. end expiratory wheezing. Cardiac examination is normal. On spirometry, FEV, is 75% of predicted and improves signiflcantly following inhaled albuterol. Which of the following is the most likely cause of this patient's respiratory failure? Which of the following tests will help predict this patient's (A) Decreased ventilatory drive responsiveness to inhaled glucocorticoids? (B) Hypoxemic respiratory failure (A) Bronchial challenge testing (C) Neuromuscularweakness (B) Diflusing capacity for carbon monoxide (D) Pulmonary embolism (C) Fractional exhaled nitric oxide (D) Pulse oximetry Item 96 An B4-year old man is evaluated 3 days after he was admit tr ted to the ICU with a right lower lobe inflltrate and presumed tr Item 94 A 44-year-old woman is evaluated 1 day after right mas- sepsis. On the day of admission, the patient vomited, aspi- rated, and developed respiratory distress. In the emergency tectomy for breast cancer. Desaturations throughout the department, temperature was 38.3'C (100.9'F) ; tachypnea, night necessitated oxygen initiation. Medications are an tachycardia, hlpoxemia, and hypotension were also present. oral opioid and subcutaneous enoxaparin. Chest radiograph on admission showed an inflltrate in the On physical examination, temperature is 37.8 "C right lower lobe. lntravenous fluids, supplemental oxygen by (100.0'F), blood pressure is 140/60 mm Hg, pulse rate is nasal cannula, and broad-spectrum antibiotics were given. 90/min, and respiration rate is 28lmin. Oxygen saturation Over the nexl24 hours, the patient improved rapidly. is 93'l" breathing oxygen, 6 L/min by nasal cannula. The On today's physical examination, temperature is 37.1 "C patient has shallow breathing with splinting. Lung examina- (98.8 'F), blood pressure is 138/80 mm Hg, pulse rate is tion reveals diminished breath sounds at the right lung base, 66lmin, and respiration rate is 16lmin. Oxygen saturation is dullness on percussion, egophony in the right lower lobe, 95'7, with the patient breathing ambient air. and rhonchi. The remainder of the examination is normal. The patient's leukocyte count is 6,000/pL (O x fOg/L) Chest radiograph shows plate like opacities in the with a normal differential. lung bases consistent with atelectasis. Sputum and blood cultures are negative. Which of the following is the most appropriate Which of the following is the most appropriate antibiotic management? management? (A) Bronchoscopy (A) Continue antibiotics for 4 additional days (B) Inhaled albuterol (B) Continue antibiotics for 7 additional days (C) Inhaled N acetylcysteine (C) Continue antibiotics for 10 additional days (D) Pain management (D) Discontinueantibiotics

Which of the following is the most appropriate Which of the following is the most appropriate antibiotic management? management? (A) Bronchoscopy (A) Continue antibiotics for 4 additional days (B) Inhaled albuterol (B) Continue antibiotics for 7 additional days (C) Inhaled N acetylcysteine (C) Continue antibiotics for 10 additional days (D) Pain management (D) Discontinueantibiotics tr Item 95 A 33-year-old woman is evaluated in the emergency Item 97 A 62-year old man is evaluated for chronic cough pro- ductive ofthin clear sputum and dyspnea on exertion that department for respiratory failure. She has a 1-week his- tory of ascending lower-extremity weakness and pares- has worsened over the last 2 years. He has a 54 pack-year thesia. She has developed progressive dyspnea over the smoking history. Medical history is otherwise unremark- past 48 hours. able, and he takes no medications. 115

Self-Assessment Test vr .D On physical examination, vital signs are normal. The (C) Repeat chest CT in 6 months t^ patient coughs during the examination, and mild expir- (D) Surgical resection UI atory wheezing is heard over the posterior lung flelds. (D Ut Cardiac examination is normal. vt (D Chest radiograph shows hyperinflated lungs with a flattened diaphragm without inflltrates. Item 100 A 69-year-old man is evaluated in the hospital for short- tr { .D Spirometry shows an FEVr/FVC ratio of 0.65 and an ness of breath 24 hours after admission for left inferior la FEV, of 52% of predicted without a signiflcant bronchodi- pubic ramus fracture. Medical history is otherwise unre- lator response. markable, and he takes no medications. On physical examination, the patient is confused. Tem Which of the following is the most likely diagnosis? perature is 38.2'C (100.8'F), blood pressure is 104/68 mm (A) Asthma Hg, pulse rate is 110/min, and respiration rate is 26lmin. Oxygen saturation is 907, breathing oxygen, 3 L/min by (B) Bronchiectasis nasal cannula. There are crackles at both lung bases. Pete (C) COPD chiae are present over the neck and upper trunk. (D) Desquamative interstitial pneumonia Chest radiograph reveals patchy inflltrates at the bases.

vr .D On physical examination, vital signs are normal. The (C) Repeat chest CT in 6 months t^ patient coughs during the examination, and mild expir- (D) Surgical resection UI atory wheezing is heard over the posterior lung flelds. (D Ut Cardiac examination is normal. vt (D Chest radiograph shows hyperinflated lungs with a flattened diaphragm without inflltrates. Item 100 A 69-year-old man is evaluated in the hospital for short- tr { .D Spirometry shows an FEVr/FVC ratio of 0.65 and an ness of breath 24 hours after admission for left inferior la FEV, of 52% of predicted without a signiflcant bronchodi- pubic ramus fracture. Medical history is otherwise unre- lator response. markable, and he takes no medications. On physical examination, the patient is confused. Tem Which of the following is the most likely diagnosis? perature is 38.2'C (100.8'F), blood pressure is 104/68 mm (A) Asthma Hg, pulse rate is 110/min, and respiration rate is 26lmin. Oxygen saturation is 907, breathing oxygen, 3 L/min by (B) Bronchiectasis nasal cannula. There are crackles at both lung bases. Pete (C) COPD chiae are present over the neck and upper trunk. (D) Desquamative interstitial pneumonia Chest radiograph reveals patchy inflltrates at the bases. Which of the following is the most likely diagnosis? tr Item 98 A 72-year-old man is evaluated flor exertional dyspnea of (A) Air embolism (B) Fat embolism syndrome 1 year's duration and recent onset oforthopnea. He has dia- betes mellitus, hypertension, and coronary artery disease. (C) Hospital-acquired pneumonia Medications are atorvastatin, aspirin, lisinopril, metopro- (D) Pulmonary embolism lol, and metformin. On physical examination, blood pressure is 150/82 mm Hg; the remaining vital signs are normal. Jugular venous pressure is elevated. An S., is present. Pulmonary examination reveals occasional crackles. There is 2+ pitting edema to the knees. Item 101 A 42-year-old man with 6 months of progressive dyspnea tr \ is diagnosed with chronic thromboembolic pulmonary A chest radiograph shows an enlarged cardiac silhou- hypertension following right heart catheterization and ette and pulmonary vascular congestion. pulmonary artery angiography. Medical history is other- An echocardiogram reveals a left ventricular ejection wise unremarkable, and he takes no medications. fraction of20% and a right ventricular systolic pressure of Apixaban is initiated. 50 mm Hg. Which ofthe following isthe most appropriate management? Which of the following is the most likely cause of the patient's pulmonary hypertension? (A) Add riociguat (B) Balloon pulmonary angioplasty evaluation (A) Chronic thromboembolic pulmonary hypertension (C) Surgicalthromboendarterectomyevaluation (B) Idiopathicpulmonaryarterialhypertension (D) No additional treatment (C) Interstitial lung disease (D) Left ventricular failure Item 102 I

Which of the following is the most likely diagnosis? tr Item 98 A 72-year-old man is evaluated flor exertional dyspnea of (A) Air embolism (B) Fat embolism syndrome 1 year's duration and recent onset oforthopnea. He has dia- betes mellitus, hypertension, and coronary artery disease. (C) Hospital-acquired pneumonia Medications are atorvastatin, aspirin, lisinopril, metopro- (D) Pulmonary embolism lol, and metformin. On physical examination, blood pressure is 150/82 mm Hg; the remaining vital signs are normal. Jugular venous pressure is elevated. An S., is present. Pulmonary examination reveals occasional crackles. There is 2+ pitting edema to the knees. Item 101 A 42-year-old man with 6 months of progressive dyspnea tr \ is diagnosed with chronic thromboembolic pulmonary A chest radiograph shows an enlarged cardiac silhou- hypertension following right heart catheterization and ette and pulmonary vascular congestion. pulmonary artery angiography. Medical history is other- An echocardiogram reveals a left ventricular ejection wise unremarkable, and he takes no medications. fraction of20% and a right ventricular systolic pressure of Apixaban is initiated. 50 mm Hg. Which ofthe following isthe most appropriate management? Which of the following is the most likely cause of the patient's pulmonary hypertension? (A) Add riociguat (B) Balloon pulmonary angioplasty evaluation (A) Chronic thromboembolic pulmonary hypertension (C) Surgicalthromboendarterectomyevaluation (B) Idiopathicpulmonaryarterialhypertension (D) No additional treatment (C) Interstitial lung disease (D) Left ventricular failure Item 102 I A 32-year-old woman is evaluated for an asthma exacerba Item 99 tion. She previously had well controlled asthma. She has A 55-year old man presents for follow-up evaluation l week increased the use of her maintenance inhaler and is using '! after an emergency department visit for abdominal pain. A her rescue medication four times daily, but her symptoms CT scan of the abdomen showed a 7-mm lung nodule in the persist. She reports no fever, chills, chest pain, or puru- right lower lobe. No previous images of the chest are avail lent sputum. She has no history of intubation, emergency able. The patient's abdominal pain has since resolved. He is a department visits, or hospitalizations for asthma and has lifelong nonsmoker and has no occupational or recreational adhered to her medication regimen. She is a nonsmoker. exposure to carcinogens. Family history is unremarkable. Medications are inhaled budesonide and albuterol. On physical examination, vital signs and other exam- On physical examination, respiration rate is 25lmin; ination flndings are normal. the remainder of vital signs are normal. Oxygen saturation is A dedicated thin-section chest CT scan demonstrates a 96% with the patient breathing ambient air. The patient is not 7 mm noncalcifled nodule with smooth contours. The rest using accessory muscles of respiration and is able to speak in of the chest CT scan is unremarkable. full sentences. There is scattered expiratory wheezing.

A 32-year-old woman is evaluated for an asthma exacerba Item 99 tion. She previously had well controlled asthma. She has A 55-year old man presents for follow-up evaluation l week increased the use of her maintenance inhaler and is using '! after an emergency department visit for abdominal pain. A her rescue medication four times daily, but her symptoms CT scan of the abdomen showed a 7-mm lung nodule in the persist. She reports no fever, chills, chest pain, or puru- right lower lobe. No previous images of the chest are avail lent sputum. She has no history of intubation, emergency able. The patient's abdominal pain has since resolved. He is a department visits, or hospitalizations for asthma and has lifelong nonsmoker and has no occupational or recreational adhered to her medication regimen. She is a nonsmoker. exposure to carcinogens. Family history is unremarkable. Medications are inhaled budesonide and albuterol. On physical examination, vital signs and other exam- On physical examination, respiration rate is 25lmin; ination flndings are normal. the remainder of vital signs are normal. Oxygen saturation is A dedicated thin-section chest CT scan demonstrates a 96% with the patient breathing ambient air. The patient is not 7 mm noncalcifled nodule with smooth contours. The rest using accessory muscles of respiration and is able to speak in of the chest CT scan is unremarkable. full sentences. There is scattered expiratory wheezing. Which of the following is the most appropriate next step in Which of the following is the most appropriate treatment? management? (A) Doxycycline, S-day course (A) Bronchoscopy with biopsy (B) Intravenous methylprednisone, followed by a S-day (B) Fluorodeoxyglucose PET/CT prednisone course

Which of the following is the most appropriate next step in Which of the following is the most appropriate treatment? management? (A) Doxycycline, S-day course (A) Bronchoscopy with biopsy (B) Intravenous methylprednisone, followed by a S-day (B) Fluorodeoxyglucose PET/CT prednisone course 116

Self-Assessment Test tl (C) Prednisone, S-daycourse On physical examination, vital signs are normal. Lung o (D) Prednisone, 14-daycourse examination reveals bibasilar crackles. There is no acces- (u (E) Switch to budesonide-formoterol sory muscle use. Prior sputum cultures have grown Pseudomonas l,l ta aeruginosa and Haemophilus porainflue nzae. (l, ut tr Item 103 A 72-year-old woman is evaluated for exacerbation of Chest radiograph reveals chronic interstitial markings but no acute change. ut o, bronchiectasis symptoms over the past 3 days. Chronic t productive cough has worsened in frequency and severity, Which of the following is the most appropriate treatment? and her sputum has increased in amount, become thicker, (A) Azithromycin and changed in color from white to dark yellow. She has (B) Ciprofloxacin been using albuterol and hypertonic saline nebulization (C) Inhaled dornase alfa with a positive expiratory pressure device three times daily since her symptoms increased. (D) Prednisone 117

Answers and Critiques Item 1 tr Answer: A Educational Objective: Prevent delirium with early f,tY POIT{TS . Measures to decrease the risk of delirium include mobilization. early mobilization, preservation of nocturnal sleep, The most :rppropriate nlanagement is carly mobilization adequate pain management, orientation of the (Option A). Delirium is characterizecl lry an acute change patient, provision ofvisual and hearing aids, and in cognitive functioning occurring over hours to days. ruitl.r minimization of nonessential medications. fluctuations during the course of the day F.eatures t-rf delir r Except in treating alcohol withdrawal, pharmacologic ra (l, ium inclucle inattentiolr, disorganizecl thinking. executive strategies are ineffective in the prevention and treatment ET dysfunction, altered level of conscior-rsncss (lethargy or of delirium. hypervigilance), perceptual clisturbance's (hallucinatitins rJ or delusions), altered psychomotor activity (hyperactivityl Bibliography t, hypoactivity, or alternating periods ot' hyperactivitl,' ancl .! Blair CJ, Mehmood T, Rudnick M. et al. Nonphrrmlcologic and medication vt hypoactivity), sleep wakc disturbances, and labile moocl. It minimization strategies lbr the prevention and treatment ol lCU delir (l, ium: A nirrrative review. J lntensive Care Med. 2019;3,1:183 190. Il']MID: is extrernely common in patients in the ICU and is associ 296994671 doitt} .tt77 I 0885066618771528 rn ated with increased length ol lCU stay, nturbidity, morlality. = and cognitive impairment. Risk factors fbr delirium ir.rclude preexisting demer-rtil, l.rypertension. alcol.rolism, ancl high Item 2 Answer: C se\erity ol illness on ICU admissior.r. Patients shoulcl be Educational Obiective: Treat obstructive sleep apnea monitored rcgularly and assessed using scales such as the with an oral appliance. Confusion Assessment N4ethod-lCU (CAM ICU) or the lnten sive Care l)elirium Screening Checklist (ICI)SC). Me:rsures The most appropriate treatment alternative to continuous to decrease thc'risk of deliriurn inclucle early mobilization, positive airway pressure (CPAP) in this patient is an oral preservation of'nocturnal sleep, adequate p:rin managemenl. appliance (Option C). This patient has symptomatic obstruc orientation of the patient, provision of visual and hearing tive sleep apnea (OSA) of'moderate severity. OSA severity aids, ancl minimization ol nonessential medications. Fiarly improves with weight loss, so all patients with overweight mobilization, consisting of interruption of'sedation fbllowecl or obesity should be counseled accordingly. In minimally by physical and occupltional therapy in the earliest days of symptomatic patients with mild OSA, weight loss might critical illness, can be ellbctive fbr treating and preventing be pref'erred therapy. Additional measures that may help delirium. mild OSA include reducing alcohol intake before bedtime, Several pharmacologic strategies, including haloper avoiding sedating medications (benzodiazepines, opioids), idol (Option B), have been attemptecl to prevent delirir-rm and avoiding a supine posture if OSA is position dependent. in critically ill patients. None have proved eflective. Sev Although CPAP improves symptoms and is generally the pre eral of these medications (aripiprazole and haloperidol) ferred treatment fbr OSA, patient pret'erence or intolerance have been added to the American Geriatrics Society Beers to CPAP should prompt consideration ol other treatments. Criteria ftrr Potentially lnappropriate Meclication Use ir.r Oral appliances increase upper airway caliber primarily by Older Adults. '[hus, nrinimizing factors that are known to exerting traction to advance the mandible. Randomized con increirse the risk tbr clelirium remair.rs the main lbcus o1' trolled trials of these appliances have demonstrated good care oi critically ill patients. control of mild to moderate OSA and improvement in synrp In general, benzocliazepines such irs lorazeparr toms such as daytime sleepiness. (Option C) should not be used for treating clelirium in A hypoglossal nerve stimulator (Option A) is implanted the ICU unless needed in patients with alcohol with in the chest wall and synchronizes with the respiratory drawal or seizures. In the absence of these indications. cycle to contract the tongue muscles during inspiration. A ber-rzodiazepines such as klrazepam may increase the risk multicenter clinical trial demonstrated its elncacy in OSA, of delirium. including severe disease; however, there are criteria fbr Melakinin (Option D) is a popular nredication pre patient selection, and the procedure is not recommended scribed with an aim to maintain the sleep cycle, which for patients with a BMI greater than 32. This patient's BMI in tllrn nlay prevent delirium. The data or.r its eff'ect in of 34 would exclude him from candidacy. Although hypo pron.rotir.rg sleep or preventing deliriurn are inconsistent. glossal nerve stimulation is efficacious in select patients, it is and tl-rus it is not recommended as a routine deliriunr pre invasive and more costly than CPAP and oral appliances and ventioll strategy. is not the best initial option for this patient.

Answers and Critiques Item 1 tr Answer: A Educational Objective: Prevent delirium with early f,tY POIT{TS . Measures to decrease the risk of delirium include mobilization. early mobilization, preservation of nocturnal sleep, The most :rppropriate nlanagement is carly mobilization adequate pain management, orientation of the (Option A). Delirium is characterizecl lry an acute change patient, provision ofvisual and hearing aids, and in cognitive functioning occurring over hours to days. ruitl.r minimization of nonessential medications. fluctuations during the course of the day F.eatures t-rf delir r Except in treating alcohol withdrawal, pharmacologic ra (l, ium inclucle inattentiolr, disorganizecl thinking. executive strategies are ineffective in the prevention and treatment ET dysfunction, altered level of conscior-rsncss (lethargy or of delirium. hypervigilance), perceptual clisturbance's (hallucinatitins rJ or delusions), altered psychomotor activity (hyperactivityl Bibliography t, hypoactivity, or alternating periods ot' hyperactivitl,' ancl .! Blair CJ, Mehmood T, Rudnick M. et al. Nonphrrmlcologic and medication vt hypoactivity), sleep wakc disturbances, and labile moocl. It minimization strategies lbr the prevention and treatment ol lCU delir (l, ium: A nirrrative review. J lntensive Care Med. 2019;3,1:183 190. Il']MID: is extrernely common in patients in the ICU and is associ 296994671 doitt} .tt77 I 0885066618771528 rn ated with increased length ol lCU stay, nturbidity, morlality. = and cognitive impairment. Risk factors fbr delirium ir.rclude preexisting demer-rtil, l.rypertension. alcol.rolism, ancl high Item 2 Answer: C se\erity ol illness on ICU admissior.r. Patients shoulcl be Educational Obiective: Treat obstructive sleep apnea monitored rcgularly and assessed using scales such as the with an oral appliance. Confusion Assessment N4ethod-lCU (CAM ICU) or the lnten sive Care l)elirium Screening Checklist (ICI)SC). Me:rsures The most appropriate treatment alternative to continuous to decrease thc'risk of deliriurn inclucle early mobilization, positive airway pressure (CPAP) in this patient is an oral preservation of'nocturnal sleep, adequate p:rin managemenl. appliance (Option C). This patient has symptomatic obstruc orientation of the patient, provision of visual and hearing tive sleep apnea (OSA) of'moderate severity. OSA severity aids, ancl minimization ol nonessential medications. Fiarly improves with weight loss, so all patients with overweight mobilization, consisting of interruption of'sedation fbllowecl or obesity should be counseled accordingly. In minimally by physical and occupltional therapy in the earliest days of symptomatic patients with mild OSA, weight loss might critical illness, can be ellbctive fbr treating and preventing be pref'erred therapy. Additional measures that may help delirium. mild OSA include reducing alcohol intake before bedtime, Several pharmacologic strategies, including haloper avoiding sedating medications (benzodiazepines, opioids), idol (Option B), have been attemptecl to prevent delirir-rm and avoiding a supine posture if OSA is position dependent. in critically ill patients. None have proved eflective. Sev Although CPAP improves symptoms and is generally the pre eral of these medications (aripiprazole and haloperidol) ferred treatment fbr OSA, patient pret'erence or intolerance have been added to the American Geriatrics Society Beers to CPAP should prompt consideration ol other treatments. Criteria ftrr Potentially lnappropriate Meclication Use ir.r Oral appliances increase upper airway caliber primarily by Older Adults. '[hus, nrinimizing factors that are known to exerting traction to advance the mandible. Randomized con increirse the risk tbr clelirium remair.rs the main lbcus o1' trolled trials of these appliances have demonstrated good care oi critically ill patients. control of mild to moderate OSA and improvement in synrp In general, benzocliazepines such irs lorazeparr toms such as daytime sleepiness. (Option C) should not be used for treating clelirium in A hypoglossal nerve stimulator (Option A) is implanted the ICU unless needed in patients with alcohol with in the chest wall and synchronizes with the respiratory drawal or seizures. In the absence of these indications. cycle to contract the tongue muscles during inspiration. A ber-rzodiazepines such as klrazepam may increase the risk multicenter clinical trial demonstrated its elncacy in OSA, of delirium. including severe disease; however, there are criteria fbr Melakinin (Option D) is a popular nredication pre patient selection, and the procedure is not recommended scribed with an aim to maintain the sleep cycle, which for patients with a BMI greater than 32. This patient's BMI in tllrn nlay prevent delirium. The data or.r its eff'ect in of 34 would exclude him from candidacy. Although hypo pron.rotir.rg sleep or preventing deliriurn are inconsistent. glossal nerve stimulation is efficacious in select patients, it is and tl-rus it is not recommended as a routine deliriunr pre invasive and more costly than CPAP and oral appliances and ventioll strategy. is not the best initial option for this patient. 119

Answers and Critiques Case series have demonstrated signiflcant improve- inserti<,rn of tube thoracostomv with either mechanical or ments in apnea-hypopnea index following maxillomandib talc plcurodesis. ular advancement surgery (Option B), but in most patients Recurrence prevention is recommcnded after the sec- this procedure would not be considered a primarytreatment. ond episode of pneun.rothorax on the ipsilaterai side in PSP Evidence supporting upper airway surgical procedures to and alter the first occrlrrence in SSP dttc to the high recur treat OSA is limited. Patient selection is not standardized. rence rate (>509l). Depending on size ancl syn.rptoms, neeclle and neurocognitive outcomes are unknown or inconsistent. aspiration (Option B). observation (Option C), and oxygen Literature on uvulopalatopharyngoplasty (Option D), a and obsenation (Option D) rnould all be appropriate options soft palatal procedure, shows only limited improvements in in a patient nith a first cpisode of PSP who did not have a apnea-hypopnea index. Trial data are beginning to emerge, high risl< occupation. lkrwever, because this patient has a but at this time, the procedure should generally not be rec- high risk occupation, dcfinitive therapy shouid be pn.rvided ommended for primary treatment of OSA. fbllowing a flrst episode of PSP. D XEY POITIS f,EY POITTS Ut o Obstructive sleep apnea (OSA) severity improves with . Recurrence prevention is recommended after the sec- = .D weight loss; in minimally symptomatic patients with ond episode of pneumothorax on the ipsilateral side UI o, mild OSA, weight loss might be the preferred therapy. in primary spontaneous pneumothorax and after the tL o Although continuous positive airway pressure (CPAP) first occurrence in secondary spontaneous pneumo- fr thorax. is generally the preferred treatment for obstructive tt sleep apnea, patient preference or intolerance to CPAP . Recurrence prevention is indicated following a first .D should prompt consideration of other treatments such episode of pneumothorax in spontaneous primary UI as an oral appliance. pneumothorax in a patient with a high risk occupation.

Case series have demonstrated signiflcant improve- inserti<,rn of tube thoracostomv with either mechanical or ments in apnea-hypopnea index following maxillomandib talc plcurodesis. ular advancement surgery (Option B), but in most patients Recurrence prevention is recommcnded after the sec- this procedure would not be considered a primarytreatment. ond episode of pneun.rothorax on the ipsilaterai side in PSP Evidence supporting upper airway surgical procedures to and alter the first occrlrrence in SSP dttc to the high recur treat OSA is limited. Patient selection is not standardized. rence rate (>509l). Depending on size ancl syn.rptoms, neeclle and neurocognitive outcomes are unknown or inconsistent. aspiration (Option B). observation (Option C), and oxygen Literature on uvulopalatopharyngoplasty (Option D), a and obsenation (Option D) rnould all be appropriate options soft palatal procedure, shows only limited improvements in in a patient nith a first cpisode of PSP who did not have a apnea-hypopnea index. Trial data are beginning to emerge, high risl< occupation. lkrwever, because this patient has a but at this time, the procedure should generally not be rec- high risk occupation, dcfinitive therapy shouid be pn.rvided ommended for primary treatment of OSA. fbllowing a flrst episode of PSP. D XEY POITIS f,EY POITTS Ut o Obstructive sleep apnea (OSA) severity improves with . Recurrence prevention is recommended after the sec- = .D weight loss; in minimally symptomatic patients with ond episode of pneumothorax on the ipsilateral side UI o, mild OSA, weight loss might be the preferred therapy. in primary spontaneous pneumothorax and after the tL o Although continuous positive airway pressure (CPAP) first occurrence in secondary spontaneous pneumo- fr thorax. is generally the preferred treatment for obstructive tt sleep apnea, patient preference or intolerance to CPAP . Recurrence prevention is indicated following a first .D should prompt consideration of other treatments such episode of pneumothorax in spontaneous primary UI as an oral appliance. pneumothorax in a patient with a high risk occupation. Bibliography Bibliography Patel SR. Obstructive sleep apnea. Ann lntern Med. 2019t171:lTC8t ITC96 Tschopp JM, Bintcliffe O, Astoul P, et al. ERS task force statement: diagnosis IPMID: :]17910571 doi;10.7326lAITC201912030 and trertment ofprimary spontaneous pneumothorax. Eur Respir J. 2015; 46:321 :15. IPMID: 26lll]6751 doi:10.1183/O9031936.00219214

Bibliography Bibliography Patel SR. Obstructive sleep apnea. Ann lntern Med. 2019t171:lTC8t ITC96 Tschopp JM, Bintcliffe O, Astoul P, et al. ERS task force statement: diagnosis IPMID: :]17910571 doi;10.7326lAITC201912030 and trertment ofprimary spontaneous pneumothorax. Eur Respir J. 2015; 46:321 :15. IPMID: 26lll]6751 doi:10.1183/O9031936.00219214 tr Item 3 Answer: A Educational Objective: Manage primary spontaneous Item 4 Answer: C Educational Objective: Treat nonexertional heat stroke. tr pneumothorax in a patient with a high risk occupation. The most appropriate treatment is evaporative cooling with The most appropriate additional nranagement is cathe water mist, fans. and ice packs (Option C). Heat stroke is a ter thoracostomy fbllonecl by pleurodesis (Option A). 'lhe failure of the body's thermal regulatory system caused by patient has a spontaneous pneumothrlrax. Because he has dysf'unction. as in elderly patients taking anticholinergic no known underlying lung disease. this would be classified meclicationsi volume depletion (diuretics, insensible water as a primary spontarleous pneumothorax (l'SP). A secondary loss); or overwhelming of the system, as ir.r athletes or ntil spontirneous pneumothorirr (SSP) occurs in someone with itary rccruits r.tho train strenuously in hot, humid weather. knou,n r-rnderlying lung disease. such as COPD. the risk <lf' They rnr,ry also erperience hypotension, ndusea. and muscle recurrencc after an initial occurrence of'a PSP is 17'l;, to .54'l{, weakness. This patient has nonexertional heat stloke. lt is in the first year. Cigarettc srnoking is the most importanl generally defined by a core body ternperature abovc 40 'C risk factor fbr PSP.'lhe relative risk of a first event o{ PSP is (tOa.o 'F) along with encephalopathy. Additional compli- 22 fbld higher in mcn irnd 9 times lrighcr in u,omen who cations of heat stroke can include kidney and liver injury, smoke tobacco than in those lvho do not srnoke.-lhe patient dissemir.rated intravascular coagulation. and rhabcllnryoly- shoulcl be counseled to stop srnoking and oflered pharrna sis. The elderly are particularly vulnerable. r,r,ith added risk cologic assistance. Other risk factors include tall height and from conrorbidities ancl medications. If untreated, rnortality a low bocly mass index. 'l'reatment fbr I lirst episode of PSP in heat stroke can reach 60'/.. Treatmer-rt of nonexertional is observation, oxygen and observation. ncedle aspirrrtion, heat stroke includes evaporative cooling (with waler rnist or placcment of a srnall bore thoracostomt', depending or.r ancl fans) with or rvithout ice packs to lovuer the core tem- sylnptomatologi Definitivc treatmellt rt,ith pleuroclesis to peraturc to a safe temperature. usually 38.5 'C (101.:l "F'). prevent recurrence is usr-rally not provided until a second Evaporative cooling is eflective, noninvasive. and easily per ipsilateral event has occurred. unless thc patient's occupa fbrn.recl, and does not interf'ere with other aspects of patient tion is considered high risk. 'Ihis patient is a profbssional care. It is associated with decreased morbidity and mortality scuba diver and is at high risk ofdeath ifhe has a recurrence when used to treat elderly patients with classic heat stroke. while diving. Flying at high altitude is also considered a Centrally acting antipyretics such as acetaminophen high risk occupation. (iiven the patient's occupation, rr more (Option A) are not ef I'ective fbr heat stroke because the underly definitive rnanagement plan should be pursued tblkrwing ing mechanism does not involve a change in the hypothalamic

tr Item 3 Answer: A Educational Objective: Manage primary spontaneous Item 4 Answer: C Educational Objective: Treat nonexertional heat stroke. tr pneumothorax in a patient with a high risk occupation. The most appropriate treatment is evaporative cooling with The most appropriate additional nranagement is cathe water mist, fans. and ice packs (Option C). Heat stroke is a ter thoracostomy fbllonecl by pleurodesis (Option A). 'lhe failure of the body's thermal regulatory system caused by patient has a spontaneous pneumothrlrax. Because he has dysf'unction. as in elderly patients taking anticholinergic no known underlying lung disease. this would be classified meclicationsi volume depletion (diuretics, insensible water as a primary spontarleous pneumothorax (l'SP). A secondary loss); or overwhelming of the system, as ir.r athletes or ntil spontirneous pneumothorirr (SSP) occurs in someone with itary rccruits r.tho train strenuously in hot, humid weather. knou,n r-rnderlying lung disease. such as COPD. the risk <lf' They rnr,ry also erperience hypotension, ndusea. and muscle recurrencc after an initial occurrence of'a PSP is 17'l;, to .54'l{, weakness. This patient has nonexertional heat stloke. lt is in the first year. Cigarettc srnoking is the most importanl generally defined by a core body ternperature abovc 40 'C risk factor fbr PSP.'lhe relative risk of a first event o{ PSP is (tOa.o 'F) along with encephalopathy. Additional compli- 22 fbld higher in mcn irnd 9 times lrighcr in u,omen who cations of heat stroke can include kidney and liver injury, smoke tobacco than in those lvho do not srnoke.-lhe patient dissemir.rated intravascular coagulation. and rhabcllnryoly- shoulcl be counseled to stop srnoking and oflered pharrna sis. The elderly are particularly vulnerable. r,r,ith added risk cologic assistance. Other risk factors include tall height and from conrorbidities ancl medications. If untreated, rnortality a low bocly mass index. 'l'reatment fbr I lirst episode of PSP in heat stroke can reach 60'/.. Treatmer-rt of nonexertional is observation, oxygen and observation. ncedle aspirrrtion, heat stroke includes evaporative cooling (with waler rnist or placcment of a srnall bore thoracostomt', depending or.r ancl fans) with or rvithout ice packs to lovuer the core tem- sylnptomatologi Definitivc treatmellt rt,ith pleuroclesis to peraturc to a safe temperature. usually 38.5 'C (101.:l "F'). prevent recurrence is usr-rally not provided until a second Evaporative cooling is eflective, noninvasive. and easily per ipsilateral event has occurred. unless thc patient's occupa fbrn.recl, and does not interf'ere with other aspects of patient tion is considered high risk. 'Ihis patient is a profbssional care. It is associated with decreased morbidity and mortality scuba diver and is at high risk ofdeath ifhe has a recurrence when used to treat elderly patients with classic heat stroke. while diving. Flying at high altitude is also considered a Centrally acting antipyretics such as acetaminophen high risk occupation. (iiven the patient's occupation, rr more (Option A) are not ef I'ective fbr heat stroke because the underly definitive rnanagement plan should be pursued tblkrwing ing mechanism does not involve a change in the hypothalamic 120

Answers and Critiques tr CONT set point. Furthermore, acetamir.rophen may exacerbate compli cations such as hepatic injury and should be avoided. Malignant hlperthermia is a rare cause of'severe hyperther Item 5 Answer: B Educational Objective: Diagnose combined pulmonary tr fibrosis and emphysema. mia in response to inhaled anesthctic agents (e.g., halothane and isoflurane) or depolarizing paratytic agents (e.g., succinylcho the most likely diagnosis is combined pulmonary fibrosis and line) (Option B). When a patient with inherited susceptibility is emphysema (CPFE) (Option B), a unique pathophysiologic exposed to one of these agents, he or she may develop muscle entib/ distinct from either idiopathic pulmonary fibrosis (lPF) rigidity, rhabdomyolysis, cardiac arrhythmias, and core body or emphysema. In patients with CPF'E, the competing eflbcts temperatue elevation to 45.0'C (113.0 'F) or more. Mortality can of emphysema and fibrosis result in higher lung volumes than reach 10'X,. Treatment consists of discor-rtinuing the triggering are fbund in patients with pulmonary fibrosis alone. Similarllt agent, active cooling, and administration of the muscle relaxant the FEV,i FVC ratio in patients with CPFE may be preserved. dantrolene every 5 to 10 minutcs until muscle rigidi$ and hyper However, there appears to be an additive deleterious effect thermia resolve. Dantrolene is inellbctive in patients with severe on gas exchange properties of the lungs, resulting in a severe r^ reduction in the Drco. High resolution Cl (HRCT) is the pre- o temperature elevation not caused by malignant hyperthermia. ET lmmersion in ice water (Option D) may be necessary fbrred diagnostic modality to demonstrate upper lobe emphy in young persons with exertional heal stroke when they sema (blue arrows, left panel bekrw) and lower-lobe fibrosis (J remain severely symptomatic despite evaporative cooling, (red arrows, right panel below), as shown below. The likeli hood of the development of pulmonary hypertension in CPFFI =t but it is not flrst-line therapy because it may be complicated IE by hypothermia. In older persons with nonexertional hyper is much higher than in either COPD or IPE The presence of vt (u thermia. ice water immersion is associated r.tith increased pulm<,rnary hypertension in CPFE portends a poor prognosis. Acute interstitial pneuraonia (AIP) (Option A) is a ra1.l ut = rnortality and should not be used. idly progressing illness resulting in acute respiratory failure over TEY POIilII days to weeks. This process is clinicnlly, radiographically. and . Treatment of nonexertional heat stroke includes evap- pathologically indistinguishable fiom acute respiratory distress orative cooling (with water mist and fans) with or syndnlme. The patient's radiograph showing upper lobe emphy without ice packs to lower the core temperature to a sematous changes and lower lobe reticular and flbrotic changes safe temperature, usually 38.5'C (101.3'F). is not consistent with the airspace opacities fbund in AIP

tr CONT set point. Furthermore, acetamir.rophen may exacerbate compli cations such as hepatic injury and should be avoided. Malignant hlperthermia is a rare cause of'severe hyperther Item 5 Answer: B Educational Objective: Diagnose combined pulmonary tr fibrosis and emphysema. mia in response to inhaled anesthctic agents (e.g., halothane and isoflurane) or depolarizing paratytic agents (e.g., succinylcho the most likely diagnosis is combined pulmonary fibrosis and line) (Option B). When a patient with inherited susceptibility is emphysema (CPFE) (Option B), a unique pathophysiologic exposed to one of these agents, he or she may develop muscle entib/ distinct from either idiopathic pulmonary fibrosis (lPF) rigidity, rhabdomyolysis, cardiac arrhythmias, and core body or emphysema. In patients with CPF'E, the competing eflbcts temperatue elevation to 45.0'C (113.0 'F) or more. Mortality can of emphysema and fibrosis result in higher lung volumes than reach 10'X,. Treatment consists of discor-rtinuing the triggering are fbund in patients with pulmonary fibrosis alone. Similarllt agent, active cooling, and administration of the muscle relaxant the FEV,i FVC ratio in patients with CPFE may be preserved. dantrolene every 5 to 10 minutcs until muscle rigidi$ and hyper However, there appears to be an additive deleterious effect thermia resolve. Dantrolene is inellbctive in patients with severe on gas exchange properties of the lungs, resulting in a severe r^ reduction in the Drco. High resolution Cl (HRCT) is the pre- o temperature elevation not caused by malignant hyperthermia. ET lmmersion in ice water (Option D) may be necessary fbrred diagnostic modality to demonstrate upper lobe emphy in young persons with exertional heal stroke when they sema (blue arrows, left panel bekrw) and lower-lobe fibrosis (J remain severely symptomatic despite evaporative cooling, (red arrows, right panel below), as shown below. The likeli hood of the development of pulmonary hypertension in CPFFI =t but it is not flrst-line therapy because it may be complicated IE by hypothermia. In older persons with nonexertional hyper is much higher than in either COPD or IPE The presence of vt (u thermia. ice water immersion is associated r.tith increased pulm<,rnary hypertension in CPFE portends a poor prognosis. Acute interstitial pneuraonia (AIP) (Option A) is a ra1.l ut = rnortality and should not be used. idly progressing illness resulting in acute respiratory failure over TEY POIilII days to weeks. This process is clinicnlly, radiographically. and . Treatment of nonexertional heat stroke includes evap- pathologically indistinguishable fiom acute respiratory distress orative cooling (with water mist and fans) with or syndnlme. The patient's radiograph showing upper lobe emphy without ice packs to lower the core temperature to a sematous changes and lower lobe reticular and flbrotic changes safe temperature, usually 38.5'C (101.3'F). is not consistent with the airspace opacities fbund in AIP r In older persons with nonexertional hyperthermia, Desquamative interstitial pneumonia (Option C), a rel atively severe form of smoking related difluse parenchyrnal ice water immersion is associated with increased lung disease. may also present with progressire dyspnea and mortality and should not be used. cougl-r. Horverer, CT scans ol a patient with desquamative interstitial pneumonia would reveal diffuse ground-glass Bibliography opacification with lower lobe predominance, which is not Epstein Y Yanovich R. Heatstroke. N Engl J Med. 2019;380:2449-2459. present in this patient's imaging studies. IPMI D: 312164001 doi:10.1056/NEJMra1810762

r In older persons with nonexertional hyperthermia, Desquamative interstitial pneumonia (Option C), a rel atively severe form of smoking related difluse parenchyrnal ice water immersion is associated with increased lung disease. may also present with progressire dyspnea and mortality and should not be used. cougl-r. Horverer, CT scans ol a patient with desquamative interstitial pneumonia would reveal diffuse ground-glass Bibliography opacification with lower lobe predominance, which is not Epstein Y Yanovich R. Heatstroke. N Engl J Med. 2019;380:2449-2459. present in this patient's imaging studies. IPMI D: 312164001 doi:10.1056/NEJMra1810762 I ; : . : : ITEM 5 121

Answers and Critiques m lhe clinical presentation of lPF (Option D) can rnimic Perlorming methacholine challenge testing is not appropriate lll Cppg. llolr'o'er. pulmonarl' tunction tests nranif'est a pure because the patient's diagnosis of asthma has already been cONT restrictive pattern. A conficlent cliugr.rosis cirn be made based established with spirometry. on the presence ofa usual interstitial pneunlrlnia pattern on Montelukast (Option C) is an oral leukotriene receptor ! HRCT ol the chest in the right clinical setting. ln this patient. antagonist that has a modest bronchodilation effect and can the presence olupper lobe emphysema, in addition to lower also treat upper airway conditions such as allergic rhinitis. tobe fibrolic changes. con[irnts CPFB rather than IPli as the Patients with aspirin exacerbated respiratory disease often diagnosis. respond well to montelukast. Adding montelukast is not appropriate because the use of a daily medication is not rec I(EY POTIII ommended for intermittent asthma symptoms. o Combined pulmonary fibrosis and emphysema Not changing this patient's management (Option D) is (CPFE) is a distinct clinical entity in which fibrotic not appropriate because the use of short-acting Br-agonists lung disease (lower lobe), similar to idiopathic pulmo- without an inhaled glucocorticoid does not reduce exacer t nary fibrosis, coexists with emphysematous changes bation risk. (upper lobe) in the same patient. = .D TEY POIilIS 6 !, Bibliography . Guidelines recommend that patients with mild per IL Amariei DE. t)odia N, Deepak J, et al. Combined pulmonary librosis and sistent asthma use inhaled glucocorticoids whenever rr emphyscnu: pulmonary function testing and a pathophysiolory per an inhaled short-acting pr-agonist is used to reduce spective. Medicina (Kaunas). 2019;55. IPMID: 315099,12] doi:10.3390/ the risk of serious exacerbations and to control It medicina55090580 symptoms. .D UI . Clinicians should review correct inhaler use with Item 6 Answer: A patients who have airways disease at each visit.

m lhe clinical presentation of lPF (Option D) can rnimic Perlorming methacholine challenge testing is not appropriate lll Cppg. llolr'o'er. pulmonarl' tunction tests nranif'est a pure because the patient's diagnosis of asthma has already been cONT restrictive pattern. A conficlent cliugr.rosis cirn be made based established with spirometry. on the presence ofa usual interstitial pneunlrlnia pattern on Montelukast (Option C) is an oral leukotriene receptor ! HRCT ol the chest in the right clinical setting. ln this patient. antagonist that has a modest bronchodilation effect and can the presence olupper lobe emphysema, in addition to lower also treat upper airway conditions such as allergic rhinitis. tobe fibrolic changes. con[irnts CPFB rather than IPli as the Patients with aspirin exacerbated respiratory disease often diagnosis. respond well to montelukast. Adding montelukast is not appropriate because the use of a daily medication is not rec I(EY POTIII ommended for intermittent asthma symptoms. o Combined pulmonary fibrosis and emphysema Not changing this patient's management (Option D) is (CPFE) is a distinct clinical entity in which fibrotic not appropriate because the use of short-acting Br-agonists lung disease (lower lobe), similar to idiopathic pulmo- without an inhaled glucocorticoid does not reduce exacer t nary fibrosis, coexists with emphysematous changes bation risk. (upper lobe) in the same patient. = .D TEY POIilIS 6 !, Bibliography . Guidelines recommend that patients with mild per IL Amariei DE. t)odia N, Deepak J, et al. Combined pulmonary librosis and sistent asthma use inhaled glucocorticoids whenever rr emphyscnu: pulmonary function testing and a pathophysiolory per an inhaled short-acting pr-agonist is used to reduce spective. Medicina (Kaunas). 2019;55. IPMID: 315099,12] doi:10.3390/ the risk of serious exacerbations and to control It medicina55090580 symptoms. .D UI . Clinicians should review correct inhaler use with Item 6 Answer: A patients who have airways disease at each visit. Educational Objective: Treat mild persistent asthma with combination airway dilator and inhaled glucocorticoid. Bibliography Global Initiative for Asthma. Clobal Strate$/ Ibr Asthma Management and The most appropriate management for this patient is to add Prevention. 202i. Available from: ginasthma.org'wp contentiuploadst 2021,'0.1'GINA 2021 Main Report FIrr'AL 21 0.1 28 WMS.pdf. Accessed beclomethasone dipropionate with albuterol (Option A) May 5, 2021. during asthma symptoms. The patient has persistent asthma defined by use of her short acting Br-agonist (albuterol) more than two times weekly but not more than once per Item 7 Answer: E day. She has no comorbidities or risk factors for severe exac Educational Objective: Evaluate a small pulmonary erbation. Based on studies demonstrating that as needed nodule in a patient at low risk for malignancy. use of inhaled glucocorticoids in combination with airway dilators is noninferior to daily use of glucocorticoids and The most appropriate next step in management is no fur superior to short acting B, agonists alone, the 2020 Global ther follo'*,up (Option E). Pulmonary nodules appear on Initiative fbr Asthma guidelines recommend that patients radiography as small radiographic opacities (<3 cm in size) with mild persistent asthma use an inhaled glucocorticoid surrounded by normal lung parenchyma. These nodules whenever they use an inhaled short acting p, agonist to are asymptomatic and are found either incidentally or on reduce the risk of serious exacerbations and to control screening. 1n contrast, a focal pulmonary opacity larger than symptoms. An alternative is the inhaler combination of low 3 cm is considered a lung mass and is presumed malignant dose glucocorticoid formoterol taken as needed for symp until proved otherwise. This patient presents for evaluation tom relief. The National Asthma Education and Prevention of an incidentally fbund solid solitary pulmonary nodule. Program also recommends an inhaled glucocorticoid, either The first step in evaluation of a solitary pulmonary nodule is as a daily low dose inhaled glucocorticoid plus as needed to determine likelihood of malignancy according to clinical short acting p, agonist or as needed concomitant inhaled and radiographic features. The risk can be considered low glucocorticoid and short acting Br-agonist. In addition to intermediate, or high. This risk can be determined clinically assessing symptom control, modiflable risk f'actors, and or with quantitative prediction models such as the Brock I comorbidities, clinicians should review correct inhaler use University Lung Cancer Risk Calculators (brocku.ca/lung with patients at each visit. cancer-screening and-risk prediction/risk calculators/). Bronchial challenge testing with methacholine (Option B) Factors that help predict malignancy include smoking his is used to identiff bronchial hyperresponsiveness, a diagnos tory age, sex (female sex is associated with greater risk than tic feature of asthma. This is particularly helpful in patients male), family history of lung cancer, emphysema, asbestos whose symptoms are suggestive of asthma but fbr whom exposure, size ofthe nodule, location (upper lobe is associ other pulmonary function test results are normal. A neg ated with greater risk than is lower lobe), and nodule type. It ative response to bronchial challenge can exclude asthma; is also important to review older scans to determine whether however, a positive test can be caused by other conditions. the nodule has grown over time. In patients who have a

Educational Objective: Treat mild persistent asthma with combination airway dilator and inhaled glucocorticoid. Bibliography Global Initiative for Asthma. Clobal Strate$/ Ibr Asthma Management and The most appropriate management for this patient is to add Prevention. 202i. Available from: ginasthma.org'wp contentiuploadst 2021,'0.1'GINA 2021 Main Report FIrr'AL 21 0.1 28 WMS.pdf. Accessed beclomethasone dipropionate with albuterol (Option A) May 5, 2021. during asthma symptoms. The patient has persistent asthma defined by use of her short acting Br-agonist (albuterol) more than two times weekly but not more than once per Item 7 Answer: E day. She has no comorbidities or risk factors for severe exac Educational Objective: Evaluate a small pulmonary erbation. Based on studies demonstrating that as needed nodule in a patient at low risk for malignancy. use of inhaled glucocorticoids in combination with airway dilators is noninferior to daily use of glucocorticoids and The most appropriate next step in management is no fur superior to short acting B, agonists alone, the 2020 Global ther follo'*,up (Option E). Pulmonary nodules appear on Initiative fbr Asthma guidelines recommend that patients radiography as small radiographic opacities (<3 cm in size) with mild persistent asthma use an inhaled glucocorticoid surrounded by normal lung parenchyma. These nodules whenever they use an inhaled short acting p, agonist to are asymptomatic and are found either incidentally or on reduce the risk of serious exacerbations and to control screening. 1n contrast, a focal pulmonary opacity larger than symptoms. An alternative is the inhaler combination of low 3 cm is considered a lung mass and is presumed malignant dose glucocorticoid formoterol taken as needed for symp until proved otherwise. This patient presents for evaluation tom relief. The National Asthma Education and Prevention of an incidentally fbund solid solitary pulmonary nodule. Program also recommends an inhaled glucocorticoid, either The first step in evaluation of a solitary pulmonary nodule is as a daily low dose inhaled glucocorticoid plus as needed to determine likelihood of malignancy according to clinical short acting p, agonist or as needed concomitant inhaled and radiographic features. The risk can be considered low glucocorticoid and short acting Br-agonist. In addition to intermediate, or high. This risk can be determined clinically assessing symptom control, modiflable risk f'actors, and or with quantitative prediction models such as the Brock I comorbidities, clinicians should review correct inhaler use University Lung Cancer Risk Calculators (brocku.ca/lung with patients at each visit. cancer-screening and-risk prediction/risk calculators/). Bronchial challenge testing with methacholine (Option B) Factors that help predict malignancy include smoking his is used to identiff bronchial hyperresponsiveness, a diagnos tory age, sex (female sex is associated with greater risk than tic feature of asthma. This is particularly helpful in patients male), family history of lung cancer, emphysema, asbestos whose symptoms are suggestive of asthma but fbr whom exposure, size ofthe nodule, location (upper lobe is associ other pulmonary function test results are normal. A neg ated with greater risk than is lower lobe), and nodule type. It ative response to bronchial challenge can exclude asthma; is also important to review older scans to determine whether however, a positive test can be caused by other conditions. the nodule has grown over time. In patients who have a 122

Answers and 9,+igl9: low risk for malignancy, like this patient, a nodule (solid could be considered if the patient's symptoms are poorly con or subsolid) that is smaller than 6 mm requires no further trolled with LABA or LAMA monotherapy, but that approach follow up. has not yet been tried in this patient. Biopsy can be considered for an intermediate-risk nod- Evidence based guidelines do not endorse chronic ule. A biopsy is not indicated in this patient who is at Iow oral glucocorticoid therapy with agents such as prednisone risk lbr malignancy. tf a biopsy is indicated, bronchoscopy (Option C) because clinical trials have not shown improved (Option A) is typically used fbr lesions that are larger and outcomes with oral glucocorticoid therapy. In addition, there more central; CT guided needle biopsy (Option C) is used for is ample evidence that chronic oral glucocorticoid ther- smaller and more peripheral lesions. apy has potential for harm, including but not limited to In patients who are at high risk, optional follow up CT hypertension, hyperglycemia, osteoporosis, and susceptibil (Option B) could be performed at 12 months; however, even ity to infection. Oral glucocorticoids are recommended for in this group, the risk for malignancy in a nodule smaller short duration treatment of acute exacerbations of COPD. than 6 mm is less than 17,. Roflumilast (Option D), a selective phosphodiesterase 4 vt o Fluorodeoxyglucose PET (Option D) would not be help inhibitor, can reduce symptoms and exacerbations in ET ful because it does not accurately characterize lesions that patients with COPD who have chronic bronchitis or frequent are less than 8 mm. exacerbations; thus, it is not the initial therapy ofchoice in L' XEY POI ]ITS this patient who lacks the sputum production of chronic tt bronchitis or history of frequent exacerbations. r! o The first step in evaluation of a solitary pulmonary tt nodule is to determine the likelihood of malignancy KEY POIl{TS o according to clinical and radiographic features. . Regardless ofCOPD severity, Br-agonists and IA = . In patients who have a low risk for malignancy, a anticholinergic/antimuscarinic agents are the main- nodule that is smaller than 6 mm in size requires no stay of therapy.

low risk for malignancy, like this patient, a nodule (solid could be considered if the patient's symptoms are poorly con or subsolid) that is smaller than 6 mm requires no further trolled with LABA or LAMA monotherapy, but that approach follow up. has not yet been tried in this patient. Biopsy can be considered for an intermediate-risk nod- Evidence based guidelines do not endorse chronic ule. A biopsy is not indicated in this patient who is at Iow oral glucocorticoid therapy with agents such as prednisone risk lbr malignancy. tf a biopsy is indicated, bronchoscopy (Option C) because clinical trials have not shown improved (Option A) is typically used fbr lesions that are larger and outcomes with oral glucocorticoid therapy. In addition, there more central; CT guided needle biopsy (Option C) is used for is ample evidence that chronic oral glucocorticoid ther- smaller and more peripheral lesions. apy has potential for harm, including but not limited to In patients who are at high risk, optional follow up CT hypertension, hyperglycemia, osteoporosis, and susceptibil (Option B) could be performed at 12 months; however, even ity to infection. Oral glucocorticoids are recommended for in this group, the risk for malignancy in a nodule smaller short duration treatment of acute exacerbations of COPD. than 6 mm is less than 17,. Roflumilast (Option D), a selective phosphodiesterase 4 vt o Fluorodeoxyglucose PET (Option D) would not be help inhibitor, can reduce symptoms and exacerbations in ET ful because it does not accurately characterize lesions that patients with COPD who have chronic bronchitis or frequent are less than 8 mm. exacerbations; thus, it is not the initial therapy ofchoice in L' XEY POI ]ITS this patient who lacks the sputum production of chronic tt bronchitis or history of frequent exacerbations. r! o The first step in evaluation of a solitary pulmonary tt nodule is to determine the likelihood of malignancy KEY POIl{TS o according to clinical and radiographic features. . Regardless ofCOPD severity, Br-agonists and IA = . In patients who have a low risk for malignancy, a anticholinergic/antimuscarinic agents are the main- nodule that is smaller than 6 mm in size requires no stay of therapy. further follow up. o Initial management of COPD includes short-acting bronchodilators, but a long-acting B, agonist or long- Bibliography acting muscarinic antagonist should be added if MacMahon H, Naidich DP, Goo JM, et al. Guidelines for management of symptoms remain poorly controlled. incidental pulmonary nodules detected 0n CT imtges: from the Fleischner Society 2017. Radiolory. 2Ol7:284i228 243. [PMID: 28240562] doi:1 0.1148,'radiol.20l 7l 6l 659 Bibliography Nici L. Mammen MJ. Charbek E, et al. Pharnracologic management of chronic obstructive pulnronary diseirse. an oflicial Anterican Thoracic Society clinical practice guideline. Am J Respir Crit (lare Med. 2020; Item 8 Answer: B 201:e56 e69. IPMID: 322839601 doi:10.1164/rccm.2O2OO3 06255T

further follow up. o Initial management of COPD includes short-acting bronchodilators, but a long-acting B, agonist or long- Bibliography acting muscarinic antagonist should be added if MacMahon H, Naidich DP, Goo JM, et al. Guidelines for management of symptoms remain poorly controlled. incidental pulmonary nodules detected 0n CT imtges: from the Fleischner Society 2017. Radiolory. 2Ol7:284i228 243. [PMID: 28240562] doi:1 0.1148,'radiol.20l 7l 6l 659 Bibliography Nici L. Mammen MJ. Charbek E, et al. Pharnracologic management of chronic obstructive pulnronary diseirse. an oflicial Anterican Thoracic Society clinical practice guideline. Am J Respir Crit (lare Med. 2020; Item 8 Answer: B 201:e56 e69. IPMID: 322839601 doi:10.1164/rccm.2O2OO3 06255T Educational Objective: Treat COPD with a long-acting bronchodilator. Item 9 Answer: A The most appropriate treatment is inhaled tiotropium bro- Educational Objective: Assess thermal upper airway mide (Option B). This patient's pulmonary disease is con injury with bronchoscopy. sistent with COPD. He has a chronic cough and dyspnea on exertion, a signiflcant smoking history, a chest radiograph The nrost appropriate next step is to pertbrm brcnchriscopl. showing hyperinflation, and spirometry results demon (Option A). 'lhis paticnt sustained thcrmal injury to his strating nonreversible obstruction. Pharmacologic therapies upper airway as evidenccd by symptclms of tracheal irrila can be used to reduce symptoms, improve qualifz of life, tion, sore throat, dysphonia. and an edcmatous oropharynx. and reduce exacerbations in patients with COPD. Regard- lntensc heat can cause cclema and blistcring ftom the mouth less of COPD severity, bronchodilators are the mainstay of to the larynr. and patients with a visibly damagcd aint'ay or COPD therapy. Inhaled bronchodilators include p, agonists stridor are at high risk ol'complcte uppcr ainvrry obstruction and antimuscarinic agents. There are inhaled short and due b swelling. It is difficult to predict which patients with long acting lbrms of both grpes. Initial management includes acutc inhalalior-ral injury u,ill clcvelop completc upper lir short acting bronchodilators, but a long acting B, agonist ',vay obstruction, and even patients lvith nrinimally apparent (LABA) or a long-acting muscarinic antagonist (LAMA), such inhalational airway injury may clevelop worsenil.lg obstr-uc as tiotropium bromide, should be added if symptoms are still tion associated with intravenous h1'dration or analgesia poorly controlled. A combination LABA-LAMA can be used needecl fbr burn treatment. tbtbwing stnokc inhalatior.r, if patients have persistent symptoms despite monotherapy one third of palients develop airway edema or mucosal with either long-acting bronchodilator. sloughing fionr epithelial necrosis. Chest physiotherapl' and Inhaled glucocorticoids (Option A) can be used in com serial bronchoscopy itre frequently necessary to facilitate bination with a bronchodilator in COPD but should not be continued airwav clelrance. Other presenting sympk)nls used as monotherapy unless the patient cannot use a bron and signs of inl.ralation injury include stridor. dysphlgia, chodilator. A combination inhaled glucocorticoid LABA singed nasal hairs, ancl sooty spLltum, which sigrtal the need

Educational Objective: Treat COPD with a long-acting bronchodilator. Item 9 Answer: A The most appropriate treatment is inhaled tiotropium bro- Educational Objective: Assess thermal upper airway mide (Option B). This patient's pulmonary disease is con injury with bronchoscopy. sistent with COPD. He has a chronic cough and dyspnea on exertion, a signiflcant smoking history, a chest radiograph The nrost appropriate next step is to pertbrm brcnchriscopl. showing hyperinflation, and spirometry results demon (Option A). 'lhis paticnt sustained thcrmal injury to his strating nonreversible obstruction. Pharmacologic therapies upper airway as evidenccd by symptclms of tracheal irrila can be used to reduce symptoms, improve qualifz of life, tion, sore throat, dysphonia. and an edcmatous oropharynx. and reduce exacerbations in patients with COPD. Regard- lntensc heat can cause cclema and blistcring ftom the mouth less of COPD severity, bronchodilators are the mainstay of to the larynr. and patients with a visibly damagcd aint'ay or COPD therapy. Inhaled bronchodilators include p, agonists stridor are at high risk ol'complcte uppcr ainvrry obstruction and antimuscarinic agents. There are inhaled short and due b swelling. It is difficult to predict which patients with long acting lbrms of both grpes. Initial management includes acutc inhalalior-ral injury u,ill clcvelop completc upper lir short acting bronchodilators, but a long acting B, agonist ',vay obstruction, and even patients lvith nrinimally apparent (LABA) or a long-acting muscarinic antagonist (LAMA), such inhalational airway injury may clevelop worsenil.lg obstr-uc as tiotropium bromide, should be added if symptoms are still tion associated with intravenous h1'dration or analgesia poorly controlled. A combination LABA-LAMA can be used needecl fbr burn treatment. tbtbwing stnokc inhalatior.r, if patients have persistent symptoms despite monotherapy one third of palients develop airway edema or mucosal with either long-acting bronchodilator. sloughing fionr epithelial necrosis. Chest physiotherapl' and Inhaled glucocorticoids (Option A) can be used in com serial bronchoscopy itre frequently necessary to facilitate bination with a bronchodilator in COPD but should not be continued airwav clelrance. Other presenting sympk)nls used as monotherapy unless the patient cannot use a bron and signs of inl.ralation injury include stridor. dysphlgia, chodilator. A combination inhaled glucocorticoid LABA singed nasal hairs, ancl sooty spLltum, which sigrtal the need 123

Answers and Critiques ffl for inspection of the upper aint,a]. Immediate protection central puimonary artcries but is less sensiti\e than pulmo- E 61 the airway is indicated for patients lvith extensive lircial nary angiography or V/Q scanning in detecting CTEPH. coNT or neck burns. decrelsed level ol consciousness. or airual D din.rer (Option B) is useful for eraluating patients obstruction. Il there is any doubt about the ainvay patencli rvith suspected acute pulmonary embolism. but it has no intubation is always preflerred. ufilib, in the evaluation of patients lor CTEPH. 'lhis patient Methylprednisolone (Option B) or other glucocorti- is taking apixaban and therefbre is at very lon' risk for acute coids do not ha\e a role in treating upper airnay edema or pulmonary.embolism. In addition. his s1'mptoms are pro smoke-induced injury of the lower airways. gressive in nature, supporting a chronic condition over a Nebulized epinephrine (Option C) can transiently recurrent thromboembolic event. reduce upper ainvay edema fiom allergic or anaphylactic For paticnts with suspected CTEPII and an abnormai reactions. but it does not have a role in the treatment of V'Q lung scan. right heart catheterization and pulmonary inhalational injury. angiography (Option C) will conflrm pulmonary h1'per D Noninvasive positive pressure ventilation (Option D) tension. exclude competing diagnoses, and provide vital UT rnill not prevent this patient from developing progressire information related to potential therapli Right heart cath- E airway obstruction or clear the ainvay of debris. eterization and pulmonary angiographl' can be aroided in .D t^ patients rvith a normal V/Q scan. ancl they should not be q, f,EY POIilTS used as the initial tests in patients with suspected CTEPI L EL . Following smoke inhalational injury immediate pro- fr tection of the airway is indicated for patients with IEY POITIS extensive facial or neck burns, decreased level ofcon- o A ventilation/perfusion scan is recommended for all It patients with pulmonary hypertension to rule out sciousness, or airway obstruction. (D UI . Following smoke inhalation, one third of patients chronic thromboembolic pulmonary hypertension. develop airway edema or mucosal sloughing from . For patients with suspected chronic thromboembolic epithelial necrosis; airway inspection, bronchoscopy, pulmonary hypertension and an abnormal ventilation/ and chest physiotherapy are frequently necessary to perfusion scan, right heart catheterization and pul- facilitate continued airway clearance. monary angiography will confirm pulmonary hyper- tension, exclude competing diagnoses, and provide Bibliography vital information related to potential therapy. Sheridan RL. Fire related inhalation injury N Engl J Med. 2016:375:464 9. IPMID: 27518664] doi,tO.tOsOlNEJMral601128 Bibliography Kim NH, Delcroix M, Jais X. et al. Chronic thromboembolic pulmonary

ffl for inspection of the upper aint,a]. Immediate protection central puimonary artcries but is less sensiti\e than pulmo- E 61 the airway is indicated for patients lvith extensive lircial nary angiography or V/Q scanning in detecting CTEPH. coNT or neck burns. decrelsed level ol consciousness. or airual D din.rer (Option B) is useful for eraluating patients obstruction. Il there is any doubt about the ainvay patencli rvith suspected acute pulmonary embolism. but it has no intubation is always preflerred. ufilib, in the evaluation of patients lor CTEPH. 'lhis patient Methylprednisolone (Option B) or other glucocorti- is taking apixaban and therefbre is at very lon' risk for acute coids do not ha\e a role in treating upper airnay edema or pulmonary.embolism. In addition. his s1'mptoms are pro smoke-induced injury of the lower airways. gressive in nature, supporting a chronic condition over a Nebulized epinephrine (Option C) can transiently recurrent thromboembolic event. reduce upper ainvay edema fiom allergic or anaphylactic For paticnts with suspected CTEPII and an abnormai reactions. but it does not have a role in the treatment of V'Q lung scan. right heart catheterization and pulmonary inhalational injury. angiography (Option C) will conflrm pulmonary h1'per D Noninvasive positive pressure ventilation (Option D) tension. exclude competing diagnoses, and provide vital UT rnill not prevent this patient from developing progressire information related to potential therapli Right heart cath- E airway obstruction or clear the ainvay of debris. eterization and pulmonary angiographl' can be aroided in .D t^ patients rvith a normal V/Q scan. ancl they should not be q, f,EY POIilTS used as the initial tests in patients with suspected CTEPI L EL . Following smoke inhalational injury immediate pro- fr tection of the airway is indicated for patients with IEY POITIS extensive facial or neck burns, decreased level ofcon- o A ventilation/perfusion scan is recommended for all It patients with pulmonary hypertension to rule out sciousness, or airway obstruction. (D UI . Following smoke inhalation, one third of patients chronic thromboembolic pulmonary hypertension. develop airway edema or mucosal sloughing from . For patients with suspected chronic thromboembolic epithelial necrosis; airway inspection, bronchoscopy, pulmonary hypertension and an abnormal ventilation/ and chest physiotherapy are frequently necessary to perfusion scan, right heart catheterization and pul- facilitate continued airway clearance. monary angiography will confirm pulmonary hyper- tension, exclude competing diagnoses, and provide Bibliography vital information related to potential therapy. Sheridan RL. Fire related inhalation injury N Engl J Med. 2016:375:464 9. IPMID: 27518664] doi,tO.tOsOlNEJMral601128 Bibliography Kim NH, Delcroix M, Jais X. et al. Chronic thromboembolic pulmonary tr Item 10 Answer: D Ed ucationa I Objective: Diagnose chronic thromboem- hypertension. Eur Respir l. 2019r53. [PMID' gosqsgog] doi:10.1183/ 13993003.01915 2018

tr Item 10 Answer: D Ed ucationa I Objective: Diagnose chronic thromboem- hypertension. Eur Respir l. 2019r53. [PMID' gosqsgog] doi:10.1183/ 13993003.01915 2018 bolic pulmonary hypertension.

tr Item 10 Answer: D Ed ucationa I Objective: Diagnose chronic thromboem- hypertension. Eur Respir l. 2019r53. [PMID' gosqsgog] doi:10.1183/ 13993003.01915 2018 bolic pulmonary hypertension. The most appropriate diagnostic test is ventilation, perfusion (V,'Q) scanning (Option D) to screen fbr chronic Item 11 Answer: B Educational Objective: Treat COPD related hypoxemia tr with supplemental oxygen therapy. thromboembolic pulmonary hypertension (CTEPFI). The diagnosis of CTEPH is difticult and can be overlooked as a The most appropriate additional therapf is supplemental cause of pulmonary l.rypertension (Pt I). In patients diag- orJgen (Option B). The use of supplemental oxlgen has been nosed with PI{. evaluation tbr C'IEPH is warrantecl even shorvr.r to impnrve quality ol lif'e and decrease mortalitl- in when a history of acute pulmonary embolism is absent. patients \\.ith COPD and resting h1,-poxen.ria $'ith an arterial The incidence of CTEPH following acute pulmonary embo- Po, ol'55 mm llg (7.:l kPa) or less. or oxlgen saturation as lism is likely less than 5')1,. More than 20'7, of patients u,ith measured by pulse oximetry ol BB'1, or less. Patients u,ith cor CI'EPII do not have a previous diagnosis ol' pulntonan' pulmonale. hcart failure. or erythroc),tosis should be of I'ered embolism. 'lherefore. the diagnosis <tf CTEPTI should not the use of supplemental oxygen if Po, is 59 mm llg (7.8 kPa) automatically be excluded in patients u'ithout a history of or less or ox!'gen saturation is 89'11, or less. Some patients pulmonary cmbolism. In patients'"vho derelop or continue mav not qualily fbr oxygen at rest but ma1'desaturate during to have symptoms suggesting PH after ll months of appro sleep. exertion. or air travel. Supplemental oxygen is t_vp priate anticoagulation for pulmonarv- embol ism. screen i ng ically, prescribed if the ox)'gen saturation as measured by. for CTEPH is rvarranted. A normal VrQ scan is sufficient pulsc oximetry falls below 89')1, in these patients, but the to exclude CTEPH as its sensitivity tbr detecting chronic benefits are less deflned. thrornbus approaches 100')1,. An abnormal \t Q requires Once a patient is started on long term oxygen ther additional investigation, typically with right hcart catheter apyl they should be re evaluated alter 2 to 3 months nith a ization and pulmonary angiographl: repeat irrterial blood gas or oxygen saturation measurement C'f angiography (C'lA) of the chest (Option A) is capirble to detcrmine il the level of supplemental ox1'gen is therapeu of detecting chronic thromboembolic material within clilated tic ancl if it is still indicated.

The most appropriate diagnostic test is ventilation, perfusion (V,'Q) scanning (Option D) to screen fbr chronic Item 11 Answer: B Educational Objective: Treat COPD related hypoxemia tr with supplemental oxygen therapy. thromboembolic pulmonary hypertension (CTEPFI). The diagnosis of CTEPH is difticult and can be overlooked as a The most appropriate additional therapf is supplemental cause of pulmonary l.rypertension (Pt I). In patients diag- orJgen (Option B). The use of supplemental oxlgen has been nosed with PI{. evaluation tbr C'IEPH is warrantecl even shorvr.r to impnrve quality ol lif'e and decrease mortalitl- in when a history of acute pulmonary embolism is absent. patients \\.ith COPD and resting h1,-poxen.ria $'ith an arterial The incidence of CTEPH following acute pulmonary embo- Po, ol'55 mm llg (7.:l kPa) or less. or oxlgen saturation as lism is likely less than 5')1,. More than 20'7, of patients u,ith measured by pulse oximetry ol BB'1, or less. Patients u,ith cor CI'EPII do not have a previous diagnosis ol' pulntonan' pulmonale. hcart failure. or erythroc),tosis should be of I'ered embolism. 'lherefore. the diagnosis <tf CTEPTI should not the use of supplemental oxygen if Po, is 59 mm llg (7.8 kPa) automatically be excluded in patients u'ithout a history of or less or ox!'gen saturation is 89'11, or less. Some patients pulmonary cmbolism. In patients'"vho derelop or continue mav not qualily fbr oxygen at rest but ma1'desaturate during to have symptoms suggesting PH after ll months of appro sleep. exertion. or air travel. Supplemental oxygen is t_vp priate anticoagulation for pulmonarv- embol ism. screen i ng ically, prescribed if the ox)'gen saturation as measured by. for CTEPH is rvarranted. A normal VrQ scan is sufficient pulsc oximetry falls below 89')1, in these patients, but the to exclude CTEPH as its sensitivity tbr detecting chronic benefits are less deflned. thrornbus approaches 100')1,. An abnormal \t Q requires Once a patient is started on long term oxygen ther additional investigation, typically with right hcart catheter apyl they should be re evaluated alter 2 to 3 months nith a ization and pulmonary angiographl: repeat irrterial blood gas or oxygen saturation measurement C'f angiography (C'lA) of the chest (Option A) is capirble to detcrmine il the level of supplemental ox1'gen is therapeu of detecting chronic thromboembolic material within clilated tic ancl if it is still indicated. 124

A tr 'lhe mcthylxanthines (arninophylline and theophylline) (Option A) are nrlu'rarely usecl to treat COPD. 'lhetiphylline Chest CT (Option A) would conlirm whether a patient has a pneumothorirx or pleural eflusion. Iloruever, dcllys associated \ ,ith obtaining chest C'l' as rtell as the nced to CONT l-ras been shou,n to improvc firnctional capacity and reduce the nunrber ol exacerbationsi ltou,e\er. it has a narrorv l,r'in- transport the p:rtient to a CT scanner pose additional clinicirl dow'between therapeutic ancl ktxic dosages. Therefore it risk to this unstable patient. Alternativc rreasures thirt can is used only fbr patients witl.r advanced COPD who have be clone quickly at the bedside arc indicated to assess firr refiactory symptoms not controlled rvith stanclarcl therapy. periprocedura I compl it'rttions. Adding hrime noninvasive positire pressure ventilatior-r Needle thoracostonry (Option C) can help rel,erse thc (Option C) to oxlgen therapv in patients with persistent hemodynamic impact of a tension pncumothorax and oftcr.r hypercapnia after an acute exacerbation o{ COPD prolongs serves as a temporizing measure until a thoracostonl' is the time to readmission and de:rth. This patier.rt does not placed. However, this maneuver is :rssociated r,r,ith risk. have persistent hypercapnia ancl the use oflnoninvasive pos- including intercostal or pulmclnary vascular injury, inter itile pr-cssure ventilation is r.rot indicated at this time. costal nerve injury. and cardiac puncture or tamponade. a o h-rhalccl glucocorticoids (Option D) are typically used In addition, if tension pneumothorax is r.tot the causc of ET only in cornbination rtith a lrurg acting bronchodilator. not the l.rypotension, tl.re patient rvould unnecessarill' nced a as monotherapl,. fbr treatrncnt of COPD. Inhaled glucclcorti thor-acostomy to re crpand the lung. lt is not clear whethcr TJ coids with bronchodilator tlrcr-apy may improvc lung func tension pneumothorax has caused this patient's hypoten t tion and reduce symptonts anci exacerbations in patients si<ln, especially given that breath souncls are diminished on IE r with nrodcratc to severe COPD, but they are associated with botl.r sides. Needle thoracostomy should not be perfbrrr-red (l, an increusctl risk olpneuntr,nil. without first establishing the diagt.tosis of pneumothorax. Pneunrothclrax and vascular injury n1d)' oc'uur r|-rring vt = TEY POIl{IS needle placement. It is rarely caused by the presence of the . The use of supplemental oxygen has been shown to vr"rscnlar catheter itself. Thtts, removing the central \/enous improve quality of life and decrease mortality in patients catheter (Option D) would not addrcss the patient's hypo with COPD and resting hypoxemia with an arterial Po, fensior-r. It is reasorrable to keep the clthcter in placc r,l,l.rile of 55 mm Hg (Z.S kPa) or less, or oxygen saturation as investigating the cause o{ the patient's hypotensior.r. measured by pulse oximetry of 88% or less. XEY POIXII . Patients with cor pulmonale, heart failure, or erythrocy- o Possible reasons for sudden hypotension following tosis should be offered the use ofsupplemental oxygen if central line insertion include procedure-related Po, is 59 mm Hg (7.8 kPa) or less or oxygen saturation is hemothorax and tension pneumothorax. 89'7, or less. o Point-of-care lung ultrasonography can help rapidly Bibliography assess patients for pneumothorax and pleural fluid.

tr 'lhe mcthylxanthines (arninophylline and theophylline) (Option A) are nrlu'rarely usecl to treat COPD. 'lhetiphylline Chest CT (Option A) would conlirm whether a patient has a pneumothorirx or pleural eflusion. Iloruever, dcllys associated \ ,ith obtaining chest C'l' as rtell as the nced to CONT l-ras been shou,n to improvc firnctional capacity and reduce the nunrber ol exacerbationsi ltou,e\er. it has a narrorv l,r'in- transport the p:rtient to a CT scanner pose additional clinicirl dow'between therapeutic ancl ktxic dosages. Therefore it risk to this unstable patient. Alternativc rreasures thirt can is used only fbr patients witl.r advanced COPD who have be clone quickly at the bedside arc indicated to assess firr refiactory symptoms not controlled rvith stanclarcl therapy. periprocedura I compl it'rttions. Adding hrime noninvasive positire pressure ventilatior-r Needle thoracostonry (Option C) can help rel,erse thc (Option C) to oxlgen therapv in patients with persistent hemodynamic impact of a tension pncumothorax and oftcr.r hypercapnia after an acute exacerbation o{ COPD prolongs serves as a temporizing measure until a thoracostonl' is the time to readmission and de:rth. This patier.rt does not placed. However, this maneuver is :rssociated r,r,ith risk. have persistent hypercapnia ancl the use oflnoninvasive pos- including intercostal or pulmclnary vascular injury, inter itile pr-cssure ventilation is r.rot indicated at this time. costal nerve injury. and cardiac puncture or tamponade. a o h-rhalccl glucocorticoids (Option D) are typically used In addition, if tension pneumothorax is r.tot the causc of ET only in cornbination rtith a lrurg acting bronchodilator. not the l.rypotension, tl.re patient rvould unnecessarill' nced a as monotherapl,. fbr treatrncnt of COPD. Inhaled glucclcorti thor-acostomy to re crpand the lung. lt is not clear whethcr TJ coids with bronchodilator tlrcr-apy may improvc lung func tension pneumothorax has caused this patient's hypoten t tion and reduce symptonts anci exacerbations in patients si<ln, especially given that breath souncls are diminished on IE r with nrodcratc to severe COPD, but they are associated with botl.r sides. Needle thoracostomy should not be perfbrrr-red (l, an increusctl risk olpneuntr,nil. without first establishing the diagt.tosis of pneumothorax. Pneunrothclrax and vascular injury n1d)' oc'uur r|-rring vt = TEY POIl{IS needle placement. It is rarely caused by the presence of the . The use of supplemental oxygen has been shown to vr"rscnlar catheter itself. Thtts, removing the central \/enous improve quality of life and decrease mortality in patients catheter (Option D) would not addrcss the patient's hypo with COPD and resting hypoxemia with an arterial Po, fensior-r. It is reasorrable to keep the clthcter in placc r,l,l.rile of 55 mm Hg (Z.S kPa) or less, or oxygen saturation as investigating the cause o{ the patient's hypotensior.r. measured by pulse oximetry of 88% or less. XEY POIXII . Patients with cor pulmonale, heart failure, or erythrocy- o Possible reasons for sudden hypotension following tosis should be offered the use ofsupplemental oxygen if central line insertion include procedure-related Po, is 59 mm Hg (7.8 kPa) or less or oxygen saturation is hemothorax and tension pneumothorax. 89'7, or less. o Point-of-care lung ultrasonography can help rapidly Bibliography assess patients for pneumothorax and pleural fluid. Celli BR, \l'edzich;r JA. Update on clinical aspects of chronic obstructive pulmonary disease. N Engl J Mecl. 2019;il8l :1257 1266. I PMII), 315538371 Bibliography doi :l 0. 10.56i N IlJMral 900500 I)xrulekar B Harris T, Jarman R. The use of lung ultrirsound in acute medi cine. Acute Med. 2019:18:239 246. [PMID: :lt.ltZOSSI

Celli BR, \l'edzich;r JA. Update on clinical aspects of chronic obstructive pulmonary disease. N Engl J Mecl. 2019;il8l :1257 1266. I PMII), 315538371 Bibliography doi :l 0. 10.56i N IlJMral 900500 I)xrulekar B Harris T, Jarman R. The use of lung ultrirsound in acute medi cine. Acute Med. 2019:18:239 246. [PMID: :lt.ltZOSSI tr Item 12 Answer: B Educational Objective: Evaluate patients with shock Item 13 Answer: A using point of-care ultrasonography. Educational Objective: Treat mild persistent asthma by stepping up therapy. 'lhe n.rost appropriate next step i11 nlanagement ol shock in this patient is k.r perfbrm chest ultrusonography (Option B). Pos- The most appropriate treatment is to step up therapy by adding sible relsons for this patient's sudden hypoter.rsion include a long-acting Br-agonist (f"CgA) to the current inhaled gluco- proceclure rclatcd hernothorrtx and tension pneunrothorar. corticoid (Option A); the preferred method would be by start- In patients in shock. point of care lung ultrasonographl, can ing a combined budesonide formoterol inhaler. This patient help rapidll' assess patients fbr pneumothorax ancl pleural has mild persistent asthma with low dose inhaled glucocorti fluid. Point ol' care ultrasor.tography when placing central coid maintenance therapy and now has increasing slmptoms venous cirthcters is associated rt,ith reduced periprocedural requiring frequent use of her short acting B2-agonist (SABA) complications, including bleeciir.rg and pncutnclthorax. inhaler. A step up in therapy is indicated fbr inadequate asthma Hor,revcr, these con-rpliciitiorts still occur. lt-t this patient. control, including either use of a SABA more than twice weekly rapicl onsct of hypotension and poor lung and hexrt sounds (not related to prevention of exercise induced bronchospasm) shoulcl prolnpt the clinician to evaluate fbr intrathoracic or need for a SABA two or more times monthly for noctumal bleeding or ptreumothorax. 'lhe clir-rician can do so using symptoms. Guidelines indicate that the preferred next step is point of: care ultrasonography. [n additior.r. lung ultraso- combined therapy with a low-dose inhaled glucocorticoid and nography can quickly visttaliz.e very small amollllts of fluicl LABA in a single inhaler. When IABAs are added to inhaled r.vithin tl.re pleural space. glucocorticoids, they provide improved control and decrease

tr Item 12 Answer: B Educational Objective: Evaluate patients with shock Item 13 Answer: A using point of-care ultrasonography. Educational Objective: Treat mild persistent asthma by stepping up therapy. 'lhe n.rost appropriate next step i11 nlanagement ol shock in this patient is k.r perfbrm chest ultrusonography (Option B). Pos- The most appropriate treatment is to step up therapy by adding sible relsons for this patient's sudden hypoter.rsion include a long-acting Br-agonist (f"CgA) to the current inhaled gluco- proceclure rclatcd hernothorrtx and tension pneunrothorar. corticoid (Option A); the preferred method would be by start- In patients in shock. point of care lung ultrasonographl, can ing a combined budesonide formoterol inhaler. This patient help rapidll' assess patients fbr pneumothorax ancl pleural has mild persistent asthma with low dose inhaled glucocorti fluid. Point ol' care ultrasor.tography when placing central coid maintenance therapy and now has increasing slmptoms venous cirthcters is associated rt,ith reduced periprocedural requiring frequent use of her short acting B2-agonist (SABA) complications, including bleeciir.rg and pncutnclthorax. inhaler. A step up in therapy is indicated fbr inadequate asthma Hor,revcr, these con-rpliciitiorts still occur. lt-t this patient. control, including either use of a SABA more than twice weekly rapicl onsct of hypotension and poor lung and hexrt sounds (not related to prevention of exercise induced bronchospasm) shoulcl prolnpt the clinician to evaluate fbr intrathoracic or need for a SABA two or more times monthly for noctumal bleeding or ptreumothorax. 'lhe clir-rician can do so using symptoms. Guidelines indicate that the preferred next step is point of: care ultrasonography. [n additior.r. lung ultraso- combined therapy with a low-dose inhaled glucocorticoid and nography can quickly visttaliz.e very small amollllts of fluicl LABA in a single inhaler. When IABAs are added to inhaled r.vithin tl.re pleural space. glucocorticoids, they provide improved control and decrease 125

Answers and Critiques the risk of exacerbations. Administration in a single inhaler agent. as uell as albuterol as needed. Nlacrolide antibiotics is preferred because it improves adherence and may reduce (e.g.. azithroml'cin) have both inflammatory and antimicro cost compared with administration of each drug in a separate bial eflbcts. Long term rnacrolide therap)'reduces the fie inhaler. Other treatment options would include increasing the quenc)'oleracerbations in patients u,ith severe COPD and a patient's regimen to a medium-dose inhaled glucocorticoid or history. of frequent exacerbations. The major concern regard adding a leukotriene receptor antagonist to her current dose of ir.rg long term macK)lide therapy is QT prolongation, but an inhaled glucocorticoid. the risk for cardiovascular death :rssociated r,r'ith long term Azithromycin (Option B) can be used to treat upper and azithromlcin therapy is low (1 in 20.000) fbr patients n,ithout lower respiratory tract inlections and is also recommended cardiac disease. Other standard inten€ntions to reduce COPD as add on therapy given three times weekly for persistent exacerbations inclucie smoking cessatiorl. proper immuniz-ir asthma not controlled by combined moderate to high dose tions. and pulmonary rehabilitation programs. Roflurnilast. a inhaled glucocorticoids with LABA. However, this patient selective phosphodiesterase-4 inhibitor. can also be used fbr does not have symptoms that suggest infection and has not patients n'ith COPD and frequent exacerbations. There are no ta yet had a trial of combined inhaled glucocorticoid LABA head to head comparisor.rs of rof lumilast r'r'ith azithromvcin. tD therapy, making this choice incorrect. The choice of medication is determined b1' the medication's = , Use of prednisone (Option C) could be considered if the side ell'ects. drug interactions. and contraindications. o, patient does not improve with a step up in her maintenance Antiproteases. including or intitr)'psin (Option A), therapy or if her clinical symptoms become more severe. typicallf inactivate proteases that may lead to permanent n However. this would not be recommended as the initial lung injury. In patients witl-r u, ar.rtitrypsin deficiencl,, lt choice. replacing this enzyme with augmentation therapl' ma1' slon Long acting muscarinic antagonists (LAMAs) such as the progression of related emphl,sema. Hou,ever. it is costlll rD ta tiotropium (Option D) provide sustained airway dilation. does not decrease exacerbations or the rate of FE\', decline. When added to therapy fbr asthma not controlled with and is not efl'ective for treatment of patients l-hose COPD is inhaled glucocorticoid LABA combination therapy, tiotro- not caused by u,-antitrypsin deficiencl: pium has been shown to improve lung function and reduce Early observational studies suggested that metoprolol exacerbations. However. no substantial evidence shows that (Option C) used by patients rvith COPD and cardiol'ascular LAMAs should be the flrst choice for long-acting airway disease might be responsible for a reduction in COPD exacer dilation, and National Asthma Education and Prevention bations. A randonrized study shorved the re\erse, rvitlr more Program guidelines speciflcally advise against using a LAMA patients in the metoprolol arm hospitalized for acute COPD as the initial agent to step up from inhaled glucocorticoid exacerbation. There were no between group di{Ierences in controller therapy. forced expiratory volume in I second (FEV,). and the cause clf' (EY POIXIS the increased rate of COPD exacerbations remains unknown. Muco\,tic agents such as oral N acetl'lclsteine (Option D) o The preferred next step for patients with inadequately mal relieve s)'mptoms in patients u'ho produce large vol controlled mild persistent asthma on an inhaled glu- umes of sputum but have not been shou'n to decrease the cocorticoid is combined therapy with a low dose frequency of COPD exacerbations. This patient has thir.r inhaled glucocorticoid and long-acting Br-agonist in a secretions and will not beneflt from N acetylcysteine. single inhaler. TEV POIII . Administration of a glucocorticoid and long,acting o Long-term macrolide therapy reduces the frequency .

the risk of exacerbations. Administration in a single inhaler agent. as uell as albuterol as needed. Nlacrolide antibiotics is preferred because it improves adherence and may reduce (e.g.. azithroml'cin) have both inflammatory and antimicro cost compared with administration of each drug in a separate bial eflbcts. Long term rnacrolide therap)'reduces the fie inhaler. Other treatment options would include increasing the quenc)'oleracerbations in patients u,ith severe COPD and a patient's regimen to a medium-dose inhaled glucocorticoid or history. of frequent exacerbations. The major concern regard adding a leukotriene receptor antagonist to her current dose of ir.rg long term macK)lide therapy is QT prolongation, but an inhaled glucocorticoid. the risk for cardiovascular death :rssociated r,r'ith long term Azithromycin (Option B) can be used to treat upper and azithromlcin therapy is low (1 in 20.000) fbr patients n,ithout lower respiratory tract inlections and is also recommended cardiac disease. Other standard inten€ntions to reduce COPD as add on therapy given three times weekly for persistent exacerbations inclucie smoking cessatiorl. proper immuniz-ir asthma not controlled by combined moderate to high dose tions. and pulmonary rehabilitation programs. Roflurnilast. a inhaled glucocorticoids with LABA. However, this patient selective phosphodiesterase-4 inhibitor. can also be used fbr does not have symptoms that suggest infection and has not patients n'ith COPD and frequent exacerbations. There are no ta yet had a trial of combined inhaled glucocorticoid LABA head to head comparisor.rs of rof lumilast r'r'ith azithromvcin. tD therapy, making this choice incorrect. The choice of medication is determined b1' the medication's = , Use of prednisone (Option C) could be considered if the side ell'ects. drug interactions. and contraindications. o, patient does not improve with a step up in her maintenance Antiproteases. including or intitr)'psin (Option A), therapy or if her clinical symptoms become more severe. typicallf inactivate proteases that may lead to permanent n However. this would not be recommended as the initial lung injury. In patients witl-r u, ar.rtitrypsin deficiencl,, lt choice. replacing this enzyme with augmentation therapl' ma1' slon Long acting muscarinic antagonists (LAMAs) such as the progression of related emphl,sema. Hou,ever. it is costlll rD ta tiotropium (Option D) provide sustained airway dilation. does not decrease exacerbations or the rate of FE\', decline. When added to therapy fbr asthma not controlled with and is not efl'ective for treatment of patients l-hose COPD is inhaled glucocorticoid LABA combination therapy, tiotro- not caused by u,-antitrypsin deficiencl: pium has been shown to improve lung function and reduce Early observational studies suggested that metoprolol exacerbations. However. no substantial evidence shows that (Option C) used by patients rvith COPD and cardiol'ascular LAMAs should be the flrst choice for long-acting airway disease might be responsible for a reduction in COPD exacer dilation, and National Asthma Education and Prevention bations. A randonrized study shorved the re\erse, rvitlr more Program guidelines speciflcally advise against using a LAMA patients in the metoprolol arm hospitalized for acute COPD as the initial agent to step up from inhaled glucocorticoid exacerbation. There were no between group di{Ierences in controller therapy. forced expiratory volume in I second (FEV,). and the cause clf' (EY POIXIS the increased rate of COPD exacerbations remains unknown. Muco\,tic agents such as oral N acetl'lclsteine (Option D) o The preferred next step for patients with inadequately mal relieve s)'mptoms in patients u'ho produce large vol controlled mild persistent asthma on an inhaled glu- umes of sputum but have not been shou'n to decrease the cocorticoid is combined therapy with a low dose frequency of COPD exacerbations. This patient has thir.r inhaled glucocorticoid and long-acting Br-agonist in a secretions and will not beneflt from N acetylcysteine. single inhaler. TEV POIII . Administration of a glucocorticoid and long,acting o Long-term macrolide therapy reduces the frequency . Br-agonist in a single inhaler is preferred because it of exacerbations in patients with severe COPD and a improves adherence and may reduce cost compared history of frequent exacerbations. with administration of each drug in a separate inhaler.

Br-agonist in a single inhaler is preferred because it of exacerbations in patients with severe COPD and a improves adherence and may reduce cost compared history of frequent exacerbations. with administration of each drug in a separate inhaler. Bibliography Bibliography \trmeersch K. Gabrovska N,l. Aumann J. et al. Azithrom)cin during acute Cloutier MM. Dixon AE. Krishnan JA. et al. Managing asthnra in adolescents chronic obstructive pulnronary disease exacerb;rtions requiring hospi and adults, 2020 asthma guideline update from the National Asthma t.lization (BACE). i\ multicenter. randomized. double blind. placebcr Education and Prevention Progrum. JAMA. 2020:32.1:2301 2317. [PMID: controlled trial. Am J Respir Crit Care N,lecl. 2019:200:857 868. IPMID, 332700951 &)i: l0.l0Oti jama .2O2O.'21974 310,16,1051 doi:10.116,1 rccm.201901 009.1OC

Bibliography Bibliography \trmeersch K. Gabrovska N,l. Aumann J. et al. Azithrom)cin during acute Cloutier MM. Dixon AE. Krishnan JA. et al. Managing asthnra in adolescents chronic obstructive pulnronary disease exacerb;rtions requiring hospi and adults, 2020 asthma guideline update from the National Asthma t.lization (BACE). i\ multicenter. randomized. double blind. placebcr Education and Prevention Progrum. JAMA. 2020:32.1:2301 2317. [PMID: controlled trial. Am J Respir Crit Care N,lecl. 2019:200:857 868. IPMID, 332700951 &)i: l0.l0Oti jama .2O2O.'21974 310,16,1051 doi:10.116,1 rccm.201901 009.1OC tr Item 14 Answer: B Educational Objective: Prevent COPD exacerbations Item 15 Answer: B Ed ucationa I Objective: Treat recurrent symptomatic tr with long-term azithromycin therapy. malignant pleural effusion with an indwelting pleural catheter. Addition ol'azithromycin (Option B) may help decrease the fiequency ol'this patient's COPD exacerbations. The p:rtient's 'lhe most appropriate management fbr this patient is place medications are a combination inhaled glucocorticoid, a ment of an indwelling pleural catheter (lPC) (Option B). 'the long acting B, agonist. and a long acting alttinruscarinic: cliagnosis of a ntalignant pleural eflusion signifles advanced 126

Answers and Critiques tr CONT, disease and overall poor prognosis (usually 4.7 months fiorn the time of'diagr-rosis). In these patients. the goal ol manage ment is relief o1'symptoms. Several therapeutic options exist, sarcoidosis, a granulomatous disease of unknown cause that can aflect any organ system but most commonly aflects the iungs. Sarcoidosis aflects Blacks more frequently than Whites and treatment decisions should be basecl on symptoms, prog- and typically occurs in younger patients. Many patients are nosis. degree of anticipated lung re expansiorr, and patient asymptomatic, and lung involvement is found incidentally petformance status. The patient has tr recurrent symptomatic on a chest radiograph obtained for other reasons. Pulmonary malignant pleural eflusion that requires definitire manage- sarcoidosis is classifled into four stages based on appearance ment gir'en the rapidi! of recurrence. h-ritial treatrnent choices on chest radiograph: stage I, bilateral hilar lymphadenopa include IPC and chernicai pleurodesis r,vith ta1c, and either thy; stage II, bilateral hilar lymphadenopathy with pulmonary may be used as first-line treatment in patients rvith expand inflltrates; stage III, parenchymal inflltrates alone; and stage able lung. In this patient, however, because there is evidence lV, pulmonary flbrosis with parenchymal distortion or bullae. of incomplete lung expansion on his post thoracentesis radio For patients with stage I disease, clinical diagnosis based on graphs, the treatment of choice is lPC. lncomplete expansicln a classic presentation is a cost ellective strate5/, with pretest t! €, of the lung is common in malignant pleural effusion. It is probabiliff approaching 99.95'/u. The overall prognosis ofstage ET diagnosed rvith eiti.rer pleural m:rnometry (measurement of I pulmonary sarcoidosis is excellent, with spontaneous regres intrapleural pressures during a thoracentesis) or. as in this sion of radiographic abnormalities observed in most patients. L' patient, evidence of incomplete re erpansion (air replacing Diagnosis of pulmonary sarcoidosis, with a few excep t, the drained pleural eflusion) on a post thor:rcentesis chest tions, typically requires bronchoscopic biopsy (Option A), .E radiograph. Nonexpandable lung has a variety of causes, with tissue obtained from a lymph node or from the pulmo vt (u including pleural thickening, pleural tumor, septations, nary parenchyma. The diagnosis is made by the flnding of non caseating granulomas with exclusion ol potential mimicking ta loculations. and endobronchial obstruction. = Chemical pleurodesis (Option A) refers to obliteratior.r infbctions (mycobacteria, fungi), exclusion of other systemic of the pleural space u.ith a sclerosing agent, typically talc. granulomatous diseases, and involvement of more than one Talc can be introducecl through a thoracostomy tube (talc organ system. The absence of respiratory and constitutional slurry) or during a thoracoscopy (talc poudrage). Successful symptoms makes infectious and malignant causes unlikely. pleurodesis requires apposition o1'the parietal and visceral Clinical presentations of sarcoidosis that do not require a pleural surfaces, r,rrhich limits the use of this treatment in biopsy include asymptomatic stage I pulmonary sarcoidosis patients with an unexpanded lung. (absence of fevers, malaise, or night sweats to suggest a malig Repeat therapeutic thoracentesis (Option C) is appropriate nancy); Lofgren syndrome (bilateral hilar lymphadenopathy, fbr patients rvith poor prognosis (<3 months) and slow reaccu migratory po$arthralgia, erythema nodosum, and fever); and mulation ol'fluid. lt would not be the best choice for this patient Heerfordt syndrome (anterior uveitis, parotiditis, fever, and because oI'the rapiditl of symptomatic fluid reaccumulation. facial nerve palsy). This as),'mptomatic patient with stage I Surgical decortication (Option D) is not used as first pulmonary sarcoidosis does not need a bronchoscopic biopsy. line treatment for recurrent malignant plettral eflusion The primary treatment for symptomatic pulmonary sar- because of its associated costs and morbidity. coidosis is systemic glucocorticoids. Methotrexate (Option B) may be used for patients who cannot tolerate glucocorticoids t(tY PorilIs due to adverse eflects or those who continue to have dis . Initial treatment of a malignant pleural effusion in abling symptoms despite glucocorticoid treatment. I\4etho patients with expandable lung includes either an trexate may also be used as a glucocorticoid sparing therapy indwelling pulmonary catheter or chemical pleuro- to limit adverse effects from long-term use of glucocorti desis with talc. coids. Neither glucocor-ticoids nor methotrexate is indicated o In patients with a malignant pleural effusion and a for asymptomatic stage I pulmonary sarcoidosis. Glucocorticoids, typically prednisone (Option C), are nonexpanding lung, an indwelling pulmonary catheter is the treatment of choice. the mainstay of therapy for sarcoidosis. However, initial treatment is usually limited to symptomatic patients with pulmonary/extrapulmonary organ dysfunction. Patients Bibliography who require long term glucocorticoids are fiequently tran- Feller Kopman Dl, Reddy CB. DeCamp MM, et al. tr4anagement of malignant pleural effusions. an official ATS/STSi STR clinical practice glideline. Am sitioned to glucocorticoid-sparing agents such as methotrex- J Respir Crit Care Med. 2018;198:839 8'19. [PMID: 30272503] doi:10.1164/ ate or leflunomide. Treatment with prednisone would not be rccm.20l807 1415ST the most appropriate initial treatment for this asymptomatic patient with stage I disease.

tr CONT, disease and overall poor prognosis (usually 4.7 months fiorn the time of'diagr-rosis). In these patients. the goal ol manage ment is relief o1'symptoms. Several therapeutic options exist, sarcoidosis, a granulomatous disease of unknown cause that can aflect any organ system but most commonly aflects the iungs. Sarcoidosis aflects Blacks more frequently than Whites and treatment decisions should be basecl on symptoms, prog- and typically occurs in younger patients. Many patients are nosis. degree of anticipated lung re expansiorr, and patient asymptomatic, and lung involvement is found incidentally petformance status. The patient has tr recurrent symptomatic on a chest radiograph obtained for other reasons. Pulmonary malignant pleural eflusion that requires definitire manage- sarcoidosis is classifled into four stages based on appearance ment gir'en the rapidi! of recurrence. h-ritial treatrnent choices on chest radiograph: stage I, bilateral hilar lymphadenopa include IPC and chernicai pleurodesis r,vith ta1c, and either thy; stage II, bilateral hilar lymphadenopathy with pulmonary may be used as first-line treatment in patients rvith expand inflltrates; stage III, parenchymal inflltrates alone; and stage able lung. In this patient, however, because there is evidence lV, pulmonary flbrosis with parenchymal distortion or bullae. of incomplete lung expansion on his post thoracentesis radio For patients with stage I disease, clinical diagnosis based on graphs, the treatment of choice is lPC. lncomplete expansicln a classic presentation is a cost ellective strate5/, with pretest t! €, of the lung is common in malignant pleural effusion. It is probabiliff approaching 99.95'/u. The overall prognosis ofstage ET diagnosed rvith eiti.rer pleural m:rnometry (measurement of I pulmonary sarcoidosis is excellent, with spontaneous regres intrapleural pressures during a thoracentesis) or. as in this sion of radiographic abnormalities observed in most patients. L' patient, evidence of incomplete re erpansion (air replacing Diagnosis of pulmonary sarcoidosis, with a few excep t, the drained pleural eflusion) on a post thor:rcentesis chest tions, typically requires bronchoscopic biopsy (Option A), .E radiograph. Nonexpandable lung has a variety of causes, with tissue obtained from a lymph node or from the pulmo vt (u including pleural thickening, pleural tumor, septations, nary parenchyma. The diagnosis is made by the flnding of non caseating granulomas with exclusion ol potential mimicking ta loculations. and endobronchial obstruction. = Chemical pleurodesis (Option A) refers to obliteratior.r infbctions (mycobacteria, fungi), exclusion of other systemic of the pleural space u.ith a sclerosing agent, typically talc. granulomatous diseases, and involvement of more than one Talc can be introducecl through a thoracostomy tube (talc organ system. The absence of respiratory and constitutional slurry) or during a thoracoscopy (talc poudrage). Successful symptoms makes infectious and malignant causes unlikely. pleurodesis requires apposition o1'the parietal and visceral Clinical presentations of sarcoidosis that do not require a pleural surfaces, r,rrhich limits the use of this treatment in biopsy include asymptomatic stage I pulmonary sarcoidosis patients with an unexpanded lung. (absence of fevers, malaise, or night sweats to suggest a malig Repeat therapeutic thoracentesis (Option C) is appropriate nancy); Lofgren syndrome (bilateral hilar lymphadenopathy, fbr patients rvith poor prognosis (<3 months) and slow reaccu migratory po$arthralgia, erythema nodosum, and fever); and mulation ol'fluid. lt would not be the best choice for this patient Heerfordt syndrome (anterior uveitis, parotiditis, fever, and because oI'the rapiditl of symptomatic fluid reaccumulation. facial nerve palsy). This as),'mptomatic patient with stage I Surgical decortication (Option D) is not used as first pulmonary sarcoidosis does not need a bronchoscopic biopsy. line treatment for recurrent malignant plettral eflusion The primary treatment for symptomatic pulmonary sar- because of its associated costs and morbidity. coidosis is systemic glucocorticoids. Methotrexate (Option B) may be used for patients who cannot tolerate glucocorticoids t(tY PorilIs due to adverse eflects or those who continue to have dis . Initial treatment of a malignant pleural effusion in abling symptoms despite glucocorticoid treatment. I\4etho patients with expandable lung includes either an trexate may also be used as a glucocorticoid sparing therapy indwelling pulmonary catheter or chemical pleuro- to limit adverse effects from long-term use of glucocorti desis with talc. coids. Neither glucocor-ticoids nor methotrexate is indicated o In patients with a malignant pleural effusion and a for asymptomatic stage I pulmonary sarcoidosis. Glucocorticoids, typically prednisone (Option C), are nonexpanding lung, an indwelling pulmonary catheter is the treatment of choice. the mainstay of therapy for sarcoidosis. However, initial treatment is usually limited to symptomatic patients with pulmonary/extrapulmonary organ dysfunction. Patients Bibliography who require long term glucocorticoids are fiequently tran- Feller Kopman Dl, Reddy CB. DeCamp MM, et al. tr4anagement of malignant pleural effusions. an official ATS/STSi STR clinical practice glideline. Am sitioned to glucocorticoid-sparing agents such as methotrex- J Respir Crit Care Med. 2018;198:839 8'19. [PMID: 30272503] doi:10.1164/ ate or leflunomide. Treatment with prednisone would not be rccm.20l807 1415ST the most appropriate initial treatment for this asymptomatic patient with stage I disease. Item 16 Answer: D t(EY P0rt{rt Educational Obiective: Manage asymptomatic stage I . Clinical presentations of sarcoidosis that do not require pulmonary sarcoidosis. a biopsy include asymptomatic stage I pulmonary sar coidosis, Lofgren syndrome, and Heerfordt syndrome. The most appropriate management for this patient is observa (Continued) tion (Option D). The patient most likely has stage I pulmonary

Item 16 Answer: D t(EY P0rt{rt Educational Obiective: Manage asymptomatic stage I . Clinical presentations of sarcoidosis that do not require pulmonary sarcoidosis. a biopsy include asymptomatic stage I pulmonary sar coidosis, Lofgren syndrome, and Heerfordt syndrome. The most appropriate management for this patient is observa (Continued) tion (Option D). The patient most likely has stage I pulmonary 127

Answers and Critiques l(EY POltlIS (ontinwd) TEY POITI' . The overall prognosis of stage I pulmonary sarcoidosis . For patients with asthma symptoms and a normal is excellent, with spontaneous regression of radio- spirometry a positive bronchial challenge test followed graphic abnormalities observed in most patients. by relief of symptoms with standard asthma therapy confirms the diagnosis of asthma. Bibliography . A negative bronchial challenge test excludes the diag- Ungprasert P. Ryu lH, Matteson EL. Clinical manifestrtions. diagnosis, nosis of asthma in most Patients. and treatment of sarcoidosis. Mayr Clin Proc lnnov Qual Outcomes. 2019r3:i158 375. IPMID, 31.185575] doi:10.1016,j.ma)'ocpiqo.2019. 0.1.006 Bibliography (i)ates AL, Wanger J, Cockcroft DW et al; Bronchoprovocation Testing Tirsk lbrce: Kai-Hekon Carlsen. ERS technical sttndtrd on bronchi:rl chal Item 17 Answer: D lenge testing: general considerations ancl pertilrmance of methacholinc D challenge tests. Eur Respir J. 2017;49. IPN'lln, 28,1612901 doi:10.1183r t^ Educational Objective: Diagnose asthma with bronchial 13993003.01526 2016 challenge testing. = .D Ut o, CL The most appropriate management for this patient is methacholine challenge testing (Option D). Confirma- tion of reversible airflow obstruction is a cornerstone Item 18 Answer: C Educational Objective: Treat neutropenic sepsis with tr rt of asthma diagnosis, and spirometry should be per- an appropriate duration of antibiotic therapy.

l(EY POltlIS (ontinwd) TEY POITI' . The overall prognosis of stage I pulmonary sarcoidosis . For patients with asthma symptoms and a normal is excellent, with spontaneous regression of radio- spirometry a positive bronchial challenge test followed graphic abnormalities observed in most patients. by relief of symptoms with standard asthma therapy confirms the diagnosis of asthma. Bibliography . A negative bronchial challenge test excludes the diag- Ungprasert P. Ryu lH, Matteson EL. Clinical manifestrtions. diagnosis, nosis of asthma in most Patients. and treatment of sarcoidosis. Mayr Clin Proc lnnov Qual Outcomes. 2019r3:i158 375. IPMID, 31.185575] doi:10.1016,j.ma)'ocpiqo.2019. 0.1.006 Bibliography (i)ates AL, Wanger J, Cockcroft DW et al; Bronchoprovocation Testing Tirsk lbrce: Kai-Hekon Carlsen. ERS technical sttndtrd on bronchi:rl chal Item 17 Answer: D lenge testing: general considerations ancl pertilrmance of methacholinc D challenge tests. Eur Respir J. 2017;49. IPN'lln, 28,1612901 doi:10.1183r t^ Educational Objective: Diagnose asthma with bronchial 13993003.01526 2016 challenge testing. = .D Ut o, CL The most appropriate management for this patient is methacholine challenge testing (Option D). Confirma- tion of reversible airflow obstruction is a cornerstone Item 18 Answer: C Educational Objective: Treat neutropenic sepsis with tr rt of asthma diagnosis, and spirometry should be per- an appropriate duration of antibiotic therapy. tt formed on all patients with suspected asthma. For some No change in treitment (Option C) is rnost appropriirte E (D patients, however, airflow obstruction is not present for this patient. In patients \\'ith neutropenic lever. it is UI during the initial spirometry, and a bronchial challenge al'"r,:rys appropriate to provide empiric gram-positive iln(l test is indicated to evaluate for bronchial hyperreactivity, gram negative coverage as an initial approach. Coverage which supports an asthma diagnosis. The test is usually firr nrethicillin resistant Staphylococ'cu.s oureus should be performed with inhaled methacholine, although other considered if the patient is henrodynanrically unstable. bttt stimuli (exercise, mannitol) also have been validated. it can be discontinuecl alter 2 to 3 d.rys if culture datr irre Bronchial challenge tests measure spirometry following tun reveali ng. Notatior.rol' previous i nf ections. resistance pat a controlled inhaled stimulus; a positive test is indicated terns, and local antibiograms should guide decisions on the by a drop in the measured FEV,. llthe result is negative, initial regimen, althor-rgh carbapenems or extended range it is unlikely that the patient has asthma, but a positive penicillin-p-lactamase inhibitors are r reasonable ernpiric result in isolation is not specific enough to diagnose choice lbr most pirtients. N4ost neutropenic fevers hal,e no asthma. Therefbre, to confirm the diagnosis, patients knorvn source. In situations in lvhich no pathogen is iclenti with a positive methacholine challenge test and sugges fied. antibiotic discontinuation is largell'contingent on t\\() tive asthma symptoms must also respond clinically to criteria: resolution of fever and impro\ienlent of the patient's treatment with asthma therapies. This patient's typical absolute neutrophil count to more than 500 ii,rL (0.5 x 10", L). symptoms and improvement with standard asthma ther Indications fbr modifying a patierlt's antibiotic coverage apy would indicate asthma if the methacholine challenge include identificatior.r of an inf'ectir)us source. escalation test result were positive. of therapy for persistent fever orur,orsening clinical status. Although initiating a trial of asthma treatment with and, it-t some cases. transition to au oral regimen fbr patients budesonide salmeterol or fluticasone (Options A, B) could leaving the hospital. Because this patient does not rneet an), be considered, guidelines indicate that it is preferable to of these criteria. sw,itching liom piperacillin tazobactan.r to first establish a diagnosis to avoid prescribing unnecessary imipenem-cilastatin (Option A) woulcl not be indicated. or incorrect treatment. It is more difficult to establish the This patient is hemodynamically stable. appears clini diagnosis of asthma once the patient is taking controller cally inrproved. and is afebrile, but the absolute neutnrphil medications. count has not rccovered. Antibiotics should be continuecl Measurement of the fractional exhaled nitric oxide until either the absolute neutrophil count recovers or the (FeNO) (Option C) in an exhaled breath sample provides a patient has con-rpletecl a full conrse of ar.rtibiotic therapy. noninvasive way to quantify eosinophilic airway inflam whichever is longest. Some guidelines suggest discontinuing mation and serves as a complementary tool in the man- antibiotics after 4B to 72 hours in patients without fever who agement of lung diseases, in particular, asthma. However, are improvir-rg and have no clear source lbr infection, regirrcl the role of FeNO in the diagnosis of asthma has not been less of neutrophil recovery Becausc this patient has been established. Although an elevated FeNO is characteristic af'ebrile for or.rly 24 hours and her absolute, neutrophil count of type 2 airway inflammation, FeNO is also elevated has not recorered, it would not be appropriate to discontirrue in disorders such as eosinophilic bronchitis, atopy, and antibiotics (Option B) at this time. allergic rhinitis and is not elevated in some asthma phe The risk of lungemia is incre:rsed in patients wl.ro notypes. Spirometry remains the flrst test of choice to remain neutropenic and febrile for ntore tl-ran 7 days. If a diagnose asthma. patierlt remains f'ebrile fbr more than ,1 days, addition of an

tt formed on all patients with suspected asthma. For some No change in treitment (Option C) is rnost appropriirte E (D patients, however, airflow obstruction is not present for this patient. In patients \\'ith neutropenic lever. it is UI during the initial spirometry, and a bronchial challenge al'"r,:rys appropriate to provide empiric gram-positive iln(l test is indicated to evaluate for bronchial hyperreactivity, gram negative coverage as an initial approach. Coverage which supports an asthma diagnosis. The test is usually firr nrethicillin resistant Staphylococ'cu.s oureus should be performed with inhaled methacholine, although other considered if the patient is henrodynanrically unstable. bttt stimuli (exercise, mannitol) also have been validated. it can be discontinuecl alter 2 to 3 d.rys if culture datr irre Bronchial challenge tests measure spirometry following tun reveali ng. Notatior.rol' previous i nf ections. resistance pat a controlled inhaled stimulus; a positive test is indicated terns, and local antibiograms should guide decisions on the by a drop in the measured FEV,. llthe result is negative, initial regimen, althor-rgh carbapenems or extended range it is unlikely that the patient has asthma, but a positive penicillin-p-lactamase inhibitors are r reasonable ernpiric result in isolation is not specific enough to diagnose choice lbr most pirtients. N4ost neutropenic fevers hal,e no asthma. Therefbre, to confirm the diagnosis, patients knorvn source. In situations in lvhich no pathogen is iclenti with a positive methacholine challenge test and sugges fied. antibiotic discontinuation is largell'contingent on t\\() tive asthma symptoms must also respond clinically to criteria: resolution of fever and impro\ienlent of the patient's treatment with asthma therapies. This patient's typical absolute neutrophil count to more than 500 ii,rL (0.5 x 10", L). symptoms and improvement with standard asthma ther Indications fbr modifying a patierlt's antibiotic coverage apy would indicate asthma if the methacholine challenge include identificatior.r of an inf'ectir)us source. escalation test result were positive. of therapy for persistent fever orur,orsening clinical status. Although initiating a trial of asthma treatment with and, it-t some cases. transition to au oral regimen fbr patients budesonide salmeterol or fluticasone (Options A, B) could leaving the hospital. Because this patient does not rneet an), be considered, guidelines indicate that it is preferable to of these criteria. sw,itching liom piperacillin tazobactan.r to first establish a diagnosis to avoid prescribing unnecessary imipenem-cilastatin (Option A) woulcl not be indicated. or incorrect treatment. It is more difficult to establish the This patient is hemodynamically stable. appears clini diagnosis of asthma once the patient is taking controller cally inrproved. and is afebrile, but the absolute neutnrphil medications. count has not rccovered. Antibiotics should be continuecl Measurement of the fractional exhaled nitric oxide until either the absolute neutrophil count recovers or the (FeNO) (Option C) in an exhaled breath sample provides a patient has con-rpletecl a full conrse of ar.rtibiotic therapy. noninvasive way to quantify eosinophilic airway inflam whichever is longest. Some guidelines suggest discontinuing mation and serves as a complementary tool in the man- antibiotics after 4B to 72 hours in patients without fever who agement of lung diseases, in particular, asthma. However, are improvir-rg and have no clear source lbr infection, regirrcl the role of FeNO in the diagnosis of asthma has not been less of neutrophil recovery Becausc this patient has been established. Although an elevated FeNO is characteristic af'ebrile for or.rly 24 hours and her absolute, neutrophil count of type 2 airway inflammation, FeNO is also elevated has not recorered, it would not be appropriate to discontirrue in disorders such as eosinophilic bronchitis, atopy, and antibiotics (Option B) at this time. allergic rhinitis and is not elevated in some asthma phe The risk of lungemia is incre:rsed in patients wl.ro notypes. Spirometry remains the flrst test of choice to remain neutropenic and febrile for ntore tl-ran 7 days. If a diagnose asthma. patierlt remains f'ebrile fbr more than ,1 days, addition of an 128

Answers and Critiques tr CONI. antifungal agent such as voriconazole (Option D) is war ranted if'the patient's neutropenia is expected to last beyond muscle rigidity, rhabdon.ryolysis. and arrhythntias.'l'reat ment includes cessatiol'l of the triggering agent. activc 7 days and no alternative source fbr the inf'ection has been cooling. and administration of dantrolene (Option D). 'lhis identified. Because this patient is no longer febrile. addition patient has not received agents known to trigger nralignant of an antifirngal agent is not ir.rdicated. hyperthermia. ar.rd the patient's symptoms ilre not consis I(EY POtilT tent with this diagnosis.

tr CONI. antifungal agent such as voriconazole (Option D) is war ranted if'the patient's neutropenia is expected to last beyond muscle rigidity, rhabdon.ryolysis. and arrhythntias.'l'reat ment includes cessatiol'l of the triggering agent. activc 7 days and no alternative source fbr the inf'ection has been cooling. and administration of dantrolene (Option D). 'lhis identified. Because this patient is no longer febrile. addition patient has not received agents known to trigger nralignant of an antifirngal agent is not ir.rdicated. hyperthermia. ar.rd the patient's symptoms ilre not consis I(EY POtilT tent with this diagnosis. . In patients with neutropenic fever, antibiotics should I(EY POITII uzually be continued until either the absolute neutrophil o Neuroleptic malignant syndrome is characterized by count recovers (>SOOlpL [O.S x forlL]) or the patient has fever, mental status changes, muscle rigidity, and completed a full course of antibiotic therapy, which- dysautonomia and is seen with both first-generation ever is longest. antipsychotics and newer atypical antipsychotics and antiemetics. t^ {l, Bibliography . Treatment of neuroleptic malignant sl,ndrome includes ET Cantwell L, Perkins J. Infectious disease emergencies in oncologr patients. Emerg Med Clin North Am. 2018136:795 810. [PMID: 30297005] doi:lo. discontinuation ofthe triggering agent, active cooling, 1016/i.emc.2018.06.009 and supportive care. (., -,E Bibliography .E tt tr Item 19 Answer: B Educationa I Objective: Treat neuroleptic malignant Ware MR, Feller DB, Hall KL. Neuroleptic malignant syndrome: diagnosis and management. Prim Care Companion CNS Disord. 2018;20. [PMID: 29325237) doi: 10.4088/ PCC. I 7r02185 (u .A = syndrome.

. In patients with neutropenic fever, antibiotics should I(EY POITII uzually be continued until either the absolute neutrophil o Neuroleptic malignant syndrome is characterized by count recovers (>SOOlpL [O.S x forlL]) or the patient has fever, mental status changes, muscle rigidity, and completed a full course of antibiotic therapy, which- dysautonomia and is seen with both first-generation ever is longest. antipsychotics and newer atypical antipsychotics and antiemetics. t^ {l, Bibliography . Treatment of neuroleptic malignant sl,ndrome includes ET Cantwell L, Perkins J. Infectious disease emergencies in oncologr patients. Emerg Med Clin North Am. 2018136:795 810. [PMID: 30297005] doi:lo. discontinuation ofthe triggering agent, active cooling, 1016/i.emc.2018.06.009 and supportive care. (., -,E Bibliography .E tt tr Item 19 Answer: B Educationa I Objective: Treat neuroleptic malignant Ware MR, Feller DB, Hall KL. Neuroleptic malignant syndrome: diagnosis and management. Prim Care Companion CNS Disord. 2018;20. [PMID: 29325237) doi: 10.4088/ PCC. I 7r02185 (u .A = syndrome. The most appropriate initial trettment is discontinuation of Item 20 Answer: D risperidone (Option B). This p:rtient developed neuroleptic Ed u catio n a I Obj ective: Treat smoking-related diffuse malignant syndrome as a result of risperidone (an atypi parenchymal lung disease. cal antipsychotic) and prontethazine (an antientetic agent). Neuroleptic nralignant syndronre is characterized by fbver. This patient has smoking related diffuse parenchymal lung mental status changes, muscle rigidity, and dysautonomia. disease (DPLD), and smoking cessation is the most appro The syndrome is seen botlr with first-generation antipsy, priate treatment (Option D). There are several DPLDs that chotics and with newer atypical antipsychotics ,nd anti, occur almost exclusively in persons who are current smok emetics. lt is most common at times of medication initiation ers. The pathologz from smoking-related DPLD includes or escalation <lf medication doses. [t can also bc caused by respiratory bronchiolitis associated interstitial Iung disease rapid r,r,ithdrawal of dopaminergic medications. ln addition (RB-ILD), desquamative interstitial pneumonia (OIP), pul to discontinuation of the triggering agents, active cooling monary Langerhans cell histiocytosis (PLCH), and smoking and supportivc care (including intravenous fluids) ntay be related interstitial flbrosis (SRIF). Smoking in conjunction used. The mortality rate associated with neuroleptic malig with other endogenous or exogenous factors may also con- nant syndrome may exceed l0')1,. tribute to idiopathic pulmonary flbrosis as well as com Serotor-rir-r syndrome is most commonly associated with bined pulmonary flbrosis and emphysema. Physiologically, the use ol selective serotonin reuptake inhibibrs (SSRls) smoking-related DPLD may have obstructive, restrictive, such as fluoxetine (Option A) and is rypically precipitated or mixed defects. This patient has a restrictive defect. Dlco by the addition of a seconcl medication that aflects the is reduced in all patients with DPLD, including smoking release or uptake of serotonin. Serotonin syndrome is char- related DPLD. Findings on high-resolution CT (HRCT) acterized by nrental status changes, dysautonomia, hyper can often help distinguish between the various types of thermia. nryoclonus. and hyperreflexia. The two leatures smoking related DPLD. This patient's HRCT flndings of that are most helptul in distinguishing serotollill syndrome lower-lobe-predominant ground-glass opacities suggest DIP. from neuroleptic malignant syndrome are the presence of RB-ILD is characterized by patchy ground-glass opacities hyperref lexia and myoclonus. I n itial managemeut incl udes with flne centrilobular nodules. PLCH, in contrast, is char removal o1'the ofl'ending agents ar.rd supportive care. includ acterized by diffuse thin walled cysts and nodular lesions ing benzodiazepines. in the mid- and upper lung zones. SRIF mimics RBILD on Cyproheptadine (Option C) rnay also be usecl ofl label chest radiograph; however, it is pathologically distinct, with fbr serokrnin syndrome if symptoms persist despite ben deposition of hyalinized collagen in alveolar septa and mini- zodiazepines. Because tl.ris pltient cloes not hirve serotonin mal inflammation. For all smoking related DPLDs, smoking syndrome. these rnedications are not appropriate. cessation is the cornerstone of treatment. Patients should Malignant hyperthermil is an autosomal dominant receive behavioral counseling and at least one of seven condition resulting from deranged intracellular calcium FDA-approved treatments for smoking cessation. metabolism in response to inhaled anesthetic irgents and Glucocorticoids (Option A) may be required in severe succinylcholine. It is characterized by severe hyperthermia. disease or refractory cases of smoking related DPLD, but

The most appropriate initial trettment is discontinuation of Item 20 Answer: D risperidone (Option B). This p:rtient developed neuroleptic Ed u catio n a I Obj ective: Treat smoking-related diffuse malignant syndrome as a result of risperidone (an atypi parenchymal lung disease. cal antipsychotic) and prontethazine (an antientetic agent). Neuroleptic nralignant syndronre is characterized by fbver. This patient has smoking related diffuse parenchymal lung mental status changes, muscle rigidity, and dysautonomia. disease (DPLD), and smoking cessation is the most appro The syndrome is seen botlr with first-generation antipsy, priate treatment (Option D). There are several DPLDs that chotics and with newer atypical antipsychotics ,nd anti, occur almost exclusively in persons who are current smok emetics. lt is most common at times of medication initiation ers. The pathologz from smoking-related DPLD includes or escalation <lf medication doses. [t can also bc caused by respiratory bronchiolitis associated interstitial Iung disease rapid r,r,ithdrawal of dopaminergic medications. ln addition (RB-ILD), desquamative interstitial pneumonia (OIP), pul to discontinuation of the triggering agents, active cooling monary Langerhans cell histiocytosis (PLCH), and smoking and supportivc care (including intravenous fluids) ntay be related interstitial flbrosis (SRIF). Smoking in conjunction used. The mortality rate associated with neuroleptic malig with other endogenous or exogenous factors may also con- nant syndrome may exceed l0')1,. tribute to idiopathic pulmonary flbrosis as well as com Serotor-rir-r syndrome is most commonly associated with bined pulmonary flbrosis and emphysema. Physiologically, the use ol selective serotonin reuptake inhibibrs (SSRls) smoking-related DPLD may have obstructive, restrictive, such as fluoxetine (Option A) and is rypically precipitated or mixed defects. This patient has a restrictive defect. Dlco by the addition of a seconcl medication that aflects the is reduced in all patients with DPLD, including smoking release or uptake of serotonin. Serotonin syndrome is char- related DPLD. Findings on high-resolution CT (HRCT) acterized by nrental status changes, dysautonomia, hyper can often help distinguish between the various types of thermia. nryoclonus. and hyperreflexia. The two leatures smoking related DPLD. This patient's HRCT flndings of that are most helptul in distinguishing serotollill syndrome lower-lobe-predominant ground-glass opacities suggest DIP. from neuroleptic malignant syndrome are the presence of RB-ILD is characterized by patchy ground-glass opacities hyperref lexia and myoclonus. I n itial managemeut incl udes with flne centrilobular nodules. PLCH, in contrast, is char removal o1'the ofl'ending agents ar.rd supportive care. includ acterized by diffuse thin walled cysts and nodular lesions ing benzodiazepines. in the mid- and upper lung zones. SRIF mimics RBILD on Cyproheptadine (Option C) rnay also be usecl ofl label chest radiograph; however, it is pathologically distinct, with fbr serokrnin syndrome if symptoms persist despite ben deposition of hyalinized collagen in alveolar septa and mini- zodiazepines. Because tl.ris pltient cloes not hirve serotonin mal inflammation. For all smoking related DPLDs, smoking syndrome. these rnedications are not appropriate. cessation is the cornerstone of treatment. Patients should Malignant hyperthermil is an autosomal dominant receive behavioral counseling and at least one of seven condition resulting from deranged intracellular calcium FDA-approved treatments for smoking cessation. metabolism in response to inhaled anesthetic irgents and Glucocorticoids (Option A) may be required in severe succinylcholine. It is characterized by severe hyperthermia. disease or refractory cases of smoking related DPLD, but 129

Answers and Critiques they should not be instituted in the absence of smoking present with acute respiratory failure, it is important to cessation. evaluate fbr cardiogenic causes. Erraluation should include Immunosuppressant therapies are occasionally used an assessment fbr volume overkrad (jugular venous dis in selected patients with interstitial lung disease. Metho- ter.rtion. S,. peripheral edema). an ECG, echocardiographl'. trexate (Option B) is not used and is not recommended for and measurement of B.type natriuretic peptides and serial patients with DIP or other DPLDs. Methotrexate, particularly serum troponins. Although cardiac contusion can lead to chronic low dose methotrexate. is associated with a small heart failure from valvular injury or cardiac dysfunction. but not insigniflcant risk of pulmonary toxicity, including this patient does not have any erridence thus far to suppod hypersensitivity pneumonitis, organizing pneumonia, acute the diagnosis of pulmonary edema. interstitial pneumonia, and pulmonary flbrosis. Patients rvith pulmonary emboiism (Option D) may Pirfenidone (Option C) is an antiflbrotic agent that present r,vith chest pain, dyspnea, and tachypnea. Chest is FDA approved for the treatment of idiopathic pulmo radiograph may demonstrate peripheral, wedge shaped nary flbrosis. It does not have a role in the management of opacities. but most often the chest radiograph is normal. (,t smoking related DPLD in general or DIP speciflcally. This patient's clinical course is most consistent rt ith ARDS. € .D (EY POIXTS rtY Pollrl UI o, . There are several diffuse parenchymal lung diseases . The diagnosis of acute respiratory distress syndrome EL that occur almost exclusively in persons who are cur- (ARDS) is based on the onset of respiratory failure n rent smokers. within l week of known ARDS insult; bilateral opaci- o For all smoking-related diffuse parenchymal lung ties on chest imaging consistent with pulmonary tt diseases, smoking cessation is the cornerstone of edema; respiratory failure not related to cardiac fail- .D l,} ure or volume overload; and arterial Por/Fto, ratio less treatment. than 300 on at least 5 cm HrO positive end expiratory Bibliography pressure. Kumar A, Cherian SV Vassallo R, et al. Current concepts in pathogenesis, diagnosis, and management of smoking related interstitial lung Bibliography diseases. Chest. 2018;154:394,108. IPMID: 29222007] doi:10.1016/j.chest. 2017.11.023 Thompson B! Chambers RC, Liu KD. Acute respiratory distress syndrome. N Engl J l,led. 2017;377:562 572. IPMID: 28792873) doi:10.1056/NEJMra 1608077

they should not be instituted in the absence of smoking present with acute respiratory failure, it is important to cessation. evaluate fbr cardiogenic causes. Erraluation should include Immunosuppressant therapies are occasionally used an assessment fbr volume overkrad (jugular venous dis in selected patients with interstitial lung disease. Metho- ter.rtion. S,. peripheral edema). an ECG, echocardiographl'. trexate (Option B) is not used and is not recommended for and measurement of B.type natriuretic peptides and serial patients with DIP or other DPLDs. Methotrexate, particularly serum troponins. Although cardiac contusion can lead to chronic low dose methotrexate. is associated with a small heart failure from valvular injury or cardiac dysfunction. but not insigniflcant risk of pulmonary toxicity, including this patient does not have any erridence thus far to suppod hypersensitivity pneumonitis, organizing pneumonia, acute the diagnosis of pulmonary edema. interstitial pneumonia, and pulmonary flbrosis. Patients rvith pulmonary emboiism (Option D) may Pirfenidone (Option C) is an antiflbrotic agent that present r,vith chest pain, dyspnea, and tachypnea. Chest is FDA approved for the treatment of idiopathic pulmo radiograph may demonstrate peripheral, wedge shaped nary flbrosis. It does not have a role in the management of opacities. but most often the chest radiograph is normal. (,t smoking related DPLD in general or DIP speciflcally. This patient's clinical course is most consistent rt ith ARDS. € .D (EY POIXTS rtY Pollrl UI o, . There are several diffuse parenchymal lung diseases . The diagnosis of acute respiratory distress syndrome EL that occur almost exclusively in persons who are cur- (ARDS) is based on the onset of respiratory failure n rent smokers. within l week of known ARDS insult; bilateral opaci- o For all smoking-related diffuse parenchymal lung ties on chest imaging consistent with pulmonary tt diseases, smoking cessation is the cornerstone of edema; respiratory failure not related to cardiac fail- .D l,} ure or volume overload; and arterial Por/Fto, ratio less treatment. than 300 on at least 5 cm HrO positive end expiratory Bibliography pressure. Kumar A, Cherian SV Vassallo R, et al. Current concepts in pathogenesis, diagnosis, and management of smoking related interstitial lung Bibliography diseases. Chest. 2018;154:394,108. IPMID: 29222007] doi:10.1016/j.chest. 2017.11.023 Thompson B! Chambers RC, Liu KD. Acute respiratory distress syndrome. N Engl J l,led. 2017;377:562 572. IPMID: 28792873) doi:10.1056/NEJMra 1608077 tr Item 21 Answer: A Educational Objective: Diagnose acute respiratory Item 22 Answer: A distress syndrome. Educational Objective: Treat shift-work sleep disorder. The most likell' cliagnosis is acute respiratory distress syn The most appropriate management is education and coun- drome (ARDS) (Option A). The diagnosis of ARDS is based seling (Option A). As much as one fifth of the American on the 2012 Berlin criteria: onset urithin 1 week of'knort,r-r work force maintains a job schedule outside of usual day ARDS insult (most are r,r,ithin 72 hours); bilateral opaci shift hours. Although some people acclimate well to this ties on chest imaging consistent rn,ith pulmonary edenra; schedule, many experience excessive sleepiness, mood per respiratory failure not related to cardiac f'ailure or r,.olurne turbations, and neurocognitive dysfunction. Symptoms per overload; arlerial Pori Fro, ratio less than 300 on at least 5 cm sisting at least 3 months meet the criteria for shift work ll,O positive end expiratory pressure (PEEP). Once criteria sleep disorder. Management should flrst include counseling are met. the severitl' of ARDS is based on the arterial P<t,r' that takes into consideration eliminating shift work. If this Fto, ratio: mild, >200 to <300: moderate, 100 to 200; severe. is not feasible, then education about symptom management <100. This patient meets the diagnostic criteria for n-ioderate should be pursued. This patient has difficulty falling asleep ARDS. Her Po,r'Fur, ratio is 132. This palier-rt likely l-ras ARDS after her nighttime shift. Education on avoidance of direct secondary to trauma. sunlight in the ear$ morning (using sunglasses or a dark l)iffuse alveolar hemorrhage (Option B) is the result of bedroom) and avoidance of exertion, eating, and alcohol bleeding into the alveolar spaces secondary to the disruption consumption before the moming sleep period should be ol'the alreolar capillary basement membrane. N,{ost patients provided. Daytime sleepiness may respond to use of caffein present with hemoptysis. altl.rough this might be absent and ated beverages, bright light exposure during the work shift, the diagrrosis neveftheless sugEested lry the appearance of and if feasible, a short (eO-minute) nap, perhaps during a neu,-diftuse or fbcal inliltrates and firlling hemogtobin level. meal break. Considering tl.re relationship of the trauma to the onset of Home sleep apnea testing (Option B), which uses respi respiratory distress and absence clf hernopt_vsis. ARDS is a ratory tools and/or noninvasive measurements of vascular nrore likelv diagnosis. tone, pulse oximetry and an accelerometer to detect posture, Acute cardiogenic pulnronary edema (Option C) can is indicated when there is strong pretest evidence ofobstruc present as hypoxemic respiratory failure. In patients who tive sleep apnea. The suspicion ofobstructive sleep apnea in

tr Item 21 Answer: A Educational Objective: Diagnose acute respiratory Item 22 Answer: A distress syndrome. Educational Objective: Treat shift-work sleep disorder. The most likell' cliagnosis is acute respiratory distress syn The most appropriate management is education and coun- drome (ARDS) (Option A). The diagnosis of ARDS is based seling (Option A). As much as one fifth of the American on the 2012 Berlin criteria: onset urithin 1 week of'knort,r-r work force maintains a job schedule outside of usual day ARDS insult (most are r,r,ithin 72 hours); bilateral opaci shift hours. Although some people acclimate well to this ties on chest imaging consistent rn,ith pulmonary edenra; schedule, many experience excessive sleepiness, mood per respiratory failure not related to cardiac f'ailure or r,.olurne turbations, and neurocognitive dysfunction. Symptoms per overload; arlerial Pori Fro, ratio less than 300 on at least 5 cm sisting at least 3 months meet the criteria for shift work ll,O positive end expiratory pressure (PEEP). Once criteria sleep disorder. Management should flrst include counseling are met. the severitl' of ARDS is based on the arterial P<t,r' that takes into consideration eliminating shift work. If this Fto, ratio: mild, >200 to <300: moderate, 100 to 200; severe. is not feasible, then education about symptom management <100. This patient meets the diagnostic criteria for n-ioderate should be pursued. This patient has difficulty falling asleep ARDS. Her Po,r'Fur, ratio is 132. This palier-rt likely l-ras ARDS after her nighttime shift. Education on avoidance of direct secondary to trauma. sunlight in the ear$ morning (using sunglasses or a dark l)iffuse alveolar hemorrhage (Option B) is the result of bedroom) and avoidance of exertion, eating, and alcohol bleeding into the alveolar spaces secondary to the disruption consumption before the moming sleep period should be ol'the alreolar capillary basement membrane. N,{ost patients provided. Daytime sleepiness may respond to use of caffein present with hemoptysis. altl.rough this might be absent and ated beverages, bright light exposure during the work shift, the diagrrosis neveftheless sugEested lry the appearance of and if feasible, a short (eO-minute) nap, perhaps during a neu,-diftuse or fbcal inliltrates and firlling hemogtobin level. meal break. Considering tl.re relationship of the trauma to the onset of Home sleep apnea testing (Option B), which uses respi respiratory distress and absence clf hernopt_vsis. ARDS is a ratory tools and/or noninvasive measurements of vascular nrore likelv diagnosis. tone, pulse oximetry and an accelerometer to detect posture, Acute cardiogenic pulnronary edema (Option C) can is indicated when there is strong pretest evidence ofobstruc present as hypoxemic respiratory failure. In patients who tive sleep apnea. The suspicion ofobstructive sleep apnea in 130

Answers and Critiques a young woman of normal weight is low; in addition, her that include honeycombing and ground glass opaciflcation. main symptoms are difflculty falling asleep and associated Inhalation ofcoal dust lvithout substantial anlounts ofsilica daytime sleepiness. If the patient's symptoms persist after can result in nodular opacities and eventually massive pul conservative therapy, in-laboratory polysomnography could monilrv fibrosis. These findings are currently less commot.t be considered for a more comprehensive evaluation. because ol improved nrine saf'ery* standards. Pleural effusions Modaflnil (Option C), a novel stimulant, is approved to are llot commonly seen. treat shift work sleep disorder. It should be considered only lnhalation r l hard metal dusts can result in pneumo after conservative measures have failed. Modafinil is limited coniosis. l}posure to the hard metal cobalt (Option C) may by cost and adverse effects, including headache, anxiety, and occur during the procc'ssing ofcobalt or the use ofcobalt by (rarely) serious skin reactions. dian.urnd polishers. Cobalt exposure can result in accumula Hypnotic medications such as zolpidem (Option D) tion of rlveolar mircrophages and multinucleated giant cells have been used to promote daytime sleep but are of varying in the alveolar space, known as giant cell pneumonia. Chest eflectiveness and pose a risk of carryover effects into the imagirrg nray show nodular and reticular opacities and small |a o, work period. Pharmacologic agents are considered second cystic spaces. Pleural elFusions Are uncommon. ET line treatments to counseling, education. and other non- Silicosis describes a spectrum ol fibrotic Ir-rng disease pharmacologic interventions. that results from exposure to silica dust (Option D). Any (J XEY POI lIIS occupation that disturbs the earth's crlrst involves potential !, risk. Workers in industries that cut orgrind silica containing tu o Conservative strategies for shift work sleep disorder to materials. perform sandblasting, or conduct lrydraulic fiack vl promote wakefulness include caffeinated beverages, ir.rg fiir natural gas are at risk. On chest imaging, the disease o B bright-light exposure during the work shift, and short preserlts with grcluncl glass, nodular, interstitial, or fibrotic l naps during breaks. infiltrutes. Pleural eflusions are uncommon with silicosis. . Conservative strategies for shift work sleep disorder to (EY POIilIS promote sleep include avoidance of direct sunlight in o Malignant mesothelioma is associated with occupa- the early morning and avoidance of exertion, eating, tional asbestos exposure in up to 70% ofcases; the and alcohol consumption before the morning sleep radiographic manifestation is usually a unilateral period. pleural effusion or pleural thickening.

a young woman of normal weight is low; in addition, her that include honeycombing and ground glass opaciflcation. main symptoms are difflculty falling asleep and associated Inhalation ofcoal dust lvithout substantial anlounts ofsilica daytime sleepiness. If the patient's symptoms persist after can result in nodular opacities and eventually massive pul conservative therapy, in-laboratory polysomnography could monilrv fibrosis. These findings are currently less commot.t be considered for a more comprehensive evaluation. because ol improved nrine saf'ery* standards. Pleural effusions Modaflnil (Option C), a novel stimulant, is approved to are llot commonly seen. treat shift work sleep disorder. It should be considered only lnhalation r l hard metal dusts can result in pneumo after conservative measures have failed. Modafinil is limited coniosis. l}posure to the hard metal cobalt (Option C) may by cost and adverse effects, including headache, anxiety, and occur during the procc'ssing ofcobalt or the use ofcobalt by (rarely) serious skin reactions. dian.urnd polishers. Cobalt exposure can result in accumula Hypnotic medications such as zolpidem (Option D) tion of rlveolar mircrophages and multinucleated giant cells have been used to promote daytime sleep but are of varying in the alveolar space, known as giant cell pneumonia. Chest eflectiveness and pose a risk of carryover effects into the imagirrg nray show nodular and reticular opacities and small |a o, work period. Pharmacologic agents are considered second cystic spaces. Pleural elFusions Are uncommon. ET line treatments to counseling, education. and other non- Silicosis describes a spectrum ol fibrotic Ir-rng disease pharmacologic interventions. that results from exposure to silica dust (Option D). Any (J XEY POI lIIS occupation that disturbs the earth's crlrst involves potential !, risk. Workers in industries that cut orgrind silica containing tu o Conservative strategies for shift work sleep disorder to materials. perform sandblasting, or conduct lrydraulic fiack vl promote wakefulness include caffeinated beverages, ir.rg fiir natural gas are at risk. On chest imaging, the disease o B bright-light exposure during the work shift, and short preserlts with grcluncl glass, nodular, interstitial, or fibrotic l naps during breaks. infiltrutes. Pleural eflusions are uncommon with silicosis. . Conservative strategies for shift work sleep disorder to (EY POIilIS promote sleep include avoidance of direct sunlight in o Malignant mesothelioma is associated with occupa- the early morning and avoidance of exertion, eating, tional asbestos exposure in up to 70% ofcases; the and alcohol consumption before the morning sleep radiographic manifestation is usually a unilateral period. pleural effusion or pleural thickening. Bibliography o Mesothelioma can have a long latent period, extend- Reis C. Staats R. Pellegrino P, et al. The prevalence ofexcessive sleepiness is ing into decades after asbestos exposure; therefore, it higher in shift workers than in patients with obstructive sleep apnca. is essential to obtain a thorough employment history. J Sleep Res. 2O2O ;29 :e1307 3. [PMI D: l]23959041 doi: 10. I I I 1 rjsr. 13071]

Bibliography o Mesothelioma can have a long latent period, extend- Reis C. Staats R. Pellegrino P, et al. The prevalence ofexcessive sleepiness is ing into decades after asbestos exposure; therefore, it higher in shift workers than in patients with obstructive sleep apnca. is essential to obtain a thorough employment history. J Sleep Res. 2O2O ;29 :e1307 3. [PMI D: l]23959041 doi: 10. I I I 1 rjsr. 13071] Bibliography Item 23 tr Ed ucationa I Objective Answer: A : Diagnose asbestos- related lung Solbes E, tlarper RW. Biological responses to asbestos inhalation and patho genesis ofasbestos related benign and malignant disease. J Investig Mcd. 2018:66 :7 21 7 27. IPMID | 293068691 doi : I 0. I 136/jim 201 7 000628 disease. 'lhc most likely <lccupational erposure is asbestos (Option A). Item 24 Answer: A The nrost likely cliagnosis in this patient is rn:rlignant meso Educational Objective: Diagnose allergic asthma tl.relionra. an aggressive tumor arising front ntesothelial cells. phenotype. i\,,lalignant mesotlrelionra is associated rvith occupational asbestos exposllre in up to 7O"1, <tt'cases. Ptrtients can have The most appropriate diagnostic test for this patient is mea a long latent period, extending into decadc's, befbre man surement of the absolute blood eosinophil count (Option A) . ifesting the disease. Therefore. it is essential b obtain a The patient presents with symptoms suggestive of allergic thoror.rgh emplovment history,: including the use of respira asthma; establishing this asthma phenotype can help direct tor)'protective equipment at the uorkplace. Piitients usually therapy. Clinical characteristics suggesting a type 2 asthma present with chest pain, dyspnea. cough, and restrictive gas phenotype include atopy, seasonal exacerbations, hay fever, exchange abnornralityl The radiographic manif'estation is and allergen sensitization. Biomarker evaluation in these usualll,' a unilaterll pleural ellusion or pleural thickening. patients often demonstrates serum or sputum eosinophilia C'l' is the primary modalitl fbr the diagnosis and staging and/or high IgE levels. This patient has a normal IgE level, ol rnalignant mesothelioma. Prognosis is poor, rvith most but this does not preclude type 2 asthma. Obtaining a blood paticnts dying of local extension of the disease and respira absolute eosinophil count will help establish the phenotype. tory lailure within l2 to 1B rnonths of diagnosis. In patients with severe disease, elevated levels of IgE and lnhalatior.r of coal dust (Option B) may result in coal eosinophils are therapeutic targets for biologic therapies. u'orker's pneumoconi<-lsis. Coal dust n-riry contain high Several types of biologic therapies are available that are concentrations ot silica ancl silicirtes, rthich can result in a directed against type 2 inflammation, targeting pathways rapidly progressivc lung disease with imaging characteristics involved in activation of eosinophils and IgE production.

Bibliography Item 23 tr Ed ucationa I Objective Answer: A : Diagnose asbestos- related lung Solbes E, tlarper RW. Biological responses to asbestos inhalation and patho genesis ofasbestos related benign and malignant disease. J Investig Mcd. 2018:66 :7 21 7 27. IPMID | 293068691 doi : I 0. I 136/jim 201 7 000628 disease. 'lhc most likely <lccupational erposure is asbestos (Option A). Item 24 Answer: A The nrost likely cliagnosis in this patient is rn:rlignant meso Educational Objective: Diagnose allergic asthma tl.relionra. an aggressive tumor arising front ntesothelial cells. phenotype. i\,,lalignant mesotlrelionra is associated rvith occupational asbestos exposllre in up to 7O"1, <tt'cases. Ptrtients can have The most appropriate diagnostic test for this patient is mea a long latent period, extending into decadc's, befbre man surement of the absolute blood eosinophil count (Option A) . ifesting the disease. Therefore. it is essential b obtain a The patient presents with symptoms suggestive of allergic thoror.rgh emplovment history,: including the use of respira asthma; establishing this asthma phenotype can help direct tor)'protective equipment at the uorkplace. Piitients usually therapy. Clinical characteristics suggesting a type 2 asthma present with chest pain, dyspnea. cough, and restrictive gas phenotype include atopy, seasonal exacerbations, hay fever, exchange abnornralityl The radiographic manif'estation is and allergen sensitization. Biomarker evaluation in these usualll,' a unilaterll pleural ellusion or pleural thickening. patients often demonstrates serum or sputum eosinophilia C'l' is the primary modalitl fbr the diagnosis and staging and/or high IgE levels. This patient has a normal IgE level, ol rnalignant mesothelioma. Prognosis is poor, rvith most but this does not preclude type 2 asthma. Obtaining a blood paticnts dying of local extension of the disease and respira absolute eosinophil count will help establish the phenotype. tory lailure within l2 to 1B rnonths of diagnosis. In patients with severe disease, elevated levels of IgE and lnhalatior.r of coal dust (Option B) may result in coal eosinophils are therapeutic targets for biologic therapies. u'orker's pneumoconi<-lsis. Coal dust n-riry contain high Several types of biologic therapies are available that are concentrations ot silica ancl silicirtes, rthich can result in a directed against type 2 inflammation, targeting pathways rapidly progressivc lung disease with imaging characteristics involved in activation of eosinophils and IgE production. 131

Answers and Critiques Use of antibody therapies in eligible patients with severe asthma. 'lhis syndrome occurs in patients \\'ithout preex persistent allergic asthma despite standard therapy reduces isting asthmir following a single. high level exposure to symptoms, exacerbations, and need for oral glucocorticoids. fumes. gases. or vapors. The diagnosis requires er,idence of An o,-antitrypsin level (Option B) should be obtained asthmatic s!'mptoms fbr at least 3 months after the exposure once in all patients with chronic obstructive pulmonary and is confirmed by airway obstruction or bronchial h1'per disease. A pattern of basilar emphysema, associated liver reactivit]'. the SDS includes infbrmation on the properties disease or panniculitis, or a strong family history of emphy of each chemical on site, along rvith the ph1-sical. health. sema in patients with COPD suggests possible cr 1 anti- and environmental hcaltl-r hazards: protective nreasures; trypsin deflciency, but none of these features is sufficiently and safetl'precautions frlr handling, sk)ring, and transport sensitive for the condition. Routine testing is not indicated ing the chemical. In the United States. the Occupational in patients with asthma. Safetl' and Health Administration requires emplovers to Patients with allergic bronchopulmonary aspergillosis make this ir.rfbrmation available upon request lor emplol'ees (ABPA) present with difncult to control asthma, produc- rtho r.r'ork with potentially harmful chenricals. Cleaning UI tive cough, and expectoration of mucus plugs. Commonly products contain volatile chemicals, and acute and chronic accepted diagnostic criteria include elevated IgE levels, pos- inhalation exposures pose respiratory health risks. includ- = .D tl itive skin tests to Asperyillus antigens, increased Aspergillus- ing astl.rma. A list ol agents that can cause occupational o, specific IgE and IgG levels, and either central bronchiectasis asthma is available at: \ rw\ r.cdc.goY r1iosh topics asthnla EL or inflltrates. This patient does not have the clinical pheno- exposures.html. a.l type of ABPA, radiographic flndings, or elevated IgE level If thc patient's sympbms beconre chronic and occupa suggesting ABPA. Measuring Aspergillus-specific IgE level tional asthma is strongly suspected. a combination of objec lrE (Option C) is not indicated. tire evidence of asthma u'ith specific immunologic or skin .D t^ Identifying the presence of atopy can identify an prick testing (Option A) fbr the suspected agent, when avail allergic asthma phenotype in a patient with respiratory able, has a high predictive value for diirgnosis. Additional symptoms. Atopic status can be measured by skin prick tests to evaluate lor occupational respiratory illnesses rna!' testing or measurement of allergen-speciflc IgE testing include bronchoprovocation testing and. in select patients. (Option D). Skin prick testing is rapid, simple, and rel specific inhalational challenges. atively inexpensive. Measurement of immunoglobulin- Bronchoscopy (Option B) does not hare a role in the speciflc IgE is more expensive but not more accurate. diagnosis ot reactive ainvays dysfunction s1'ndronre. It may' However, the flrst management step for this patient is to be considered ilthe clinical picture is at1'pical u,ith concerns measure the total blood eosinophil count to determine his fbr pneumonia or alveolitis. Horver,er. it u'ould not precede asthma phenotype. a rer.ier,v of the SDS r,r,hene'ner an occuprltional lung disease is suspected. rrY P0trlt ln patients rtith clinical symptoms suggestive of o Clinical characteristics suggesting a type 2 asthma bronchospastic disease but n'ith normal spirometr),. phenotype include atopy, seasonal exacerbations, hay bronchoprovocation rvith a methacholine challengc test fever, and allergen sensitization. (Option C) can be used to identifl' bronchial hyperre o For patients with symptoms suggestive of type 2 asthma sponsiveness. Bronchial challenge testing uses a con phenotype, measurement of IgE levels and total eosino trolled inhaled stimulus to induce bronchospasm in phil count canbe used to confirm this asthma phenotype association u'ith spirometr)'r a positive test is indicated and direct therapy. by a drop in the measured FEV,. Due to the risk of an exaggerated response as well as dilflculties u,ith interpreta Bibliography tion. metl-racholine challenge testing is contraindicated in patients r,vith airflou' lirnitation (FE\'<60"i, ol predicted McGregor MC, Krings JG, Nair B et al. Role of biologics in asthma. Am l Respir Crit Care Med. 2019;199:433-445. [PMID: 30525902] doi:10.1164/ or FE\', <1.5 [. ir.r adults). In this patient u'ith an fiE\ir of rccm.201810-1944CI 55'1, of predicted, methacl.roline challenge testing uould be inappropriate. Item 25 Answer: D XEY POIXI Educational Objective: Evaluate occupational lung o When an occupational lung disease is suspected, disease using the employer Safety Data Sheet. clinicians should request a Safety Data Sheet (SDS) The most appropriate next diagnostic step is review of the from the patient's employer; the SDS details chemical Saf'ety Data Sheet (SDS) (Option D). The patient's history properties and known health risks associated with suggests a discrete temporal relationship to an acciden- substances at the workplace. tal irritant exposure and onset of respiratory symptonls consistent with a diagnosis of reactive airways dysfunc Bibliography Rosenman K, Reilly MJ, Pechter E, et al. Cleaning products and work-related tion syndrome. Reactive airways dysfunction syndrome is asthma, 10 year update. J Occup Environ Med. 2020;62:130 137. [PMID: a well described subset of irritant induced occupational 318957371 doi:1O.1O97lJoM.0O0000OOOOOO1771

Use of antibody therapies in eligible patients with severe asthma. 'lhis syndrome occurs in patients \\'ithout preex persistent allergic asthma despite standard therapy reduces isting asthmir following a single. high level exposure to symptoms, exacerbations, and need for oral glucocorticoids. fumes. gases. or vapors. The diagnosis requires er,idence of An o,-antitrypsin level (Option B) should be obtained asthmatic s!'mptoms fbr at least 3 months after the exposure once in all patients with chronic obstructive pulmonary and is confirmed by airway obstruction or bronchial h1'per disease. A pattern of basilar emphysema, associated liver reactivit]'. the SDS includes infbrmation on the properties disease or panniculitis, or a strong family history of emphy of each chemical on site, along rvith the ph1-sical. health. sema in patients with COPD suggests possible cr 1 anti- and environmental hcaltl-r hazards: protective nreasures; trypsin deflciency, but none of these features is sufficiently and safetl'precautions frlr handling, sk)ring, and transport sensitive for the condition. Routine testing is not indicated ing the chemical. In the United States. the Occupational in patients with asthma. Safetl' and Health Administration requires emplovers to Patients with allergic bronchopulmonary aspergillosis make this ir.rfbrmation available upon request lor emplol'ees (ABPA) present with difncult to control asthma, produc- rtho r.r'ork with potentially harmful chenricals. Cleaning UI tive cough, and expectoration of mucus plugs. Commonly products contain volatile chemicals, and acute and chronic accepted diagnostic criteria include elevated IgE levels, pos- inhalation exposures pose respiratory health risks. includ- = .D tl itive skin tests to Asperyillus antigens, increased Aspergillus- ing astl.rma. A list ol agents that can cause occupational o, specific IgE and IgG levels, and either central bronchiectasis asthma is available at: \ rw\ r.cdc.goY r1iosh topics asthnla EL or inflltrates. This patient does not have the clinical pheno- exposures.html. a.l type of ABPA, radiographic flndings, or elevated IgE level If thc patient's sympbms beconre chronic and occupa suggesting ABPA. Measuring Aspergillus-specific IgE level tional asthma is strongly suspected. a combination of objec lrE (Option C) is not indicated. tire evidence of asthma u'ith specific immunologic or skin .D t^ Identifying the presence of atopy can identify an prick testing (Option A) fbr the suspected agent, when avail allergic asthma phenotype in a patient with respiratory able, has a high predictive value for diirgnosis. Additional symptoms. Atopic status can be measured by skin prick tests to evaluate lor occupational respiratory illnesses rna!' testing or measurement of allergen-speciflc IgE testing include bronchoprovocation testing and. in select patients. (Option D). Skin prick testing is rapid, simple, and rel specific inhalational challenges. atively inexpensive. Measurement of immunoglobulin- Bronchoscopy (Option B) does not hare a role in the speciflc IgE is more expensive but not more accurate. diagnosis ot reactive ainvays dysfunction s1'ndronre. It may' However, the flrst management step for this patient is to be considered ilthe clinical picture is at1'pical u,ith concerns measure the total blood eosinophil count to determine his fbr pneumonia or alveolitis. Horver,er. it u'ould not precede asthma phenotype. a rer.ier,v of the SDS r,r,hene'ner an occuprltional lung disease is suspected. rrY P0trlt ln patients rtith clinical symptoms suggestive of o Clinical characteristics suggesting a type 2 asthma bronchospastic disease but n'ith normal spirometr),. phenotype include atopy, seasonal exacerbations, hay bronchoprovocation rvith a methacholine challengc test fever, and allergen sensitization. (Option C) can be used to identifl' bronchial hyperre o For patients with symptoms suggestive of type 2 asthma sponsiveness. Bronchial challenge testing uses a con phenotype, measurement of IgE levels and total eosino trolled inhaled stimulus to induce bronchospasm in phil count canbe used to confirm this asthma phenotype association u'ith spirometr)'r a positive test is indicated and direct therapy. by a drop in the measured FEV,. Due to the risk of an exaggerated response as well as dilflculties u,ith interpreta Bibliography tion. metl-racholine challenge testing is contraindicated in patients r,vith airflou' lirnitation (FE\'<60"i, ol predicted McGregor MC, Krings JG, Nair B et al. Role of biologics in asthma. Am l Respir Crit Care Med. 2019;199:433-445. [PMID: 30525902] doi:10.1164/ or FE\', <1.5 [. ir.r adults). In this patient u'ith an fiE\ir of rccm.201810-1944CI 55'1, of predicted, methacl.roline challenge testing uould be inappropriate. Item 25 Answer: D XEY POIXI Educational Objective: Evaluate occupational lung o When an occupational lung disease is suspected, disease using the employer Safety Data Sheet. clinicians should request a Safety Data Sheet (SDS) The most appropriate next diagnostic step is review of the from the patient's employer; the SDS details chemical Saf'ety Data Sheet (SDS) (Option D). The patient's history properties and known health risks associated with suggests a discrete temporal relationship to an acciden- substances at the workplace. tal irritant exposure and onset of respiratory symptonls consistent with a diagnosis of reactive airways dysfunc Bibliography Rosenman K, Reilly MJ, Pechter E, et al. Cleaning products and work-related tion syndrome. Reactive airways dysfunction syndrome is asthma, 10 year update. J Occup Environ Med. 2020;62:130 137. [PMID: a well described subset of irritant induced occupational 318957371 doi:1O.1O97lJoM.0O0000OOOOOO1771 132

I Answers and Critiques Item 26 Answer: D Bibliography l-ederer DJ, Martinez FJ. ldiopathic pulmonary fibrosis. N Ilngl J Med. 2018; Ed u catio na I Obj ective : Diagnose diffu se parenchymal 378:1811 1823. [PMID: 29742380] doi:10.1056/NElMra1705751 lung disease.

Item 26 Answer: D Bibliography l-ederer DJ, Martinez FJ. ldiopathic pulmonary fibrosis. N Ilngl J Med. 2018; Ed u catio na I Obj ective : Diagnose diffu se parenchymal 378:1811 1823. [PMID: 29742380] doi:10.1056/NElMra1705751 lung disease. The most appropriate diagnostic test to perform next is high resolution chest CT (HRCT) (Option D). This patient has symptoms and clinical flndings suggestive of a diffuse Item 27 Answer: C Educational Objective: Treat pulmonary embolism in a tr parenchymal lung disease (DPLD). Nonproductive cough pregnant woman. and dyspnea are the most common presenting symptoms of 'lhe mclst appropritte treatnlent is l<.rw molecular weight DPLD. Findings on chest auscultation can be variable, but heparin (Option C). The Americrn Society of Henrir the presence ofinspiratory dry crackles and clubbing is com tolog, (ASII) 20lB guidelincs fbr nriinagement ol venous patible with a DPLD such as idiopathic pulmonary flbrosis. tl-rromboembolisn-r in the context of pregntncy recont Other flndings supporting the diagnosis of DPLD include l,l nrend low molecular weight heparin (LMWIl). LiVIWtl is o, chest radiograph showing small lung volumes, unexplained stror, gly recommcnded orcr unfractionated heparin (UFH). bibasilar inflltrates, restrictive physiolory, and a reduced ET r\ntitl.rronrbotic therapy markedly rcduces rlrtrt:rlity in Dlco. HRCT will help conflrm the diagnosis of DPLD and nonpregrlant and pregnant patients with acute venous L' may also narrow the differential diagnosis. For example, thrombocmbolism (V'lE). l-MWtl is at least as eflbctive as =l the addition of expiratory images can help diagnose small Uf ii in thc treatment of V'l'lr in pregnant patients. and tlte .E airway disease, and prone images can help exclude depen- t risks of irleeding are similar with the two agents. Extencled (u dent atelectasis as a potential confounder. In an appropriate tuse of UF-[J during pregnillrcv is associated with a risk <tf clinical setting, typical HRCT flndings may obviate the need UI = osteoporotic f'racture ot2.')'l;,. There is limited clata on bone for lung biopsy. health irr pregnant \ romen rcceiving t.N4WIl. but in non The findings on HRCT highly correlate with histopa- pregnant \ (xlen thc risk o1'fracture appears tti be higher in thologr identifled on open lung biopsy; consequently, biopsy women receiving UIH contpared with LN,4WH. In additiorr. is not uniformly required to establish a diagnosis. Lung the risk of heparir.r induced tl.rromhocytopenia is higher biopsy, either bronchoscopic (Option A) or surgical, may be in nonpregnant women treated lvith UI,'I1 contpared r,r,ith considered in settings in which pulmonary function tests LMWH (2.7')i, r,ersus 0'){,). !'inall1,. thc ASH guideline r.rotes and HRCT are insufficient to make a diagnosis. that the closing of LMWH is nrore prediclable thirn UFII. and In the evaluation of dyspnea, cardiopulmonary exercise laboratory testing is generally unnecessary, n.raking treat testing (Option B) can be helpful if the initial evaluation nlent more convenient. is unrevealing, deconditioning is a possibiliry or multiple There is linritccl data on the safbty of the direct oral problems may be contributing to dyspnea. However, this anticoagulants (clabigatran, apixaban, ecloxaban, and rivar patient's symptoms, chest radiograph, and spirometry sug oxaban) (Options A, D) in pregnant \!on1er1. Since tl.rey are gest a DPLD. Cardiopulmonary exercise testing will not add likely to cross the placenta ancl their reproductive efi'ects in to the diagnostic yield. humans are unknown, the ASI I gr.ricicline does not reconr CT angiography (Option C) of the chest will also provide mend ther.n {br pregr.rant w'ornen. Finally, dabigirtran is n<tt a reasonable assessment of the pulmonary parenchyma and is approvecl as rnonotherapy tor \iTE; it lnust be preceded lry the diagnostic modality of choice for pulmonary embolism, an heparin therapy. unlikely diagnosis for a patient with dyspnea progressing over Fondaparir.rux (Option B) is not recomnrenclecl fbr first 7 months. In addition, contrast is not needed for the delin- line therupy o1 Vl'ti in pregnancy because this drug l.ras eation ol DPLDs and adds the unnecessary risk of contrast been reported to cross the placenta ir.r small ant<tunts. and induced nephropathy. Although the addition of contrast can cxperience $,ith fbndaparintrx in pregllallcy is very lintited help delineate mediastinal lymphadenopathy, there is no sug- (especiallv dr.rring the first trimester). gestion of Iymphadenopathy on this patient's chest radiograph. Vitanrin K antigonists such as warl'arin (Option E) arc Evaluation with transthoracic echocardiogram (Option E) not cclnsiclered acceptable therapy for pregnancy associatecl can be used to exclude left sided heart failure and assess lor V'fE. Warfarin crosses the placenta ancl has the potential pulmonary hypertension. This patient, however, does not to callse teratogenicity. pregnancy loss, fetal bleeding, and have any clinical or radiologic signs of heart failure (elevated neurodevelopmental deficits. Irr pregnant patients with V'l't.|. central venous pressure, S.,, edema, cardiomegaly, pulmo acceptable irlternltives are available. Warfarin is recon-r nary congestion) or pulmonary hypertension (flxed splitting mended irr pregnant women with rnechanical heart valves of Sr, prominent venous o wave, enlarged central pulmonary if the dose is less thiur 5 mg daily. arteries, and prominent right ventricle). XEY POITTI XEY POITT . In pregnant patients, low-molecular-weight heparin o In a patient with a clinical picture suggestive of diffuse is the preferred treatment for venous thromboembo- parenchymal lung disease, high-resolution CT is the lism disease' most appropriate diagnostic test. (continued)

The most appropriate diagnostic test to perform next is high resolution chest CT (HRCT) (Option D). This patient has symptoms and clinical flndings suggestive of a diffuse Item 27 Answer: C Educational Objective: Treat pulmonary embolism in a tr parenchymal lung disease (DPLD). Nonproductive cough pregnant woman. and dyspnea are the most common presenting symptoms of 'lhe mclst appropritte treatnlent is l<.rw molecular weight DPLD. Findings on chest auscultation can be variable, but heparin (Option C). The Americrn Society of Henrir the presence ofinspiratory dry crackles and clubbing is com tolog, (ASII) 20lB guidelincs fbr nriinagement ol venous patible with a DPLD such as idiopathic pulmonary flbrosis. tl-rromboembolisn-r in the context of pregntncy recont Other flndings supporting the diagnosis of DPLD include l,l nrend low molecular weight heparin (LMWIl). LiVIWtl is o, chest radiograph showing small lung volumes, unexplained stror, gly recommcnded orcr unfractionated heparin (UFH). bibasilar inflltrates, restrictive physiolory, and a reduced ET r\ntitl.rronrbotic therapy markedly rcduces rlrtrt:rlity in Dlco. HRCT will help conflrm the diagnosis of DPLD and nonpregrlant and pregnant patients with acute venous L' may also narrow the differential diagnosis. For example, thrombocmbolism (V'lE). l-MWtl is at least as eflbctive as =l the addition of expiratory images can help diagnose small Uf ii in thc treatment of V'l'lr in pregnant patients. and tlte .E airway disease, and prone images can help exclude depen- t risks of irleeding are similar with the two agents. Extencled (u dent atelectasis as a potential confounder. In an appropriate tuse of UF-[J during pregnillrcv is associated with a risk <tf clinical setting, typical HRCT flndings may obviate the need UI = osteoporotic f'racture ot2.')'l;,. There is limited clata on bone for lung biopsy. health irr pregnant \ romen rcceiving t.N4WIl. but in non The findings on HRCT highly correlate with histopa- pregnant \ (xlen thc risk o1'fracture appears tti be higher in thologr identifled on open lung biopsy; consequently, biopsy women receiving UIH contpared with LN,4WH. In additiorr. is not uniformly required to establish a diagnosis. Lung the risk of heparir.r induced tl.rromhocytopenia is higher biopsy, either bronchoscopic (Option A) or surgical, may be in nonpregnant women treated lvith UI,'I1 contpared r,r,ith considered in settings in which pulmonary function tests LMWH (2.7')i, r,ersus 0'){,). !'inall1,. thc ASH guideline r.rotes and HRCT are insufficient to make a diagnosis. that the closing of LMWH is nrore prediclable thirn UFII. and In the evaluation of dyspnea, cardiopulmonary exercise laboratory testing is generally unnecessary, n.raking treat testing (Option B) can be helpful if the initial evaluation nlent more convenient. is unrevealing, deconditioning is a possibiliry or multiple There is linritccl data on the safbty of the direct oral problems may be contributing to dyspnea. However, this anticoagulants (clabigatran, apixaban, ecloxaban, and rivar patient's symptoms, chest radiograph, and spirometry sug oxaban) (Options A, D) in pregnant \!on1er1. Since tl.rey are gest a DPLD. Cardiopulmonary exercise testing will not add likely to cross the placenta ancl their reproductive efi'ects in to the diagnostic yield. humans are unknown, the ASI I gr.ricicline does not reconr CT angiography (Option C) of the chest will also provide mend ther.n {br pregr.rant w'ornen. Finally, dabigirtran is n<tt a reasonable assessment of the pulmonary parenchyma and is approvecl as rnonotherapy tor \iTE; it lnust be preceded lry the diagnostic modality of choice for pulmonary embolism, an heparin therapy. unlikely diagnosis for a patient with dyspnea progressing over Fondaparir.rux (Option B) is not recomnrenclecl fbr first 7 months. In addition, contrast is not needed for the delin- line therupy o1 Vl'ti in pregnancy because this drug l.ras eation ol DPLDs and adds the unnecessary risk of contrast been reported to cross the placenta ir.r small ant<tunts. and induced nephropathy. Although the addition of contrast can cxperience $,ith fbndaparintrx in pregllallcy is very lintited help delineate mediastinal lymphadenopathy, there is no sug- (especiallv dr.rring the first trimester). gestion of Iymphadenopathy on this patient's chest radiograph. Vitanrin K antigonists such as warl'arin (Option E) arc Evaluation with transthoracic echocardiogram (Option E) not cclnsiclered acceptable therapy for pregnancy associatecl can be used to exclude left sided heart failure and assess lor V'fE. Warfarin crosses the placenta ancl has the potential pulmonary hypertension. This patient, however, does not to callse teratogenicity. pregnancy loss, fetal bleeding, and have any clinical or radiologic signs of heart failure (elevated neurodevelopmental deficits. Irr pregnant patients with V'l't.|. central venous pressure, S.,, edema, cardiomegaly, pulmo acceptable irlternltives are available. Warfarin is recon-r nary congestion) or pulmonary hypertension (flxed splitting mended irr pregnant women with rnechanical heart valves of Sr, prominent venous o wave, enlarged central pulmonary if the dose is less thiur 5 mg daily. arteries, and prominent right ventricle). XEY POITTI XEY POITT . In pregnant patients, low-molecular-weight heparin o In a patient with a clinical picture suggestive of diffuse is the preferred treatment for venous thromboembo- parenchymal lung disease, high-resolution CT is the lism disease' most appropriate diagnostic test. (continued) 133

Answers and l f EY POltTt (onflnucd) f,EY POIilI5 . Because there are limited data on the safety of direct o Point of-care thoracic ultrasonography can determine oral anticoagulants and fondaparinux in pregnancy, the presence or absence of a pneumothorax or pleural they are not recommended. effusion and can characterize the lung parenchyma to aid in the detection of heart failure or pneumonia. Bibliography o Point-of-care thoracic ultrasonography is particularly Bates SM, Rajasekhar A, Middeldorp S, et al. American Society of Hematolos, 2018 guidelines fbr m:rnagement of venous thromboembolism: venous helpful for critically ill patients when the use of thromboembolism in the context ofpregnancy. Blood Adv 2018;2:3317 imaging techniques requiring transport would delay 3359. IPMID: 30482767] doi:10.1182,rbloodadvances.2O18O248O2 diagnosis.

f EY POltTt (onflnucd) f,EY POIilI5 . Because there are limited data on the safety of direct o Point of-care thoracic ultrasonography can determine oral anticoagulants and fondaparinux in pregnancy, the presence or absence of a pneumothorax or pleural they are not recommended. effusion and can characterize the lung parenchyma to aid in the detection of heart failure or pneumonia. Bibliography o Point-of-care thoracic ultrasonography is particularly Bates SM, Rajasekhar A, Middeldorp S, et al. American Society of Hematolos, 2018 guidelines fbr m:rnagement of venous thromboembolism: venous helpful for critically ill patients when the use of thromboembolism in the context ofpregnancy. Blood Adv 2018;2:3317 imaging techniques requiring transport would delay 3359. IPMID: 30482767] doi:10.1182,rbloodadvances.2O18O248O2 diagnosis. D ut tr Item 28 Answer: A Educational Objective: Diagnose the cause of acute Bibliography Mayo PH, Copetti R, Feller-Kopman D, et al. Thoracic ultrasonography: a narrative review. Intensive Care Med. 2019;45:1200 1211. IPMID: E respiratory deterioration in a critically ill patient with 314180601 doi:10.1007,'s00lil.l 019-05725 8 o bedside thoracic ultrasonography. U) o, CL n The most appropriate next step is to perform bedside ultraso- nography (Option A). Point-of-care thoracic ultrasonography provides a noninvasive means of rapidly assessing the lungs, Item 29 Answer: D Educational Objective: Diagnose small cell lung cancer. tr It pleura. and diaphragm. It is particularly helpful fbr critically The most likely diagrrosis is small cell lung cancer (Option D). E (D ill patients when the use of imaging techniques requiring There are fvvo major classes ol lung cancer: non-small cell UI transpoft would delay diagnosis. Thoracic ultrasonography lung cancer (NSCLC) and small cell lung cancer (SCI-C). can determine the presence or absence ofa pneumothorax or Small cell lung cancer typically presents as bulky symptom- pleural effusion and can characterize the lung parenchyma to atic masses with mediastinal involvement. It originates from aid in the detection of heart failure or pneumonia. Potential neuroendocrine cell precursors and is characterized by rapid causes ofworsening gas exchange include increasing pleural growth and early metastases. Extrathoracic spread is present effusion, developnrent of a pneumothorax, and worsening o1 in75'/"to B0'1, of patients at initial diagnosis. Symptom onset underlying pneumonia or heart failure, all ol which can be is rapid (typically <B 12 weeks) and inclucles cough. wheez rapidly assessed using point of:care ultrasonography. ing, dyspnea. hemoptysis, weight loss. fatigue. anorexia. CT of the chest (Option B) is an option, but it will take and manil'estations of paraneoplastic syndromes. The most longer to perform than bedside thoracic ultrasonography, frequent paraneoplastic syndrome is the syndrome of inap which will delay diagnosis and will also require transport of propriate antidiuretic hormone secretion (SIADH). This syn an unstable patient. drome results from production of antidiuretic hormone by The use of paralytic agents such as cisatracurium malignant cells. Other paraneoplastic syndromes associ (Option C) in patients u,ith severe acute respiratory distress ated with SCI-C include Cushing syndrome, Lambert Baton disorder (ARDS) may improve oxygenation. decrease venti syndrome, encephalomyelitis, and sensory neuropathy. This lator induced lung injury. and reduce mortality. lndications patient has a lung mass with bulky mediastinal lymphade inclucle agitation, unclesired movement, and ventilator dys- nopathy and hyponatren.ria (secondary to SIADH). making synchrony. Hou,ever, use of these agents is not fi rst line ther sn.rall cell lung cancer the most likely diagnosis. apy lor these conditions and is typically initiated only when Approximately 80'2, of' lung cancer cases are NSCLC. sedation and analgesia fail to control these symptoms. How. which is divided into adenocarcinoma. squamous cell carci ever, this patient has not yet been diagnosed with ARDS, and noma. and large cell carcinoma. Adenocarcinoma (Option A) there is likely anothcr more easily re'"ersible cause fbr this is the most common NSCLC and accounts for almost all lung patient's acute decline that can be diagnosed with bedside cancer diagnoses in nonsmokers. The most frequent location thoracic ultrasonographl: of adenocarcinoma is in the peripheral aspects of thc lung Tension pneumothorax should be suspectecl in patients parenchyma as a solitary nodule or mass. Squamous cell presenting with signi ficant cardiorespiratory distress (wors carcinoma is the second most common subtype of NSCI.C. It ening dyspnea, hypotension, absent breath sounds on one correlates highly l,r,ith smoking history and usually originates side, tracheal deviation, and distended neck veins). A ten- in the central airways. Large cell carcinoma (Option C) is an sion pneumothorax that is large and hemodynamically undifferentiated carcinoma and characteristically prcsents signiticant should be managed by emergent needle thoracos as a peripheral mass with prominent necrosis. Adenocar tomy (Option D) lollowed by thoracostomy tube placement cinoma and large cell carcinoma are not associated with and hospitalization. The patient's findings do not fully sup SIADH reluted hl ponatremil. port the diagnosis of tension pncumothorax, and emer Fibrosing mediastinitis (Option B) is a rare complication gent needle thoracostomy is not indicated. Bedside thoracic of previous histoplasmosis. It is characterized by an excessive ultrasonography may quickly providc a diagnosis and guide fibrotic reaction in the mediastinum and can cause compres- appropriate therapy. sion of adjaccnt structurcs, such as thc airways, vessels, and

D ut tr Item 28 Answer: A Educational Objective: Diagnose the cause of acute Bibliography Mayo PH, Copetti R, Feller-Kopman D, et al. Thoracic ultrasonography: a narrative review. Intensive Care Med. 2019;45:1200 1211. IPMID: E respiratory deterioration in a critically ill patient with 314180601 doi:10.1007,'s00lil.l 019-05725 8 o bedside thoracic ultrasonography. U) o, CL n The most appropriate next step is to perform bedside ultraso- nography (Option A). Point-of-care thoracic ultrasonography provides a noninvasive means of rapidly assessing the lungs, Item 29 Answer: D Educational Objective: Diagnose small cell lung cancer. tr It pleura. and diaphragm. It is particularly helpful fbr critically The most likely diagrrosis is small cell lung cancer (Option D). E (D ill patients when the use of imaging techniques requiring There are fvvo major classes ol lung cancer: non-small cell UI transpoft would delay diagnosis. Thoracic ultrasonography lung cancer (NSCLC) and small cell lung cancer (SCI-C). can determine the presence or absence ofa pneumothorax or Small cell lung cancer typically presents as bulky symptom- pleural effusion and can characterize the lung parenchyma to atic masses with mediastinal involvement. It originates from aid in the detection of heart failure or pneumonia. Potential neuroendocrine cell precursors and is characterized by rapid causes ofworsening gas exchange include increasing pleural growth and early metastases. Extrathoracic spread is present effusion, developnrent of a pneumothorax, and worsening o1 in75'/"to B0'1, of patients at initial diagnosis. Symptom onset underlying pneumonia or heart failure, all ol which can be is rapid (typically <B 12 weeks) and inclucles cough. wheez rapidly assessed using point of:care ultrasonography. ing, dyspnea. hemoptysis, weight loss. fatigue. anorexia. CT of the chest (Option B) is an option, but it will take and manil'estations of paraneoplastic syndromes. The most longer to perform than bedside thoracic ultrasonography, frequent paraneoplastic syndrome is the syndrome of inap which will delay diagnosis and will also require transport of propriate antidiuretic hormone secretion (SIADH). This syn an unstable patient. drome results from production of antidiuretic hormone by The use of paralytic agents such as cisatracurium malignant cells. Other paraneoplastic syndromes associ (Option C) in patients u,ith severe acute respiratory distress ated with SCI-C include Cushing syndrome, Lambert Baton disorder (ARDS) may improve oxygenation. decrease venti syndrome, encephalomyelitis, and sensory neuropathy. This lator induced lung injury. and reduce mortality. lndications patient has a lung mass with bulky mediastinal lymphade inclucle agitation, unclesired movement, and ventilator dys- nopathy and hyponatren.ria (secondary to SIADH). making synchrony. Hou,ever, use of these agents is not fi rst line ther sn.rall cell lung cancer the most likely diagnosis. apy lor these conditions and is typically initiated only when Approximately 80'2, of' lung cancer cases are NSCLC. sedation and analgesia fail to control these symptoms. How. which is divided into adenocarcinoma. squamous cell carci ever, this patient has not yet been diagnosed with ARDS, and noma. and large cell carcinoma. Adenocarcinoma (Option A) there is likely anothcr more easily re'"ersible cause fbr this is the most common NSCLC and accounts for almost all lung patient's acute decline that can be diagnosed with bedside cancer diagnoses in nonsmokers. The most frequent location thoracic ultrasonographl: of adenocarcinoma is in the peripheral aspects of thc lung Tension pneumothorax should be suspectecl in patients parenchyma as a solitary nodule or mass. Squamous cell presenting with signi ficant cardiorespiratory distress (wors carcinoma is the second most common subtype of NSCI.C. It ening dyspnea, hypotension, absent breath sounds on one correlates highly l,r,ith smoking history and usually originates side, tracheal deviation, and distended neck veins). A ten- in the central airways. Large cell carcinoma (Option C) is an sion pneumothorax that is large and hemodynamically undifferentiated carcinoma and characteristically prcsents signiticant should be managed by emergent needle thoracos as a peripheral mass with prominent necrosis. Adenocar tomy (Option D) lollowed by thoracostomy tube placement cinoma and large cell carcinoma are not associated with and hospitalization. The patient's findings do not fully sup SIADH reluted hl ponatremil. port the diagnosis of tension pncumothorax, and emer Fibrosing mediastinitis (Option B) is a rare complication gent needle thoracostomy is not indicated. Bedside thoracic of previous histoplasmosis. It is characterized by an excessive ultrasonography may quickly providc a diagnosis and guide fibrotic reaction in the mediastinum and can cause compres- appropriate therapy. sion of adjaccnt structurcs, such as thc airways, vessels, and 134

Answers and Critiques [[ esophagus. I--ibrosing mediastirritis usually alfects youl.rger Treatment with wartarin (Option D) has also not llJ prrtients. slon,ly progresses over 2 to 5 years, and has calci- shown any beneflt and is associated with an increased risk coNr fications on inlaging. 'lhus. it is iin unlikely cliagnosis irr this of mortality in patients who lack other indications fbr anti- patient. coagulation.

[[ esophagus. I--ibrosing mediastirritis usually alfects youl.rger Treatment with wartarin (Option D) has also not llJ prrtients. slon,ly progresses over 2 to 5 years, and has calci- shown any beneflt and is associated with an increased risk coNr fications on inlaging. 'lhus. it is iin unlikely cliagnosis irr this of mortality in patients who lack other indications fbr anti- patient. coagulation. I(EY POIl{T I(EY POIXTS r Small cell lung cancer typically presents as bulky . Therapy with pirfenidone or nintedanib decreases the symptomatic masses with mediastinal involvement, rate of progression of idiopathic pulmonary fibrosis and is associated with paraneoplastic syndromes- but is not curative. most frequently, the syndrome of inappropriate anti- r In patients with idiopathic pulmonary fibrosis, lung diuretic hormone secretion. transplantation is a life-prolonging therapy for those without comorbidities that may otherwise limit life Bibliography ut expectancy. o \\hng S, Zimmermann S. Plrikh K, et al. Current diagnosis and mJl.lilgement of small cell lung clncer. Mayo Clin Proc. 2019;94:1599 1622. IPMID: ET 1113782351 doi:10.1016/j.mayocp.20l9.01.O3.1 Bibliography Lederer Dl. l\.,lartinez FJ. ldiopathic pulnronary librosis. N Engl J Med. 2018: f-, 378:1811 1823. IPMID: 297.12380] doi: 10.1056 rNI'.J N4ra1705751 t =t Item 30 Answer: B t! UI Educational Objective: Treat idiopathic pulmonary a, Item 31 fibrosis.

I(EY POIl{T I(EY POIXTS r Small cell lung cancer typically presents as bulky . Therapy with pirfenidone or nintedanib decreases the symptomatic masses with mediastinal involvement, rate of progression of idiopathic pulmonary fibrosis and is associated with paraneoplastic syndromes- but is not curative. most frequently, the syndrome of inappropriate anti- r In patients with idiopathic pulmonary fibrosis, lung diuretic hormone secretion. transplantation is a life-prolonging therapy for those without comorbidities that may otherwise limit life Bibliography ut expectancy. o \\hng S, Zimmermann S. Plrikh K, et al. Current diagnosis and mJl.lilgement of small cell lung clncer. Mayo Clin Proc. 2019;94:1599 1622. IPMID: ET 1113782351 doi:10.1016/j.mayocp.20l9.01.O3.1 Bibliography Lederer Dl. l\.,lartinez FJ. ldiopathic pulnronary librosis. N Engl J Med. 2018: f-, 378:1811 1823. IPMID: 297.12380] doi: 10.1056 rNI'.J N4ra1705751 t =t Item 30 Answer: B t! UI Educational Objective: Treat idiopathic pulmonary a, Item 31 fibrosis. The most appropriate treatment is antiflbrotic therapy with Answer: D Educational Objective: Minimize sedation in ventilated tr vt = E patients in the ICU. pirfenidone (Option B). This patient has idiopathic pulmo nary fibrosis (lPF). Patients with IPF present with chronic The most approprirte managemcnt is to hold the sedation shortness of breath and a dry cough. Patients typically have and analgesia inlusions (Option D). I.'or acutely hospital bibasilar inspiratory Velcro like crackles, and clubbing is ized patients ventilated fbr more than 24 hours, guidelines common. The prevalence of disease increases with age. A suggest protocols to reducc sedation. Sedative analgesic confldent diagnosis can be made based on the presence nredic:rtions can cause excess sedation iincl may prolor-rg of typical symptoms and a usual interstitial pneumonia the duration of mechanical ventilation. ln randomizcd clin- pattern on a high resolution CT scan of the chest. IPF is ical trials, two strategies have been showr] to be ellcctive in progressive, with a median survival of :l to 5 years after reducir.rg the duration olmechanical ventilation and its asso diagnosis. ln 2014 the FDA approved two medications: pir- ciated complication. The first strategy consists of intenrrit fenidone, an antiflbrotic agent, and nintedanib, a tyrosine tcnt intravenous administration of analgcsia witl-rout sed- kinase inhibitor, for use in patients with IPF. In clinical atires (analgesia first approacl'r). A secor-rd strategy cor-rsists triais the two agents were found to have comparable effl of daily' interruption of' continuous intusior-r of ar.ralgesics cacy in mitigating the rate of FVC decline by approximately and sedatives. !'ariltions of these protocols exist. including 50'1, over the course of 1 year. They have also shown some targeting Iight sedation. The oplimal strategy is not knowr-r, eflicacy in reducing severe respiratory events such as acute and guidelines o{ler no prelerencc due to insufficient data. exacerbations and hospitalization. Common side efl'ects but a1l have in comnron periocls oltinte in rvhich the patient are anorexia, nausea, photosensitivity (pirfenidone), and is arvakc. When implcmentecl routinely, probcols that lirnit diarrhea (nintedanib). Although these medications delay sedatiot't or allow spontaneolls awakening n,ill decrease the IPF progression, they are not curative. Relerral to a pulm lengtl.t of rnechanical ventilation. ICU stall and incicience of onologist or interstitial lung disease center may be appro delirium. In this cleeply sedatecl patient. stopping seclation priate belbre initiating treatment with these medications. and analgesics now will allow the fastest clecrease in rnedi Lung transplantation is a life prolonging therapy for those cation levels. thus lllou,ing:lsscssnlent ol thc patient. without comorbidities that may otherwise limit life expec- Titrirtion of sedutior.r medication (Option A) lt,ill also tancy. Early referral ol eligible patients to a transplant lead to arousal. Ilowever, thc time to rcach steacly state center is appropriate given the unpredictability of disease rfter decrcasing thc infusion rltc of a sedative is prolongecl progression. (7 half livcs). thr.rs ;lrolonging thc time until an appropriate A clinical trial of N acetylcysteine monotherapy nenroklgic cxaminirt iol1. (Option A) did not show any beneflt in patients with IPF. Elcctroencephalography (Option B) rcmains a kcy diag Interferon y and endothelin antagonists have also been nostic tool firr critically ill palicnts with uncxplained altered fbund to be ineffective. rnental status becarlsc the ir-rcictcnce of noncoruulsive sei A combination regimen ol prednisone with azathio zures l.rirs bcen repurtcd to be as high as .'l:l'/;, in critically ill prine and N acetylcysteine (Option C) is associated with an patienls wilh enccphalopathy. But the first step shor-rld be to increase in mortality in lPF. Hence, treatment guidelines fbr stop the medication cllects befbre initiating other diagr.rostic IPF make a strong recommendation against its use. cv:rluations.

The most appropriate treatment is antiflbrotic therapy with Answer: D Educational Objective: Minimize sedation in ventilated tr vt = E patients in the ICU. pirfenidone (Option B). This patient has idiopathic pulmo nary fibrosis (lPF). Patients with IPF present with chronic The most approprirte managemcnt is to hold the sedation shortness of breath and a dry cough. Patients typically have and analgesia inlusions (Option D). I.'or acutely hospital bibasilar inspiratory Velcro like crackles, and clubbing is ized patients ventilated fbr more than 24 hours, guidelines common. The prevalence of disease increases with age. A suggest protocols to reducc sedation. Sedative analgesic confldent diagnosis can be made based on the presence nredic:rtions can cause excess sedation iincl may prolor-rg of typical symptoms and a usual interstitial pneumonia the duration of mechanical ventilation. ln randomizcd clin- pattern on a high resolution CT scan of the chest. IPF is ical trials, two strategies have been showr] to be ellcctive in progressive, with a median survival of :l to 5 years after reducir.rg the duration olmechanical ventilation and its asso diagnosis. ln 2014 the FDA approved two medications: pir- ciated complication. The first strategy consists of intenrrit fenidone, an antiflbrotic agent, and nintedanib, a tyrosine tcnt intravenous administration of analgcsia witl-rout sed- kinase inhibitor, for use in patients with IPF. In clinical atires (analgesia first approacl'r). A secor-rd strategy cor-rsists triais the two agents were found to have comparable effl of daily' interruption of' continuous intusior-r of ar.ralgesics cacy in mitigating the rate of FVC decline by approximately and sedatives. !'ariltions of these protocols exist. including 50'1, over the course of 1 year. They have also shown some targeting Iight sedation. The oplimal strategy is not knowr-r, eflicacy in reducing severe respiratory events such as acute and guidelines o{ler no prelerencc due to insufficient data. exacerbations and hospitalization. Common side efl'ects but a1l have in comnron periocls oltinte in rvhich the patient are anorexia, nausea, photosensitivity (pirfenidone), and is arvakc. When implcmentecl routinely, probcols that lirnit diarrhea (nintedanib). Although these medications delay sedatiot't or allow spontaneolls awakening n,ill decrease the IPF progression, they are not curative. Relerral to a pulm lengtl.t of rnechanical ventilation. ICU stall and incicience of onologist or interstitial lung disease center may be appro delirium. In this cleeply sedatecl patient. stopping seclation priate belbre initiating treatment with these medications. and analgesics now will allow the fastest clecrease in rnedi Lung transplantation is a life prolonging therapy for those cation levels. thus lllou,ing:lsscssnlent ol thc patient. without comorbidities that may otherwise limit life expec- Titrirtion of sedutior.r medication (Option A) lt,ill also tancy. Early referral ol eligible patients to a transplant lead to arousal. Ilowever, thc time to rcach steacly state center is appropriate given the unpredictability of disease rfter decrcasing thc infusion rltc of a sedative is prolongecl progression. (7 half livcs). thr.rs ;lrolonging thc time until an appropriate A clinical trial of N acetylcysteine monotherapy nenroklgic cxaminirt iol1. (Option A) did not show any beneflt in patients with IPF. Elcctroencephalography (Option B) rcmains a kcy diag Interferon y and endothelin antagonists have also been nostic tool firr critically ill palicnts with uncxplained altered fbund to be ineffective. rnental status becarlsc the ir-rcictcnce of noncoruulsive sei A combination regimen ol prednisone with azathio zures l.rirs bcen repurtcd to be as high as .'l:l'/;, in critically ill prine and N acetylcysteine (Option C) is associated with an patienls wilh enccphalopathy. But the first step shor-rld be to increase in mortality in lPF. Hence, treatment guidelines fbr stop the medication cllects befbre initiating other diagr.rostic IPF make a strong recommendation against its use. cv:rluations. 135

llfryg=la_c1iliru es tr CONI. A heatl CT (Option C) is unlikely to yield any relevant infbrmation in this patient. A neurologic exarnination, litr A rl-reumatoid eflirsion (Option D) is typically an inflamrnatory eflusion with a low pH (<7.2), a low glucose '"vhicl-r sedation should be held, should guide tl.re decision to level (<40 mgtcll- [2.2 mrnol,'Ll), and an elevated LD]t level. perform any inraging studies. t(EY POttrs I(EY POIilTS . A chylothorax is diagnosed by a triglyceride level o Sedative-analgesic medications can cause excess greater than 110 mg/dl (1.24 mmol/L), and it is typi- sedation and may prolong the duration of mechanical cally a lymphocytic predominant exudative effusion. ventilation. . The most common nontraumatic cause of chylothorax o For acutely hospitalized patients ventilated for more is malignancy, of which lymphoma is the most com- than24 hours, guidelines suggest protocols to reduce sedation. Bibliography UI Bibliography I.tller Kopman D, Light R. Pleural disease. n'Engl J Med. 2018r378:7,10 751. (D IPMID' 294661 4ol doi:10. l056 \EJVral103503 = Ervin lN, Rentes VC, I)ibble ER, et al. Evidence based practices for acute UI respiratory failure and acute respiratory distress syndrome: A systematic o, review of reviews. Chest. 2020;158:2381 -2393. [PM I D: 32682771] doi:10. 1016/j.chest.2020.06.080 tL r! Item 33 Answer: B Educational Objective: Diagnose idiopathic pulmonary tt .D l^ tr Item 32 Answer: B Educational Objective: Diagnose a chylothorax. fibrosis.

tr CONI. A heatl CT (Option C) is unlikely to yield any relevant infbrmation in this patient. A neurologic exarnination, litr A rl-reumatoid eflirsion (Option D) is typically an inflamrnatory eflusion with a low pH (<7.2), a low glucose '"vhicl-r sedation should be held, should guide tl.re decision to level (<40 mgtcll- [2.2 mrnol,'Ll), and an elevated LD]t level. perform any inraging studies. t(EY POttrs I(EY POIilTS . A chylothorax is diagnosed by a triglyceride level o Sedative-analgesic medications can cause excess greater than 110 mg/dl (1.24 mmol/L), and it is typi- sedation and may prolong the duration of mechanical cally a lymphocytic predominant exudative effusion. ventilation. . The most common nontraumatic cause of chylothorax o For acutely hospitalized patients ventilated for more is malignancy, of which lymphoma is the most com- than24 hours, guidelines suggest protocols to reduce sedation. Bibliography UI Bibliography I.tller Kopman D, Light R. Pleural disease. n'Engl J Med. 2018r378:7,10 751. (D IPMID' 294661 4ol doi:10. l056 \EJVral103503 = Ervin lN, Rentes VC, I)ibble ER, et al. Evidence based practices for acute UI respiratory failure and acute respiratory distress syndrome: A systematic o, review of reviews. Chest. 2020;158:2381 -2393. [PM I D: 32682771] doi:10. 1016/j.chest.2020.06.080 tL r! Item 33 Answer: B Educational Objective: Diagnose idiopathic pulmonary tt .D l^ tr Item 32 Answer: B Educational Objective: Diagnose a chylothorax. fibrosis. The most likely diagnosis is idiopathic pulmonary flbrosis 'lhe most lil<ely dilgnosis is chylotlrorar (Option B). Chy (lPF) (Option B). IPF is associated with the histopathologic lotl-rorax refers to thc presence of chylc w,ithin the pleural appearance of usual interstitial pneumonia, the most com- space. Chylothorax hls both trauntatic uncl nontraumatic mon idiopathic form of diffuse parenchymal lung disease causes. The nrost corrmon traumatic cxuse is thoracic surgerl: (DPLD). It typically presents in patients between 50 and Esophagostomy carries tlie highest risk fbllorvecl by medias 70 years of age who have a greater than 6 month duration tinirl lyrnph node dissection. mediastinal tum<tr resectiorr. of a dry cough and dyspnea on exertion. History will reveal and any surgery involving the lorver neck and ntediastinurn. no potential cause for the development of flbrosis, and lung The most cofflrnon nontraumatic cause is malignancy,, of examination is notable for Velcro-like inspiratory crackles which lynphonta is the nlost commolt. Other pclssible non that are predominant at the bases. Clubbing is present in up traumatic causcs inclucle lymphatic disorclers and chylous to 50'2, of patients. The best diagnostic test is high resolution ascites. In patients with nontraumatic cases. the mechanism CT (HRCT) of the chest, which may show abnormalities such ol.the chylothorax varies with the underlying cause. In this as bilateral, peripheral, and basal predominant septal line patient it is most likely secondary to contpressive obstruction thickening with honeycomb changes. The most appropriate due to bulky lyrnplradenopathll Chest prrin lnd fever are rare next step in this patient's management is to discuss the in patients lvith ch1'lothorux, but the presence oi'fer,er may patient's diagnosis in a multidisciplinary meeting involving represent an unclerlying lymphoma. Clrl,krus ef lirsions have a a thoracic radiologist, a pathologist, and a pulmonologist; a high protein concentration nlaking lhent exudafes by Light's multidisciplinary discussion may yield a confldent diagnosis criteria. 'lhe explanatior.r for elevated protein in a chylotrs of IPFI, without the need for a lung biopsy. ettusion is unknowlr.'lhe pleural fluicl lactate dehydrogenase Patients with cryptogenic organizing pneumonia (COP) (LDH) is fypically kl.tr ref lecti're of'a trallsudxte. If elevated, it (Option A) typically present with cough, fever, and malaise otten reflects thc unclerlving callse of thc eflusion. such as a for 6 to 8 weeks. Initial chest radiographs will demonstrate rnalignanclr A chylothorax is diagnosecl lty a trigl),ceride level patchy opacities that mimic pneumonia, and as a result, greater than ll0 mg'dL (1.24 mmol L). ancl it is fypically a patients are often initially misdiagnosed with community- lympl-rocytic predominant eflusior.r. Although chylothorax is acquired pneumonia and treated with standard antibiot- often milky in appearance, irs is a clrolcsterol efiusion. it can ics. HRCT scans will demonstrate ground-glass opacities appear serous or sanguineous. or areas of alveolar consolidation resembling an infectious A cholesterol eflirsion (Option A) is diagnosed lry pneumonia, but flndings can include peripheral nodules and a pleural fluicl cholesterol level grextcr thill 200 mg,/dl. nodules along the bronchovascular bundle. This patient's (5.t8 mmolr'L). (lholesterol effusions are cluite rare and wher.r age, long duration of symptoms, and honeycomb changes on present are most commonly associated r,r,,ith tuberculosis. HRCT scan do not flt the clinical picture of COP rheumatoid eflirsions. ar.rd other chronic pleural effusions. Nonspeciflc interstitial pneumonia (NSIP) (Option C) Empyema (Option C) is incorrect as the patient has no is the most common DPLD associated with autoimmune clir-rical I'eatures of infection (fever, chest pain, leukocytosis). disorders, but it can occasionally be idiopathic. NSIP affects In addition, empyema is not milky in appearance and is typ a younger population than IPFI. HRCT scans will demon ically associated with a low pleural f luid pl I and low glucose. strate bilateral lower-lobe reticular changes and an absence

The most likely diagnosis is idiopathic pulmonary flbrosis 'lhe most lil<ely dilgnosis is chylotlrorar (Option B). Chy (lPF) (Option B). IPF is associated with the histopathologic lotl-rorax refers to thc presence of chylc w,ithin the pleural appearance of usual interstitial pneumonia, the most com- space. Chylothorax hls both trauntatic uncl nontraumatic mon idiopathic form of diffuse parenchymal lung disease causes. The nrost corrmon traumatic cxuse is thoracic surgerl: (DPLD). It typically presents in patients between 50 and Esophagostomy carries tlie highest risk fbllorvecl by medias 70 years of age who have a greater than 6 month duration tinirl lyrnph node dissection. mediastinal tum<tr resectiorr. of a dry cough and dyspnea on exertion. History will reveal and any surgery involving the lorver neck and ntediastinurn. no potential cause for the development of flbrosis, and lung The most cofflrnon nontraumatic cause is malignancy,, of examination is notable for Velcro-like inspiratory crackles which lynphonta is the nlost commolt. Other pclssible non that are predominant at the bases. Clubbing is present in up traumatic causcs inclucle lymphatic disorclers and chylous to 50'2, of patients. The best diagnostic test is high resolution ascites. In patients with nontraumatic cases. the mechanism CT (HRCT) of the chest, which may show abnormalities such ol.the chylothorax varies with the underlying cause. In this as bilateral, peripheral, and basal predominant septal line patient it is most likely secondary to contpressive obstruction thickening with honeycomb changes. The most appropriate due to bulky lyrnplradenopathll Chest prrin lnd fever are rare next step in this patient's management is to discuss the in patients lvith ch1'lothorux, but the presence oi'fer,er may patient's diagnosis in a multidisciplinary meeting involving represent an unclerlying lymphoma. Clrl,krus ef lirsions have a a thoracic radiologist, a pathologist, and a pulmonologist; a high protein concentration nlaking lhent exudafes by Light's multidisciplinary discussion may yield a confldent diagnosis criteria. 'lhe explanatior.r for elevated protein in a chylotrs of IPFI, without the need for a lung biopsy. ettusion is unknowlr.'lhe pleural fluicl lactate dehydrogenase Patients with cryptogenic organizing pneumonia (COP) (LDH) is fypically kl.tr ref lecti're of'a trallsudxte. If elevated, it (Option A) typically present with cough, fever, and malaise otten reflects thc unclerlving callse of thc eflusion. such as a for 6 to 8 weeks. Initial chest radiographs will demonstrate rnalignanclr A chylothorax is diagnosecl lty a trigl),ceride level patchy opacities that mimic pneumonia, and as a result, greater than ll0 mg'dL (1.24 mmol L). ancl it is fypically a patients are often initially misdiagnosed with community- lympl-rocytic predominant eflusior.r. Although chylothorax is acquired pneumonia and treated with standard antibiot- often milky in appearance, irs is a clrolcsterol efiusion. it can ics. HRCT scans will demonstrate ground-glass opacities appear serous or sanguineous. or areas of alveolar consolidation resembling an infectious A cholesterol eflirsion (Option A) is diagnosed lry pneumonia, but flndings can include peripheral nodules and a pleural fluicl cholesterol level grextcr thill 200 mg,/dl. nodules along the bronchovascular bundle. This patient's (5.t8 mmolr'L). (lholesterol effusions are cluite rare and wher.r age, long duration of symptoms, and honeycomb changes on present are most commonly associated r,r,,ith tuberculosis. HRCT scan do not flt the clinical picture of COP rheumatoid eflirsions. ar.rd other chronic pleural effusions. Nonspeciflc interstitial pneumonia (NSIP) (Option C) Empyema (Option C) is incorrect as the patient has no is the most common DPLD associated with autoimmune clir-rical I'eatures of infection (fever, chest pain, leukocytosis). disorders, but it can occasionally be idiopathic. NSIP affects In addition, empyema is not milky in appearance and is typ a younger population than IPFI. HRCT scans will demon ically associated with a low pleural f luid pl I and low glucose. strate bilateral lower-lobe reticular changes and an absence 136

Answers and Critiques I of honeycombing, but they can also demonstrate areas of Dexamethasone (Option D) has been shown to have a ground glass opaciflcation. In this patient, the lack of an role in prophylaxis fbr high altitude-related illnesses ancl underlying autoimmune disease, older age, and HRCT flnd- as treatment for high altitude cerebral edema but not fbr ings are not consistent with NSIP IlAPE. Respiratory bronchiolitis-associated interstitial lung Furosemide (Option E) is a loop diuretic that is com disease (RB ILD) (Option D) is the histopathologic diagnosis monly used in pulmonary edema secondary to heart fail associated with the HRCT flnding of centrilobular micro- urc. However, the typical patient with HAPE is not volume I nodular disease in current smokers. On physiologic testing, overloaded. The use ofdiuretics in these patients has no role RB ILD may have combined restriction and obstruction. in HAPE and may cause harnr by depleting intravascular The patient is not an active smoker, which argues against volume and further reducing oxygen delivery to hypoxic RB ILD. tissues. I(EY POITII I(EY POITI la . Idiopathic pulmonary fibrosis presents in patients . Treatment of high-altitude pulmonary edema focuses (l, between 50 and 70 years of age, greater than 6 months' on promptly reducing the pulmonary artery pressure; ET

I(EY POITII I(EY POITI la . Idiopathic pulmonary fibrosis presents in patients . Treatment of high-altitude pulmonary edema focuses (l, between 50 and 70 years of age, greater than 6 months' on promptly reducing the pulmonary artery pressure; ET duration ofa dry cough and dyspnea on exertion, the patient should be given supplemental oxygen and IJ Velcrolike crackles, clubbing (50%), and honeycomb advised to descend to a lower altitude as soon as pos- .E, changes on HRCT scans. sible and to limit physical exertion and cold exposure. E lg r (l, Bibliography Bibliography Lederer DJ, Martinez FJ. Idiopathic pulmonary fibrosis. N Engl J Med. Luks AM, Swenson ER, Bdrtsch P Acute high altitude sickness. Eur Respir vt = 2018;378:1811 1823. IPMID: 297423801 doi:10.1056/NEJMra17}575l Rev. 2017;26. [PMID: 28143S79] doi:lO.ll83/1600Q617.0096-2016

duration ofa dry cough and dyspnea on exertion, the patient should be given supplemental oxygen and IJ Velcrolike crackles, clubbing (50%), and honeycomb advised to descend to a lower altitude as soon as pos- .E, changes on HRCT scans. sible and to limit physical exertion and cold exposure. E lg r (l, Bibliography Bibliography Lederer DJ, Martinez FJ. Idiopathic pulmonary fibrosis. N Engl J Med. Luks AM, Swenson ER, Bdrtsch P Acute high altitude sickness. Eur Respir vt = 2018;378:1811 1823. IPMID: 297423801 doi:10.1056/NEJMra17}575l Rev. 2017;26. [PMID: 28143S79] doi:lO.ll83/1600Q617.0096-2016 Item 34 Answer: C Educational Objective: Treat high-altitude pulmonary Item 35 Answer: D Educational Objective: Treat sepsis with a balanced tr edema. crystalloid solution.

Item 34 Answer: C Educational Objective: Treat high-altitude pulmonary Item 35 Answer: D Educational Objective: Treat sepsis with a balanced tr edema. crystalloid solution. The most appropriate additional treatment is descent to a 'll.re most appropriate resuscitative treatment for this patient krwcr altitude (Option C) as soon as possible. The patient is lactated Ringer solution (Option D). The patient most is experiencing high altitucle pulmonary edema (HAPE), likely has sepsis or septic shock based on a source of infec which is caused by exagqerutecl hypoxic pulmonary vaso tion. I'ever. hypotension. tachycardia, and altered mentation. constriction and abnormally high pulmonary artery and Sepsis and septic shock are medical emergencies, and treat capillary pressures. The resulting leal<age ol edema fluid ment with fluid resuscitation begins immediately. Guidelines into the alveolus causes l.rypoxemia and may evoke an recommend that in the resuscitation {iom sepsis inducecl inflamnratory response. Risks fbr this disorder include rapid hypoperfusion, at least l)0 mllkg of'intravenous crystalloicl asccnt to altitudes greater than 2.500 meters (-8200 feet). fluid be given within the first ll hours with either balanced tl.rc actual altitude attained, time spent at altitude, and a crystalloid solution such as lactated Ringer solutionor O.9"/,' history of high-altitude illness. The typical symptoms of saline. However. a large 2018 clinical trial demonstrated that HAPE (cough, shortness ofbreath. and fatigue) can be dif among critically il1 adults. thc use of a balanced crystalloid ficult to distinguish from pneumonia. As HAPE progresses, s<ilution fbr intravenous fluid aclministration resulted in patients can develop pink fiothy sputum. hemoptysis. ancl a lorner rate of the con.rposite outcome of death fiom any life threatening hypoxemia. Trextmenl oIHAPE focuses on callse. new renal replacement thcrapy, or persistent renal promptly reducing the pulmonary artery pressure. This can dysfunction than the use o1 0.9'l, saline. lvith an absolute bc done by providing supplcn.rcntal oxygen. limiting the dillerence of 1.1'1,. patient's physical exertion and cold exposure, and advising 'lhree large trials have evaluated the benefits of albu the patient to descend to a lowcr altitude as soon as pos rnin administration (Option A) compared with crystalloid sible. 'lhis patient has received supplemental oxygen and solutions. Although prespecificd subgroup analyses in two should descend to a lower altitude. Some clinicians suggest of the trials initially suggested that albumin may impnrve thc use ol nifedipine as adjunctive therapy, but there is a survival over crystalloids in patients with septic shock. more paucity of'data to confirm its benefit. recent meta-analyses suggest otherwise. Because albumin Acetazolamide (Option A) is commonly used fbr prcr is significantly more expensive than crystalloid solutions, phylaxis against HAPE, but it has no role in treatment. it is not recommended lbr routine use in resuscitatior.r of Ceftriaxone (Option B) would be appropriate if the patients lvith septic shock. patient had a concurrent pneumonia along with HAPE. Bicarbonate solutions (Option B) are not recommended However, given the symptoms and timing of onset in this as a standard part of sepsis or septic shock resuscitation otherwise healthy patient, there is notlring to suggest a con and would not benefit this patient. f'lven in patients with an current pneumonia or the need fbr antibiotics. increased anion gap acidosis, administration of bicarbonate

The most appropriate additional treatment is descent to a 'll.re most appropriate resuscitative treatment for this patient krwcr altitude (Option C) as soon as possible. The patient is lactated Ringer solution (Option D). The patient most is experiencing high altitucle pulmonary edema (HAPE), likely has sepsis or septic shock based on a source of infec which is caused by exagqerutecl hypoxic pulmonary vaso tion. I'ever. hypotension. tachycardia, and altered mentation. constriction and abnormally high pulmonary artery and Sepsis and septic shock are medical emergencies, and treat capillary pressures. The resulting leal<age ol edema fluid ment with fluid resuscitation begins immediately. Guidelines into the alveolus causes l.rypoxemia and may evoke an recommend that in the resuscitation {iom sepsis inducecl inflamnratory response. Risks fbr this disorder include rapid hypoperfusion, at least l)0 mllkg of'intravenous crystalloicl asccnt to altitudes greater than 2.500 meters (-8200 feet). fluid be given within the first ll hours with either balanced tl.rc actual altitude attained, time spent at altitude, and a crystalloid solution such as lactated Ringer solutionor O.9"/,' history of high-altitude illness. The typical symptoms of saline. However. a large 2018 clinical trial demonstrated that HAPE (cough, shortness ofbreath. and fatigue) can be dif among critically il1 adults. thc use of a balanced crystalloid ficult to distinguish from pneumonia. As HAPE progresses, s<ilution fbr intravenous fluid aclministration resulted in patients can develop pink fiothy sputum. hemoptysis. ancl a lorner rate of the con.rposite outcome of death fiom any life threatening hypoxemia. Trextmenl oIHAPE focuses on callse. new renal replacement thcrapy, or persistent renal promptly reducing the pulmonary artery pressure. This can dysfunction than the use o1 0.9'l, saline. lvith an absolute bc done by providing supplcn.rcntal oxygen. limiting the dillerence of 1.1'1,. patient's physical exertion and cold exposure, and advising 'lhree large trials have evaluated the benefits of albu the patient to descend to a lowcr altitude as soon as pos rnin administration (Option A) compared with crystalloid sible. 'lhis patient has received supplemental oxygen and solutions. Although prespecificd subgroup analyses in two should descend to a lower altitude. Some clinicians suggest of the trials initially suggested that albumin may impnrve thc use ol nifedipine as adjunctive therapy, but there is a survival over crystalloids in patients with septic shock. more paucity of'data to confirm its benefit. recent meta-analyses suggest otherwise. Because albumin Acetazolamide (Option A) is commonly used fbr prcr is significantly more expensive than crystalloid solutions, phylaxis against HAPE, but it has no role in treatment. it is not recommended lbr routine use in resuscitatior.r of Ceftriaxone (Option B) would be appropriate if the patients lvith septic shock. patient had a concurrent pneumonia along with HAPE. Bicarbonate solutions (Option B) are not recommended However, given the symptoms and timing of onset in this as a standard part of sepsis or septic shock resuscitation otherwise healthy patient, there is notlring to suggest a con and would not benefit this patient. f'lven in patients with an current pneumonia or the need fbr antibiotics. increased anion gap acidosis, administration of bicarbonate 137

Answers and Critiques [Il solution is not associated u,ith improved outcomes and can The indolence of ground glass noduies and their very llJ Sxvs adverse eflects such as hypocalcemia. hypercapnia. and low metabolic activity also makes fluorodeoxyglucose PET coNT QT prolongation. less useful (Option C); PET scans in this setting can show Guidelines recommend against using hydroryethyl false positive results. starches (HESs) (Option C) fbr intravascular volume replace Resection (Option D) would not be recommended at ment in patients rvith sepsis or septic shock due to a lack of this point because it would subject the patient to a surgery data shou,it-tg superiority to crystalloid solutions and salety that may be unnecessary given the indeterminate nature concerns. A nefi,r,ork meta-analysis fbcused on acute resus ofthe nodule. citation of patients ruith sepsis or septic shock found that XEY POIlIT HESs resulted in a higher risk of death and need fbr renal replacement therapy compared u,ith crystalloids. o An incidentally found ground-glass (subsolid) pulmo nary nodule 6 mm or larger necessitates follow up I(EY POIl{TS chest CT at 6 to 12 months; if it persists but is UI . Sepsis and septic shock are medical emergencies, and unchanged in size, CT should be repeated at2-year E fluid resuscitation should begin immediately. intervals for 5 years. .D U! o Guidelines recommend that in the resuscitation from o, sepsis-induced hypoperfusion, at least 30 ml/kg of Bibliography CL MacMahon H, Naidich DB Goo JM. et al. Guidelines for management of n intravenous crystalloid fluid be given within the first incidental pulmonary nodules detected on CT images: from the 3 hours. Fleischner Society 2017. Radiolo$,: 2017:281:228 2.13. IP]\,llD: 282.105621 .st doi :1 0. 1148i radiol.2017 1 61 659 E (D Bibliography UI Semler MW, Self WH, Wanderer JP et al; SMART Investigators and the Pragmatic Critical Care Research Group. Balanced crystalloids versus saline in critically ill adults. N Engl J Med. 2018;378:829 839. IPMID: Item 37 Answer: B 294859251 doi:10.1056i NEJMoaul1584 Ed u cati o na I O bj ective : Evaluate suspected pulmonary hypertension.

[Il solution is not associated u,ith improved outcomes and can The indolence of ground glass noduies and their very llJ Sxvs adverse eflects such as hypocalcemia. hypercapnia. and low metabolic activity also makes fluorodeoxyglucose PET coNT QT prolongation. less useful (Option C); PET scans in this setting can show Guidelines recommend against using hydroryethyl false positive results. starches (HESs) (Option C) fbr intravascular volume replace Resection (Option D) would not be recommended at ment in patients rvith sepsis or septic shock due to a lack of this point because it would subject the patient to a surgery data shou,it-tg superiority to crystalloid solutions and salety that may be unnecessary given the indeterminate nature concerns. A nefi,r,ork meta-analysis fbcused on acute resus ofthe nodule. citation of patients ruith sepsis or septic shock found that XEY POIlIT HESs resulted in a higher risk of death and need fbr renal replacement therapy compared u,ith crystalloids. o An incidentally found ground-glass (subsolid) pulmo nary nodule 6 mm or larger necessitates follow up I(EY POIl{TS chest CT at 6 to 12 months; if it persists but is UI . Sepsis and septic shock are medical emergencies, and unchanged in size, CT should be repeated at2-year E fluid resuscitation should begin immediately. intervals for 5 years. .D U! o Guidelines recommend that in the resuscitation from o, sepsis-induced hypoperfusion, at least 30 ml/kg of Bibliography CL MacMahon H, Naidich DB Goo JM. et al. Guidelines for management of n intravenous crystalloid fluid be given within the first incidental pulmonary nodules detected on CT images: from the 3 hours. Fleischner Society 2017. Radiolo$,: 2017:281:228 2.13. IP]\,llD: 282.105621 .st doi :1 0. 1148i radiol.2017 1 61 659 E (D Bibliography UI Semler MW, Self WH, Wanderer JP et al; SMART Investigators and the Pragmatic Critical Care Research Group. Balanced crystalloids versus saline in critically ill adults. N Engl J Med. 2018;378:829 839. IPMID: Item 37 Answer: B 294859251 doi:10.1056i NEJMoaul1584 Ed u cati o na I O bj ective : Evaluate suspected pulmonary hypertension. Item 35 Answer: A The most appropriate diagnostic test to perfbrm is echo cardiography (Option B). Approximately 10% of patients Educational Objective: Evaluate an S-mm ground-glass (subsolid) pulmonary nodule with serial CT scans. with systemic sclerosis develop pulmonary arterial hypertension (PAH), a signiflcant cause of morbidity and The most appropriate management is chest CT every mortality. Symptoms of pulmonary hypertension (PH) are 2 years for 5 years (OptionA). The patient has an indeter nonspeciflc; thus, the average time from symptom onset to minate pulmonary nodule and requires further follow up diagnosis can exceed 2 years. Symptoms include exertional evaluation. Pulmonary nodules can be classifled as solid dyspnea or lightheadedness, Iower extremity edema, chest or subsolid. The subsolid nodule classification is further pain, palpitations, and in some cases, syncope. Findings subdivided into pure ground-glass nodules and part- on physical examination frequently include an accentu solid nodules. The evaluation of pure ground glass nod- ated or persistently split Sr. A holosystolic tricuspid regurgi ules is informed primarily by nodule size. An incidentally tant murmur, jugular venous distention, a right ventricular found ground-glass nodule of 6 mm or larger necessitates heave, hepatomegaly, ascites, and peripheral edema occur in follow up chest CT at 6 to 12 months. If the nodule persists the face of progressive right ventricular failure. Pulmonary but is unchanged in size, as in this patient, chest CT should flndings reflect underlying lung disease when present. If be repeated at2 year intervals for 5 years. Earlierfollow up PAH is suspected, transthoracic echocardiography should be is unlikely to affect the outcome of these characteristically pursued. Echocardiography provides an estimation of mean indolent lesions. Studies have shown that an average of 3 pulmonary artery systolic pressure and assessment of both to 4 years is typically required to establish growth or, less right and left heart size and function. If the echocardiogram commonly, to diagnose a developing invasive carcinoma. suggests PH, the patient should be referred for further evalu- Many ground glass nodules resolve spontaneouslybecause ation, including right heart catheterization. In patients with they can also be from infectious or inflammatory causes. systemic sclerosis, guidelines suggest annual screening with If the nodule resolves, no further follow up is needed. If echocardiography for PH. the nodule grows or develops a solid component, biopsy or CT angiography (Option A) can be used to evaluate resection is recommended. for the presence of acute pulmonary embolism. Since the Ground glass nodules are associated with more indo- patient's symptoms are progressive over months, the like lent histologic Iesions (e.g., adenocarcinoma in situ and Iihood of acute pulmonary embolism is very low. CT angi minimally invasive adenocarcinoma), which require longer ography is not the best initial diagnostic test for this patient. follow up to determine whether they are benign. Thus, it Patients with systemic sclerosis are at increased risk is not appropriate to perform follow-up CT at 12 months fbr developing coronary artery disease and interstitial lung (Option B) with no further testing if the scan is normal. disease. In a patient with progressive dyspnea, both diseases

Item 35 Answer: A The most appropriate diagnostic test to perfbrm is echo cardiography (Option B). Approximately 10% of patients Educational Objective: Evaluate an S-mm ground-glass (subsolid) pulmonary nodule with serial CT scans. with systemic sclerosis develop pulmonary arterial hypertension (PAH), a signiflcant cause of morbidity and The most appropriate management is chest CT every mortality. Symptoms of pulmonary hypertension (PH) are 2 years for 5 years (OptionA). The patient has an indeter nonspeciflc; thus, the average time from symptom onset to minate pulmonary nodule and requires further follow up diagnosis can exceed 2 years. Symptoms include exertional evaluation. Pulmonary nodules can be classifled as solid dyspnea or lightheadedness, Iower extremity edema, chest or subsolid. The subsolid nodule classification is further pain, palpitations, and in some cases, syncope. Findings subdivided into pure ground-glass nodules and part- on physical examination frequently include an accentu solid nodules. The evaluation of pure ground glass nod- ated or persistently split Sr. A holosystolic tricuspid regurgi ules is informed primarily by nodule size. An incidentally tant murmur, jugular venous distention, a right ventricular found ground-glass nodule of 6 mm or larger necessitates heave, hepatomegaly, ascites, and peripheral edema occur in follow up chest CT at 6 to 12 months. If the nodule persists the face of progressive right ventricular failure. Pulmonary but is unchanged in size, as in this patient, chest CT should flndings reflect underlying lung disease when present. If be repeated at2 year intervals for 5 years. Earlierfollow up PAH is suspected, transthoracic echocardiography should be is unlikely to affect the outcome of these characteristically pursued. Echocardiography provides an estimation of mean indolent lesions. Studies have shown that an average of 3 pulmonary artery systolic pressure and assessment of both to 4 years is typically required to establish growth or, less right and left heart size and function. If the echocardiogram commonly, to diagnose a developing invasive carcinoma. suggests PH, the patient should be referred for further evalu- Many ground glass nodules resolve spontaneouslybecause ation, including right heart catheterization. In patients with they can also be from infectious or inflammatory causes. systemic sclerosis, guidelines suggest annual screening with If the nodule resolves, no further follow up is needed. If echocardiography for PH. the nodule grows or develops a solid component, biopsy or CT angiography (Option A) can be used to evaluate resection is recommended. for the presence of acute pulmonary embolism. Since the Ground glass nodules are associated with more indo- patient's symptoms are progressive over months, the like lent histologic Iesions (e.g., adenocarcinoma in situ and Iihood of acute pulmonary embolism is very low. CT angi minimally invasive adenocarcinoma), which require longer ography is not the best initial diagnostic test for this patient. follow up to determine whether they are benign. Thus, it Patients with systemic sclerosis are at increased risk is not appropriate to perform follow-up CT at 12 months fbr developing coronary artery disease and interstitial lung (Option B) with no further testing if the scan is normal. disease. In a patient with progressive dyspnea, both diseases 138

Answers and Critiques should be considered. However, this patient's findings of Two small randomized controlled trials showed that increased jugular venous distention, persistently split S2, and eszopiclone (Option C) administered early in the course of tricuspid regurgitant murmur suggest PAH. The patient's continuous positive airway pressure (CPAP) Ied to mod- pulmonary examination and chest radiograph are normal. est improvements in CPAP adherence. However, the role of An exercise stress test (Option C) or pulmonary function such hlpnotic agents in promoting CPAP adherence remains testing (Option D) may be indicated if the patient's echo controversial. Their use later in the course of PAP, as in this cardiogram is unremarkable, but neither is the best initial patient, is unknown, and the risk for adverse effects may choice in light of her physical examination flndings. outweigh their beneflt. Modaflnil (Option D) is a stimulant medication that KEY PO I ilTS can be used for residual excessive sleepiness in patients with . Physical examination findings of pulmonary hyper OSA who are using PAP optimally. The patient's adherence tension may include accentuated or persistently split to PAP therapy is not yet known, so it is not appropriate to Sr, holosystolic tricuspid regurgitant murmur, jugular prescribe modaflnil. ta (l, venous distention, right ventricular heave, hepatomeg XEY POITIS CT aly, ascites, and peripheral edema. o Transthoracic echocardiography is indicated in . The treatment response for patients with sleep apnea IJ depends on adherence to positive airway pressure .E, patients with suspected pulmonary hlpertension. therapy and should be assessed in all patients. G UI Bibliography o Download of adherence data from the positive airway q, Jiang Y Turk MA, Pope JE. l.'actors associated with pulmonary arterial pressure device yields important information about UI hypertension (PAH) in systemic sclerosis (SSc). Autoimmun Rev 2020; use that can be discussed with the patient with sleep = 19:102602. [PMID: 326594761 doi:10.1016/j.autrev.2020.102602 apnea to explore barriers and formulate a plan to pro- mote adherence. Item 38 Answer: A Educational Objective: Assess adherence to positive Bibliography airway pressure therapy. Patil SII Ayappa IA, Caples SM, et al. Treatment of adult obstructive sleep apnea with positive airway pressure: an American Academy of Sleep Medicine clinical practice guideline. J Clin Sleep Med. 2019;15:335 343. The most appropriate management is to assess the patient's [PMID: 30736887] doi:10.5664/jcsm.7640 adherence to positive airway pressure (PAP) therapy (Option A). This patient has severe, symptomatic obstructive sleep apnea (OSA), for which PAP is preferred therapy. The response to treatment depends on adherence; a substantial proportion of patients, particularly early in the course of therapy, do Item 39 Ed ucationa I Objective Answer: B : Diagnose a complicated tr parapneumonic effusion. not use PAP as intended (all night, every night). Symptom burden probably drives adherence, but for those who lack 'Ihe diagnostic test that will be most helpful in directing motivation, educational programs can help, as can direct therapy is pleural fliiid pLI (Option B). the patient pres to-patient reports wirelessly transmitted from the device to ents with severe community-acquired pneurmonia and smartphones or computers. Adherence might be improved an associateci pleural efiusion (parapneumonic ellusion). by addressing common adverse effects. Side eflects such as A parapneumonic effusion can be either uncomplicated xerostomia and nasal dryness and congestion can be amelio- (sterile and free flowing) or complicated (infected or loc rated by in line humidiflcation. Intranasal glucocorticoids or ulated). An uncomplicated eflusion is typically small anci anticholinergics may be useful for recalcitrant nasal conges can resolve cln its ou,n. A complicated parapneumonic tion or rhinitis. Modifled pressure proflles that slightly reduce effusion occurs when there has been bacterial iuvasiotr pressure on exhalation may enhance comfort. Proper mask across the pleural mesothelium, stimulating a significant flt enhances comfort and mitigates air leak. PAP interfaces, inflammatory response. A diagnostic thoracentesis should ranging fiom nasal pillows that sit at the nasal openings to be perfirnned to assess the pleural effusion. A itarapneu nasal masks that cover the nose to oronasal (full face) masks monic eflitsion is considered complicated n'hen an exuda that cover the nose and mouth, are frequently updated and tive eflusion has either or both of the follorving character improved and may improve adherence. Download of data istics: p11 less than 7.2 (or glucose <ztO mgrdl [2.2 mmol,L] from the PAP device yields important information about use in the absence of pll data) or evidence ot'micror..rrganisnl that the physician can discuss with the patient to explore invasion by culture or Gram stain. ln the setting of'stis barriers and formulate a plan to promote adherence. pected infection, a pleural fluid pI{ level of less than 7'2 Bilevel positive ainvay pressure (Option B) is consid- is the best inclicator of a complicated pler-rral etlirsion that ered preferred therapy in hypoventilation syndromes such requires clrainage. Ultrasonography also has bee'n fbur.rd as those associated with neuromuscular disease or severe use{ul in the determination of a complicatecl pilrapneu- COPD, but little evidence supports its superiority in promot nronic effusion and has a sensitivity of 69"1,' and speciflcity ing treatment adherence for OSA. rr1 90"., rn hcn cornpleritl is sccn.

should be considered. However, this patient's findings of Two small randomized controlled trials showed that increased jugular venous distention, persistently split S2, and eszopiclone (Option C) administered early in the course of tricuspid regurgitant murmur suggest PAH. The patient's continuous positive airway pressure (CPAP) Ied to mod- pulmonary examination and chest radiograph are normal. est improvements in CPAP adherence. However, the role of An exercise stress test (Option C) or pulmonary function such hlpnotic agents in promoting CPAP adherence remains testing (Option D) may be indicated if the patient's echo controversial. Their use later in the course of PAP, as in this cardiogram is unremarkable, but neither is the best initial patient, is unknown, and the risk for adverse effects may choice in light of her physical examination flndings. outweigh their beneflt. Modaflnil (Option D) is a stimulant medication that KEY PO I ilTS can be used for residual excessive sleepiness in patients with . Physical examination findings of pulmonary hyper OSA who are using PAP optimally. The patient's adherence tension may include accentuated or persistently split to PAP therapy is not yet known, so it is not appropriate to Sr, holosystolic tricuspid regurgitant murmur, jugular prescribe modaflnil. ta (l, venous distention, right ventricular heave, hepatomeg XEY POITIS CT aly, ascites, and peripheral edema. o Transthoracic echocardiography is indicated in . The treatment response for patients with sleep apnea IJ depends on adherence to positive airway pressure .E, patients with suspected pulmonary hlpertension. therapy and should be assessed in all patients. G UI Bibliography o Download of adherence data from the positive airway q, Jiang Y Turk MA, Pope JE. l.'actors associated with pulmonary arterial pressure device yields important information about UI hypertension (PAH) in systemic sclerosis (SSc). Autoimmun Rev 2020; use that can be discussed with the patient with sleep = 19:102602. [PMID: 326594761 doi:10.1016/j.autrev.2020.102602 apnea to explore barriers and formulate a plan to pro- mote adherence. Item 38 Answer: A Educational Objective: Assess adherence to positive Bibliography airway pressure therapy. Patil SII Ayappa IA, Caples SM, et al. Treatment of adult obstructive sleep apnea with positive airway pressure: an American Academy of Sleep Medicine clinical practice guideline. J Clin Sleep Med. 2019;15:335 343. The most appropriate management is to assess the patient's [PMID: 30736887] doi:10.5664/jcsm.7640 adherence to positive airway pressure (PAP) therapy (Option A). This patient has severe, symptomatic obstructive sleep apnea (OSA), for which PAP is preferred therapy. The response to treatment depends on adherence; a substantial proportion of patients, particularly early in the course of therapy, do Item 39 Ed ucationa I Objective Answer: B : Diagnose a complicated tr parapneumonic effusion. not use PAP as intended (all night, every night). Symptom burden probably drives adherence, but for those who lack 'Ihe diagnostic test that will be most helpful in directing motivation, educational programs can help, as can direct therapy is pleural fliiid pLI (Option B). the patient pres to-patient reports wirelessly transmitted from the device to ents with severe community-acquired pneurmonia and smartphones or computers. Adherence might be improved an associateci pleural efiusion (parapneumonic ellusion). by addressing common adverse effects. Side eflects such as A parapneumonic effusion can be either uncomplicated xerostomia and nasal dryness and congestion can be amelio- (sterile and free flowing) or complicated (infected or loc rated by in line humidiflcation. Intranasal glucocorticoids or ulated). An uncomplicated eflusion is typically small anci anticholinergics may be useful for recalcitrant nasal conges can resolve cln its ou,n. A complicated parapneumonic tion or rhinitis. Modifled pressure proflles that slightly reduce effusion occurs when there has been bacterial iuvasiotr pressure on exhalation may enhance comfort. Proper mask across the pleural mesothelium, stimulating a significant flt enhances comfort and mitigates air leak. PAP interfaces, inflammatory response. A diagnostic thoracentesis should ranging fiom nasal pillows that sit at the nasal openings to be perfirnned to assess the pleural effusion. A itarapneu nasal masks that cover the nose to oronasal (full face) masks monic eflitsion is considered complicated n'hen an exuda that cover the nose and mouth, are frequently updated and tive eflusion has either or both of the follorving character improved and may improve adherence. Download of data istics: p11 less than 7.2 (or glucose <ztO mgrdl [2.2 mmol,L] from the PAP device yields important information about use in the absence of pll data) or evidence ot'micror..rrganisnl that the physician can discuss with the patient to explore invasion by culture or Gram stain. ln the setting of'stis barriers and formulate a plan to promote adherence. pected infection, a pleural fluid pI{ level of less than 7'2 Bilevel positive ainvay pressure (Option B) is consid- is the best inclicator of a complicated pler-rral etlirsion that ered preferred therapy in hypoventilation syndromes such requires clrainage. Ultrasonography also has bee'n fbur.rd as those associated with neuromuscular disease or severe use{ul in the determination of a complicatecl pilrapneu- COPD, but little evidence supports its superiority in promot nronic effusion and has a sensitivity of 69"1,' and speciflcity ing treatment adherence for OSA. rr1 90"., rn hcn cornpleritl is sccn. 139

Answers and Critiques tr CONI. r\ pleural fluid lactate dehl'drogenirse (l-DH) (Option A) level greater than tno thirds ol the r.rpper limit of normal tbr serum l.DH may support the diagnosis o1'an exudate in this warrn up and warming cold air before inhalation (e.g.. with a mask or scarf), are also recommended. In contrast. the 2020 Asthma Guideline Update from the National Asthma Edu patient, but it is nonspecific ancl nray simply be an indicat<tr cation and Prevention Program has continued the previous of inf lammation rather than infection olthe pleural space. recommendation of as-needed SABA-only use for this group Pleural fluid procalcitonin measurement (Option C) has of patients. bcen studied as a metl.rod to cliflercntiate parapneumonic Use of single-agent LABAs such as salmeterol (Option A) and tuberculous pleural efi'usior.rs fiom other causes of exu is not recommended because of a demonstrated increased datir,e effusions and to dillbrentiate parapneumonic fronl risk of asthma-related death when used without a simulta tuberculous pleural effusions. Ilouever. studies hare failed neous controller medication. Clinical trial results show that to demonstrate the value ol procalcitonin measurement. and LABAs used with inhaled glucocorticoids do not significantly it is not recommended. increase the risk of asthma related hospitalization, intuba 'Itrtal protein measLlremcnts (Option D) are helpiul in D tion, or death compared with inhaled glucocorticoids alone. t characterizing the pleural fluid as exudative by Light's crite and they result in signiflcantly lewer asthma exacerbations. E ria (ratio ofpleural-fluid protein to serum protein level >0.5). Daily use of low dose inhaled glucocorticoids (Option B) .D th However. total pleural fluicl protein measurements do r.rot would expose this patient to a signiflcantly higher total o, dilterentiate betlveen a complicatcd and an uncomplicated dose of inhaled glucocorticoids compared with as-needed EL parapneumonic eflusion. use. In addition, if daily inhaled controller medication a.t with a glucocorticoid is prescribed. it should usually be XEY POIIII l! accompanied by a SABA before exercise and as needed for r In the setting of suspected infection, a pleural fluid quick relief. .D tt pH Ievel of less than 7.2 (or glucose <40 mg/dl In patients with asthma, inhaled ipratropium (Option D) [z.z mmol/L] in the absence of pH data) is the best is generally not used for quick relief because of its delayed indicator of a complicated pleural effusion that onset and peak action of15 minutes and 1 to 2 hours, respec- requires drainage. tively. A SABA is preferred to ipratropium, either with a daily inhaled glucocorticoid or administered with an inhaled Bibliography glucocorticoid. F'eller Kopman D, Light R. Pleural disease. N Engl I Med. 2Ol8;378:74O 751. IPMID: 29466t461 doi:10.1056tNEJMra1.103503 f,EY POIXTS r Exercise induced bronchoconstriction is an acute. measurable airway obstruction that occurs in response Item 40 Answer: C to exercise. Educational Objective: Manage exercise-induced bron- choconstriction. . Global Initiative for Asthma guidelines recommend that initial pharmacologic therapy for exercise induced The most appropriate management is to begin budesonide- bronchoconstriction should consist of a daily inhaled formoterol 5 to 20 minutes before exercise (Option C). glucocorticoid plus a short-acting p, agonist or low- Exercise-induced bronchoconstriction (EIB) is acute, measur dose budesonide-formoterol before exercise, whereas able airway obstruction that occurs in response to exercise. It the National Asthma Education and Prevention Frogram is one of the most common triggers of symptoms in patients recommends a short-acting Br-agonist. with known asthma. It also occurs in patients without asthma (typically, elite athletes) during periods of high-intensity exer Bibliography cise. Environmental factors such as cold. dry air, exposure to Clobal Initiati\e for Asthma. Clobal Strate$/ for Asthma Management and high levels of trichloramines in swimming pools, and inhala Prevention. 2021. Arailable from: ginasthma.org, $'p content uploads tion of airborne particulates and ozone can play a key role in 2021,04,GINA 2021 Main Repon FINAL 21 0.1 28 \A/MS.pdf. Accessed May 5. 2021. precipitating symptoms. For safery current Global Initiative for Asthma (GINA) guidelines no longer recommend treat- ment of intermittent asthma, including EIB, with a short- Item 41 Answer: B acting Br-agonist (SABA) alone. All adults should receive a glucocorticoid-containing controller treatment to reduce Educational Objective: Treat anaphylaxis. tr their risk of serious exacerbations and to control symptoms. 'lhe most appropriate treatment is epinephrine (Option B). The glucocorticoid controller medication can be administered This patient has anaphllaxis {ntm a }lr-nrenoptera sting. Ana either as regular daily treatment or, in milder asthma, as phllaxis is a serere reaction causccl b1. acute mediator release the combination glucocorticoid formoterol taken whenever ir.rto the circulation. usuallv triggcred b1 tgE linked immunrr needed for asthma relief. Accordingly, GINA guidelines rec logic responses to specific ftrods. rledications. insect \enom. ommend a daily inhaled glucocorticoid plus a SABA before latex. or other antigens but sonretintes occurring without an exercise or low-dose budesonide formoterol before exer allergic trigger. The mediator release results in various clinical cise. Nonpharmacologic measures, including pre exercise manilbstations. including pruritus. hypotension, tachycardia,

tr CONI. r\ pleural fluid lactate dehl'drogenirse (l-DH) (Option A) level greater than tno thirds ol the r.rpper limit of normal tbr serum l.DH may support the diagnosis o1'an exudate in this warrn up and warming cold air before inhalation (e.g.. with a mask or scarf), are also recommended. In contrast. the 2020 Asthma Guideline Update from the National Asthma Edu patient, but it is nonspecific ancl nray simply be an indicat<tr cation and Prevention Program has continued the previous of inf lammation rather than infection olthe pleural space. recommendation of as-needed SABA-only use for this group Pleural fluid procalcitonin measurement (Option C) has of patients. bcen studied as a metl.rod to cliflercntiate parapneumonic Use of single-agent LABAs such as salmeterol (Option A) and tuberculous pleural efi'usior.rs fiom other causes of exu is not recommended because of a demonstrated increased datir,e effusions and to dillbrentiate parapneumonic fronl risk of asthma-related death when used without a simulta tuberculous pleural effusions. Ilouever. studies hare failed neous controller medication. Clinical trial results show that to demonstrate the value ol procalcitonin measurement. and LABAs used with inhaled glucocorticoids do not significantly it is not recommended. increase the risk of asthma related hospitalization, intuba 'Itrtal protein measLlremcnts (Option D) are helpiul in D tion, or death compared with inhaled glucocorticoids alone. t characterizing the pleural fluid as exudative by Light's crite and they result in signiflcantly lewer asthma exacerbations. E ria (ratio ofpleural-fluid protein to serum protein level >0.5). Daily use of low dose inhaled glucocorticoids (Option B) .D th However. total pleural fluicl protein measurements do r.rot would expose this patient to a signiflcantly higher total o, dilterentiate betlveen a complicatcd and an uncomplicated dose of inhaled glucocorticoids compared with as-needed EL parapneumonic eflusion. use. In addition, if daily inhaled controller medication a.t with a glucocorticoid is prescribed. it should usually be XEY POIIII l! accompanied by a SABA before exercise and as needed for r In the setting of suspected infection, a pleural fluid quick relief. .D tt pH Ievel of less than 7.2 (or glucose <40 mg/dl In patients with asthma, inhaled ipratropium (Option D) [z.z mmol/L] in the absence of pH data) is the best is generally not used for quick relief because of its delayed indicator of a complicated pleural effusion that onset and peak action of15 minutes and 1 to 2 hours, respec- requires drainage. tively. A SABA is preferred to ipratropium, either with a daily inhaled glucocorticoid or administered with an inhaled Bibliography glucocorticoid. F'eller Kopman D, Light R. Pleural disease. N Engl I Med. 2Ol8;378:74O 751. IPMID: 29466t461 doi:10.1056tNEJMra1.103503 f,EY POIXTS r Exercise induced bronchoconstriction is an acute. measurable airway obstruction that occurs in response Item 40 Answer: C to exercise. Educational Objective: Manage exercise-induced bron- choconstriction. . Global Initiative for Asthma guidelines recommend that initial pharmacologic therapy for exercise induced The most appropriate management is to begin budesonide- bronchoconstriction should consist of a daily inhaled formoterol 5 to 20 minutes before exercise (Option C). glucocorticoid plus a short-acting p, agonist or low- Exercise-induced bronchoconstriction (EIB) is acute, measur dose budesonide-formoterol before exercise, whereas able airway obstruction that occurs in response to exercise. It the National Asthma Education and Prevention Frogram is one of the most common triggers of symptoms in patients recommends a short-acting Br-agonist. with known asthma. It also occurs in patients without asthma (typically, elite athletes) during periods of high-intensity exer Bibliography cise. Environmental factors such as cold. dry air, exposure to Clobal Initiati\e for Asthma. Clobal Strate$/ for Asthma Management and high levels of trichloramines in swimming pools, and inhala Prevention. 2021. Arailable from: ginasthma.org, $'p content uploads tion of airborne particulates and ozone can play a key role in 2021,04,GINA 2021 Main Repon FINAL 21 0.1 28 \A/MS.pdf. Accessed May 5. 2021. precipitating symptoms. For safery current Global Initiative for Asthma (GINA) guidelines no longer recommend treat- ment of intermittent asthma, including EIB, with a short- Item 41 Answer: B acting Br-agonist (SABA) alone. All adults should receive a glucocorticoid-containing controller treatment to reduce Educational Objective: Treat anaphylaxis. tr their risk of serious exacerbations and to control symptoms. 'lhe most appropriate treatment is epinephrine (Option B). The glucocorticoid controller medication can be administered This patient has anaphllaxis {ntm a }lr-nrenoptera sting. Ana either as regular daily treatment or, in milder asthma, as phllaxis is a serere reaction causccl b1. acute mediator release the combination glucocorticoid formoterol taken whenever ir.rto the circulation. usuallv triggcred b1 tgE linked immunrr needed for asthma relief. Accordingly, GINA guidelines rec logic responses to specific ftrods. rledications. insect \enom. ommend a daily inhaled glucocorticoid plus a SABA before latex. or other antigens but sonretintes occurring without an exercise or low-dose budesonide formoterol before exer allergic trigger. The mediator release results in various clinical cise. Nonpharmacologic measures, including pre exercise manilbstations. including pruritus. hypotension, tachycardia, 140

Answers and Critiques tr CONT ancl rin\ray compromise rvith bnrnchocollstriction. lnitial tl-eatment ol anaphylaxis is with cpinephrine. rvhich m:ry in this patient are unclear and may involve more than one substance. However, a primary cotrsideration is ol-li oid toxicitll with a background o[ access to methadone, be administered intramuscularly or intravenously. N,lech anisrns ot action of epinephrine include vasoconstriction, respiratory depression, miotic pupils, depressed level o1 respiratory smooth rnuscle relaxatiorr. and stabilization of' consciousness, and a transient response of the respiratory dc'granulating inflammatory cells. Sonre patients, such as this ratc to naloxone. In acldition to icler.rtifying the agents or one, require repeat doses o1'epinephrine or even an intrave classes of drugs taken, care o1'patients r,vho have takett irt.t t nous epinephrine infusion if anaphylaxis persists. Patients overdose is primarily supportive: maintenance ol irinvay should be girren supplenlentll oxygen and watched closely lbr patency and ventilatior.r is critically important in prtients signs of irir',t,ay compr<-lmise, sucl-r as stridor or obstruction with decreased mental status. 'lhis patient's inabilit_v tcr clue to a srtollen tongue, r'r,hich ma!' require intubation tcr protect the ainr,ay and concern tbr aspiration necessitate nlaintain ainvay patency: Patients often require fiuid resus lirway intubation. citation, with or lvithout vilsopressor- therapy. Factors that Flumazenil (Option B), an antagor.rist of the benzodi tt o increase risk fbr biphasic an:rphyhxis (anaphylaxis occurring azepine receptor. is generally not indicated in patients with ET I 72 l.ururs after resolution of'thc initial episode) inclucle a depressed consciousness clue kr polysubstance intoxication severe initial episode and a rrecd tilr more than one dose o1 because it can precipitate rn ithdrawal seizures. Furthermure, IJ epinephrine. When snch risk erists, or when there is risk o1' because the respiratory depressant efi'ects of benzodiaze !E' anlphylaxis fatality due to coexisting carcliovascular disease or pines are pr-oportionally small relative to those of'opioids. IE lack of'access to epinephrinc or cnlcrgenL)'services, extended reversal witl-r flumazenil rvill not ber.refit a patient \\,itll r

tr CONT ancl rin\ray compromise rvith bnrnchocollstriction. lnitial tl-eatment ol anaphylaxis is with cpinephrine. rvhich m:ry in this patient are unclear and may involve more than one substance. However, a primary cotrsideration is ol-li oid toxicitll with a background o[ access to methadone, be administered intramuscularly or intravenously. N,lech anisrns ot action of epinephrine include vasoconstriction, respiratory depression, miotic pupils, depressed level o1 respiratory smooth rnuscle relaxatiorr. and stabilization of' consciousness, and a transient response of the respiratory dc'granulating inflammatory cells. Sonre patients, such as this ratc to naloxone. In acldition to icler.rtifying the agents or one, require repeat doses o1'epinephrine or even an intrave classes of drugs taken, care o1'patients r,vho have takett irt.t t nous epinephrine infusion if anaphylaxis persists. Patients overdose is primarily supportive: maintenance ol irinvay should be girren supplenlentll oxygen and watched closely lbr patency and ventilatior.r is critically important in prtients signs of irir',t,ay compr<-lmise, sucl-r as stridor or obstruction with decreased mental status. 'lhis patient's inabilit_v tcr clue to a srtollen tongue, r'r,hich ma!' require intubation tcr protect the ainr,ay and concern tbr aspiration necessitate nlaintain ainvay patency: Patients often require fiuid resus lirway intubation. citation, with or lvithout vilsopressor- therapy. Factors that Flumazenil (Option B), an antagor.rist of the benzodi tt o increase risk fbr biphasic an:rphyhxis (anaphylaxis occurring azepine receptor. is generally not indicated in patients with ET I 72 l.ururs after resolution of'thc initial episode) inclucle a depressed consciousness clue kr polysubstance intoxication severe initial episode and a rrecd tilr more than one dose o1 because it can precipitate rn ithdrawal seizures. Furthermure, IJ epinephrine. When snch risk erists, or when there is risk o1' because the respiratory depressant efi'ects of benzodiaze !E' anlphylaxis fatality due to coexisting carcliovascular disease or pines are pr-oportionally small relative to those of'opioids. IE lack of'access to epinephrinc or cnlcrgenL)'services, extended reversal witl-r flumazenil rvill not ber.refit a patient \\,itll r observation ol up to 6 hours ur longer nray be w,arranted. i mpending respiratory fai lure. o ,\ntihistamines that antzrgonizc the H, receptor. such as Naloxone (Option C) is ar.r opioid antidote that can be ut = diphenhydramine (Option A), and the H., receptor. such as ad m i n istered intravenous 11,, i n t ra nr uscu I arlyr, intranasa I 11,: tarnotidine (Option C), are often given in tl.re setting of ana and endotracheally. If respiratory depression measurably phylaxis. IIowever, they are ot little proven benefit beyond irnproves, naloxone can be given in repeated doses or as ar.r reliet'ol pr:uritus and skin eruptions such as urticaria. They intravenous infusion until the opioid is sufliciently metabo clcl not afl'ect respiratory smooth muscle or vascular tone. lized and cleared. ln rnany instances, naloxone can avert the Glucocorticoids such as methylprednisolone (Option D) need fbr mechanical ventilirtiou. In this patient. hou,ever. rrre of ten given fbr anaphylaxis. but their e{ficacy in this set intubation is necessary because ol his apparent inability to ting is not lrell proved. Furthernrore. their delayed onset <l1 protect the ainva1,. ilction renders them ineflbctive in the nranagement of earll, Providing lTigher ler,els ol supplernental oxlgen (Option D) and acute signs and symptorxs. could modestly raise the prtient's bkroci or1'gen levels but Other vasopressors, such as n<lrepinephrine (Option E), will not afl'ect the primary underlying problerns o1'alveolar rnight be useful fbr persistelrt hypotension and shock but hypoventilation and inability to prolect the ainvay fionr ckl not crlrrect impairment til other organ systems, such as aspiratiolt. the respiratory system. Repeat dosing ofepinephrine, rather TEY POIf,T5 than aclministration ol norepinephrine, is the appropriate intervention for this patiellt. . Opioid overdose should be suspected in patients with respiratory depression, miotic pupils, and depressed I(EY POIXIS level of consciousness. . Epinephrine is the treatment ol'choice for anaphylaxis. o In addition to seeking to identiflz the specific agents or . If anaphylaxis persists after an initial epinephrine dose, classes of drugs taken, care of overdose patients is pri- repeat doses may be needed. marily supportive; maintenance of airway patency and ventilation is critically important in patients with Bibliography decreased mental status. Shaker MS, Wallace DV Golden DBK, et ll; Collabor:rtors. Anaphylaxis ir 2020 practice parameter update, systematic review and Grading of Recommendations, Assessment, [)evelopment and Eva]uation (GRADE) Bibliography dnalysis. J Allergy Clin Immunol. 2020;145:1082 1123. IPMID: 320012531 Skolnik A, Monas J. The crashing toxicolos, patient. Emerg Med Clin North doi : 10.1016 /j.jaci. 2020.Ol.Ol7 Am. 2020;38:841 856. [PMID: 32981621] doi 10.1O16/i.emc.2020.06.014

observation ol up to 6 hours ur longer nray be w,arranted. i mpending respiratory fai lure. o ,\ntihistamines that antzrgonizc the H, receptor. such as Naloxone (Option C) is ar.r opioid antidote that can be ut = diphenhydramine (Option A), and the H., receptor. such as ad m i n istered intravenous 11,, i n t ra nr uscu I arlyr, intranasa I 11,: tarnotidine (Option C), are often given in tl.re setting of ana and endotracheally. If respiratory depression measurably phylaxis. IIowever, they are ot little proven benefit beyond irnproves, naloxone can be given in repeated doses or as ar.r reliet'ol pr:uritus and skin eruptions such as urticaria. They intravenous infusion until the opioid is sufliciently metabo clcl not afl'ect respiratory smooth muscle or vascular tone. lized and cleared. ln rnany instances, naloxone can avert the Glucocorticoids such as methylprednisolone (Option D) need fbr mechanical ventilirtiou. In this patient. hou,ever. rrre of ten given fbr anaphylaxis. but their e{ficacy in this set intubation is necessary because ol his apparent inability to ting is not lrell proved. Furthernrore. their delayed onset <l1 protect the ainva1,. ilction renders them ineflbctive in the nranagement of earll, Providing lTigher ler,els ol supplernental oxlgen (Option D) and acute signs and symptorxs. could modestly raise the prtient's bkroci or1'gen levels but Other vasopressors, such as n<lrepinephrine (Option E), will not afl'ect the primary underlying problerns o1'alveolar rnight be useful fbr persistelrt hypotension and shock but hypoventilation and inability to prolect the ainvay fionr ckl not crlrrect impairment til other organ systems, such as aspiratiolt. the respiratory system. Repeat dosing ofepinephrine, rather TEY POIf,T5 than aclministration ol norepinephrine, is the appropriate intervention for this patiellt. . Opioid overdose should be suspected in patients with respiratory depression, miotic pupils, and depressed I(EY POIXIS level of consciousness. . Epinephrine is the treatment ol'choice for anaphylaxis. o In addition to seeking to identiflz the specific agents or . If anaphylaxis persists after an initial epinephrine dose, classes of drugs taken, care of overdose patients is pri- repeat doses may be needed. marily supportive; maintenance of airway patency and ventilation is critically important in patients with Bibliography decreased mental status. Shaker MS, Wallace DV Golden DBK, et ll; Collabor:rtors. Anaphylaxis ir 2020 practice parameter update, systematic review and Grading of Recommendations, Assessment, [)evelopment and Eva]uation (GRADE) Bibliography dnalysis. J Allergy Clin Immunol. 2020;145:1082 1123. IPMID: 320012531 Skolnik A, Monas J. The crashing toxicolos, patient. Emerg Med Clin North doi : 10.1016 /j.jaci. 2020.Ol.Ol7 Am. 2020;38:841 856. [PMID: 32981621] doi 10.1O16/i.emc.2020.06.014 tr Item 42 Answer: A Educational Objective: Treat unprotected airway with Item 43 Answer: D endotracheal intubation. Educational Objective: Diagnose occupational asthma. The most appropriate treatment is erldotracheal intubation The most likely diagnosis is occupational asthma (Option D). (Option A). This patient has a tttxic syndrclme manifesting This patient presents with one of the most common types of as respiratory depression, ancl therc is concern fbr possi occupational asthma, bakers' asthma. Occupational asthma ble aspiration. 'lhe circumstances of the toxic syndrome includes both asthma caused by exposure to sensitizing or

tr Item 42 Answer: A Educational Objective: Treat unprotected airway with Item 43 Answer: D endotracheal intubation. Educational Objective: Diagnose occupational asthma. The most appropriate treatment is erldotracheal intubation The most likely diagnosis is occupational asthma (Option D). (Option A). This patient has a tttxic syndrclme manifesting This patient presents with one of the most common types of as respiratory depression, ancl therc is concern fbr possi occupational asthma, bakers' asthma. Occupational asthma ble aspiration. 'lhe circumstances of the toxic syndrome includes both asthma caused by exposure to sensitizing or 141

Anslvgrs and Critiques \ irritant substances in the workplace and preexisting asthma Item 44 Answer: B t that is exacerbated by these same factors. Typical sensitizing Educational Objective: Treat COPD with lung volume agents are high molecular weight substances. such as pro- reduction surgery. teins, that induce an IgE-mediated immunologic response. In bakers' asthma, exposure to proteins in wheat and rye The most appropriate therapy for this patient is lung r,'olume l I flour is a likely cause. Once sensitized, patients may react reduction surgery (Option B). Lung volume reduction sur to very low levels ofexposure. A key clinical indicator is the gery improves quality of life, exercise tolerance, pulmonary relationship of symptoms to work exposure: patients often function, and survival in patients rvith emphysema. The \ improve on weekends and during time away trom work. National Emphysema Treatment l'rial also fbund that suc 1 Spirometry before and after workplace exposures is a cost cess relied on ideal patient selection. Ideal patients are those effective way to conflrm a suspected diagnosis of occupa- 'a,ith upper-lobe-predominant en.rphyserna, FEVI and Dt.rrt tional asthma. Alternatively, serial peak flow measurements of' 2o"/,, of predicted or higher, and low exercise tolerance D can be used. In addition to pharmacologic therapy. treat after completion of pulmonary rehabilitation. Patients with u) ment consists of reducing exposure to the offending agent an FEV, of less than 20'1, of predicted. a Dt-t:o of less than 20'X, € .D through workplace modiflcations or removing patients from of predicted, or non upper lobe predominant disease had .A the workplace entirely. high mortality rates. Bronchoscopic surgery is also a possible o, Acute bronchitis (Option A) is a lower respiratory tract therapeutic option. Caref'ully selected patients rt'ho received cl- infection of the large airways, often caused by viral patho endobronchial valve therapy have a greater likelihood of an f.t gens. lt is often preceded by symptoms of upper respiratory increase in their FEV, of 15')(, or greater, significant improve tract infection such as headache. sore throat. and rhinitis. ments in their 6 minute walk distances, and improrements .Er Most cases of acute bronchitis are self-limiting and resolve in their dyspnea. .D UI within 1 to 3 weeks. Although this patient's symptoms are Macrolide antibiotics such as azithromlcin (Option A) similar to those of bronchitis, the symptom duration and have anti-inflammatory and antimicrobial effects. Long improvement away from the workplace suggest a different term macrolide therapy may reduce the frequency of exac cause. erbations when prescribed to patients n'ith severe COPD Acute hypersensitivity pneumonitis (Option B) is also and a history of frequent exacerbations. Chronic antibiotic I caused by inhalation of sensitizing antigens, but it leads therapy is not indicated for most patients'with COPD. and to a markedly diflerent clinical syndrome than occupa- this patient has no indication for chronic antibiotic therapy. l tional asthma. lt is characterized by fever. cough, and Roflumilast (Option C) is a selective phosphodiesterase 4 fatigue within 12 hours of a major exposure to an inciting inhibitor that is used to reduce chronic symptoms and the antigen. lnspiratory crackles are heard during physical frequency of exacerbations in patients with severe COPD examination. who have either primarily symptoms of chronic bronchitis Allergic bronchopulmonary aspergillosis (ABPA) or frequent exacerbations. This patient rtith symptoms and (Option C) is an ongoing immunologic response to inhaled radiographic flndings most consistent nith emphysema and Aspergillus. The reaction leads to persistent eosinophilic no history offiequent exacerbations does not have an indi- airway inflammation, increased IgE levels, and eventually cation for roflumilast therapy. i tissue damage with airway remodeling. Diagnostic criteria The patient had a minimum oxygen saturation of 90'1, include the presence of asthma, elevated IgE levels, posi during a 6 minute walk test. Supplemental oxygen therapy I

irritant substances in the workplace and preexisting asthma Item 44 Answer: B t that is exacerbated by these same factors. Typical sensitizing Educational Objective: Treat COPD with lung volume agents are high molecular weight substances. such as pro- reduction surgery. teins, that induce an IgE-mediated immunologic response. In bakers' asthma, exposure to proteins in wheat and rye The most appropriate therapy for this patient is lung r,'olume l I flour is a likely cause. Once sensitized, patients may react reduction surgery (Option B). Lung volume reduction sur to very low levels ofexposure. A key clinical indicator is the gery improves quality of life, exercise tolerance, pulmonary relationship of symptoms to work exposure: patients often function, and survival in patients rvith emphysema. The \ improve on weekends and during time away trom work. National Emphysema Treatment l'rial also fbund that suc 1 Spirometry before and after workplace exposures is a cost cess relied on ideal patient selection. Ideal patients are those effective way to conflrm a suspected diagnosis of occupa- 'a,ith upper-lobe-predominant en.rphyserna, FEVI and Dt.rrt tional asthma. Alternatively, serial peak flow measurements of' 2o"/,, of predicted or higher, and low exercise tolerance D can be used. In addition to pharmacologic therapy. treat after completion of pulmonary rehabilitation. Patients with u) ment consists of reducing exposure to the offending agent an FEV, of less than 20'1, of predicted. a Dt-t:o of less than 20'X, € .D through workplace modiflcations or removing patients from of predicted, or non upper lobe predominant disease had .A the workplace entirely. high mortality rates. Bronchoscopic surgery is also a possible o, Acute bronchitis (Option A) is a lower respiratory tract therapeutic option. Caref'ully selected patients rt'ho received cl- infection of the large airways, often caused by viral patho endobronchial valve therapy have a greater likelihood of an f.t gens. lt is often preceded by symptoms of upper respiratory increase in their FEV, of 15')(, or greater, significant improve tract infection such as headache. sore throat. and rhinitis. ments in their 6 minute walk distances, and improrements .Er Most cases of acute bronchitis are self-limiting and resolve in their dyspnea. .D UI within 1 to 3 weeks. Although this patient's symptoms are Macrolide antibiotics such as azithromlcin (Option A) similar to those of bronchitis, the symptom duration and have anti-inflammatory and antimicrobial effects. Long improvement away from the workplace suggest a different term macrolide therapy may reduce the frequency of exac cause. erbations when prescribed to patients n'ith severe COPD Acute hypersensitivity pneumonitis (Option B) is also and a history of frequent exacerbations. Chronic antibiotic I caused by inhalation of sensitizing antigens, but it leads therapy is not indicated for most patients'with COPD. and to a markedly diflerent clinical syndrome than occupa- this patient has no indication for chronic antibiotic therapy. l tional asthma. lt is characterized by fever. cough, and Roflumilast (Option C) is a selective phosphodiesterase 4 fatigue within 12 hours of a major exposure to an inciting inhibitor that is used to reduce chronic symptoms and the antigen. lnspiratory crackles are heard during physical frequency of exacerbations in patients with severe COPD examination. who have either primarily symptoms of chronic bronchitis Allergic bronchopulmonary aspergillosis (ABPA) or frequent exacerbations. This patient rtith symptoms and (Option C) is an ongoing immunologic response to inhaled radiographic flndings most consistent nith emphysema and Aspergillus. The reaction leads to persistent eosinophilic no history offiequent exacerbations does not have an indi- airway inflammation, increased IgE levels, and eventually cation for roflumilast therapy. i tissue damage with airway remodeling. Diagnostic criteria The patient had a minimum oxygen saturation of 90'1, include the presence of asthma, elevated IgE levels, posi during a 6 minute walk test. Supplemental oxygen therapy I tive skin tests to Aspergillus antigens, increased pulmonary (Option D) improves quality of life and decreases mortality 1

irritant substances in the workplace and preexisting asthma Item 44 Answer: B t that is exacerbated by these same factors. Typical sensitizing Educational Objective: Treat COPD with lung volume agents are high molecular weight substances. such as pro- reduction surgery. teins, that induce an IgE-mediated immunologic response. In bakers' asthma, exposure to proteins in wheat and rye The most appropriate therapy for this patient is lung r,'olume l I flour is a likely cause. Once sensitized, patients may react reduction surgery (Option B). Lung volume reduction sur to very low levels ofexposure. A key clinical indicator is the gery improves quality of life, exercise tolerance, pulmonary relationship of symptoms to work exposure: patients often function, and survival in patients rvith emphysema. The \ improve on weekends and during time away trom work. National Emphysema Treatment l'rial also fbund that suc 1 Spirometry before and after workplace exposures is a cost cess relied on ideal patient selection. Ideal patients are those effective way to conflrm a suspected diagnosis of occupa- 'a,ith upper-lobe-predominant en.rphyserna, FEVI and Dt.rrt tional asthma. Alternatively, serial peak flow measurements of' 2o"/,, of predicted or higher, and low exercise tolerance D can be used. In addition to pharmacologic therapy. treat after completion of pulmonary rehabilitation. Patients with u) ment consists of reducing exposure to the offending agent an FEV, of less than 20'1, of predicted. a Dt-t:o of less than 20'X, € .D through workplace modiflcations or removing patients from of predicted, or non upper lobe predominant disease had .A the workplace entirely. high mortality rates. Bronchoscopic surgery is also a possible o, Acute bronchitis (Option A) is a lower respiratory tract therapeutic option. Caref'ully selected patients rt'ho received cl- infection of the large airways, often caused by viral patho endobronchial valve therapy have a greater likelihood of an f.t gens. lt is often preceded by symptoms of upper respiratory increase in their FEV, of 15')(, or greater, significant improve tract infection such as headache. sore throat. and rhinitis. ments in their 6 minute walk distances, and improrements .Er Most cases of acute bronchitis are self-limiting and resolve in their dyspnea. .D UI within 1 to 3 weeks. Although this patient's symptoms are Macrolide antibiotics such as azithromlcin (Option A) similar to those of bronchitis, the symptom duration and have anti-inflammatory and antimicrobial effects. Long improvement away from the workplace suggest a different term macrolide therapy may reduce the frequency of exac cause. erbations when prescribed to patients n'ith severe COPD Acute hypersensitivity pneumonitis (Option B) is also and a history of frequent exacerbations. Chronic antibiotic I caused by inhalation of sensitizing antigens, but it leads therapy is not indicated for most patients'with COPD. and to a markedly diflerent clinical syndrome than occupa- this patient has no indication for chronic antibiotic therapy. l tional asthma. lt is characterized by fever. cough, and Roflumilast (Option C) is a selective phosphodiesterase 4 fatigue within 12 hours of a major exposure to an inciting inhibitor that is used to reduce chronic symptoms and the antigen. lnspiratory crackles are heard during physical frequency of exacerbations in patients with severe COPD examination. who have either primarily symptoms of chronic bronchitis Allergic bronchopulmonary aspergillosis (ABPA) or frequent exacerbations. This patient rtith symptoms and (Option C) is an ongoing immunologic response to inhaled radiographic flndings most consistent nith emphysema and Aspergillus. The reaction leads to persistent eosinophilic no history offiequent exacerbations does not have an indi- airway inflammation, increased IgE levels, and eventually cation for roflumilast therapy. i tissue damage with airway remodeling. Diagnostic criteria The patient had a minimum oxygen saturation of 90'1, include the presence of asthma, elevated IgE levels, posi during a 6 minute walk test. Supplemental oxygen therapy I tive skin tests to Aspergillus antigens, increased pulmonary (Option D) improves quality of life and decreases mortality 1 Aspergillus speciflc IgE and IgG levels, and either central fbr patients with COPD and an arterial Po,,, of 55 mm Hg bronchiectasis or infiltrates. The patient's normal Aspergillus- (7.3 kPa) or less or an oxygen saturation of 88'/n or less. For specific IgE level and chest radiograph do not support a patients with COPD and comorbidities such as erythrocyto diagnosis of ABPA. sis, heart failure, or cor pulmonale, supplemental o-rygen is reasonable if the arterial Po, is 59 mm Hg (2.8 kPa) or less or XEY POIXIS oxygen saturation is 89'X, or less. This patient does not meet . Occupational asthma includes asthma caused by the criteria for supplemental oxygen. exposure to sensitizing or irritant substances in the workplace, including high molecular-weight sub X EY PO IITII stances, such as proteins, that induce an IgE-mediated o Lung volume reduction surgery improves quality of immunologic response. life, exercise tolerance, pulmonary function. and sur- . Occupational asthma is characterized by an improve- vival in selected patients with emphysema. ment in symptoms when the patient is away from o Ideal patients for lung volume reduction therapy are work. those with upper-lobe predominant emphysema, FEV, and Dlco of20% ofpredicted or higher, and low Bibliography exercise tolerance after completion of pulmonary Cormier M. Leniidre C. Occupational asthma. tnt J Tuberc l_ung Dis. 2020r rehabilitation. l 24:8-21. Il']M ID: 32005302] doi:10.5588, ijtld.19.O301

Aspergillus speciflc IgE and IgG levels, and either central fbr patients with COPD and an arterial Po,,, of 55 mm Hg bronchiectasis or infiltrates. The patient's normal Aspergillus- (7.3 kPa) or less or an oxygen saturation of 88'/n or less. For specific IgE level and chest radiograph do not support a patients with COPD and comorbidities such as erythrocyto diagnosis of ABPA. sis, heart failure, or cor pulmonale, supplemental o-rygen is reasonable if the arterial Po, is 59 mm Hg (2.8 kPa) or less or XEY POIXIS oxygen saturation is 89'X, or less. This patient does not meet . Occupational asthma includes asthma caused by the criteria for supplemental oxygen. exposure to sensitizing or irritant substances in the workplace, including high molecular-weight sub X EY PO IITII stances, such as proteins, that induce an IgE-mediated o Lung volume reduction surgery improves quality of immunologic response. life, exercise tolerance, pulmonary function. and sur- . Occupational asthma is characterized by an improve- vival in selected patients with emphysema. ment in symptoms when the patient is away from o Ideal patients for lung volume reduction therapy are work. those with upper-lobe predominant emphysema, FEV, and Dlco of20% ofpredicted or higher, and low Bibliography exercise tolerance after completion of pulmonary Cormier M. Leniidre C. Occupational asthma. tnt J Tuberc l_ung Dis. 2020r rehabilitation. l 24:8-21. Il']M ID: 32005302] doi:10.5588, ijtld.19.O301 142

Answers and Critiques Bibliography I(IY POII{I Global Initiative for Chronic Obstructive Lung Disease. 2020 Report, Global Strategr for the Diagnosis, l\4anagement and Prevention ol (lhronic . Providing supplemental oxygen in acutely ill medical Obstructive Pulmonary Disease. goldcopd.org/wp content/uploads/ patients with normal oxygen saturation increases 2019/12/GOLD 2020 FINAL verl.2 03Dec19 WMVpdf. Accessed on January 24, 2021. mortality in a dose-dependent manner.

Bibliography I(IY POII{I Global Initiative for Chronic Obstructive Lung Disease. 2020 Report, Global Strategr for the Diagnosis, l\4anagement and Prevention ol (lhronic . Providing supplemental oxygen in acutely ill medical Obstructive Pulmonary Disease. goldcopd.org/wp content/uploads/ patients with normal oxygen saturation increases 2019/12/GOLD 2020 FINAL verl.2 03Dec19 WMVpdf. Accessed on January 24, 2021. mortality in a dose-dependent manner. Bibliography tr Item 45 Answer: D Educational Objective: Prevent hyperoxia in a critically Siemieniuk RAC. Chu I)K. Kim LH, et al. Orlgen therapy tbr acutely ill medical patients: il clinical practice guideline. BMJ. 2018:363:k.1169. IPMID: 303555671 doi: 10.1136r'bmj.k.1169 ill patient. The patient requires no aclditional oxygen management Item 46 Answer: B (Option D). A 2018 systematic review found that supple mental oxygen in patients with normal oxygen satrlration Educationa| Objective: Diagnose obstructive sleep tr vl (u increases mortality. This review fbcused on acutely ill adults apnea after anesthesia. ET with sepsis, critical illness, stroke. trauma, myocardial The most likely cause of the patient's hypoxemia is obstructive infarction, or cardiac arrest. and patients who had emer lr, sleep apnea (OSA) (Option B). OSA may be clinically recog, gency surgery. In the liberal oxygen therapy group, the E' nized for the first timc alter a procedure that entails generai median baseline oxygen saturation as measured by pulse rg anesthesia and/'or narcotics. In this situation, OSA ma1'mani, t oximetry (Spo,) was 96'1, with a range of 94"1, to 99"/,,. Com fest as repeated episodes olpostoperative hypoxemia but may o, pared with the conservative oxygen therapy group, patients also present as frank respiratory failure. This patient has risk !ta with the highest Spo. had increased in-hospital mortality, factors for OSA. including obesity, male sex, hypertension, increased 30 day mortality, and increased mortaliqr at lon" and a thick neck. Many ofthese risk factors are incorpc;rated gest follow-up. A dose-response curve was evident, with into predictive scoring algorithms to identily those individu mortality highest in trials with the greatest increase in SpOr. als before surgery. With increasing use of screening tools and Providing supplemental oxygen for patients u,ith an Spo, perioperative care pathuays, unexpected patient events due higher than 96'l, increased mortality by approximately l')1,. to undiagnosed OSA fbllowing general anesthesia or opioid Based on these results, an international expert panel pro analgesics are less common than in the past. vided tno strong recommendations: (l) an Spo: o1 96"/,, or Aspiration pneumonia (Option A) is less likely after lower should be maintained in patients receiving oxygen an elective surgical procedure, which is usually preceded therapy, and (2) oxygen therapy should not be started hrr by precautions to avoid oral intake fbr several l.rours befbre patients with acute myocardial infarction or stroke and ar.r surgery. 'Ihe normal chest radiograph after intubation and Spo, of 93"1,, or higher. 'lhese guidelines do not apply to all postintubation normalization of hypoxemia als<t rule out acute medical cnnditions. For example, higher Sao, values aspiration as a cause of acute respiratory failurc. ot nearly 100?, are likely beneficial fbr patients with carbon Pulmonary eclema (Option C). atelectasis. and pneu monoxide poisoning, clustcr headache. sickle cell crisis, or monia are among the most common reasons for reintuba- pneumothorax. tion following general anesthesia. These conditions would A nonrebreather mask (Option A) is an orygen deliv be associated with an abnormal postintubation chest radio ery method that uses a ntask, an oxygen reservoir. and graph and would not quickly resolve with intubation and a system of one-way valves that limits the mixing of the mechanical ventilalion, making them unlikely diagnoses. oxygen supply with exhaled gases and room air. As a The risk lbr poskrperative deep venolls thromboembo short-term solution ttlr significant hypoxemia, it supplics lism (VTE) is highest after 48 to 72 hours of immobilization; the highest concentration of oxygen (957,) that can be pro most postorthopedic surgery care pathuays, including pro vided to a spontaneously breathing patient. This patient longed anticoagulation as seen in this patient, are designed to has no indication for delivery ofsuch high concentrations prevent VTE. Pulmonary embolism (Option D) inrmediately of oxygen. and this thcrapy could prove to be detrimental after orthopedic surgcry ltould be unusual, as w,oulcl com lor the patient. plete resolution o{ hypoxemia immediately atter intubation. Venturi masks (Option B) consist ola device that mixes air and oxygen. The fkrw of oxygen through the device I(EY POIXT I entrains air, which results in a consistent inhaled oxygen o Obstructive sleep apnea may be clinically recognized concentration. Venturi masks are indicated for patients in for the first time after a procedure that entails general whom fixed oxygen concentrations are desired.'lhis patient anesthesia and/or narcotics and may manifest as l has no indication fbr oxygcn therapy by any means. includ repeated episodes of postoperative hypoxemia but ing Venturi mask. may also present as frank respiratory failure. The patient has normal oxygen sanrration. Oxygen, 3 Lrmin by nasal cannula (Option C). is not indicated fbrthis Bibliography patient and may increase mortality if use results in increased Tamisier R, I.-abre F, O'Donoghue F. et al. Anesthesia and sleep apnea. Sleep Spo, abore 96'X,. Med Rev 2018;,10:79 92. IPMtD: 29174558] doi:10.1016/i.smrv.2017.10.006

Bibliography tr Item 45 Answer: D Educational Objective: Prevent hyperoxia in a critically Siemieniuk RAC. Chu I)K. Kim LH, et al. Orlgen therapy tbr acutely ill medical patients: il clinical practice guideline. BMJ. 2018:363:k.1169. IPMID: 303555671 doi: 10.1136r'bmj.k.1169 ill patient. The patient requires no aclditional oxygen management Item 46 Answer: B (Option D). A 2018 systematic review found that supple mental oxygen in patients with normal oxygen satrlration Educationa| Objective: Diagnose obstructive sleep tr vl (u increases mortality. This review fbcused on acutely ill adults apnea after anesthesia. ET with sepsis, critical illness, stroke. trauma, myocardial The most likely cause of the patient's hypoxemia is obstructive infarction, or cardiac arrest. and patients who had emer lr, sleep apnea (OSA) (Option B). OSA may be clinically recog, gency surgery. In the liberal oxygen therapy group, the E' nized for the first timc alter a procedure that entails generai median baseline oxygen saturation as measured by pulse rg anesthesia and/'or narcotics. In this situation, OSA ma1'mani, t oximetry (Spo,) was 96'1, with a range of 94"1, to 99"/,,. Com fest as repeated episodes olpostoperative hypoxemia but may o, pared with the conservative oxygen therapy group, patients also present as frank respiratory failure. This patient has risk !ta with the highest Spo. had increased in-hospital mortality, factors for OSA. including obesity, male sex, hypertension, increased 30 day mortality, and increased mortaliqr at lon" and a thick neck. Many ofthese risk factors are incorpc;rated gest follow-up. A dose-response curve was evident, with into predictive scoring algorithms to identily those individu mortality highest in trials with the greatest increase in SpOr. als before surgery. With increasing use of screening tools and Providing supplemental oxygen for patients u,ith an Spo, perioperative care pathuays, unexpected patient events due higher than 96'l, increased mortality by approximately l')1,. to undiagnosed OSA fbllowing general anesthesia or opioid Based on these results, an international expert panel pro analgesics are less common than in the past. vided tno strong recommendations: (l) an Spo: o1 96"/,, or Aspiration pneumonia (Option A) is less likely after lower should be maintained in patients receiving oxygen an elective surgical procedure, which is usually preceded therapy, and (2) oxygen therapy should not be started hrr by precautions to avoid oral intake fbr several l.rours befbre patients with acute myocardial infarction or stroke and ar.r surgery. 'Ihe normal chest radiograph after intubation and Spo, of 93"1,, or higher. 'lhese guidelines do not apply to all postintubation normalization of hypoxemia als<t rule out acute medical cnnditions. For example, higher Sao, values aspiration as a cause of acute respiratory failurc. ot nearly 100?, are likely beneficial fbr patients with carbon Pulmonary eclema (Option C). atelectasis. and pneu monoxide poisoning, clustcr headache. sickle cell crisis, or monia are among the most common reasons for reintuba- pneumothorax. tion following general anesthesia. These conditions would A nonrebreather mask (Option A) is an orygen deliv be associated with an abnormal postintubation chest radio ery method that uses a ntask, an oxygen reservoir. and graph and would not quickly resolve with intubation and a system of one-way valves that limits the mixing of the mechanical ventilalion, making them unlikely diagnoses. oxygen supply with exhaled gases and room air. As a The risk lbr poskrperative deep venolls thromboembo short-term solution ttlr significant hypoxemia, it supplics lism (VTE) is highest after 48 to 72 hours of immobilization; the highest concentration of oxygen (957,) that can be pro most postorthopedic surgery care pathuays, including pro vided to a spontaneously breathing patient. This patient longed anticoagulation as seen in this patient, are designed to has no indication for delivery ofsuch high concentrations prevent VTE. Pulmonary embolism (Option D) inrmediately of oxygen. and this thcrapy could prove to be detrimental after orthopedic surgcry ltould be unusual, as w,oulcl com lor the patient. plete resolution o{ hypoxemia immediately atter intubation. Venturi masks (Option B) consist ola device that mixes air and oxygen. The fkrw of oxygen through the device I(EY POIXT I entrains air, which results in a consistent inhaled oxygen o Obstructive sleep apnea may be clinically recognized concentration. Venturi masks are indicated for patients in for the first time after a procedure that entails general whom fixed oxygen concentrations are desired.'lhis patient anesthesia and/or narcotics and may manifest as l has no indication fbr oxygcn therapy by any means. includ repeated episodes of postoperative hypoxemia but ing Venturi mask. may also present as frank respiratory failure. The patient has normal oxygen sanrration. Oxygen, 3 Lrmin by nasal cannula (Option C). is not indicated fbrthis Bibliography patient and may increase mortality if use results in increased Tamisier R, I.-abre F, O'Donoghue F. et al. Anesthesia and sleep apnea. Sleep Spo, abore 96'X,. Med Rev 2018;,10:79 92. IPMtD: 29174558] doi:10.1016/i.smrv.2017.10.006 143

Answers and Critiques tr Item 47 Answer: C Educational Objective: Evaluate a pulmonary nodule Bibliography Colarinha P \Ah1'and \r,hen to request firr A Pet Ct scan in A lung cancer patient? Rev Port Cir Cardiotorac Vasc. 2o2o Jul Sepr27:167-177. [PMID, with an integrated PET/CT scan. 33068s0s1

tr Item 47 Answer: C Educational Objective: Evaluate a pulmonary nodule Bibliography Colarinha P \Ah1'and \r,hen to request firr A Pet Ct scan in A lung cancer patient? Rev Port Cir Cardiotorac Vasc. 2o2o Jul Sepr27:167-177. [PMID, with an integrated PET/CT scan. 33068s0s1 An integrated PET/CT (Option C) should be performed next. PET utilizes the radionuclide 1B fluoro-2-deoryglucose. rvhich accumulates rt,ithin highly metabolicalll' actire cells such as cancer cells and can be visualized as discrete areas Item 48 Answer: C Educational Objective: Treat acute respiratory distress tr ol.uptake. lntegrated PET CT allon's improled localization of' syndrome with prone positioning. thc metabolic activiry PET scans are u'idely used to eraluate The most appropriate lranagelnent is prone positioning risk of maligr.rancl, in lung nodules. to stage knort'n thoracic (Option C). The patient has severe acute respiratory dis tumors. :rnd to er'aluate lor nletastatic disease from other tress s1'ndrome (ARDS) due to ittfluenza pneumonia (arte nonthoracic malignancies. Fllse positive PET scans can rial Po, Fio, = 92). Prone positioning reduces compressiolt I gl occur in other hypernretabolic conditions, such as infection of portions of the lung behind the cardiac and mediastinal € (D or inflammation. in which cells accumulate fluorodeoryglu structures and improves venlilation perfusion matching (^ cose. fralse-negative results can occur rt'hen tumors have lou, in patients with ARDS. Prone positioning for at least 12 to q, rates of metabolic activity such as carcinoid, adenocarci 16 hours daily should be considered for patients u'ith mod EL. noma in situ, and, rarel!,. metastatic kidney', prostate. or tes erate to severe ARDS \ .ith persistent h1'poxemia despite n ticular cancer. PET is not useful in cletermining maiignancy use ol lort, tidal volume ventilation and plateau pressure in lung nodules less than 8 mm it.t size; howerer, a PET C'f less than 30 cm HrO. The indications lor prone position .Et scan can help in staging and needle positioning for biopsl' ing have been variably defined, but entrl-criteria in a .D gr targets. For erample, in this patient rvith a solitary pulmo pivotal clinical trial that shor,ved benefit included: arte nary nodule. a PET,CT scan may help determine rvhether rial Por, Fto, <150; Flo2 >0.60 on positive end erpiratory,' any lymph node involvement is present that rtas not visible pressure >5 cm HrO. Study participants \,\'ere intubated on the chest CT scan. providir-rg a potentially more accessible lor less than 48 hours before initiating prone position and strategically important biopsy target. ing. Although the patient is also meeting goals for lung Endobronchial ultrasound (EBUS) (Option A) permits protective ventilation. randornized trials shou' that the visualization of mediastinal ancl hilar lymph nodes lor nee- addition of prone positioning irnproves mortalit!'in those dlc aspiration. EBUS r,vith transbronchial needle aspiratior.t patients. is the initial procedure lbr obtaining tissue from mediasti- The sedation ler'el sl.roulcl not be increased (Option A). nal and hilar lymph nodes in the diagnosis and staging of '[he patient is n.reeting goals lbr sedation and is calm and patients !\,ith known or suspected thoracic malignancy An easily' arousable. Light sedation protocols or daill' art'aket.t integrated PET,CT scan can guide where to biops-ll and it ing trials are associated with decreased length of mechanical rvould be premalure to perforn.r an EBUS-guided transbron ventilation and length of ICU sta1,. chial needle aspiration rvitl.tout this information. In patients w'ith refractorl' hl,poxemia, a recruitment For ilatients suspected of having interstitial lung disease. matleuver (Option B) '-applying a high level of CPAP a high resolution (slice thickness of'1 mm) CT (Option B) to open collapsed alveoli (e.g.. continuous pressure to should be ordered. However. because the slice interval (the 35 cm HrO foll0 seconds) has been conditionally rec distance betrveen individual slices) rvith high-resolution CT ommended. Hou,ever. a randomized control trial demon is larger than r,r'ith conventional CT. this technique "skips" strated that recruitment maneuvers in patients lvith intenal sections of the lur.rg and should not be used to eval ' moderate to severe ARDS rtas associated u'ith increased uate lung nodules. A high resolution CT scan cannot stage risk fbr barotrauma. pneunrothorax. and death compared lung cancer or guide ."r,here to biopsy: u,ith star-rdard care. Sputum cytolos/ (Option D) has a lorver sensitivity than The FACCT trial suggestcd that ercessive fluid resus EBUS guided transbronchial ncedlc aspiration for diagnosis citation is harmful to ARDS patients. l'his trial compared of lung cancer, does not procluce su{ficient sample material conservative with liberal fluid strategies based on central fbr molecular studies. and u,ill not provide needed staging venous pressure and pulmonary artery occiusion pres infbrrnation. sure (a surrogate for leit atrial pressure) in patients u,ith ARDS. Although mortality did not difTer betn'een groups. I(EY POIXIT patients ltho r'r,ere treated u,itl-r conservatir.e fluid man o PET/CT scans are widely used to evaluate risk of agement short'ed improvecl orr,genation and decreased malignancy in lung nodules, to stage known thoracic tinle on the r,entikior and in the ICU. In patients n'ho tumors, and to evaluate for metastatic disease from are hemodl'narnicall1. stable and do not have end other nonthoracic malignancies. organ hy'poperfusion. minin.rizing fluid administration o PET scans are not useful for determining malignancy is r,r,arranted. This patier.rt still requires norepinephrine blood pressure supporti diuresis is not indicated at this in lung nodules less than 8 mm in size. time (Option D).

An integrated PET/CT (Option C) should be performed next. PET utilizes the radionuclide 1B fluoro-2-deoryglucose. rvhich accumulates rt,ithin highly metabolicalll' actire cells such as cancer cells and can be visualized as discrete areas Item 48 Answer: C Educational Objective: Treat acute respiratory distress tr ol.uptake. lntegrated PET CT allon's improled localization of' syndrome with prone positioning. thc metabolic activiry PET scans are u'idely used to eraluate The most appropriate lranagelnent is prone positioning risk of maligr.rancl, in lung nodules. to stage knort'n thoracic (Option C). The patient has severe acute respiratory dis tumors. :rnd to er'aluate lor nletastatic disease from other tress s1'ndrome (ARDS) due to ittfluenza pneumonia (arte nonthoracic malignancies. Fllse positive PET scans can rial Po, Fio, = 92). Prone positioning reduces compressiolt I gl occur in other hypernretabolic conditions, such as infection of portions of the lung behind the cardiac and mediastinal € (D or inflammation. in which cells accumulate fluorodeoryglu structures and improves venlilation perfusion matching (^ cose. fralse-negative results can occur rt'hen tumors have lou, in patients with ARDS. Prone positioning for at least 12 to q, rates of metabolic activity such as carcinoid, adenocarci 16 hours daily should be considered for patients u'ith mod EL. noma in situ, and, rarel!,. metastatic kidney', prostate. or tes erate to severe ARDS \ .ith persistent h1'poxemia despite n ticular cancer. PET is not useful in cletermining maiignancy use ol lort, tidal volume ventilation and plateau pressure in lung nodules less than 8 mm it.t size; howerer, a PET C'f less than 30 cm HrO. The indications lor prone position .Et scan can help in staging and needle positioning for biopsl' ing have been variably defined, but entrl-criteria in a .D gr targets. For erample, in this patient rvith a solitary pulmo pivotal clinical trial that shor,ved benefit included: arte nary nodule. a PET,CT scan may help determine rvhether rial Por, Fto, <150; Flo2 >0.60 on positive end erpiratory,' any lymph node involvement is present that rtas not visible pressure >5 cm HrO. Study participants \,\'ere intubated on the chest CT scan. providir-rg a potentially more accessible lor less than 48 hours before initiating prone position and strategically important biopsy target. ing. Although the patient is also meeting goals for lung Endobronchial ultrasound (EBUS) (Option A) permits protective ventilation. randornized trials shou' that the visualization of mediastinal ancl hilar lymph nodes lor nee- addition of prone positioning irnproves mortalit!'in those dlc aspiration. EBUS r,vith transbronchial needle aspiratior.t patients. is the initial procedure lbr obtaining tissue from mediasti- The sedation ler'el sl.roulcl not be increased (Option A). nal and hilar lymph nodes in the diagnosis and staging of '[he patient is n.reeting goals lbr sedation and is calm and patients !\,ith known or suspected thoracic malignancy An easily' arousable. Light sedation protocols or daill' art'aket.t integrated PET,CT scan can guide where to biops-ll and it ing trials are associated with decreased length of mechanical rvould be premalure to perforn.r an EBUS-guided transbron ventilation and length of ICU sta1,. chial needle aspiration rvitl.tout this information. In patients w'ith refractorl' hl,poxemia, a recruitment For ilatients suspected of having interstitial lung disease. matleuver (Option B) '-applying a high level of CPAP a high resolution (slice thickness of'1 mm) CT (Option B) to open collapsed alveoli (e.g.. continuous pressure to should be ordered. However. because the slice interval (the 35 cm HrO foll0 seconds) has been conditionally rec distance betrveen individual slices) rvith high-resolution CT ommended. Hou,ever. a randomized control trial demon is larger than r,r'ith conventional CT. this technique "skips" strated that recruitment maneuvers in patients lvith intenal sections of the lur.rg and should not be used to eval ' moderate to severe ARDS rtas associated u'ith increased uate lung nodules. A high resolution CT scan cannot stage risk fbr barotrauma. pneunrothorax. and death compared lung cancer or guide ."r,here to biopsy: u,ith star-rdard care. Sputum cytolos/ (Option D) has a lorver sensitivity than The FACCT trial suggestcd that ercessive fluid resus EBUS guided transbronchial ncedlc aspiration for diagnosis citation is harmful to ARDS patients. l'his trial compared of lung cancer, does not procluce su{ficient sample material conservative with liberal fluid strategies based on central fbr molecular studies. and u,ill not provide needed staging venous pressure and pulmonary artery occiusion pres infbrrnation. sure (a surrogate for leit atrial pressure) in patients u,ith ARDS. Although mortality did not difTer betn'een groups. I(EY POIXIT patients ltho r'r,ere treated u,itl-r conservatir.e fluid man o PET/CT scans are widely used to evaluate risk of agement short'ed improvecl orr,genation and decreased malignancy in lung nodules, to stage known thoracic tinle on the r,entikior and in the ICU. In patients n'ho tumors, and to evaluate for metastatic disease from are hemodl'narnicall1. stable and do not have end other nonthoracic malignancies. organ hy'poperfusion. minin.rizing fluid administration o PET scans are not useful for determining malignancy is r,r,arranted. This patier.rt still requires norepinephrine blood pressure supporti diuresis is not indicated at this in lung nodules less than 8 mm in size. time (Option D). 144

Answers and Critiques TEY POIXT XEY POIXTS . Prone positioning for at least 12 hours daily should be . Hospitalized patients suspected of having obesity considered for patients with acute respiratory syn- hlpoventilation syndrome should be started on non- drome and arterial Por/Fro, <150 mm Hg, Fro, >0.60 invasive ventilation with either bilevel positive airway on positive end-expiratory pressure >5 cm HrO, who pressure or volume-targeted pressure support. have been intubated for less than 48 hours. . More than79'/. of patients with obesity hypoventila- tion syndrome have severe obstructive sleep apnea; Bibliography the diagnosis should be confirmed with polysomnog- Thompson BT, Chambers RC, Liu KD. Acute respiratory distress syndrome. N Engl J Med. 2017;377 562- 572. IPMID | 287 9287 3l doi:t}.1056/NEJMra16O8O77 raphy in a sleep laboratory. Bibliography

TEY POIXT XEY POIXTS . Prone positioning for at least 12 hours daily should be . Hospitalized patients suspected of having obesity considered for patients with acute respiratory syn- hlpoventilation syndrome should be started on non- drome and arterial Por/Fro, <150 mm Hg, Fro, >0.60 invasive ventilation with either bilevel positive airway on positive end-expiratory pressure >5 cm HrO, who pressure or volume-targeted pressure support. have been intubated for less than 48 hours. . More than79'/. of patients with obesity hypoventila- tion syndrome have severe obstructive sleep apnea; Bibliography the diagnosis should be confirmed with polysomnog- Thompson BT, Chambers RC, Liu KD. Acute respiratory distress syndrome. N Engl J Med. 2017;377 562- 572. IPMID | 287 9287 3l doi:t}.1056/NEJMra16O8O77 raphy in a sleep laboratory. Bibliography tr Item 49 Answer: B Mokhlesi B, Masa JF, Brozek lL, et al. Evaluation and management ofobesity Ut (l, hypoventilation syndrome. an official American Thoracic Society clinical Educational Objective: Treat obesity hypoventilation practice guideline. Am J Respir Crit Care Med. 2019;200:e6-e24. IPMID: ET 313687981 doi:10.1164/rccm.201905-1071ST syndrome. (J .E, Thc rnost appropriate treatment is bilerel positivc lirway pressure (llPAP) (Option B). The patient lus hypc.rclpnic respir-atory failure due to a combination of'opiates (oxyco, done) and obesity hypoventilation syndrome (OI IS), in wl-rich Item 50 Answer: B Educational Objective: Treat severe COPD with tr |E vt o roflumilast. UI the obesity has led to mechanical changes that incrcase tl.re = krad that the respiratory muscles must overconte. 'lhe addi The most appropriate treatment is roflumilast (Option B). tion ofopiates decreased the respiratory drive in I patient that This patient has COPD with Gtobal Initiative fbr Chronic hacl unclerlying hypoventilation. BPAP clelivers a higher level Obstructi,ne Lung Disease (GOLD) class D severity based on of positive airway pressure during inspiration than during his high symptom burclen and exacerbations. He is already expiration. Ir.r the acute setting, the cliflbrencc between expi receiving combination ir.rhalecl therapy with a long-acting ratory ancl inspiratory pressure l-relps the respiratory muscles p, agonist, long.-acting muscarinic antagonist, and inhaled generate app(rpriate tidal volumes. A backup respiratory rate glucocorticoid. Roflumilast. a selective phosphodiesterase can also be dcsignated to initiate breaths in patients lr,,ho have ,1 inhibitor, can reduce symptonls and exacerbations ir.r a lor,r, respiratory rate. The 2019 guidelines ft orn the American palients n,ith serere COPD who have a chronic bronchitis Thoracic Sriciety (ATS) reconrmend that hospitalized patients phenotype or frequent exacerbations. Given this patient's suspected of having OHS should be startcd on noninvasive clinical picture, he would likely benefit from the addition of ventilation u'ith either BPAP or volume targctcd pressure roflumilast. Azithnnnycin. a macrolide antibiotic, can also be support irnd continued on this therapy until they undergo used for patients with COPD and persistent exacerbations, outpaticnt evaluation for obstructive sleep apnea (OSA), idc, especially in those who are current nonsmokers. There are no ally during the first 3 months after hospital dischargc. head-to-head comparisorrs of rof lumilast with azithronrycin. Acetazolamide (Option A) is a respiratory stimulant The choice of rredication is determined by the medicatior-r's that has been usecl to improve ventilation in patients with side eflects. drug interactions, ancl contraindications. OHS. l{owcver, it does not address concurrent obstructive Nocturnal noninvasive ventilation with bilevel positive slccp apnea and can lead to electrolyte abnurmalities. Acet airway pressure (Option A) can be prescribed for patients azolamide nriry be considered as an adjuvant treatment in with concomitant obstructive sleep apnea or chronic hyper patients with refiactory OHS rvho continue to hyporrentilate capnic respiratory failure (Prn., of 52 mm Hg [O.S kPa] or even with noninvasive ventilation and weight loss. higher). ln select populations, it nray improve hospital-frc'c The ATS recommends CPAP (Option C) rather tl-ran survir,al. This pirtier-rt does r-rot meet the criteria for nocturnal BPAP as the initial treatment for stable arnbulatory adult noninvasive ventilation. patients with OtlS and concurrent sevele OSA. Importantlyi For patients with COPD. supplernental ox-vgen therapy since r.nure than 70'X, of patients with OtlS have severe OSA, (Option C) improves quality ol lifb and decreases mortality the diagr.rosis should be confirmed by polysomnography in a in patients with an arterial Pr>, of 55 nrn.r Hg (7.3 kPa) or sleep laboratory. Until that time. the A'lS recommends that less or an oxygen saturation as measured by pulse c"rximetry patients with OHS be treated with either llPAt']or volume of BB'X, or less. For patients with COPD who also have cor Irrgcle(l pressure support. pulmonale, heart lirilurc, or erythrocytosis, these thresholds lr.rtubation and invasive mechanical ventilatiott are lowered to a Po, of .59 mm Ug (z.g kPa) or less or oxygen (Option D) are an option in the care of patients with acute saturation of B9'7, or less. However, this patient does not exacerbation of'OHS. However, this patiellt can be aroused meet these criteria. ar-rd has no contraindications to BPAP 'lhtts. a tinre lin-rited Because this prtient will likely benefit from the addi- trial (l 2 hours) of BPAP. with repeated evalu:ttion <tt gas tion of roflumilast, discharging hirn 'vt'ith no additions to l.tis exchange, is warranted. treatment regimen (Option D) r,r,ould not be appropriate.

tr Item 49 Answer: B Mokhlesi B, Masa JF, Brozek lL, et al. Evaluation and management ofobesity Ut (l, hypoventilation syndrome. an official American Thoracic Society clinical Educational Objective: Treat obesity hypoventilation practice guideline. Am J Respir Crit Care Med. 2019;200:e6-e24. IPMID: ET 313687981 doi:10.1164/rccm.201905-1071ST syndrome. (J .E, Thc rnost appropriate treatment is bilerel positivc lirway pressure (llPAP) (Option B). The patient lus hypc.rclpnic respir-atory failure due to a combination of'opiates (oxyco, done) and obesity hypoventilation syndrome (OI IS), in wl-rich Item 50 Answer: B Educational Objective: Treat severe COPD with tr |E vt o roflumilast. UI the obesity has led to mechanical changes that incrcase tl.re = krad that the respiratory muscles must overconte. 'lhe addi The most appropriate treatment is roflumilast (Option B). tion ofopiates decreased the respiratory drive in I patient that This patient has COPD with Gtobal Initiative fbr Chronic hacl unclerlying hypoventilation. BPAP clelivers a higher level Obstructi,ne Lung Disease (GOLD) class D severity based on of positive airway pressure during inspiration than during his high symptom burclen and exacerbations. He is already expiration. Ir.r the acute setting, the cliflbrencc between expi receiving combination ir.rhalecl therapy with a long-acting ratory ancl inspiratory pressure l-relps the respiratory muscles p, agonist, long.-acting muscarinic antagonist, and inhaled generate app(rpriate tidal volumes. A backup respiratory rate glucocorticoid. Roflumilast. a selective phosphodiesterase can also be dcsignated to initiate breaths in patients lr,,ho have ,1 inhibitor, can reduce symptonls and exacerbations ir.r a lor,r, respiratory rate. The 2019 guidelines ft orn the American palients n,ith serere COPD who have a chronic bronchitis Thoracic Sriciety (ATS) reconrmend that hospitalized patients phenotype or frequent exacerbations. Given this patient's suspected of having OHS should be startcd on noninvasive clinical picture, he would likely benefit from the addition of ventilation u'ith either BPAP or volume targctcd pressure roflumilast. Azithnnnycin. a macrolide antibiotic, can also be support irnd continued on this therapy until they undergo used for patients with COPD and persistent exacerbations, outpaticnt evaluation for obstructive sleep apnea (OSA), idc, especially in those who are current nonsmokers. There are no ally during the first 3 months after hospital dischargc. head-to-head comparisorrs of rof lumilast with azithronrycin. Acetazolamide (Option A) is a respiratory stimulant The choice of rredication is determined by the medicatior-r's that has been usecl to improve ventilation in patients with side eflects. drug interactions, ancl contraindications. OHS. l{owcver, it does not address concurrent obstructive Nocturnal noninvasive ventilation with bilevel positive slccp apnea and can lead to electrolyte abnurmalities. Acet airway pressure (Option A) can be prescribed for patients azolamide nriry be considered as an adjuvant treatment in with concomitant obstructive sleep apnea or chronic hyper patients with refiactory OHS rvho continue to hyporrentilate capnic respiratory failure (Prn., of 52 mm Hg [O.S kPa] or even with noninvasive ventilation and weight loss. higher). ln select populations, it nray improve hospital-frc'c The ATS recommends CPAP (Option C) rather tl-ran survir,al. This pirtier-rt does r-rot meet the criteria for nocturnal BPAP as the initial treatment for stable arnbulatory adult noninvasive ventilation. patients with OtlS and concurrent sevele OSA. Importantlyi For patients with COPD. supplernental ox-vgen therapy since r.nure than 70'X, of patients with OtlS have severe OSA, (Option C) improves quality ol lifb and decreases mortality the diagr.rosis should be confirmed by polysomnography in a in patients with an arterial Pr>, of 55 nrn.r Hg (7.3 kPa) or sleep laboratory. Until that time. the A'lS recommends that less or an oxygen saturation as measured by pulse c"rximetry patients with OHS be treated with either llPAt']or volume of BB'X, or less. For patients with COPD who also have cor Irrgcle(l pressure support. pulmonale, heart lirilurc, or erythrocytosis, these thresholds lr.rtubation and invasive mechanical ventilatiott are lowered to a Po, of .59 mm Ug (z.g kPa) or less or oxygen (Option D) are an option in the care of patients with acute saturation of B9'7, or less. However, this patient does not exacerbation of'OHS. However, this patiellt can be aroused meet these criteria. ar-rd has no contraindications to BPAP 'lhtts. a tinre lin-rited Because this prtient will likely benefit from the addi- trial (l 2 hours) of BPAP. with repeated evalu:ttion <tt gas tion of roflumilast, discharging hirn 'vt'ith no additions to l.tis exchange, is warranted. treatment regimen (Option D) r,r,ould not be appropriate. 145

Answers and Critiques rEY POTTII an initial investigation. would help determine the presence o Roflumilast, a selective phosphodiesterase-4 inhibitor, ol metastatic disease within thc thorar and potential resect ability of the tumor. can reduce symptoms and exacerbations in patients with severe COPD who have a chronic bronchitis phe- XEY POIXI notype or frequent exacerbations. . In patients with radiographic evidence of advanced stage lung cancer, diagnosis and staging are best Bibliography accomplished with a single invasive test at a location labaki WW, Rosenberg SR. Chronic obstructive pulrnonary disease. Ann [ntem that will establish both the diagnosis and the stage of Med. 2o20:173:lTCt7 -ITC32. [PMID; 32745,158] doi:10.7326/AITC202008040 disease.

rEY POTTII an initial investigation. would help determine the presence o Roflumilast, a selective phosphodiesterase-4 inhibitor, ol metastatic disease within thc thorar and potential resect ability of the tumor. can reduce symptoms and exacerbations in patients with severe COPD who have a chronic bronchitis phe- XEY POIXI notype or frequent exacerbations. . In patients with radiographic evidence of advanced stage lung cancer, diagnosis and staging are best Bibliography accomplished with a single invasive test at a location labaki WW, Rosenberg SR. Chronic obstructive pulrnonary disease. Ann [ntem that will establish both the diagnosis and the stage of Med. 2o20:173:lTCt7 -ITC32. [PMID; 32745,158] doi:10.7326/AITC202008040 disease. Item 51 Bibliography F la tr Answer: B Educational Objective: Evaluate possible lung cancer Duma N. Santana Davila R, Molina JR. Non-small cell lung cancer: epidemi- ologr: screening, diagnosis, and treatment. Mayo Clin Proc. 2019:94:1623 l6-10. IPMID: 313782361 doi:10.1o16/j.mayocp.20l9.0l.0l3 with a chest CT. (D = (,t The most appropriate next step in management is CT of the o, * n chest (Option B). the patient presents r,rith a chest mass in the superior sulcus that has led to shoulder and arm pain, weakness and atrophy of the muscles of the hand. Item 52 Answer: B Educational Objective: Manage an abnormal pulse tr oximetry reading. ll and Horner syndrome (ptosis, miosis, anhidrosis). This con (D steliation of symptoms is called Pancoast syndrome and is The most appropriate nlanagement is to change the pulse vt typically caused by tumor infiltration of the brachial plexus oximetry probe to an earlobe probe (Option B). Pulse andtor extension of the tumor into the parietal pleural. ribs. oximetry' calculates the differential betrveen absorption or vertebral bodies. These tumors are typically non-small of infrared light by oxygenated and deoxl'genated blood cell iung cancer (NSCLC) and do not present \t'ith symptoms and is n,idell' used to monitor oxygenation. Conventional of dyspnea or cough until late because of their peripheral probes used on the finger, toe. and earlobe rell'on trans location. Diagnosis of these tumors can be delayed by several mission technolog,, utilizing emitting and detecting sen' months because patients ma!' first be treated for shoulder sors applied on opposing sides of the digit or earlobe. bursitis or arthritis. Superior sulcus tumors are staged the lnaccurate reirdings can be caused by vasoconstriction, same way as NSCLC elser,vhere in the chest. Initial evalua lor,r' perf'usion states. skin pigmentation. motion artifact. tion should start u/ith a full history physical examination, or nail polish. The clinician should eramine the pulse complete blood count. serum chemistry studies. and CT of oximeter u'aveform to determine if the reading is accu the chest. The presence offindings on physical examination rate: a normal signal shorvs a sharp u'aveform r,r'ith a clear (consolidation, effusion. bone tenderness. neurologic find dicrotic notch. lhe absence of a clear dicrotic notch sug ings) r.r,ill indicate advanced disease. PET can be rery helpful gests the de.,,ice is not providing an accurate reading. In a in the initial evaluation of potential lung cancer, as sereral patient lr,ith Raynaud phenomenon ar.rd clinical signs of studies have demonstrated that PET identifies unsuspected peripheral vasoconstriction. pulse oximetr!""vith a finger mediastinal involvement, distant disease, or both, 'nvhich probe is likely to be erroneous. Options include changing infbrms staging biopsies and reduces futile (noncurative) to an earlobe probe or use of reflectance techr.rolog,' u'ith a surgery The deflnitive diagnosis of lung cancer requires tis- forehead probe in u,hich the emitter and detector sensors sue histopathologl. In patients with radiographic evidence are adjacent to each other. of advanced stage disease. diagnosis and staging are best lncreasing the oxlgen therapl'to an FKr, of 0.50 (Option A) accomplished r.tith a single invasive test at a location that u'ould be appropriate only after pulse oximeter has been will establish both the diagnosis and the stage of disease. r,erifled lor accurac\,. A 2018 svstematic revie'ur, fbund that Bronchoscopy (Option A) is not a good choice for tn,o supplemental ox],gen in patients rt'ith normal oxygen satu reasons. First. to assess accessibilitl,for biops1,, a CT should ration increases mortalityi The revieu, focused on acutely ill be performed flrst. Second, in this patient the tunror is a adults',vith sepsis. critical illness. stroke. trauma. rnyocardial peripheral lesion, and the yield for peripheral lesions is typi- infarction. or cardiac arrest. and patients u'ho had emer cally loul Even ifthe lesion nere accessible by bronchoscopy gency surgery it may not be the best modaliry- if it cannot simultaneousll,' Arterial blood gases (ABGs) (Option C) should be diagnose and stage the tumor. measured to assess fbr underlying hl,percapnia in patients CT guided biopsy (Option C) is not the best choice r,r,ith a lort'FEV,. a change in mental status. acute COPD or because there has been no assessment for possible meta asthma exacerbations. cler,ated level of serum bicarbonate. static disease. Ideally one biopsy should be perfornted lor or in some patients, orygen desaturation on pulse oximetn: both stuging and diagnosis. Belore ABGs are obtained in this patient, the pulse oxin.retry Surgical resection (Option D) should not be perf'ormed reading needs to be verified by replacing the finger probe until the extent of disease has been determined. Chest CT. as r.trith an earlclbe or fbrehead probe.

Item 51 Bibliography F la tr Answer: B Educational Objective: Evaluate possible lung cancer Duma N. Santana Davila R, Molina JR. Non-small cell lung cancer: epidemi- ologr: screening, diagnosis, and treatment. Mayo Clin Proc. 2019:94:1623 l6-10. IPMID: 313782361 doi:10.1o16/j.mayocp.20l9.0l.0l3 with a chest CT. (D = (,t The most appropriate next step in management is CT of the o, * n chest (Option B). the patient presents r,rith a chest mass in the superior sulcus that has led to shoulder and arm pain, weakness and atrophy of the muscles of the hand. Item 52 Answer: B Educational Objective: Manage an abnormal pulse tr oximetry reading. ll and Horner syndrome (ptosis, miosis, anhidrosis). This con (D steliation of symptoms is called Pancoast syndrome and is The most appropriate nlanagement is to change the pulse vt typically caused by tumor infiltration of the brachial plexus oximetry probe to an earlobe probe (Option B). Pulse andtor extension of the tumor into the parietal pleural. ribs. oximetry' calculates the differential betrveen absorption or vertebral bodies. These tumors are typically non-small of infrared light by oxygenated and deoxl'genated blood cell iung cancer (NSCLC) and do not present \t'ith symptoms and is n,idell' used to monitor oxygenation. Conventional of dyspnea or cough until late because of their peripheral probes used on the finger, toe. and earlobe rell'on trans location. Diagnosis of these tumors can be delayed by several mission technolog,, utilizing emitting and detecting sen' months because patients ma!' first be treated for shoulder sors applied on opposing sides of the digit or earlobe. bursitis or arthritis. Superior sulcus tumors are staged the lnaccurate reirdings can be caused by vasoconstriction, same way as NSCLC elser,vhere in the chest. Initial evalua lor,r' perf'usion states. skin pigmentation. motion artifact. tion should start u/ith a full history physical examination, or nail polish. The clinician should eramine the pulse complete blood count. serum chemistry studies. and CT of oximeter u'aveform to determine if the reading is accu the chest. The presence offindings on physical examination rate: a normal signal shorvs a sharp u'aveform r,r'ith a clear (consolidation, effusion. bone tenderness. neurologic find dicrotic notch. lhe absence of a clear dicrotic notch sug ings) r.r,ill indicate advanced disease. PET can be rery helpful gests the de.,,ice is not providing an accurate reading. In a in the initial evaluation of potential lung cancer, as sereral patient lr,ith Raynaud phenomenon ar.rd clinical signs of studies have demonstrated that PET identifies unsuspected peripheral vasoconstriction. pulse oximetr!""vith a finger mediastinal involvement, distant disease, or both, 'nvhich probe is likely to be erroneous. Options include changing infbrms staging biopsies and reduces futile (noncurative) to an earlobe probe or use of reflectance techr.rolog,' u'ith a surgery The deflnitive diagnosis of lung cancer requires tis- forehead probe in u,hich the emitter and detector sensors sue histopathologl. In patients with radiographic evidence are adjacent to each other. of advanced stage disease. diagnosis and staging are best lncreasing the oxlgen therapl'to an FKr, of 0.50 (Option A) accomplished r.tith a single invasive test at a location that u'ould be appropriate only after pulse oximeter has been will establish both the diagnosis and the stage of disease. r,erifled lor accurac\,. A 2018 svstematic revie'ur, fbund that Bronchoscopy (Option A) is not a good choice for tn,o supplemental ox],gen in patients rt'ith normal oxygen satu reasons. First. to assess accessibilitl,for biops1,, a CT should ration increases mortalityi The revieu, focused on acutely ill be performed flrst. Second, in this patient the tunror is a adults',vith sepsis. critical illness. stroke. trauma. rnyocardial peripheral lesion, and the yield for peripheral lesions is typi- infarction. or cardiac arrest. and patients u'ho had emer cally loul Even ifthe lesion nere accessible by bronchoscopy gency surgery it may not be the best modaliry- if it cannot simultaneousll,' Arterial blood gases (ABGs) (Option C) should be diagnose and stage the tumor. measured to assess fbr underlying hl,percapnia in patients CT guided biopsy (Option C) is not the best choice r,r,ith a lort'FEV,. a change in mental status. acute COPD or because there has been no assessment for possible meta asthma exacerbations. cler,ated level of serum bicarbonate. static disease. Ideally one biopsy should be perfornted lor or in some patients, orygen desaturation on pulse oximetn: both stuging and diagnosis. Belore ABGs are obtained in this patient, the pulse oxin.retry Surgical resection (Option D) should not be perf'ormed reading needs to be verified by replacing the finger probe until the extent of disease has been determined. Chest CT. as r.trith an earlclbe or fbrehead probe. 146

Answers and Critiques m CT angiography (Option D) has signiflcantly improved In patients with hypovolemic shock, vasopressors such E 15s accuracy of evaluating pulmonary embolism. For as norepinephrine (Option B) are usually not helpful since LUNl patients who present with symptoms suspicious for an acute they do not correct the primary underlying problem and, venous thromboembolism (VTE), such as sudden drop in in the absence of adequate volume resuscitation, further oxygenation, CT angiography provides a rapid, noninvasive reduce tissue perfusion. means of diagnosis. Initiating an evaluation for VTE in this Transjugular intrahepatic portosystemic shunt (TIPS) patient should be considered only if the pulse oximetry (Option D) can help in managing acute variceal bleeding reading is verifled to be accurate. and preventing recurrent variceal hemorrhage. In patients without prwious variceal hemorrhage, hemostasis should be attempted with pharmacologic and endoscopic methods . Inaccurate pulse oximetry reading by finger probe can first. Ilthis fails, TIPS should be considered. be caused by vasoconstriction, low perfusion states, skin pigmentation, motion artifact, or nail polish. . Most patients with acute upper gastrointestinal bleed- {, r In cases of suspected inaccurate pulse oximetry by cr ing should receive a transfusion of packed red blood finger probe, changing to an earlobe probe or forehead cells to a target hemoglobin level of 7 to 9 g/dl probe is indicated. t, (70-eo gtL). EI Bibliography . In patients with portal hypertension and acute gastro- .E vl Jubran A. Pulse oximetry. Crit Care. 201519:272. [PMID: 26f79876] intestinal bleeding, transfusion to 10 g/dl (rOO glt) or (u doi:10.1186/s13054-015-0984-8 higher can rapidly increase portal pressure, putting 3 vt the patient at significant risk for rebleeding.

m CT angiography (Option D) has signiflcantly improved In patients with hypovolemic shock, vasopressors such E 15s accuracy of evaluating pulmonary embolism. For as norepinephrine (Option B) are usually not helpful since LUNl patients who present with symptoms suspicious for an acute they do not correct the primary underlying problem and, venous thromboembolism (VTE), such as sudden drop in in the absence of adequate volume resuscitation, further oxygenation, CT angiography provides a rapid, noninvasive reduce tissue perfusion. means of diagnosis. Initiating an evaluation for VTE in this Transjugular intrahepatic portosystemic shunt (TIPS) patient should be considered only if the pulse oximetry (Option D) can help in managing acute variceal bleeding reading is verifled to be accurate. and preventing recurrent variceal hemorrhage. In patients without prwious variceal hemorrhage, hemostasis should be attempted with pharmacologic and endoscopic methods . Inaccurate pulse oximetry reading by finger probe can first. Ilthis fails, TIPS should be considered. be caused by vasoconstriction, low perfusion states, skin pigmentation, motion artifact, or nail polish. . Most patients with acute upper gastrointestinal bleed- {, r In cases of suspected inaccurate pulse oximetry by cr ing should receive a transfusion of packed red blood finger probe, changing to an earlobe probe or forehead cells to a target hemoglobin level of 7 to 9 g/dl probe is indicated. t, (70-eo gtL). EI Bibliography . In patients with portal hypertension and acute gastro- .E vl Jubran A. Pulse oximetry. Crit Care. 201519:272. [PMID: 26f79876] intestinal bleeding, transfusion to 10 g/dl (rOO glt) or (u doi:10.1186/s13054-015-0984-8 higher can rapidly increase portal pressure, putting 3 vt the patient at significant risk for rebleeding. tr Item 53 Answer: C Ed ucational Objective: Treat gastrointestinal bleeding Bibliography Siau K, Hearnshaw S, Stanley AJ, et al. British Society of Gastroenterolog/ (BSG)-led multisociety consensus care bundle for the early clinical man- with packed red blood cell transfusion. agement of acute upper gastrointestinal bleeding. Fronfline Gastroenterol. 2020;11:311-323. [PMID: 32582423] doi:10.1136/flgastro 2019 101395 'lhe most appropriate treatment for this patient is trans- fusion of packed red blood cells (PRBCs) (Option C). He is Item 54 likely experiencing acute upper gastrointestinal bleeding fiom a variceal hemorrhage with subsequent hypovole- mia and hypotension. In patients with cirrhosis, variceal Answer: C Educational Objective: Treat ethylene glycol poisoning. tr hemorrhage carries a significant risk of morbidity and The most appropriate treatment is fomepizole and hemodi- mortality. Studies have demonstrated that the mortality alysis (Option C). The patient probably has ethylene glycol rate is decreased with a restrictive transfusion strateS/, toxicity. Fomepizole blocks the enzyme alcohol dehydroge- defined as a hemoglobin goal of 7 to 9 gldL (7o-9a glL), nase, which converts alcohols such as ethylene glycol and compared with a liberal transf'usion strates/. However, methanol to their toxic metabolites. Indications for hemo- dilf'erent thresholds and hemoglobin levels may trigger dialysis fbr the ingestion of ethylene glycol or methanol transfusion in actively bleeding patients who are in shock. include severe anion gap metabolic acidosis and end-organ Higher hemoglobin values may also be desirable in patients involvement (kidney impairment, visual changes). Hemodi- with acute coronary syndrome or chronic cardiovascular alysis removes the parent alcohol and its toxic metabolites. disease. ln patients with portal hypertension, transfusion It should be performed as soon as possible in confirmed to higher values (10 gldl hoO g/l-l or higher) can rapidly ethylene glycol or methanol poisoning or in suspected cases increase portal pressure, putting the patient at signiflcant associated with increased anion gap metabolic acidosis or risk for rebleeding. In addition to PRBCs, early resuscita- symptoms of end organ damage. Toxic alcohol ingestion is tion with crystalloid fluids is indicated to provide vascular typically confirmed by drug level measurements, which can support while waiting for blood products. take hours to days; hemodialysis would be appropriate now During massive variceal bleeding in which endoscopic because this patient's presentation is highly zuggestive: eth care is delayed or it is impossible to visualize the bleeding ylene glycol is found in automotive coolants; the patient has source, balloon tamponade (Option A) is an option. How- severe acidemia with an anion gap of 22 and normal glucose ever, balloon tamponade carries several risks, including and lactate levels; and the osmolal gap is elevated. esophageal rupture and ulceration, and should be used Ethanol (Option A) blocks alcohol dehydrogenase by only in cases of life-threatening hemorrhage and only competing with other alcohols. Although administration of until alternative hemostasis methods can be employed. ethanol is eflective for toxic alcohol poisoning, it is limited Although this patient has evidence of acute upper gas- by imprecise dosing, which can lead to the typical adverse trointestinal bleeding, the source of the bleeding is not effects ofethanol intoxication (e.g., sedation and behavioral yet identified and clinical flndings do not indicate uncon- disinhibition). Fomepizole (Option B) is therefore preferable trolled bleeding. to ethanol for this purpose because its dosing is precise and

tr Item 53 Answer: C Ed ucational Objective: Treat gastrointestinal bleeding Bibliography Siau K, Hearnshaw S, Stanley AJ, et al. British Society of Gastroenterolog/ (BSG)-led multisociety consensus care bundle for the early clinical man- with packed red blood cell transfusion. agement of acute upper gastrointestinal bleeding. Fronfline Gastroenterol. 2020;11:311-323. [PMID: 32582423] doi:10.1136/flgastro 2019 101395 'lhe most appropriate treatment for this patient is trans- fusion of packed red blood cells (PRBCs) (Option C). He is Item 54 likely experiencing acute upper gastrointestinal bleeding fiom a variceal hemorrhage with subsequent hypovole- mia and hypotension. In patients with cirrhosis, variceal Answer: C Educational Objective: Treat ethylene glycol poisoning. tr hemorrhage carries a significant risk of morbidity and The most appropriate treatment is fomepizole and hemodi- mortality. Studies have demonstrated that the mortality alysis (Option C). The patient probably has ethylene glycol rate is decreased with a restrictive transfusion strateS/, toxicity. Fomepizole blocks the enzyme alcohol dehydroge- defined as a hemoglobin goal of 7 to 9 gldL (7o-9a glL), nase, which converts alcohols such as ethylene glycol and compared with a liberal transf'usion strates/. However, methanol to their toxic metabolites. Indications for hemo- dilf'erent thresholds and hemoglobin levels may trigger dialysis fbr the ingestion of ethylene glycol or methanol transfusion in actively bleeding patients who are in shock. include severe anion gap metabolic acidosis and end-organ Higher hemoglobin values may also be desirable in patients involvement (kidney impairment, visual changes). Hemodi- with acute coronary syndrome or chronic cardiovascular alysis removes the parent alcohol and its toxic metabolites. disease. ln patients with portal hypertension, transfusion It should be performed as soon as possible in confirmed to higher values (10 gldl hoO g/l-l or higher) can rapidly ethylene glycol or methanol poisoning or in suspected cases increase portal pressure, putting the patient at signiflcant associated with increased anion gap metabolic acidosis or risk for rebleeding. In addition to PRBCs, early resuscita- symptoms of end organ damage. Toxic alcohol ingestion is tion with crystalloid fluids is indicated to provide vascular typically confirmed by drug level measurements, which can support while waiting for blood products. take hours to days; hemodialysis would be appropriate now During massive variceal bleeding in which endoscopic because this patient's presentation is highly zuggestive: eth care is delayed or it is impossible to visualize the bleeding ylene glycol is found in automotive coolants; the patient has source, balloon tamponade (Option A) is an option. How- severe acidemia with an anion gap of 22 and normal glucose ever, balloon tamponade carries several risks, including and lactate levels; and the osmolal gap is elevated. esophageal rupture and ulceration, and should be used Ethanol (Option A) blocks alcohol dehydrogenase by only in cases of life-threatening hemorrhage and only competing with other alcohols. Although administration of until alternative hemostasis methods can be employed. ethanol is eflective for toxic alcohol poisoning, it is limited Although this patient has evidence of acute upper gas- by imprecise dosing, which can lead to the typical adverse trointestinal bleeding, the source of the bleeding is not effects ofethanol intoxication (e.g., sedation and behavioral yet identified and clinical flndings do not indicate uncon- disinhibition). Fomepizole (Option B) is therefore preferable trolled bleeding. to ethanol for this purpose because its dosing is precise and 147

Answers and Critiques tr CONT, it lacks the adverse effects of ethanol. Fbmepizole is e.rpen sive, however, and may not be as rt,idely available as ethanol. Because ethylene glycol or methanol intoxication can risk of rapid clinical deterioration. Managing this patient in sites other than the ICU, including the emergencl. depart- ment observation unit (Option A), general medicine ttard cause sedation similar to that seen with ethanol intoxica (Option B), or an outpatient setting (Option D), places her at tion, sedative drugs such as lorazep:rm (Option D) are gener risk if there is a sudden change in clinical status in a setting ally avoided in patients with alcohol intoxication. However. that is unable to respond with the necessary personnel and in ethanol ingestion the patient should be monitored for resources for quick and efI'ective resuscitation. alcohol rvithdrar,',a1. rvhich can be fatal. Treatment of alco- ITY POIilI hol r.r,ithdral,r,al u,ith benzodiazepines such as lorazepam is appropriate. . Signs and symptoms of clinical instability, including hypotension, hypoxemia, arrhythmias, and mental IEY POIXIS status changes, may be useful in identiffing those o Ethylene Blycol and methanol toxicity should be treated patients who require intense resources or may be at ut with fomepizole. risk ofdeterioration. (D o Indications for hemodialysis in the setting of ethylene = l,l glycol or methanol toxicity include severe anion gap Bibliography q, metabolic acidosis and end-organ involvement (kidney Liu \D{, Lu Y, Carey KA, et al. Comparison ofearly warning scoring systems CL for hospitalized patients with and without infection at risk for in- a't impairment, visual changes). hospital mortality and transfer to the intensive care unit. JAMA Netw Open. 2020;3:e205191. IPMID: 32427324] doi:10.10o1,'jamanetworkopen. 2020.5191 lt Bibliography tr Kraut lA, Mullins ME. Toxic alcohols. N Engl J Med. 2018;378:270 280. .D UI IPMID: 293423921 doi:10.1056/NUMral615295 Item 56 Answer: C Ed ucationa I O bjective : Diagnose cystic fibrosis.

tr CONT, it lacks the adverse effects of ethanol. Fbmepizole is e.rpen sive, however, and may not be as rt,idely available as ethanol. Because ethylene glycol or methanol intoxication can risk of rapid clinical deterioration. Managing this patient in sites other than the ICU, including the emergencl. depart- ment observation unit (Option A), general medicine ttard cause sedation similar to that seen with ethanol intoxica (Option B), or an outpatient setting (Option D), places her at tion, sedative drugs such as lorazep:rm (Option D) are gener risk if there is a sudden change in clinical status in a setting ally avoided in patients with alcohol intoxication. However. that is unable to respond with the necessary personnel and in ethanol ingestion the patient should be monitored for resources for quick and efI'ective resuscitation. alcohol rvithdrar,',a1. rvhich can be fatal. Treatment of alco- ITY POIilI hol r.r,ithdral,r,al u,ith benzodiazepines such as lorazepam is appropriate. . Signs and symptoms of clinical instability, including hypotension, hypoxemia, arrhythmias, and mental IEY POIXIS status changes, may be useful in identiffing those o Ethylene Blycol and methanol toxicity should be treated patients who require intense resources or may be at ut with fomepizole. risk ofdeterioration. (D o Indications for hemodialysis in the setting of ethylene = l,l glycol or methanol toxicity include severe anion gap Bibliography q, metabolic acidosis and end-organ involvement (kidney Liu \D{, Lu Y, Carey KA, et al. Comparison ofearly warning scoring systems CL for hospitalized patients with and without infection at risk for in- a't impairment, visual changes). hospital mortality and transfer to the intensive care unit. JAMA Netw Open. 2020;3:e205191. IPMID: 32427324] doi:10.10o1,'jamanetworkopen. 2020.5191 lt Bibliography tr Kraut lA, Mullins ME. Toxic alcohols. N Engl J Med. 2018;378:270 280. .D UI IPMID: 293423921 doi:10.1056/NUMral615295 Item 56 Answer: C Ed ucationa I O bjective : Diagnose cystic fibrosis. tr Item 55 Answer: C Educational Objective: Assess need for critical care The most likely diagnosis is cystic fibrosis (CF) (Option C). Cystic flbrosis is an autosomal recessive genetic disorder affecting the CFTR gene. The most common genetic variant placement in a patient at high risk for sepsis. resulting in disease is AF508. The abnormal CFTR genotype 'lhe most appropriate renue fbr care of this patient is the results in abnormally thick secretions that are dilficult ICU (Option C). There are no universally accepted criteria to clear. These secretions lead to chronic bacterial infec- fbr admission to an ICU. Signs and s).mptoms of clinical tion and inflammation in the lungs, which eventually lead instabiliry including hypotension. h1'poxemia. arrhythmias. to bronchiectasis. Pulmonary symptoms include chronic and mental status changes. rnay be useful to identifl patients productive cough, recurrent sinusitis, and recurrent pul- who require intense resollrces or may be at risk of sud monary infections. Many patients also develop liver disease den deterioration. This patient has many findings to suggest (from impaired bile flow), endocrine and exocrine pan- clinical instability, including abnormal oxygen saturation, creatic insufficiency, and malabsorption. Male infertility borclerline hypotension, tachycardia, tachypnea, and altered is common. CF is most commonly diagnosed in children ment:rl status. Sepsis-3 guidelines recommend the use of after an abnormal newborn screening but is sometimes the quick Sequential Organ Failure Assessment (qSOFA) not diagnosed until adulthood. Sweat chloride testing is score, a simplified clinical scoring system that includes onl1,' the initial test for CE, with genetic testing conflrming the tlrree criteria: respiration rate of 22, rnin or greater. altered diagnosis. mentation. and systolic blood pressure 100 mm Hg or less. Allergic bronchopulmonary aspergillosis (ABPA) A qSOFA score of 2 or greater in the setting of knor,r,n or (Option A) is an ongoing immunologic response to inhaled suspected infection is used to predict increased mortalir-y* Aspergillus species that leads to persistent eosinophilic and should prompt er,'aluation for resuscitation and con airway inflammation, increased IgE levels (both total and sideration of ICU admission. Recentll,, the use of qSOFA to Aspergillus speciflc), and eventually tissue damage with predict sepsis has come under increased scrutiny given con airway remodeling. Patients present with difficult-to-control flicting studies regarding its accuracy across different patient asthma, productive cough, and expectoration of brown- populations. Other scoring systems. such as the National ish mucus plugs. Radiographs may demonstrate pulmonary Early Warning Systen.r (NEWS). may outperform qSOFA in inflltrates and bronchiectasis. The normal immunoglobu- predicting in-hospital death and need for ICU admission. lin levels and presence of chronic diarrhea make ABPA an Because there is no perfect test for identifying sepsis. scoring unlikely diagnosis in this patient. systems should not be used as the sole indicator of disease or In dr-antitrypsin deflciency (Option B), proteases that triage needs. would normally be inactivated by antiproteases (e.g., o,- this patient has evidence of'clinical instabiiiry includ antitrypsin) lead to destruction of lung tissue. This condition ing borderline abnormal oxrygen saturation, hypotension. most commonly leads to emphysema, although bronchiecta- tachycardia, tachypnea, and altered mental status. She is at sis can also occur. However, this condition is unlikely given

tr Item 55 Answer: C Educational Objective: Assess need for critical care The most likely diagnosis is cystic fibrosis (CF) (Option C). Cystic flbrosis is an autosomal recessive genetic disorder affecting the CFTR gene. The most common genetic variant placement in a patient at high risk for sepsis. resulting in disease is AF508. The abnormal CFTR genotype 'lhe most appropriate renue fbr care of this patient is the results in abnormally thick secretions that are dilficult ICU (Option C). There are no universally accepted criteria to clear. These secretions lead to chronic bacterial infec- fbr admission to an ICU. Signs and s).mptoms of clinical tion and inflammation in the lungs, which eventually lead instabiliry including hypotension. h1'poxemia. arrhythmias. to bronchiectasis. Pulmonary symptoms include chronic and mental status changes. rnay be useful to identifl patients productive cough, recurrent sinusitis, and recurrent pul- who require intense resollrces or may be at risk of sud monary infections. Many patients also develop liver disease den deterioration. This patient has many findings to suggest (from impaired bile flow), endocrine and exocrine pan- clinical instability, including abnormal oxygen saturation, creatic insufficiency, and malabsorption. Male infertility borclerline hypotension, tachycardia, tachypnea, and altered is common. CF is most commonly diagnosed in children ment:rl status. Sepsis-3 guidelines recommend the use of after an abnormal newborn screening but is sometimes the quick Sequential Organ Failure Assessment (qSOFA) not diagnosed until adulthood. Sweat chloride testing is score, a simplified clinical scoring system that includes onl1,' the initial test for CE, with genetic testing conflrming the tlrree criteria: respiration rate of 22, rnin or greater. altered diagnosis. mentation. and systolic blood pressure 100 mm Hg or less. Allergic bronchopulmonary aspergillosis (ABPA) A qSOFA score of 2 or greater in the setting of knor,r,n or (Option A) is an ongoing immunologic response to inhaled suspected infection is used to predict increased mortalir-y* Aspergillus species that leads to persistent eosinophilic and should prompt er,'aluation for resuscitation and con airway inflammation, increased IgE levels (both total and sideration of ICU admission. Recentll,, the use of qSOFA to Aspergillus speciflc), and eventually tissue damage with predict sepsis has come under increased scrutiny given con airway remodeling. Patients present with difficult-to-control flicting studies regarding its accuracy across different patient asthma, productive cough, and expectoration of brown- populations. Other scoring systems. such as the National ish mucus plugs. Radiographs may demonstrate pulmonary Early Warning Systen.r (NEWS). may outperform qSOFA in inflltrates and bronchiectasis. The normal immunoglobu- predicting in-hospital death and need for ICU admission. lin levels and presence of chronic diarrhea make ABPA an Because there is no perfect test for identifying sepsis. scoring unlikely diagnosis in this patient. systems should not be used as the sole indicator of disease or In dr-antitrypsin deflciency (Option B), proteases that triage needs. would normally be inactivated by antiproteases (e.g., o,- this patient has evidence of'clinical instabiiiry includ antitrypsin) lead to destruction of lung tissue. This condition ing borderline abnormal oxrygen saturation, hypotension. most commonly leads to emphysema, although bronchiecta- tachycardia, tachypnea, and altered mental status. She is at sis can also occur. However, this condition is unlikely given 148

Answers and Critiques the patient's constellation of pulmonary sinus, and gastro, correlation bctween baseline cortisol lerel or cortisol reser\e intestinal symptoms and lack of emphysematous changes on ancl response tcl glucocorticoid supplementatiorr does not chest imaging. support use of tl.ris measurement in lratients wilh refractory Although selective IgA deficiency (Option D) is the shock. most common primary antibody deficiency, most patients Guidelines recomntend against the use ol intravenous remain asymptomatic. IgA provides mucosal immunity; in.rmunoglobulins (lVlG) (Option C) in patients with sepsis therefore, patients with IgA deflciency are susceptible rur septic shock. Individual randomizccl studies and system to infections of the respiratory tract and, less frequently, lltic revieu,s and meta anall,ses have failed to convincingly gastrointestinal tract. Sinopulmonary infections are the (lemonstrute that the use of IVIG results in reduced rnortalitv most common presenting manifestation. Patients with IgA and are not recommended. deflciency may also develop celiac disease with associated Procalcitonin lxe:lsurement (Option D) should not be chronic diarrhea. Consideration of IgA deflciency is reason- rurdered in this patient. lts use as a therapeutic guide for able in this patient, but immunoglobulin testing is normal, initiation ol lrrtibiotics in septic patients or as a way to t^ o excluding this disorder. determine the source of irT fection in critical illness has been ET studied with conflicting results. '[he r.nost robust clata have rtY P0rrTt been shown ,when prclcalcitonin levels r,vere used to guide . The diagrosis ofcystic fibrosis should be considered rtntibiotic deescalation in patients with lolr,'er respiratory L., E in young adults with any symptom or combination of tract inf'ection. Since the test would not help guide the man a! syrnptoms such as chronic productive cough, recur- ilgement of this patient's refractory shock, it is not indicated. Ut rent sinusitis, recurrent pulmonary infections, and o bronchiectasis. fEY POIXIS t^ = o Sweat chloride testing is the initial test for cystic flbrosis, . The use of glucocorticoids in the setting of sepsis is suggested if adequate fluid resuscitation and vaso- with genetic testing confirming the diagnosis. pressor therapy are unable to restore hemodynamic stability. Bibliography Boucher RC. Muco-obstructive lung diseases. N Engl J Med. 2019;380:1941 o Guideline-recommended hydrocortisone dosage for I 9s3. [PMID: 31091375] doi:10. 1056/NUMra18t379g refractory septic shock varies from a maximum of 200 mg to 400 mg daily.

the patient's constellation of pulmonary sinus, and gastro, correlation bctween baseline cortisol lerel or cortisol reser\e intestinal symptoms and lack of emphysematous changes on ancl response tcl glucocorticoid supplementatiorr does not chest imaging. support use of tl.ris measurement in lratients wilh refractory Although selective IgA deficiency (Option D) is the shock. most common primary antibody deficiency, most patients Guidelines recomntend against the use ol intravenous remain asymptomatic. IgA provides mucosal immunity; in.rmunoglobulins (lVlG) (Option C) in patients with sepsis therefore, patients with IgA deflciency are susceptible rur septic shock. Individual randomizccl studies and system to infections of the respiratory tract and, less frequently, lltic revieu,s and meta anall,ses have failed to convincingly gastrointestinal tract. Sinopulmonary infections are the (lemonstrute that the use of IVIG results in reduced rnortalitv most common presenting manifestation. Patients with IgA and are not recommended. deflciency may also develop celiac disease with associated Procalcitonin lxe:lsurement (Option D) should not be chronic diarrhea. Consideration of IgA deflciency is reason- rurdered in this patient. lts use as a therapeutic guide for able in this patient, but immunoglobulin testing is normal, initiation ol lrrtibiotics in septic patients or as a way to t^ o excluding this disorder. determine the source of irT fection in critical illness has been ET studied with conflicting results. '[he r.nost robust clata have rtY P0rrTt been shown ,when prclcalcitonin levels r,vere used to guide . The diagrosis ofcystic fibrosis should be considered rtntibiotic deescalation in patients with lolr,'er respiratory L., E in young adults with any symptom or combination of tract inf'ection. Since the test would not help guide the man a! syrnptoms such as chronic productive cough, recur- ilgement of this patient's refractory shock, it is not indicated. Ut rent sinusitis, recurrent pulmonary infections, and o bronchiectasis. fEY POIXIS t^ = o Sweat chloride testing is the initial test for cystic flbrosis, . The use of glucocorticoids in the setting of sepsis is suggested if adequate fluid resuscitation and vaso- with genetic testing confirming the diagnosis. pressor therapy are unable to restore hemodynamic stability. Bibliography Boucher RC. Muco-obstructive lung diseases. N Engl J Med. 2019;380:1941 o Guideline-recommended hydrocortisone dosage for I 9s3. [PMID: 31091375] doi:10. 1056/NUMra18t379g refractory septic shock varies from a maximum of 200 mg to 400 mg daily. tr Item 57 Answer: B Educational Objective: Treat refractory septic shock Bibliography Rochwerg B, Oczkowski SJ, Siemieniuk RAC, et al. Corticosteroids in sepsis: an updated systematic review and meta-analysis. Crit Care with glucocorticoid therapy. Med. 2018;46:i411-1420. IPMID: 2997922t] doi:10.1097/CCM.0000 000000003262 'lhe r.nost appropriate adclitional managetnent is intravenous adtrinistration ot hydrocortisone (Option B). This patient has septic shock related to the necrotic diabetic fitot ulcer. Item 58 Answer: D Despite aggressive early resuscitation with crystalloid fluids and concomitant vasopressors, the patient's hemodynamic Ed ucationa I Obiective : Treat depression associated with montelukast. status remains unstable. 'lhe use o1'glucocorticoids ir.r the setting ofsepsis has been suggested to achieve hemodl,nantic The most appropriate treatment is to stop montelukast stability rvhen it is not achieved with intravenous lluids (Option D). After initiation of asthma therapies, patients and virsopressor therapies. A 2018 meta analysis of 42 trials should be reassessed for symptom control and medication concluded that although there was no evidence that glu tolerance. Montelukast has been associated with signiflcant cocorticoids improre mortalityl patients lvith septic shock adverse mental health effects and may be the cause of the who receive glucocorticoicls ilre more likely to h:rve reversal patient's depression. Depressive symptoms can occur in of shock within 7 days. Guidelines published by the Soci- patients with and without a previous history of depression ety of'Critical Care lt{edicine and the European Society of or other neuropsychiatric disorders. In March 2020 the FDA l n tensile Care Medicine in')017 recomnrend consicleration added a boxed warning to montelukast, strengthening pre of glucocorticoids fbr patients rvith refiirctory septic sl.rock vious warnings about behavior and mood-related changes, at a maximurn dose of 400 mg hydrocortisone daily or the including suicides, associated with this medication. The equivalent using another glucocorticoid. The 2016 Surviving FDA also advised against using montelukast for allergic rhi- Sepsis Campaigr.r guidelines recommend hydrocortisone in nitis because other flrst-line medications, such as intranasal doses up to 200 rng daily fbr refiactory shock. glucocorticoids, are widely available and more efficacious Se'ueral studies have evaluated the utility ol assessing and because many physicians are unaware of montelu- endogenous cortisol levels and cortisol reserves in patients kast's potential adverse mental health effects. This patient's with shock. Historically. utilization of cosyntropin stinrt.lation asthma symptoms are well controlled, and he has new (Option A) was widespread. llouever, failure to demonstrate symptoms and a positive Patient Health Questionnaire-2

tr Item 57 Answer: B Educational Objective: Treat refractory septic shock Bibliography Rochwerg B, Oczkowski SJ, Siemieniuk RAC, et al. Corticosteroids in sepsis: an updated systematic review and meta-analysis. Crit Care with glucocorticoid therapy. Med. 2018;46:i411-1420. IPMID: 2997922t] doi:10.1097/CCM.0000 000000003262 'lhe r.nost appropriate adclitional managetnent is intravenous adtrinistration ot hydrocortisone (Option B). This patient has septic shock related to the necrotic diabetic fitot ulcer. Item 58 Answer: D Despite aggressive early resuscitation with crystalloid fluids and concomitant vasopressors, the patient's hemodynamic Ed ucationa I Obiective : Treat depression associated with montelukast. status remains unstable. 'lhe use o1'glucocorticoids ir.r the setting ofsepsis has been suggested to achieve hemodl,nantic The most appropriate treatment is to stop montelukast stability rvhen it is not achieved with intravenous lluids (Option D). After initiation of asthma therapies, patients and virsopressor therapies. A 2018 meta analysis of 42 trials should be reassessed for symptom control and medication concluded that although there was no evidence that glu tolerance. Montelukast has been associated with signiflcant cocorticoids improre mortalityl patients lvith septic shock adverse mental health effects and may be the cause of the who receive glucocorticoicls ilre more likely to h:rve reversal patient's depression. Depressive symptoms can occur in of shock within 7 days. Guidelines published by the Soci- patients with and without a previous history of depression ety of'Critical Care lt{edicine and the European Society of or other neuropsychiatric disorders. In March 2020 the FDA l n tensile Care Medicine in')017 recomnrend consicleration added a boxed warning to montelukast, strengthening pre of glucocorticoids fbr patients rvith refiirctory septic sl.rock vious warnings about behavior and mood-related changes, at a maximurn dose of 400 mg hydrocortisone daily or the including suicides, associated with this medication. The equivalent using another glucocorticoid. The 2016 Surviving FDA also advised against using montelukast for allergic rhi- Sepsis Campaigr.r guidelines recommend hydrocortisone in nitis because other flrst-line medications, such as intranasal doses up to 200 rng daily fbr refiactory shock. glucocorticoids, are widely available and more efficacious Se'ueral studies have evaluated the utility ol assessing and because many physicians are unaware of montelu- endogenous cortisol levels and cortisol reserves in patients kast's potential adverse mental health effects. This patient's with shock. Historically. utilization of cosyntropin stinrt.lation asthma symptoms are well controlled, and he has new (Option A) was widespread. llouever, failure to demonstrate symptoms and a positive Patient Health Questionnaire-2 149

Answers and Critiques result suggesting depression; therefore, montelukast should the flon' of fluid through a tube is dictated in part b1' the be discontinued, and the patient should be monitored for radius ancl length of the tube. If rte apply this to \enous improvement in his depressive symptoms, which typically access catheters. choosir-rg a device that is sl.rort and has a resolve if medication related. Other adverse effects include n'ide dianreter lumeu r,r,ill maximize flo\l'rates through the anaphylaxis, angioedema, dizziness, dyspepsia, muscle catheter fbr r,olume resuscitation. weakness, and elevated transaminases occurring in less Altl.rough a peripherally inserted central catheter (PICC) than 2% ofall patients. The occurrence ofeosinophilic gran- Iine (Option A) or triple lumen catheter (Option D) might ulomatosis with polyangiitis has been described in patients seem more dr-rrable thall a peripheral IV line. their long taking antileukotriene agents, but most cases occur follow- lengtl.r and narro\\' gauge lumens significantll' limit the ing discontinuation of glucocorticoids for severe asthma maximal flou.rate of infused fluids. tn fact. most 18 gauge and may simply represent an uncovering of a previously IV catheters hare a mirximal flow rate that lar erceeds that undiagnosed condition. It remains unclear if this adverse of a PICC lir.re and is comparable to that of all three catheters event is caused by the drug. combined in a triple lumen catheter. In addition. femoral (/) Escitalopram (Option A) is a selective serotonin insertion ot lV catheters should be:rvt-rided ilpossible due to € (D reuptake inhibitor used to treat depression and anxiety in i ncreasecl risk o{' infec tion and th ron.rbosis.

result suggesting depression; therefore, montelukast should the flon' of fluid through a tube is dictated in part b1' the be discontinued, and the patient should be monitored for radius ancl length of the tube. If rte apply this to \enous improvement in his depressive symptoms, which typically access catheters. choosir-rg a device that is sl.rort and has a resolve if medication related. Other adverse effects include n'ide dianreter lumeu r,r,ill maximize flo\l'rates through the anaphylaxis, angioedema, dizziness, dyspepsia, muscle catheter fbr r,olume resuscitation. weakness, and elevated transaminases occurring in less Altl.rough a peripherally inserted central catheter (PICC) than 2% ofall patients. The occurrence ofeosinophilic gran- Iine (Option A) or triple lumen catheter (Option D) might ulomatosis with polyangiitis has been described in patients seem more dr-rrable thall a peripheral IV line. their long taking antileukotriene agents, but most cases occur follow- lengtl.r and narro\\' gauge lumens significantll' limit the ing discontinuation of glucocorticoids for severe asthma maximal flou.rate of infused fluids. tn fact. most 18 gauge and may simply represent an uncovering of a previously IV catheters hare a mirximal flow rate that lar erceeds that undiagnosed condition. It remains unclear if this adverse of a PICC lir.re and is comparable to that of all three catheters event is caused by the drug. combined in a triple lumen catheter. In addition. femoral (/) Escitalopram (Option A) is a selective serotonin insertion ot lV catheters should be:rvt-rided ilpossible due to € (D reuptake inhibitor used to treat depression and anxiety in i ncreasecl risk o{' infec tion and th ron.rbosis. l,t adults. Adding an antidepressant to this patient's regimen is Intraosseous administration of fluid (Option C) is n.rost o, not necessary because the montelukast may be the cause of commonly indicated r.r'hen IV access is not avarilable. Irr CL the patient's depression and discontinuation of the medica- man)'situations. placement of an intraosseous needle der-ice n tion may resolve his symptoms. in the hurnerus or tibia is eas!,. and its short. large-bore .(t Controller medications such as salmeterol or lumen allon's lbr rapid adn-rinistration ot'lV fluids. Honever. (D budesonide formoterol (Options B, C) can be stepped up this patient has IV access. and the cler.ice is contraindicated Ut or down with the goal of maintaining symptom control and in patients with conditions such as osteogenesis imperf'ecttr. minimizing medication exposure. Stepping up this patient's osteopenia. and osteoporosis because placement ofthe nee treatment regimen with additional controller medications is dle mal increase fiacture risk. Iu addition. placemer.rt of not indicated because his asthma symptoms are well con- a needle in ir bone tl-ritt is fractured or has iilreadl' been trolled. Instead, his therapy should be stepped down, and irccessed. or where a previous intraosseous device placement the first drug to be discontinued is montelukast. r,r'as recently per{brmed. is contraindicated. .\n l8-gauge peripheral I\t line has similar maritnal flon'rates irnd is pre XEY POIf,IS tbrred in this patient. o After initiation of asthma therapies, patients should be reassessed for symptom control and medication rtY P0r1rr tolerance. . For rapid and large-volume fluid administration, o Montelukast should be discontinued in patients with choosing an access device that is short and has a wide-diameter lumen will maximize flow rates. symptoms sugEestive of depression.

l,t adults. Adding an antidepressant to this patient's regimen is Intraosseous administration of fluid (Option C) is n.rost o, not necessary because the montelukast may be the cause of commonly indicated r.r'hen IV access is not avarilable. Irr CL the patient's depression and discontinuation of the medica- man)'situations. placement of an intraosseous needle der-ice n tion may resolve his symptoms. in the hurnerus or tibia is eas!,. and its short. large-bore .(t Controller medications such as salmeterol or lumen allon's lbr rapid adn-rinistration ot'lV fluids. Honever. (D budesonide formoterol (Options B, C) can be stepped up this patient has IV access. and the cler.ice is contraindicated Ut or down with the goal of maintaining symptom control and in patients with conditions such as osteogenesis imperf'ecttr. minimizing medication exposure. Stepping up this patient's osteopenia. and osteoporosis because placement ofthe nee treatment regimen with additional controller medications is dle mal increase fiacture risk. Iu addition. placemer.rt of not indicated because his asthma symptoms are well con- a needle in ir bone tl-ritt is fractured or has iilreadl' been trolled. Instead, his therapy should be stepped down, and irccessed. or where a previous intraosseous device placement the first drug to be discontinued is montelukast. r,r'as recently per{brmed. is contraindicated. .\n l8-gauge peripheral I\t line has similar maritnal flon'rates irnd is pre XEY POIf,IS tbrred in this patient. o After initiation of asthma therapies, patients should be reassessed for symptom control and medication rtY P0r1rr tolerance. . For rapid and large-volume fluid administration, o Montelukast should be discontinued in patients with choosing an access device that is short and has a wide-diameter lumen will maximize flow rates. symptoms sugEestive of depression. Bibliography Bibliography Berman DJ. Schiavi A. Frank Slvl. et al. Factors that influence llo$'through Voelker R. Boxed warning for allergl drug. IAMA. 2020:323:12:16. [PMID: intraYascul:rr catheters: the clinical relevance ol Poiseuille's lau: 3')2592791 doi: I 0. 1001/jama.2020.'1040 Transfusion. 2020160:1410 l.l17. IPMID: 3')6131721doi:l0.lll1 trf:15898

Bibliography Bibliography Berman DJ. Schiavi A. Frank Slvl. et al. Factors that influence llo$'through Voelker R. Boxed warning for allergl drug. IAMA. 2020:323:12:16. [PMID: intraYascul:rr catheters: the clinical relevance ol Poiseuille's lau: 3')2592791 doi: I 0. 1001/jama.2020.'1040 Transfusion. 2020160:1410 l.l17. IPMID: 3')6131721doi:l0.lll1 trf:15898 tr Item 59 Answer: B Educational Objective: Manage intravenous access for Item 60 Answer: A Educational Obiective: Diagnose ascending cholangitis. tr patients in shock. '[he rnost likell' diagnosis is acute ascending cholirngi Fbr this patient. the most appropriate additional intra\e tis (Option A). The presence of cholangitis is heralded b1, nous (lV) access is a secor.rd 18 gauge pcripheral IV catheter the onset of the Charcot triad (ter,er. jaundice. and right in the arm (Option B). The patient has developed hemor upper quadrant abdorninal pain) or Re1'nolcls pentad rhagic shock. Patients u/ith osteogenesis intperfecta have an (Charcot triad plus h1'potension and altered nrcntal sta increased propensitl'for bleeding due to dysfunctionrrl inter- tus). as secn in this piitient. Diirgnostic imaging revealing actions between platelets and endothelial cel1s. ln adclition, signs of biliary obstruction further supports the diagnosis. collagen defects can lead to increased fragility ot capillary Cholangitis is potentialll, lif'e threatening. Initial risk strat beds. Patients lvith hemorrhagic shock should be managed illcation. blsed on ser,eritl, and multiplicin' of involvement with volume repletion, and IV crystalloid solution should be of other organ svstenls. is used to guide treatmcnt ol:rcutc initiated r.r,hile waiting fbr blood products. This patient has ascending cholangitis. In this paticnt. aggressive cry.stalloicl a single peripheral IV n,ith rvhich to start resuscitation, but resuscitation ar-rd antibiritic therapl' targeting gram negative a second access point should be obtained in case the first IV Lnterobctc'terioceoe shonld be aclntinistered. Identified becomes dysl'unctional. According to the law of l,oiseuille. common bile duct slones should be rentoved urgently

tr Item 59 Answer: B Educational Objective: Manage intravenous access for Item 60 Answer: A Educational Obiective: Diagnose ascending cholangitis. tr patients in shock. '[he rnost likell' diagnosis is acute ascending cholirngi Fbr this patient. the most appropriate additional intra\e tis (Option A). The presence of cholangitis is heralded b1, nous (lV) access is a secor.rd 18 gauge pcripheral IV catheter the onset of the Charcot triad (ter,er. jaundice. and right in the arm (Option B). The patient has developed hemor upper quadrant abdorninal pain) or Re1'nolcls pentad rhagic shock. Patients u/ith osteogenesis intperfecta have an (Charcot triad plus h1'potension and altered nrcntal sta increased propensitl'for bleeding due to dysfunctionrrl inter- tus). as secn in this piitient. Diirgnostic imaging revealing actions between platelets and endothelial cel1s. ln adclition, signs of biliary obstruction further supports the diagnosis. collagen defects can lead to increased fragility ot capillary Cholangitis is potentialll, lif'e threatening. Initial risk strat beds. Patients lvith hemorrhagic shock should be managed illcation. blsed on ser,eritl, and multiplicin' of involvement with volume repletion, and IV crystalloid solution should be of other organ svstenls. is used to guide treatmcnt ol:rcutc initiated r.r,hile waiting fbr blood products. This patient has ascending cholangitis. In this paticnt. aggressive cry.stalloicl a single peripheral IV n,ith rvhich to start resuscitation, but resuscitation ar-rd antibiritic therapl' targeting gram negative a second access point should be obtained in case the first IV Lnterobctc'terioceoe shonld be aclntinistered. Identified becomes dysl'unctional. According to the law of l,oiseuille. common bile duct slones should be rentoved urgently 150

Answers and Critiques tr CONT, r,rrith endoscopic rctrograde cholangiopancreatographl. in patients w'ith cholirngitis, after rvhich elective cholecystec torny shor.rld be perlbrmed during the initial hospitalization instability rnuscle and ocular clonus, ancl hyperretlexia. l'reatment includes supportive measurcs, such as avoidance of arry {urther serotonergic agents, ancl seclation with berl' or within 2 weeks [o reduce the risk of complications. h.r zodiazepines to reduce agitation. Sedalion bhints autonornic patients who are not surgical cu-rdidales. endoscopic sphinc- surges and reduces the rnuscle activity tl.rat contributes to terotonl/ can be perfbrmed to fircilitate tl-re passage of addi hyperthermia. Cyproheptadine, an antihistamine lvith anti tional cornrnon bilc duct stones. serotonergic activit),, is used tifi label as an antidote in sercr Acute cholecystitis (Option B) can also present r,r,ith tonin syndrorne in patients who do not respond to benzodi fever and abdominal pain, and laboratory studies may show azepine ther:rpy. Its efiectiveness has not beer.r establishecl in leukocytosis; liver chemistries arc not ele'uated in ullcom clinical trials. and use is based on expefi opinion arld crse plicated acute cholecystitis. 'lhe diagr-rosis can be made by series. lt is available onl1, in pill and syrup fbrmulatiorts so ultrasonography shorving gallbladder wall thickcning andi nMst be adrninistered orally rthich is sclmetimes a challellge or edcma, which is not present in this patier-rt. in uncoopcral ive patients. a (l, '[he diagnosis of'acute pancreatitis (Option C) requires Because hyperthemia il1 serotonin syndrome is r con ET t\,\,o cll'the lollor.r,ing three criteria: (l) acute <tnset abdom sequencc of excessir,e rnuscle activity. the centrall-v acting inal pain charactcristic of pancreatitis (sevcrc, persistent antipyretic acetaminophen (Option A) lvill not allbct tem \, Ibr hours to days. and epigastric in location, olten radiating perature elcvatior-r in this patient. In extrerne cases of'hyper- 'ct to the back); (2) serum lipase or amylase levcls clcvated to thermia, intubation and neuromuscular blockade might be E ll, thrcc to five times the upper limit o{'normal: und (3) charac indicated. t! teristic radiographic findings on contrast-elthancecl CT. This Fentanyl (Option B) is also a serotonin receptor agonist o pirtient's presentation ol septic shock and cholcstasis is not and shiluld bc avoided as a sedative analgesic agent in the ta = E consistent r.r,ith acute pancreatitis. patient with scrotonin syndrome. Pyogenic liver abscesses (Option D) are conrplications ln pal ients who have taken sympathonrimetic agents such ol biliary tract inf'ections or portal venous spreacl ol intra as cocaine or anrphetamines. benzodiazepines are the corner- abdominal infections such as diverticulitis. Patients u,ith stone of therapy fbr agitirtior.r. p Blocker nrcdications such as pyogcnic liver abscesses present with I'ever and right proprar-rolol (Option D) sltoutd be ar,'oidecl in patients with upper cluadrant abd<lrninal pain. An abscess car.r typically cocaine toxicity because they block the B adrenergic recrptors be detected lvith ultrasonography. 'lhe patient's prcsentatior.r lrrd theoretically leale the activated o rcceptors unopposed, does not fit the clinical picture ofpyogenic liver absccss. leading b severe lrypertension. ln this case. t he patient's bl<xrci pressure does not require acute intervention. ar-rd sedation,,r,ill XEY POITTS probably rccluce blood pressure independently. o The presence of cholangitis is heralded by the onset of fever, jaundice, and right-upper-quadrant abdominal (rY POrf,IS " Pain. o Common signs and symptoms of serotonin syndrome . Common bile duct stones should be removed urgently include mental status changes, hyperthermia, diapho- with endoscopic retrograde cholangiopancreatography resis, tremor, autonomic instability, muscle and ocular in patients with acute cholangitis. clonus, and hyperreflexia. o Treatment of serotonin syndrome includes supportive Bibliography measures, such as avoidance of any further serotoner- Manes G, Paspatis C, Aabrkken L, et al. Endoscopic management ofcommon gic agents, and sedation with benzodiazepines to bile duct stones: European Society ofCastrointestinal Endoscopy (ESGE) guideline. Endoscopy. 2019 51:472 491. IPMID: 30943551] doi:10.1055/ reduce agitation. a 0862 0346 Bibliography Werneke U, Truedson-Martiniussen P, Wikstrom H, et al. Serotonin syn-

tr CONT, r,rrith endoscopic rctrograde cholangiopancreatographl. in patients w'ith cholirngitis, after rvhich elective cholecystec torny shor.rld be perlbrmed during the initial hospitalization instability rnuscle and ocular clonus, ancl hyperretlexia. l'reatment includes supportive measurcs, such as avoidance of arry {urther serotonergic agents, ancl seclation with berl' or within 2 weeks [o reduce the risk of complications. h.r zodiazepines to reduce agitation. Sedalion bhints autonornic patients who are not surgical cu-rdidales. endoscopic sphinc- surges and reduces the rnuscle activity tl.rat contributes to terotonl/ can be perfbrmed to fircilitate tl-re passage of addi hyperthermia. Cyproheptadine, an antihistamine lvith anti tional cornrnon bilc duct stones. serotonergic activit),, is used tifi label as an antidote in sercr Acute cholecystitis (Option B) can also present r,r,ith tonin syndrorne in patients who do not respond to benzodi fever and abdominal pain, and laboratory studies may show azepine ther:rpy. Its efiectiveness has not beer.r establishecl in leukocytosis; liver chemistries arc not ele'uated in ullcom clinical trials. and use is based on expefi opinion arld crse plicated acute cholecystitis. 'lhe diagr-rosis can be made by series. lt is available onl1, in pill and syrup fbrmulatiorts so ultrasonography shorving gallbladder wall thickcning andi nMst be adrninistered orally rthich is sclmetimes a challellge or edcma, which is not present in this patier-rt. in uncoopcral ive patients. a (l, '[he diagnosis of'acute pancreatitis (Option C) requires Because hyperthemia il1 serotonin syndrome is r con ET t\,\,o cll'the lollor.r,ing three criteria: (l) acute <tnset abdom sequencc of excessir,e rnuscle activity. the centrall-v acting inal pain charactcristic of pancreatitis (sevcrc, persistent antipyretic acetaminophen (Option A) lvill not allbct tem \, Ibr hours to days. and epigastric in location, olten radiating perature elcvatior-r in this patient. In extrerne cases of'hyper- 'ct to the back); (2) serum lipase or amylase levcls clcvated to thermia, intubation and neuromuscular blockade might be E ll, thrcc to five times the upper limit o{'normal: und (3) charac indicated. t! teristic radiographic findings on contrast-elthancecl CT. This Fentanyl (Option B) is also a serotonin receptor agonist o pirtient's presentation ol septic shock and cholcstasis is not and shiluld bc avoided as a sedative analgesic agent in the ta = E consistent r.r,ith acute pancreatitis. patient with scrotonin syndrome. Pyogenic liver abscesses (Option D) are conrplications ln pal ients who have taken sympathonrimetic agents such ol biliary tract inf'ections or portal venous spreacl ol intra as cocaine or anrphetamines. benzodiazepines are the corner- abdominal infections such as diverticulitis. Patients u,ith stone of therapy fbr agitirtior.r. p Blocker nrcdications such as pyogcnic liver abscesses present with I'ever and right proprar-rolol (Option D) sltoutd be ar,'oidecl in patients with upper cluadrant abd<lrninal pain. An abscess car.r typically cocaine toxicity because they block the B adrenergic recrptors be detected lvith ultrasonography. 'lhe patient's prcsentatior.r lrrd theoretically leale the activated o rcceptors unopposed, does not fit the clinical picture ofpyogenic liver absccss. leading b severe lrypertension. ln this case. t he patient's bl<xrci pressure does not require acute intervention. ar-rd sedation,,r,ill XEY POITTS probably rccluce blood pressure independently. o The presence of cholangitis is heralded by the onset of fever, jaundice, and right-upper-quadrant abdominal (rY POrf,IS " Pain. o Common signs and symptoms of serotonin syndrome . Common bile duct stones should be removed urgently include mental status changes, hyperthermia, diapho- with endoscopic retrograde cholangiopancreatography resis, tremor, autonomic instability, muscle and ocular in patients with acute cholangitis. clonus, and hyperreflexia. o Treatment of serotonin syndrome includes supportive Bibliography measures, such as avoidance of any further serotoner- Manes G, Paspatis C, Aabrkken L, et al. Endoscopic management ofcommon gic agents, and sedation with benzodiazepines to bile duct stones: European Society ofCastrointestinal Endoscopy (ESGE) guideline. Endoscopy. 2019 51:472 491. IPMID: 30943551] doi:10.1055/ reduce agitation. a 0862 0346 Bibliography Werneke U, Truedson-Martiniussen P, Wikstrom H, et al. Serotonin syn- tr Item 61 Answer: C Ed ucationa I Objective: Treat serotonin syndrome. drome: a clinical review ol current controversies. J Integr Neurosci. 2o2O;t9 :719 727. IPMID: 333788461 doi:10.31083/j.jin.2020.04.314

tr Item 61 Answer: C Ed ucationa I Objective: Treat serotonin syndrome. drome: a clinical review ol current controversies. J Integr Neurosci. 2o2O;t9 :719 727. IPMID: 333788461 doi:10.31083/j.jin.2020.04.314 'lhe nrost appropriate treatment is lorazepam (Option C) Item 62 Answer: D intt-avenoush'. This patient has serotonin syndrome. Risk Educational Objective: Diagnose sleep apnea with factors lbr serotonin syndrome include use of selective sero polysomnography. toniu rcuptake inhibikrrs and other medications (sometimes morc tlran one) that increase nervous systelx serotonin The most appropriate management is polysomnography in activity. T1.tis patient takes paroxetinc. a selective serotollill a sleep Iaboratory (Option D). Objective testing is required rettpt:rke inhibitor. l-ramadol ancl cocaine also increlrse sercl fbr a diagnosis of obstructive sleep apnea (OSA) and central tonin relcase in the central nervous system. Conrnron signs sleep apnea (CSA). In laboratory polysomnography is the gold and syrnptoms ol serotonin syndrome inclucle mental sta standard test for mission critical workers, patients with com tus changes, hyperthenni:r. diaphoresis. tremor. ilutonomic plicated OSA, and patients with comorbid conditions such as 151

Answers and Critiques heart failure, neuromuscular disease, and advanced pulmo- moderate to severe symptoms (e.g.. ha'ning to rtalk more nary disease in which diagnostic and treatment algorithms slou,ly than others of same age due to breathlessness. having are more complex. This patient has risk factors for both OSA to stop to catch breath when walking tin level ground at own (male sex, snoring, overweight) and CSA (heart failure and pace. or having more severe breathlessness) and fbr patients atrial flbrillation). Once the tlpe of apnea is clarifled during experiencing at least one COPD exacerbation per year, par- the diagnostic portion of po$somnography, the technician ticularly in those recentl)/ hospitalized after an exacerbation. may then use the most appropriate mode of positive airway Ti.ris patient meets the criteria fbr pulnronary rehabilitation. pressure therapy and assess the response to treatment. o, Antitrypsin augmentation therapy (Option A) can An actigraph (Option A), a small device worn on the slow the progression ol emphysema in patients with a,- wrist, uses an accelerometer and an ambient light sensor antitrypsin deficiencli but it is not eflective ibr the treatment to objectively measure disrupted sleep patterns and sleep ol COPD in p:rtients rt,itl.ront o, antitrypsin deficiency. An wake cycles over multiple days and nights. Actigraphy is not crr antitrypsin level shoulcl be obtained once in all patients D a substitute for a home sleep study or polysomnography and with COPD. If cr,-antitrypsin deficiency is diagnosed, ra cannot diagnose sleep apnea syndromes. augmentatiolr therapy might be indicatecl. It rtould be pre- Home sleep apnea testing (Option B) should be used in rnature to provide augmentation therapy lvithout first mea = .D UI patients without comorbid cardiopulmonary disease who suring the n, antitrypsin level. o, are likely to have OSA of at least moderate severity, such as The National lJrnphysema Treatment Trial (NETT) o. a middle-aged man with obesity who snores loudly, pauses demonstratecl that patients with upper lobe-predonrinant a-t breathing, and gasps during sleep. emphysenra :rr.rd signific:rnt exercise Iimitations even after Overnight pulse oximetry (Option C) is poorly discrim participation in a pulmonary rehabilitation program had lt inative to diagnose OSA, but in those who are asymptomatic improved cluality' ol life. exercise tolerance, pulnronary .D vt with a low pretest probability, normal overnight oximetry fur.rction, ancl sunival with lung volume reduction surgery might be reassuring and support the decision to avoid fur- (Option B). This patient has homogenous emphysema, and ther testing. The patient has daytime sleepiness, which is a there is no evidence of exercise limitations. strong indication for treatment of sleep-disordered breath The patient had a rninirnum oxygen saturation of B9't, ing. Further screening with overnight oximetry will not add during a 6 minute u,alk test. Supplemental oxygen therapy reliably important diagnostic information, nor will it alter (Option D) improves quality of lif'e and decreases mortality the decision to treat. fbr patients With COPD and a Po, of 55 mm Hg (7.3 kPa) or less or an oxygen saturation of BS'X, or less. For patients with f,EY POIXI COPD and certain comorbiclities such as erythrocytosis. . In-laboratory polysomnography is the gold standard sleep heart failr"rre. or cor pulnronale, supplenrental oxygen is rer apnea test for mission-critical workers, patients with sonable if'the Po, is 59 mnr llg (7.8 kPa) or less or the oxygen complicated obstructive sleep apnea, and patients with saturation is B9'7, or less. 'lhis patient does not meet criteria comortrid condidons such as heart failure, nzuromuscu- fbr supplemetltal ox),gen. Iar disease, and adanced pulmonary disease in which rtY P0rilTs diagnostic and treatment algorithms are more complex. . Pulmonary rehabilitation has numerous benefits in Bibliography patients with COPD, including reduced symptoms, Kapur VK. Auckley DH, Chowdhuri S, et al. Clinical practice guideline for improved quality of life, and decreased frequency of diagnostic testing for adult obstructive sleep apnea, an American hospitalizations. Academy of Sleep Medicine clinical practice guideline. J Clin Sleep Med. 2Ol7 :13:479 504. [PMID: 28162150] doi:10.5664/jcsm.6506 . Addition of pulmonary rehabilitation should be con- sidered for patients with COPD and moderate to severe symptoms and patients experiencing at least

heart failure, neuromuscular disease, and advanced pulmo- moderate to severe symptoms (e.g.. ha'ning to rtalk more nary disease in which diagnostic and treatment algorithms slou,ly than others of same age due to breathlessness. having are more complex. This patient has risk factors for both OSA to stop to catch breath when walking tin level ground at own (male sex, snoring, overweight) and CSA (heart failure and pace. or having more severe breathlessness) and fbr patients atrial flbrillation). Once the tlpe of apnea is clarifled during experiencing at least one COPD exacerbation per year, par- the diagnostic portion of po$somnography, the technician ticularly in those recentl)/ hospitalized after an exacerbation. may then use the most appropriate mode of positive airway Ti.ris patient meets the criteria fbr pulnronary rehabilitation. pressure therapy and assess the response to treatment. o, Antitrypsin augmentation therapy (Option A) can An actigraph (Option A), a small device worn on the slow the progression ol emphysema in patients with a,- wrist, uses an accelerometer and an ambient light sensor antitrypsin deficiencli but it is not eflective ibr the treatment to objectively measure disrupted sleep patterns and sleep ol COPD in p:rtients rt,itl.ront o, antitrypsin deficiency. An wake cycles over multiple days and nights. Actigraphy is not crr antitrypsin level shoulcl be obtained once in all patients D a substitute for a home sleep study or polysomnography and with COPD. If cr,-antitrypsin deficiency is diagnosed, ra cannot diagnose sleep apnea syndromes. augmentatiolr therapy might be indicatecl. It rtould be pre- Home sleep apnea testing (Option B) should be used in rnature to provide augmentation therapy lvithout first mea = .D UI patients without comorbid cardiopulmonary disease who suring the n, antitrypsin level. o, are likely to have OSA of at least moderate severity, such as The National lJrnphysema Treatment Trial (NETT) o. a middle-aged man with obesity who snores loudly, pauses demonstratecl that patients with upper lobe-predonrinant a-t breathing, and gasps during sleep. emphysenra :rr.rd signific:rnt exercise Iimitations even after Overnight pulse oximetry (Option C) is poorly discrim participation in a pulmonary rehabilitation program had lt inative to diagnose OSA, but in those who are asymptomatic improved cluality' ol life. exercise tolerance, pulnronary .D vt with a low pretest probability, normal overnight oximetry fur.rction, ancl sunival with lung volume reduction surgery might be reassuring and support the decision to avoid fur- (Option B). This patient has homogenous emphysema, and ther testing. The patient has daytime sleepiness, which is a there is no evidence of exercise limitations. strong indication for treatment of sleep-disordered breath The patient had a rninirnum oxygen saturation of B9't, ing. Further screening with overnight oximetry will not add during a 6 minute u,alk test. Supplemental oxygen therapy reliably important diagnostic information, nor will it alter (Option D) improves quality of lif'e and decreases mortality the decision to treat. fbr patients With COPD and a Po, of 55 mm Hg (7.3 kPa) or less or an oxygen saturation of BS'X, or less. For patients with f,EY POIXI COPD and certain comorbiclities such as erythrocytosis. . In-laboratory polysomnography is the gold standard sleep heart failr"rre. or cor pulnronale, supplenrental oxygen is rer apnea test for mission-critical workers, patients with sonable if'the Po, is 59 mnr llg (7.8 kPa) or less or the oxygen complicated obstructive sleep apnea, and patients with saturation is B9'7, or less. 'lhis patient does not meet criteria comortrid condidons such as heart failure, nzuromuscu- fbr supplemetltal ox),gen. Iar disease, and adanced pulmonary disease in which rtY P0rilTs diagnostic and treatment algorithms are more complex. . Pulmonary rehabilitation has numerous benefits in Bibliography patients with COPD, including reduced symptoms, Kapur VK. Auckley DH, Chowdhuri S, et al. Clinical practice guideline for improved quality of life, and decreased frequency of diagnostic testing for adult obstructive sleep apnea, an American hospitalizations. Academy of Sleep Medicine clinical practice guideline. J Clin Sleep Med. 2Ol7 :13:479 504. [PMID: 28162150] doi:10.5664/jcsm.6506 . Addition of pulmonary rehabilitation should be con- sidered for patients with COPD and moderate to severe symptoms and patients experiencing at least tr Item 63 Answer: C Educational Objective: Treat COPD with pulmonary one exacerbation per year, particularly in those recently hospitalized after an exacerbation. rehabilitation. Bibliography The lnost appropriate treatment is pulmonary rehabilitation t-abaki WW Rosenberg SR Chronic obstructive pulmonary disease. Ann lntem (Option C). Tl-ris patient has been hospitalized fbr a COPD Med. 2o20:173:lTC17 ITC32. [PMID: 3z4s4s8] doi:10.7326/AITC202008040

tr Item 63 Answer: C Educational Objective: Treat COPD with pulmonary one exacerbation per year, particularly in those recently hospitalized after an exacerbation. rehabilitation. Bibliography The lnost appropriate treatment is pulmonary rehabilitation t-abaki WW Rosenberg SR Chronic obstructive pulmonary disease. Ann lntem (Option C). Tl-ris patient has been hospitalized fbr a COPD Med. 2o20:173:lTC17 ITC32. [PMID: 3z4s4s8] doi:10.7326/AITC202008040 exacerbatior-t and is ready for discharge. The most important next step is to optimize her therapy. Pulmonary rehabilita tion integrates exercise training, education. ancl nutritional Item 64 Answer: C and social support lbr patients with chronic lung conditions. Educational Objective: Treat an acute COPD exacerbation It has numerous benefits, ir.rcluding reduced symptoms, with glucocurticoids. improved quality of lif.e, and decreased frequency of'hospi talizations, in patients with COPD. Addition of pulmonary The most appropriate treatment is prednisone (Option C). rehabilitation is recommended ft)r patients with COPD and The goals ofl treatment of an acute COPD exacerbation are 152

Answers and Critiques to relieve acute symptoms and to prevent future exacer clifiuse skeletal muscle acti'",ation that r-esults fiom intracel bations. If the patient has hypoxia, supplemental oxygen lr-rlar calcium release. It is triggerecl ntost often bv ir-rhaled should be used to maintain an oxygen saturation of 88% to anesthetics and the depolarizing neuromuscular blocker suc 92'1,. Noninvasive or invasive mechanical ventilation may be cir.rylcholine. Presenting signs and symptoms reflect hyper necessary ifventilation or oxygenation is inadequate. Acute nret:rbolism and include r.r.rusclc rigidity (including nlasscter symptoms should be treated with short-acting Br-agonists muscle rigidity), tachycard ia, tachypnea, I aboratory eviclence with or without anticholinergic agents. Glucocorticoids are ol' rhabckrmyolysis (elevated serunr creatine kinase, potas a mainstay of the treatment of COPD exacerbations because sium. and phosphorus levels rnd myoglobinuria), and tem they can improve FEV, and hypoxia; decrease the need for perxture that can be strikingly higli..15.0'C (113.0'F) or hospitalization when used early; and decrease the frequency rnore. Mortali!,'c:rn reach 10'.1,. Treatment consists of discor-r of treatment failures, length of stay, and time to subsequent tinuing the triggering agent. activc coolir.rg. and adrninistrn exacerbations. Short courses of lower dose oral glucocorti- tion ol the muscle relarant clrrntrolene every 5 to 10 minutes coids (prednisone 40 mg/d for 5 days) have been found to be until muscle rigidif_v" ar-rd hypertl.rermia resolve. Dantrolene vt o equivalent to higher doses, longer courses, and intravenous interfbres rn'ith intracellular calciun-r relcase and is consid ET administration. ered an antidote to nralignant hyperll.rermia. Patients should Supplemental oxygen therapy should be used for be rnonitored in the ICU tbr 2.,1 l.rours fbllowing an episode o1 rY, patients with acute COPD exacerbations to maintain an rnalignant hyperthermia. 'E oxygen saturation of 88"h to 92"1,. This patient is maintaining Acetaminophen (Option A) acts as an autipyretic IE oxygen saturation greater than BB'1, while receiving oxygen through central nervous svstenr n.rcchanisms. It is inefl'ec t,l (l, through a standard nasal cannula; thus, a high-flow nasal tive at controlling ferer in rnalignant hyperthermia, nhich UI cannula (Option A) is unnecessary. is generated from activatir.rn olskeletal muscles. = For patients with acute hypercapnic respiratory failure Cyproheptadine (Option B). a serotonin and histanrine with acidosis due to a COPD exacerbation, noninvasive ven- antagonist. is sometimes r-rsed oft label to treat serotonin tilation with bilevel positive airway pressure (Option B) can syndrome. Serotonin syndronrc is a lcss serrcre hyperthernric improve symptoms and reduce intubation rates, Iength of reaction triglered by simultaneous use of two or ntore rled hospital stay, and mortality. However, this patient has ade ications that afl'ect release or reuptake of serotonin. Unlil<e : quate ventilation (as evidenced by her normal pH and Pco, neuroleptic malignant syndrome. serotonin syndrome usu levels) and does not require noninvasive ventilation. ally includes hyperrcflcxia and rnyoclonus, does not result A sputum culture (Option D) is not routinely obtained in muscle rigiditll and generally resolves spontaneously af ter in patients with a COPD exacerbation because the results 24 hours. Cyproheptadine does not have tr role in the trc'at rarely affect management. rnent ol malignant hy'perthenria. lhe calcium channcl blocker diltiazem (Option D) f,EY POIlIIS blocks calcium influx into vascul:rr and cardiac muscle cells o Glucocorticoids are a mainstay of the treatment of irut r,r,onld not alfect the calcir-rn'r dl,srcgulation of the sl<e le COPD exacerbations because they can improve FEV, tal muscles that occurs in malignilt.tt hyperthermia. and hypoxia; decrease the need for hospitalization I(EY POITIS when used early; and decrease the frequency oftreat ment failures, Iength of stay, and time to subsequent . Malignant hyperthermia is a rare cause of severe exacerbations. hyperthermia in response to inhaled anesthetic agents . In patients with COPD exacerbation, short courses of or depolarizing paralytic agents such as succinylcho- line, resulting in muscle rigidity, rhabdomyolysis, car- lower-dose oral glucocorticoids (prednisone 40 mg/d diac arrhlthmias, and significant core body temperature for 5 days) have been found to be equivalent to higher elevation. doses, longer courses, and intravenous administration. o Treatment of malignant hyperthermia consists of dis Bibliography continuing the triggering agent, active cooling, and Dobler CC, Morrow AS, Beuschel B, et al. Pharmacologic therapies in administration of the muscle relaxant dantrolene. patients with exacerbation of chronic obstructive pulmonary disease: A systematic review with meta-analysis. Ann Intern Med,. 2020;772:413 422. [PMID: 32092762) doit7}.7326 lM19 -3OO7 Bibliography Hopkins PM, Girard T, Dalay S, et al. Malignant hypedhermia 2020: guideline from the Association of Anaesthetists. Anaesthesia. 202l:76:655-664. IPMID, 33399225] doi:1O.1111/anae.15317 Item 65 tr Answer: C Ed ucatio na I O bjective: Treat malignant hyperthermia. Item 66 Answer: A The most appropriate treatnlent is dantrolene (Option C). Educational Objective: Diagnose central sleep apnea. This patient has developed rnalignant hyperthermia alter receiving succinylcholine. Malignant hyperthermia is a rare The most likely diagnosis is central sleep apnea (CSA) autosomal dominant inheritecl disorder cl-raracterized bV (Option A). the clinical history risk factors in the form

to relieve acute symptoms and to prevent future exacer clifiuse skeletal muscle acti'",ation that r-esults fiom intracel bations. If the patient has hypoxia, supplemental oxygen lr-rlar calcium release. It is triggerecl ntost often bv ir-rhaled should be used to maintain an oxygen saturation of 88% to anesthetics and the depolarizing neuromuscular blocker suc 92'1,. Noninvasive or invasive mechanical ventilation may be cir.rylcholine. Presenting signs and symptoms reflect hyper necessary ifventilation or oxygenation is inadequate. Acute nret:rbolism and include r.r.rusclc rigidity (including nlasscter symptoms should be treated with short-acting Br-agonists muscle rigidity), tachycard ia, tachypnea, I aboratory eviclence with or without anticholinergic agents. Glucocorticoids are ol' rhabckrmyolysis (elevated serunr creatine kinase, potas a mainstay of the treatment of COPD exacerbations because sium. and phosphorus levels rnd myoglobinuria), and tem they can improve FEV, and hypoxia; decrease the need for perxture that can be strikingly higli..15.0'C (113.0'F) or hospitalization when used early; and decrease the frequency rnore. Mortali!,'c:rn reach 10'.1,. Treatment consists of discor-r of treatment failures, length of stay, and time to subsequent tinuing the triggering agent. activc coolir.rg. and adrninistrn exacerbations. Short courses of lower dose oral glucocorti- tion ol the muscle relarant clrrntrolene every 5 to 10 minutes coids (prednisone 40 mg/d for 5 days) have been found to be until muscle rigidif_v" ar-rd hypertl.rermia resolve. Dantrolene vt o equivalent to higher doses, longer courses, and intravenous interfbres rn'ith intracellular calciun-r relcase and is consid ET administration. ered an antidote to nralignant hyperll.rermia. Patients should Supplemental oxygen therapy should be used for be rnonitored in the ICU tbr 2.,1 l.rours fbllowing an episode o1 rY, patients with acute COPD exacerbations to maintain an rnalignant hyperthermia. 'E oxygen saturation of 88"h to 92"1,. This patient is maintaining Acetaminophen (Option A) acts as an autipyretic IE oxygen saturation greater than BB'1, while receiving oxygen through central nervous svstenr n.rcchanisms. It is inefl'ec t,l (l, through a standard nasal cannula; thus, a high-flow nasal tive at controlling ferer in rnalignant hyperthermia, nhich UI cannula (Option A) is unnecessary. is generated from activatir.rn olskeletal muscles. = For patients with acute hypercapnic respiratory failure Cyproheptadine (Option B). a serotonin and histanrine with acidosis due to a COPD exacerbation, noninvasive ven- antagonist. is sometimes r-rsed oft label to treat serotonin tilation with bilevel positive airway pressure (Option B) can syndrome. Serotonin syndronrc is a lcss serrcre hyperthernric improve symptoms and reduce intubation rates, Iength of reaction triglered by simultaneous use of two or ntore rled hospital stay, and mortality. However, this patient has ade ications that afl'ect release or reuptake of serotonin. Unlil<e : quate ventilation (as evidenced by her normal pH and Pco, neuroleptic malignant syndrome. serotonin syndrome usu levels) and does not require noninvasive ventilation. ally includes hyperrcflcxia and rnyoclonus, does not result A sputum culture (Option D) is not routinely obtained in muscle rigiditll and generally resolves spontaneously af ter in patients with a COPD exacerbation because the results 24 hours. Cyproheptadine does not have tr role in the trc'at rarely affect management. rnent ol malignant hy'perthenria. lhe calcium channcl blocker diltiazem (Option D) f,EY POIlIIS blocks calcium influx into vascul:rr and cardiac muscle cells o Glucocorticoids are a mainstay of the treatment of irut r,r,onld not alfect the calcir-rn'r dl,srcgulation of the sl<e le COPD exacerbations because they can improve FEV, tal muscles that occurs in malignilt.tt hyperthermia. and hypoxia; decrease the need for hospitalization I(EY POITIS when used early; and decrease the frequency oftreat ment failures, Iength of stay, and time to subsequent . Malignant hyperthermia is a rare cause of severe exacerbations. hyperthermia in response to inhaled anesthetic agents . In patients with COPD exacerbation, short courses of or depolarizing paralytic agents such as succinylcho- line, resulting in muscle rigidity, rhabdomyolysis, car- lower-dose oral glucocorticoids (prednisone 40 mg/d diac arrhlthmias, and significant core body temperature for 5 days) have been found to be equivalent to higher elevation. doses, longer courses, and intravenous administration. o Treatment of malignant hyperthermia consists of dis Bibliography continuing the triggering agent, active cooling, and Dobler CC, Morrow AS, Beuschel B, et al. Pharmacologic therapies in administration of the muscle relaxant dantrolene. patients with exacerbation of chronic obstructive pulmonary disease: A systematic review with meta-analysis. Ann Intern Med,. 2020;772:413 422. [PMID: 32092762) doit7}.7326 lM19 -3OO7 Bibliography Hopkins PM, Girard T, Dalay S, et al. Malignant hypedhermia 2020: guideline from the Association of Anaesthetists. Anaesthesia. 202l:76:655-664. IPMID, 33399225] doi:1O.1111/anae.15317 Item 65 tr Answer: C Ed ucatio na I O bjective: Treat malignant hyperthermia. Item 66 Answer: A The most appropriate treatnlent is dantrolene (Option C). Educational Objective: Diagnose central sleep apnea. This patient has developed rnalignant hyperthermia alter receiving succinylcholine. Malignant hyperthermia is a rare The most likely diagnosis is central sleep apnea (CSA) autosomal dominant inheritecl disorder cl-raracterized bV (Option A). the clinical history risk factors in the form 153

Answers and Critiques of medical comorbidities, and respiratory tracing from the patient has acute hypercapnic respiratory lailure due to an polysomnogram are most compatible with CSA. CSA is exacerbation of COPD. Patients who develop acute respira deflned by pauses in breathing due to a loss ofoutput from tory acidosis are the subgroup most likely to benefit from an the central respiratory generators in the brainstem to the inirial trial of BPAP BPAP delivers a higher level of positive muscles that make up the respiratory pump. CSA is typically ainvay pressure during inspiration than during expiration. associated with comorbid conditions, most commonly heart Tidal volume is proportional with the dillerence betlteen failure. Other risk factors include atrial flbrillation and opi the inspiratory and expiratory pressures. BPAP oflloads the oid use. The respiratory tracing from the polysomnogram respiratory muscles and augments minute ventilation by shows the classic conflguration ofCheyne Stokes breathing helping the respiratory muscle generate an adequate tidal in CSA, with a crescendo decrescendo pattern of airflow volume. Although she may eventually require mechanical and intervening breathing pauses as blood carbon dioxide ventilation. BPAP is the flrst intervention because in patients tension falls and the stimulus to breathe dissipates. \ ,ith COPD it reduces work of breathing, need for intuba D Although obstructive sleep apnea (OSA) (Option B) tion. hospital length of stay. and mortality. lrl can coexist with CSA, this patient lacks some important Continuous positive airway pressure (CPAP) (Option B) E risk factors (obesity and a thick neck). Respiratory flow in delirrers a constant airway pressure during inspiration and .D vt OSA would demonstrate cessation of airflow rather than the expiration. No additional pressure above the lerel of CPAP a, waxing and waning of ventilation seen here. In OSA, the full is provided, and therefbre tidal volume is not augmented. CL polysomnogram tracing would show continued respiratory Patients must initiate every breath. Although CPAP can be n effort of the rib cage and abdomen despite lack of airflow. used in patients with hypercapnic respiratory lailure due This patient's presentation is more consistent with CSA. to pulmonary qdema or obstructive sleep apnea. in patients ll Sleep-related hlpoventilation (Option C) syndromes are wi{h COPD. BPAP has the strongest evidence supporting (D la associated with advanced COPD, obesity, restrictive lung dis- improved patiedt ouS:omes-''r eases related to lgphoscoliosis or neuromuscular disorders, The patient.had respiratory acidosis: thus strategies and other diseases. Sustained reductions in oxyhemoglobin to augment tidal r,olume and support work of breathing saturation (<90% for at least 5 minutes or >30% total sleep time are needed. l{igh flow nasal cannula (Option C) allor.ts a by oximetry or polysomnography) in the setting of a compat- decrease in the work ofbreathing and in dead spacei ho$I ible medical condition signi$z a hlpoventilation syrrdrome. ever, it does not augment tidal volumes. This modaliry* has OSA may or may not be an associated feature. The patient's not been studied in severe hypercapnia from acute exacer clinical picture and Cheyne-Stokes respiratory tracing are not bations of COPD. consistent with sleep-related hypoventilation qmdrome. Patients with acute exacerbation of COPD who do not Approximately 10% of OSA patients treated with posi- have contraindications to BPAP should have a time limited tive airwaypressure (PAP) exhibit "treatment emergent CSA' trial (<2 hours) to assess whether clinical response has (Option D), the signiflcance of which is a matter of debate. occurred. The rationale is that if the patient responds, out In many patients, the central apneas dissipate as patients comes are better. If there is no improvement, intubation acclimate to PAP therapy. This patient has no evidence of and mechanical ventilation (Option D) should be instituted OSA and is not receiving treatment with PAB making this because delays are associated with increased mortalig an untenable diagnosis. I(EY POtilTS XEY POITIS . Patients with COPD who develop acute respiratory aci- . Central sleep apnea is defined by pauses in breathing dosis are the subgroup most likely to benefit from an ini due to a loss of output from the central respiratory tial trial ofnoninvasive bilevel positive airway pressure. generators in the brainstem to the muscles that make . In patients with acute hypercapnic respiratory failure up the respiratory pump. due to COPD, noninvasive bilevel positive airway o Central sleep apnea is most commonly associated with pressure reduces work ofbreathing, need for intuba- heart failure, atrial fibrillation, and opioid use. tion, hospital length of stay, and mortality. : Bibliography Bibliography Costanzo MR. Central sleep apnea in patients with heaft failure how to Rochwerg B, Brochard L, Elliott MW, et al. Oflicial ERS/ATS clinical practice screen, how to treat. Curr Heart Fail Rep.2O2O;77:277-ZAZ. [PMID, guidelines: noninvasive ventilation for acute respiratory failure. Eur : 328036411 doi:10.1007/s11897 O2O OO172-O Respir J. 2017;50. [PMID: 28860265 j doi:10.1183i 1399 3OO3.02426 2076

of medical comorbidities, and respiratory tracing from the patient has acute hypercapnic respiratory lailure due to an polysomnogram are most compatible with CSA. CSA is exacerbation of COPD. Patients who develop acute respira deflned by pauses in breathing due to a loss ofoutput from tory acidosis are the subgroup most likely to benefit from an the central respiratory generators in the brainstem to the inirial trial of BPAP BPAP delivers a higher level of positive muscles that make up the respiratory pump. CSA is typically ainvay pressure during inspiration than during expiration. associated with comorbid conditions, most commonly heart Tidal volume is proportional with the dillerence betlteen failure. Other risk factors include atrial flbrillation and opi the inspiratory and expiratory pressures. BPAP oflloads the oid use. The respiratory tracing from the polysomnogram respiratory muscles and augments minute ventilation by shows the classic conflguration ofCheyne Stokes breathing helping the respiratory muscle generate an adequate tidal in CSA, with a crescendo decrescendo pattern of airflow volume. Although she may eventually require mechanical and intervening breathing pauses as blood carbon dioxide ventilation. BPAP is the flrst intervention because in patients tension falls and the stimulus to breathe dissipates. \ ,ith COPD it reduces work of breathing, need for intuba D Although obstructive sleep apnea (OSA) (Option B) tion. hospital length of stay. and mortality. lrl can coexist with CSA, this patient lacks some important Continuous positive airway pressure (CPAP) (Option B) E risk factors (obesity and a thick neck). Respiratory flow in delirrers a constant airway pressure during inspiration and .D vt OSA would demonstrate cessation of airflow rather than the expiration. No additional pressure above the lerel of CPAP a, waxing and waning of ventilation seen here. In OSA, the full is provided, and therefbre tidal volume is not augmented. CL polysomnogram tracing would show continued respiratory Patients must initiate every breath. Although CPAP can be n effort of the rib cage and abdomen despite lack of airflow. used in patients with hypercapnic respiratory lailure due This patient's presentation is more consistent with CSA. to pulmonary qdema or obstructive sleep apnea. in patients ll Sleep-related hlpoventilation (Option C) syndromes are wi{h COPD. BPAP has the strongest evidence supporting (D la associated with advanced COPD, obesity, restrictive lung dis- improved patiedt ouS:omes-''r eases related to lgphoscoliosis or neuromuscular disorders, The patient.had respiratory acidosis: thus strategies and other diseases. Sustained reductions in oxyhemoglobin to augment tidal r,olume and support work of breathing saturation (<90% for at least 5 minutes or >30% total sleep time are needed. l{igh flow nasal cannula (Option C) allor.ts a by oximetry or polysomnography) in the setting of a compat- decrease in the work ofbreathing and in dead spacei ho$I ible medical condition signi$z a hlpoventilation syrrdrome. ever, it does not augment tidal volumes. This modaliry* has OSA may or may not be an associated feature. The patient's not been studied in severe hypercapnia from acute exacer clinical picture and Cheyne-Stokes respiratory tracing are not bations of COPD. consistent with sleep-related hypoventilation qmdrome. Patients with acute exacerbation of COPD who do not Approximately 10% of OSA patients treated with posi- have contraindications to BPAP should have a time limited tive airwaypressure (PAP) exhibit "treatment emergent CSA' trial (<2 hours) to assess whether clinical response has (Option D), the signiflcance of which is a matter of debate. occurred. The rationale is that if the patient responds, out In many patients, the central apneas dissipate as patients comes are better. If there is no improvement, intubation acclimate to PAP therapy. This patient has no evidence of and mechanical ventilation (Option D) should be instituted OSA and is not receiving treatment with PAB making this because delays are associated with increased mortalig an untenable diagnosis. I(EY POtilTS XEY POITIS . Patients with COPD who develop acute respiratory aci- . Central sleep apnea is defined by pauses in breathing dosis are the subgroup most likely to benefit from an ini due to a loss of output from the central respiratory tial trial ofnoninvasive bilevel positive airway pressure. generators in the brainstem to the muscles that make . In patients with acute hypercapnic respiratory failure up the respiratory pump. due to COPD, noninvasive bilevel positive airway o Central sleep apnea is most commonly associated with pressure reduces work ofbreathing, need for intuba- heart failure, atrial fibrillation, and opioid use. tion, hospital length of stay, and mortality. : Bibliography Bibliography Costanzo MR. Central sleep apnea in patients with heaft failure how to Rochwerg B, Brochard L, Elliott MW, et al. Oflicial ERS/ATS clinical practice screen, how to treat. Curr Heart Fail Rep.2O2O;77:277-ZAZ. [PMID, guidelines: noninvasive ventilation for acute respiratory failure. Eur : 328036411 doi:10.1007/s11897 O2O OO172-O Respir J. 2017;50. [PMID: 28860265 j doi:10.1183i 1399 3OO3.02426 2076 tr Item 67 Answer: A Educational Objective: Treat acute exacerbation of Item 68 Answer: A Educational Objective: Manage newly recognized sepsis tr COPD with bilevel positive airway pressure ventilation. with the hour-l care bundle. The most appropriate treatment is a trial of noninvasive The most appropriate management for this patient is to staft bilevel positive airway pressure (BPAP) (Option A). The antibiotic therapy (Option A). The patient may have sepsis

tr Item 67 Answer: A Educational Objective: Treat acute exacerbation of Item 68 Answer: A Educational Objective: Manage newly recognized sepsis tr COPD with bilevel positive airway pressure ventilation. with the hour-l care bundle. The most appropriate treatment is a trial of noninvasive The most appropriate management for this patient is to staft bilevel positive airway pressure (BPAP) (Option A). The antibiotic therapy (Option A). The patient may have sepsis 154

Answers and Critiques tr CONT, based on tachycardia, t'ever, and hl,potension in the setting ol a known or suspected infbction. The diagr, osis ol septic shock may be confirmed by the results of laboratory sfudies and of lung cancer through reduction in smoking is the most important way to reduce the burden of disease. Survival rates are directly linked to cancer stage at the time of diag response to fluid resuscitation. in 2018 the Surviving Sepsis nosis. Many lung cancers are diagnosed at a late stage; thus, Campaign pubiished revised guidelines suglesting that phy several randomized clinical trials have evaluated screening sicians administer specific bundled care to patients within measures. The randomized National Lung Screening Trial t hour of'sepsis recognition. The hour 1 bundle includes ini (NLST) compared LDCT screening with chest radiography tiating lluid resuscitatioll. obtaining blood cultures, checking over 3 years among patients ages 55 to 74 years with at least serum lactate level, and administering appropriate antibiotics. a 30 pack year history of smoking who currently smoked In this patient, fluid resuscitation has been initiated, blood cul or had quit in the past 15 years. The trial showed a relative tures have beer.r obtair.red, and serum lactate level is pending; mortality reduction of 20% in the LDCT screening group. the only other item in the bundle that needs to be addressed is The U.S. Preventive Services Task Force (USPSTF) and other the immediate administration of appropriate antibiotics. societies now recommend LDCT screening for lung cancer in (,I o Chest radiography (Option B) is often indicated to iden- high-risk populations. The USPSTF recommends screening ET tify the source of sepsis. This patient has rhonchi on exam patients ages 50 through B0 years who have no symptoms ination. raising the possibility that pneumonia is the source of lung cancer, have at least a 2O-pack-year smoking his- rYt ol int'ection. However, obtaining a chest radiograph should tory and are current smokers or have quit within the Iast !, not take priority over administering empiric antibiotics in 15 years. Cessation of screening should also be considered C' this patient rt ith presumed sepsis, because delays in admin in those who have not smoked in 15 years, those with lim rrt (l, istration reduce patient survival. ited life expectancy, and those who would not be candi- (a Indications for intubation (Option C) include signifl- dates for or would not be willing to undergo surgery This = cant hypoxia, inability to ventilate properly, and airway com patient is at high risk because of her age and smoking history promise. Although this patient's respiration rate is elevated, and should undergo annual LDCT. Screening has potential he is not hypoxic and he has no indication of impending harms, including the consequences of evaluating abnormal airrvay compromise or ventilatory lailure. Therefbre, intuba-. results (additional tests and procedures), radiation exposure, tion is no1 indicated. patient distress, and overdiagnosis. It is desirable that lung In patients with suspected sepsis and hypotension, early cancer screening take place in a center that has radiologic, resuscitation with 30 mlrkg of crystalloid solution is indi- diagnostic, and treatment capabilities similar to those of cated and should be performed as part of the hour-l bundle. centers involved in the NLST. Vasopressor suppofi is indicated if hypotension or organ per- Chest radiography (Option A) and sputum cytologz fusion persists following adequate fluid resuscitation. Norepi- (Option D) are not recommended for lung cancer screening. nephrine (Option D) is the preferred vasopressor because of Several clinical trials have found no mortality beneflt to its ability to improve both vascular tone and myocardial per screening with either method. formance without significantly increasing the risk of arrhyth- Fluorodeoxyglucose PET (Option B) plays a role in mias. In this patient, response to crystalloid resuscitation evaluating patients once a pulmonary nodule or mass is should be assessed before vasopressor support is provided. identifled on CT. It does not have a role in routine lung cancer screening. There is moderate certainty that annual screening o Initiating fluid resuscitation, obtaining blood cultures, for lung cancer with LDCT is of net benefit in asymp checking serum lactate level, and administering tomatic persons who are at high risk for lung cancer. appropriate antibiotics is recommended within t hour This patient fulfills all the criteria for benefiting from of sepsis recognition. LDCT lung cancer screening. Not offering LDCT lung . In patients with sepsis, delays in administration of cancer screening (Option E) may result in unnecessary empiric antibiotics are associated with reduced early mortality. patient survival.

tr CONT, based on tachycardia, t'ever, and hl,potension in the setting ol a known or suspected infbction. The diagr, osis ol septic shock may be confirmed by the results of laboratory sfudies and of lung cancer through reduction in smoking is the most important way to reduce the burden of disease. Survival rates are directly linked to cancer stage at the time of diag response to fluid resuscitation. in 2018 the Surviving Sepsis nosis. Many lung cancers are diagnosed at a late stage; thus, Campaign pubiished revised guidelines suglesting that phy several randomized clinical trials have evaluated screening sicians administer specific bundled care to patients within measures. The randomized National Lung Screening Trial t hour of'sepsis recognition. The hour 1 bundle includes ini (NLST) compared LDCT screening with chest radiography tiating lluid resuscitatioll. obtaining blood cultures, checking over 3 years among patients ages 55 to 74 years with at least serum lactate level, and administering appropriate antibiotics. a 30 pack year history of smoking who currently smoked In this patient, fluid resuscitation has been initiated, blood cul or had quit in the past 15 years. The trial showed a relative tures have beer.r obtair.red, and serum lactate level is pending; mortality reduction of 20% in the LDCT screening group. the only other item in the bundle that needs to be addressed is The U.S. Preventive Services Task Force (USPSTF) and other the immediate administration of appropriate antibiotics. societies now recommend LDCT screening for lung cancer in (,I o Chest radiography (Option B) is often indicated to iden- high-risk populations. The USPSTF recommends screening ET tify the source of sepsis. This patient has rhonchi on exam patients ages 50 through B0 years who have no symptoms ination. raising the possibility that pneumonia is the source of lung cancer, have at least a 2O-pack-year smoking his- rYt ol int'ection. However, obtaining a chest radiograph should tory and are current smokers or have quit within the Iast !, not take priority over administering empiric antibiotics in 15 years. Cessation of screening should also be considered C' this patient rt ith presumed sepsis, because delays in admin in those who have not smoked in 15 years, those with lim rrt (l, istration reduce patient survival. ited life expectancy, and those who would not be candi- (a Indications for intubation (Option C) include signifl- dates for or would not be willing to undergo surgery This = cant hypoxia, inability to ventilate properly, and airway com patient is at high risk because of her age and smoking history promise. Although this patient's respiration rate is elevated, and should undergo annual LDCT. Screening has potential he is not hypoxic and he has no indication of impending harms, including the consequences of evaluating abnormal airrvay compromise or ventilatory lailure. Therefbre, intuba-. results (additional tests and procedures), radiation exposure, tion is no1 indicated. patient distress, and overdiagnosis. It is desirable that lung In patients with suspected sepsis and hypotension, early cancer screening take place in a center that has radiologic, resuscitation with 30 mlrkg of crystalloid solution is indi- diagnostic, and treatment capabilities similar to those of cated and should be performed as part of the hour-l bundle. centers involved in the NLST. Vasopressor suppofi is indicated if hypotension or organ per- Chest radiography (Option A) and sputum cytologz fusion persists following adequate fluid resuscitation. Norepi- (Option D) are not recommended for lung cancer screening. nephrine (Option D) is the preferred vasopressor because of Several clinical trials have found no mortality beneflt to its ability to improve both vascular tone and myocardial per screening with either method. formance without significantly increasing the risk of arrhyth- Fluorodeoxyglucose PET (Option B) plays a role in mias. In this patient, response to crystalloid resuscitation evaluating patients once a pulmonary nodule or mass is should be assessed before vasopressor support is provided. identifled on CT. It does not have a role in routine lung cancer screening. There is moderate certainty that annual screening o Initiating fluid resuscitation, obtaining blood cultures, for lung cancer with LDCT is of net benefit in asymp checking serum lactate level, and administering tomatic persons who are at high risk for lung cancer. appropriate antibiotics is recommended within t hour This patient fulfills all the criteria for benefiting from of sepsis recognition. LDCT lung cancer screening. Not offering LDCT lung . In patients with sepsis, delays in administration of cancer screening (Option E) may result in unnecessary empiric antibiotics are associated with reduced early mortality. patient survival. . Annual lung cancer screening should be performed Bibliography in patients aged 50 through 80 years who have no Lely MM, Evans LE, Rhodes A. The surviving sepsis campaign bundle: 2018 update [Editorial]. Intensive Care Med. 2018;44:925-928. [PMID: symptoms of lung cancer, have at least a 20-pack-year 296755661 doi:10.1007/s00134 018 5085-0 smoking history and are current smokers or have quit within the last 15 years. Item 69 Answer: C o Cessation oflung cancer screening should be con- Educational Objective: Screen for lung cancer in a sidered in those who have not smoked in 15 years, patient at high risk. those with limited life expectancy, and those who would not be candidates for or would not be willing The most appropriate lung cancer screening test to per- to undergo surgery. form is low-dose chest CT (LDCT) (Option C). Prevention

. Annual lung cancer screening should be performed Bibliography in patients aged 50 through 80 years who have no Lely MM, Evans LE, Rhodes A. The surviving sepsis campaign bundle: 2018 update [Editorial]. Intensive Care Med. 2018;44:925-928. [PMID: symptoms of lung cancer, have at least a 20-pack-year 296755661 doi:10.1007/s00134 018 5085-0 smoking history and are current smokers or have quit within the last 15 years. Item 69 Answer: C o Cessation oflung cancer screening should be con- Educational Objective: Screen for lung cancer in a sidered in those who have not smoked in 15 years, patient at high risk. those with limited life expectancy, and those who would not be candidates for or would not be willing The most appropriate lung cancer screening test to per- to undergo surgery. form is low-dose chest CT (LDCT) (Option C). Prevention 155

Answers and Critiques Bibliography patient. hou€l,er. the absence of any identifiable pathogen Mazzone PJ, Silvestri GA, Patel S, et al. Screening for lung cancer: CHEST on bronchoalveolar lavage cultures as well as localization ol guideline and expert panel report. Chest. 2018;153:954-985. [PMID: infiltrates to the radiation field r-r-rle out this diagnosis. 29374573) doi:10.1016/j.chest.2018.01.016 Hypersensitivi$/ pnellmonitis (tlP) (Option B) results fiom exposure to a wide variety of antigens that provoke Item 70 an exaggerated immune response in susceptible persons. tr Answer: D Ed ucationa l Objective : Diagnose radiation pneumonitis. High resolution CT scan will shol,r' micronoduies ancl ground giass opacities. Flowever, tl.re absence of a discrete The most likely diagnosis, based on the patient's clinical and exposure and radiologic findings confined to the prel'ious radiologic picture. is radiation pneunlonitis (Option D). Tvp radiation field do not fit the clinical picture of HP. ically developing 4 to 12 neeks af ter completion of radiother There is no clinical su5gestiot.t of volume or,erload in apy. the lung opacities can cross rnultiple lobes (as showr1: this patient: hence. pulmonerry edema (Option C) is not the red arrolvs point to the major fissure separating the right likely cause. ln addition, pulmonary edema typically results l,I middle and lower lobes) and :rppear delir.reated by "straight in bilateral symmetric radiographic infiltrates. (D lines" corresponding to the radiation fleld (as show'n, bor = t(EY POilarS UT dered by green lines). g, . Patients with radiation pneumonitis typically develop CL cough, shortness of breath, and radiographic ffiltrates ..t 4 to 12 weeks after radiation exposure.

Bibliography patient. hou€l,er. the absence of any identifiable pathogen Mazzone PJ, Silvestri GA, Patel S, et al. Screening for lung cancer: CHEST on bronchoalveolar lavage cultures as well as localization ol guideline and expert panel report. Chest. 2018;153:954-985. [PMID: infiltrates to the radiation field r-r-rle out this diagnosis. 29374573) doi:10.1016/j.chest.2018.01.016 Hypersensitivi$/ pnellmonitis (tlP) (Option B) results fiom exposure to a wide variety of antigens that provoke Item 70 an exaggerated immune response in susceptible persons. tr Answer: D Ed ucationa l Objective : Diagnose radiation pneumonitis. High resolution CT scan will shol,r' micronoduies ancl ground giass opacities. Flowever, tl.re absence of a discrete The most likely diagnosis, based on the patient's clinical and exposure and radiologic findings confined to the prel'ious radiologic picture. is radiation pneunlonitis (Option D). Tvp radiation field do not fit the clinical picture of HP. ically developing 4 to 12 neeks af ter completion of radiother There is no clinical su5gestiot.t of volume or,erload in apy. the lung opacities can cross rnultiple lobes (as showr1: this patient: hence. pulmonerry edema (Option C) is not the red arrolvs point to the major fissure separating the right likely cause. ln addition, pulmonary edema typically results l,I middle and lower lobes) and :rppear delir.reated by "straight in bilateral symmetric radiographic infiltrates. (D lines" corresponding to the radiation fleld (as show'n, bor = t(EY POilarS UT dered by green lines). g, . Patients with radiation pneumonitis typically develop CL cough, shortness of breath, and radiographic ffiltrates ..t 4 to 12 weeks after radiation exposure. It o Pulmonary toxicity of immune checkpoint inhibitors .= D may also manifest as radiation recall pneumonitis, a vl variant of radiation pneumonitis, in areas of previous radiation exposure.

It o Pulmonary toxicity of immune checkpoint inhibitors .= D may also manifest as radiation recall pneumonitis, a vl variant of radiation pneumonitis, in areas of previous radiation exposure. I, Bibliography Jain V Berman AT. Radiation pneumonitis: old problem, new tricks. Cancers .a I * (Basel). 2018;10. [PMID: 29970850] doi:10.3390/cancersl0070222 a- lr .. \* Item 71 Answer: A Educational Objective: Evaluate a pleural effusion in tr the ICU.

a- lr .. \* Item 71 Answer: A Educational Objective: Evaluate a pleural effusion in tr the ICU. The most appropriate diagnostic test to perform is bedside thoracic ultrasonography (Option A). The patient is present irrg with septic shock and hypoxemic respiratory failure. Her presentation is secondary to a nlultifbcal pneumonia with The classic symptoms are clyspnea on exertion. non- an associated left pleural eflusion. Once a pleural effusion productive cough, and hvpoxemia; low grade fevers are also is detected on chest radiograph, bedside thoracic ultraso common. A subset of patients develop radiation flbrosis 6 to nography can be used to characterize the fluid and the l2 months after treatment. Immune checkpoint inhibitors f'easibility of drainage. Thoracic point of-care ultrasonog sttch as pembroluzimab are inrmunomodulatory drugs that raphy is a helpful addition particularly in patients n,ho are are r,r,idely used in the managenrent of adranced malignan semirecumbent, such as those who are critically iil. and does cies. including non-small cell lung cancer. Although they not necessitate transporting the patient fron.r the ICU or have signiflcant clinical benefits, these drugs are also associ interrupting resuscitation. Thoracic ultrasonography allor.r,s ated with significant adverse efl'ects, including pneumonitis. fbr the easy identiflcation of a fiee flolving or loculated ln contrast to radiatior-r pneumonitis, immune checkpoint pleural effusion and can dift'erentiate befween solid masses inhibitor related pneumollitis usually does not cross lung and loculated eflusions. The presence of a locuiated pleural fissures. Pulmonary toxicity of imnrune checkpoint inl.rib effusion in the setting of severe community acquired pneu itors may also manifest as radiatior.r recall pneumonitis, a monia would be an indication fbr diagnostic sampling and variant ol radiation pneuntonitis. which manifests in areas drainage of the e{Iusior.r. of previous radiation exposure. Radiation recall pneumonitis Aclvantages of CT imaging n,ith contrast (Option B) can occur \ rith multiple other chemotl-rerapeutic agents. include the ability to detect small arroulrts of pler.rral fluid; cven years after radiation therapy assessment of coexisting intrirthoracic abnormalities such Hospital acquired pneumonia (Option A) is an inlport as pulmonary masses and malignant pleural disease: and ant consideration in any intnrune compromised patient identification of an empyerra, as enhancement of the with new symptoms and radiographic inflltrates. ln this pleura around the fluid creates a lenticular shaped opacity.

The most appropriate diagnostic test to perform is bedside thoracic ultrasonography (Option A). The patient is present irrg with septic shock and hypoxemic respiratory failure. Her presentation is secondary to a nlultifbcal pneumonia with The classic symptoms are clyspnea on exertion. non- an associated left pleural eflusion. Once a pleural effusion productive cough, and hvpoxemia; low grade fevers are also is detected on chest radiograph, bedside thoracic ultraso common. A subset of patients develop radiation flbrosis 6 to nography can be used to characterize the fluid and the l2 months after treatment. Immune checkpoint inhibitors f'easibility of drainage. Thoracic point of-care ultrasonog sttch as pembroluzimab are inrmunomodulatory drugs that raphy is a helpful addition particularly in patients n,ho are are r,r,idely used in the managenrent of adranced malignan semirecumbent, such as those who are critically iil. and does cies. including non-small cell lung cancer. Although they not necessitate transporting the patient fron.r the ICU or have signiflcant clinical benefits, these drugs are also associ interrupting resuscitation. Thoracic ultrasonography allor.r,s ated with significant adverse efl'ects, including pneumonitis. fbr the easy identiflcation of a fiee flolving or loculated ln contrast to radiatior-r pneumonitis, immune checkpoint pleural effusion and can dift'erentiate befween solid masses inhibitor related pneumollitis usually does not cross lung and loculated eflusions. The presence of a locuiated pleural fissures. Pulmonary toxicity of imnrune checkpoint inl.rib effusion in the setting of severe community acquired pneu itors may also manifest as radiatior.r recall pneumonitis, a monia would be an indication fbr diagnostic sampling and variant ol radiation pneuntonitis. which manifests in areas drainage of the e{Iusior.r. of previous radiation exposure. Radiation recall pneumonitis Aclvantages of CT imaging n,ith contrast (Option B) can occur \ rith multiple other chemotl-rerapeutic agents. include the ability to detect small arroulrts of pler.rral fluid; cven years after radiation therapy assessment of coexisting intrirthoracic abnormalities such Hospital acquired pneumonia (Option A) is an inlport as pulmonary masses and malignant pleural disease: and ant consideration in any intnrune compromised patient identification of an empyerra, as enhancement of the with new symptoms and radiographic inflltrates. ln this pleura around the fluid creates a lenticular shaped opacity. 156

Answers and Critiques tr CONI. Ilrx,vcver. CT imaging requires thc patient to be removed tiom the ICU and exposes the lratient to irradiatior,. A lateral decubitus film (Option C) would also difibren arrgiography rvould not be part <tt tl.re initial battery of tests, and transporting this unstable patient nould pose additional risk. tiate between a free flowing and a loculated pleural eflusion. Puhnonary artery catheters (Option B) have lost favor I lowever. it is now rarely uscd in the ICU because bedside ability in recent years because several large studies and ultrasonography is easy to access ancl to use. In addition, a mcta analyses suggest no benefit to patients. and in some Iateral decubitus fllm would not dernclnstrate the feasibilitv cirses suggest increased risk, r,rrhen they are used to guide of drainage as ultrasound does. thcraplr The use of a pulnronary xrtery c:ttheter for henro Finallyl a thoracic MRI (Option D) car-r e{fectilely display d-v-'nanlic monitoring ma)r bc reasonable rt hen the diagnosis plcural tumors, chest r,r,all invasion. spir-ral cord invasion. r-cmains uncefiain or the pttient has not responded to resus and pleural effusions. Hou'cver, it is not as useful as thorzrcic citation efibrts. ultrasonography and C'f fbr evaluation of parapneumonic the AH A recommencls t ritnsthoracic echocardiograpl.ry eltusions, it is expensive, and it requires the patient to be as the initial noninvasive in-raging test following a chest vt €, moved from the ICU. radiograph. lf the trar.rsthoracic echocarcliogram fails to pro ET vide adequate images or the diagr.rosis remains uncertain, I(EY POtilTS the Al.lA recommends cc.rnsidering transesophageal echocar (J o Thoracic ultrasonography allows for the easy identifi- diography (Option C). T' cation of a free flowing or loculated pleural effusion E as and can differentiate between solid masses and locu- fEY POIXT vt lated effusions. o The initial evaluation of cardiogenic shock includes o,

tr CONI. Ilrx,vcver. CT imaging requires thc patient to be removed tiom the ICU and exposes the lratient to irradiatior,. A lateral decubitus film (Option C) would also difibren arrgiography rvould not be part <tt tl.re initial battery of tests, and transporting this unstable patient nould pose additional risk. tiate between a free flowing and a loculated pleural eflusion. Puhnonary artery catheters (Option B) have lost favor I lowever. it is now rarely uscd in the ICU because bedside ability in recent years because several large studies and ultrasonography is easy to access ancl to use. In addition, a mcta analyses suggest no benefit to patients. and in some Iateral decubitus fllm would not dernclnstrate the feasibilitv cirses suggest increased risk, r,rrhen they are used to guide of drainage as ultrasound does. thcraplr The use of a pulnronary xrtery c:ttheter for henro Finallyl a thoracic MRI (Option D) car-r e{fectilely display d-v-'nanlic monitoring ma)r bc reasonable rt hen the diagnosis plcural tumors, chest r,r,all invasion. spir-ral cord invasion. r-cmains uncefiain or the pttient has not responded to resus and pleural effusions. Hou'cver, it is not as useful as thorzrcic citation efibrts. ultrasonography and C'f fbr evaluation of parapneumonic the AH A recommencls t ritnsthoracic echocardiograpl.ry eltusions, it is expensive, and it requires the patient to be as the initial noninvasive in-raging test following a chest vt €, moved from the ICU. radiograph. lf the trar.rsthoracic echocarcliogram fails to pro ET vide adequate images or the diagr.rosis remains uncertain, I(EY POtilTS the Al.lA recommends cc.rnsidering transesophageal echocar (J o Thoracic ultrasonography allows for the easy identifi- diography (Option C). T' cation of a free flowing or loculated pleural effusion E as and can differentiate between solid masses and locu- fEY POIXT vt lated effusions. o The initial evaluation of cardiogenic shock includes o, o Thoracic point-of-care ultrasonography is a helpful laboratory testing for myocardial ischemia and heart vt = E failure, chest radiography, electrocardiography, and addition particularly in patients who are semirecum- bent, such as those who are critically ill, and does not transthoracic echocardiography. necessitate moving the patient from the ICU. Bibliography van Diepen S, Katz JN Albert NM, et al; American Heart Association Council Bibliography on Clinical Cardiolory; Council on Cardiovascuiar and Stroke Porcel JM. Chest imaging for the diagnosis ol complicated parapneumonic Nursing; Council on Quality of Care and Outcomes Research; effusions. Curr Opin Pulm Med. 2018;24:398 402. [PMID: 295175871 and Mission: Lifeline. Contemporary management of cardiogenic doi:10.1097/MCP000000000000048s shock: A scientific statement from the American Heart Association. Circulation. 2Ol7 ;136:e232 e268. [PMID: 28923988] doi:10.1161 /CIR. 0000000000000s2s

o Thoracic point-of-care ultrasonography is a helpful laboratory testing for myocardial ischemia and heart vt = E failure, chest radiography, electrocardiography, and addition particularly in patients who are semirecum- bent, such as those who are critically ill, and does not transthoracic echocardiography. necessitate moving the patient from the ICU. Bibliography van Diepen S, Katz JN Albert NM, et al; American Heart Association Council Bibliography on Clinical Cardiolory; Council on Cardiovascuiar and Stroke Porcel JM. Chest imaging for the diagnosis ol complicated parapneumonic Nursing; Council on Quality of Care and Outcomes Research; effusions. Curr Opin Pulm Med. 2018;24:398 402. [PMID: 295175871 and Mission: Lifeline. Contemporary management of cardiogenic doi:10.1097/MCP000000000000048s shock: A scientific statement from the American Heart Association. Circulation. 2Ol7 ;136:e232 e268. [PMID: 28923988] doi:10.1161 /CIR. 0000000000000s2s tr Item72 Answer: D Ed u cati o na I O bjective : Evaluate shock with transthoracic echocardiography. Item 73 Answer: D Educational Objective: Prevent malnutrition in a Thc most appropriate managcmcnt is transthoracic echo critically ill patient. cardiography (Option D). This patient has f'eatures consis tcnt with cardiogenic shock (cool extremities, pulmonary 'lhe most appropriate manag(rment is ki stop enteral nutri crackles. jugular venous distention, altered mental status, tiorr and start parenteral nutrition (Option D). I\4alnutrition oliguria). Cardiogenic shocl< occurs rn,hen a primary cardiac in critically ill patients leacls; to increased morbidity and insult causes decreased cardiac output. ln addition to a phys mortality Al1 patier.rts adn.ritled to the ICU should have a ical examination, the American Heart Association (AHA) nutritional evaluation. EnteraL nutrition should start within recommends laboratory testing for myocardial ischemia and 24 to ,18 hours of adrnission in critically ill patients. Gtticle heart failure. chest radiographli electrocardiographyi and lines recommend that parenr:eral nutrition to achie'ne full transthoracic echocardiography. A tr:rnsthoracic echocar nr-rtritional goals should be started only alter 7 to 10 days of diogram provides infbrn-ration on heart size, systolic and inability to achieve tnore th:rn 60')1, of ener$/ and protein diastolic function, regional wall motion abnormalities, and requirements by tl-re enteral route alone. It.titiating parenterill valvular disease. Regional wall motion abnormalities suggest nutrition before 7 to 10 days in critically ill patients on some coronary artery disease. and changes in the myocardium can enteral nutrition does not improvc outcomes and may be sLlggest conditions such as cardiac anryloid. Echocardiogrrr dctrinrental to the pltient. phy rnay also provide prognostic inlirrnration. Megestrol acetate (Option A) is an appetite stin-rulant In the absence of contrair.rdications. additional imaging that has been used in paticnts rvith carrcer related anorexia \\,ith C'l'angiography (Option A) is ;ippropriate if pulmonnry cachexia and in older rrdultr; rt'ith failure to thrive. This embolism is considered high probabilityl CT angiography patient's ir-rabili[,' to meet h'ir caloric needs is related tct has significantly improvecl the accuracy of evaluating pul intolerance of enteral feeding:; as cvidcnced by bloating and monary embolism and could bc considered in this patient enresis, not anorexia. if the initial tests do not support n.ryocardial int'arction rtr Methylnaltrexone (Optio,n B) is indicated to managc other cardiac causes of' this patient's shock. Hou,ever, C'l' const\ration related to opiatt:s. Although the patient uses

tr Item72 Answer: D Ed u cati o na I O bjective : Evaluate shock with transthoracic echocardiography. Item 73 Answer: D Educational Objective: Prevent malnutrition in a Thc most appropriate managcmcnt is transthoracic echo critically ill patient. cardiography (Option D). This patient has f'eatures consis tcnt with cardiogenic shock (cool extremities, pulmonary 'lhe most appropriate manag(rment is ki stop enteral nutri crackles. jugular venous distention, altered mental status, tiorr and start parenteral nutrition (Option D). I\4alnutrition oliguria). Cardiogenic shocl< occurs rn,hen a primary cardiac in critically ill patients leacls; to increased morbidity and insult causes decreased cardiac output. ln addition to a phys mortality Al1 patier.rts adn.ritled to the ICU should have a ical examination, the American Heart Association (AHA) nutritional evaluation. EnteraL nutrition should start within recommends laboratory testing for myocardial ischemia and 24 to ,18 hours of adrnission in critically ill patients. Gtticle heart failure. chest radiographli electrocardiographyi and lines recommend that parenr:eral nutrition to achie'ne full transthoracic echocardiography. A tr:rnsthoracic echocar nr-rtritional goals should be started only alter 7 to 10 days of diogram provides infbrn-ration on heart size, systolic and inability to achieve tnore th:rn 60')1, of ener$/ and protein diastolic function, regional wall motion abnormalities, and requirements by tl-re enteral route alone. It.titiating parenterill valvular disease. Regional wall motion abnormalities suggest nutrition before 7 to 10 days in critically ill patients on some coronary artery disease. and changes in the myocardium can enteral nutrition does not improvc outcomes and may be sLlggest conditions such as cardiac anryloid. Echocardiogrrr dctrinrental to the pltient. phy rnay also provide prognostic inlirrnration. Megestrol acetate (Option A) is an appetite stin-rulant In the absence of contrair.rdications. additional imaging that has been used in paticnts rvith carrcer related anorexia \\,ith C'l'angiography (Option A) is ;ippropriate if pulmonnry cachexia and in older rrdultr; rt'ith failure to thrive. This embolism is considered high probabilityl CT angiography patient's ir-rabili[,' to meet h'ir caloric needs is related tct has significantly improvecl the accuracy of evaluating pul intolerance of enteral feeding:; as cvidcnced by bloating and monary embolism and could bc considered in this patient enresis, not anorexia. if the initial tests do not support n.ryocardial int'arction rtr Methylnaltrexone (Optio,n B) is indicated to managc other cardiac causes of' this patient's shock. Hou,ever, C'l' const\ration related to opiatt:s. Although the patient uses 157

Answers and Critiques treatment in a large trial of patients with heart lailure tr CONI. opiates. the presence of liquicl fcces in the osktmy bag and the presencc ol bouel sountls irrgue against constipation as ir causc ol intolerirnce. deflned by a left ventricular ejection fraction less than 45'X,. Continuous positive airway pressure (CPAP) (Option B) In criticalll, i1l patients. incre:rsit.tg fiber in thc enteral is effective at maintaining upper airway patency in obstruc diet (Option C) can decrease cliarrhea and itnprovc tolerance tive sleep apnea (OSA) but is generally ineffective in treating to enteral nutriticln. Ilortever, bloating and etttesis are the CSA, a disorder of ventilatory control. In fact, when CPAP result of her intolerance to clltertl fbeding. In addition, a is used in the treatment of obstructive sleep apnea, it can more ulgent need nou'is the provisiot-t of adeqr-rlte nutrition. occasionally result in CSA (a condition called treatment emergent central sleep apnea). CPAP may be appropriate in f,EV P0tt{Tt some patients with combined CSA and OSA, as determined o Enteral nutrition should start within 24 to 48 hours of by polysomnography. admission in critically ill patients. The patient has nonspeciflc fatigue and tiredness. o In critically ill patients, supplemental parenteral nutri- Modaflnil (Option C) is used to combat excessive sleepiness UI tion should be started after 7 to 10 days of inability to associated with hypersomnia syndromes, such as narco € .D achieve more than 60olo of enerry and protein require- lepsy, and residual sleepiness associated with OSA despite vt ments by the enteral route alone. adequate CPAP therapy. A stimulant medication is not indi q, cated for this patient. TL n Bibliography McClave SA, Taylor BE, Martindale RG, et al; Society of Critical Care f,EY POITI

treatment in a large trial of patients with heart lailure tr CONI. opiates. the presence of liquicl fcces in the osktmy bag and the presencc ol bouel sountls irrgue against constipation as ir causc ol intolerirnce. deflned by a left ventricular ejection fraction less than 45'X,. Continuous positive airway pressure (CPAP) (Option B) In criticalll, i1l patients. incre:rsit.tg fiber in thc enteral is effective at maintaining upper airway patency in obstruc diet (Option C) can decrease cliarrhea and itnprovc tolerance tive sleep apnea (OSA) but is generally ineffective in treating to enteral nutriticln. Ilortever, bloating and etttesis are the CSA, a disorder of ventilatory control. In fact, when CPAP result of her intolerance to clltertl fbeding. In addition, a is used in the treatment of obstructive sleep apnea, it can more ulgent need nou'is the provisiot-t of adeqr-rlte nutrition. occasionally result in CSA (a condition called treatment emergent central sleep apnea). CPAP may be appropriate in f,EV P0tt{Tt some patients with combined CSA and OSA, as determined o Enteral nutrition should start within 24 to 48 hours of by polysomnography. admission in critically ill patients. The patient has nonspeciflc fatigue and tiredness. o In critically ill patients, supplemental parenteral nutri- Modaflnil (Option C) is used to combat excessive sleepiness UI tion should be started after 7 to 10 days of inability to associated with hypersomnia syndromes, such as narco € .D achieve more than 60olo of enerry and protein require- lepsy, and residual sleepiness associated with OSA despite vt ments by the enteral route alone. adequate CPAP therapy. A stimulant medication is not indi q, cated for this patient. TL n Bibliography McClave SA, Taylor BE, Martindale RG, et al; Society of Critical Care f,EY POITI Medicine. Guidelines for the provision and assessment of nutrition sup o The initial management of central sleep apnea should lt port therapy in the adult critically ill patient: Society of Critical Care target modifiable risk factors such as the reduction or .D Medicine (SCCM) and American Society for Parenteral and Enteral ut Nutrition (A.S.P.E.N.). JPEN J Parenter Enteral Nutr. 2016;40:159 211. elimination of opioids or medical optimization of IPMID : 267730771 doi:10.117l0148 6O7t75621863 heart failure.

Medicine. Guidelines for the provision and assessment of nutrition sup o The initial management of central sleep apnea should lt port therapy in the adult critically ill patient: Society of Critical Care target modifiable risk factors such as the reduction or .D Medicine (SCCM) and American Society for Parenteral and Enteral ut Nutrition (A.S.P.E.N.). JPEN J Parenter Enteral Nutr. 2016;40:159 211. elimination of opioids or medical optimization of IPMID : 267730771 doi:10.117l0148 6O7t75621863 heart failure. Item 74 Answer: D Bibliography Wasef S, Mir S, Ryan C, et al. Treatment for patients with sleep apnea on Educational Objective: Treat opioid-related sleep apnea. opioids for chronic pain: results of the Opsatb trial. I Clin Sleep Med. 2021:17 :819-824. IPMID: 33382032] doi:10..5664 rjcsm.9064 The most appropriate treatment is a pain rehabilitation pro gram (Option D). A sleep study showed that this patient has central sleep apnea (CSA). CSA is deflned by pauses in air- Item 75 Answer: D flow due to loss ofoutput from the central respiratory gener- Educational Objective: Treat an acute COPD exacertation ators in the brainstem to the respiratory muscles, resulting in with azithromycin. lack ofrespiratory effort. There are few clinical trials proving a role for speciflc treatment of CSA, so initial management The most appropriate additional treatment is oral azithro- should target modiflable risk factors. For example, reduction mycin (Option D). Infectious agents in COPD exacerbations or elimination of opioids improves CSA. Medical optimiza- are often viral but can be bacterial. The most common bac tion of heart failure (with drugs or devices, optimizing fluid terial causes include Streptococcus pneumoniae, Haemo- balance in the setting of volume overload, or surgery such philus influenzae, Moroxella catorrhalis, and Mycoplasma as valve repair or cardiac transplantation) has been shown pneumoniae. Antibiotics are indicated in patients who have to improve CSA. This patient's CSA is most likely related to increased sputum purulence and either increased dyspnea use of opioid analgesics. Because initial management of CSA or increased sputum volume, as well as in patients who should target modiflable risk factors, a pain rehabilitation require invasive or noninvasive mechanical ventilation. program to help the patient curtail opioid use is appropriate. The recommended duration of antibiotic therapy is 5 days. Additionally, a more appropriate long term pain manage The antibiotic used should be based on local bacterial ment stratery is needed to improve her qualig of life. How resistance patterns; common initial treatments include ever, adherence to a pain management plan that includes amoxicillin with clavulanic acid and macrolide and opioid reduction may be difficult and failure is frequent. tetracycline antibiotics. Thus, azithromycin would be an Adaptive servo ventilation (ASV) (Option A) is a form appropriate treatment for this patient. of positive airway pressure therapy that effectively sup The methylxanthines (aminophylline and theophylline) presses CSA. Small observational studies suggest that it has are now rarely used to treat COPD. Theophylline (Option A) some efficacy in opioid-induced CSA, but controlled trials has been shown to improve functional capacity and reduce are lacking to demonstrate improvements in important out the number of exacerbations. However, it has a narrow win- comes. Although a trial of ASV may be warranted in some dow between therapeutic and toxic dosages and therefore patients with opioid related CSA, it should be preceded by is used only for patients with advanced COPD who have an attempt to reduce opioid use and to try other treatments refractory symptoms not controlled using standard therapy. with proven efficacy and safety. Consideration should also Studies of the use of either aminophylline or theophylline be given to an increased risk ofdeath associated with ASV during acute exacerbations have shown no beneflt.

Item 74 Answer: D Bibliography Wasef S, Mir S, Ryan C, et al. Treatment for patients with sleep apnea on Educational Objective: Treat opioid-related sleep apnea. opioids for chronic pain: results of the Opsatb trial. I Clin Sleep Med. 2021:17 :819-824. IPMID: 33382032] doi:10..5664 rjcsm.9064 The most appropriate treatment is a pain rehabilitation pro gram (Option D). A sleep study showed that this patient has central sleep apnea (CSA). CSA is deflned by pauses in air- Item 75 Answer: D flow due to loss ofoutput from the central respiratory gener- Educational Objective: Treat an acute COPD exacertation ators in the brainstem to the respiratory muscles, resulting in with azithromycin. lack ofrespiratory effort. There are few clinical trials proving a role for speciflc treatment of CSA, so initial management The most appropriate additional treatment is oral azithro- should target modiflable risk factors. For example, reduction mycin (Option D). Infectious agents in COPD exacerbations or elimination of opioids improves CSA. Medical optimiza- are often viral but can be bacterial. The most common bac tion of heart failure (with drugs or devices, optimizing fluid terial causes include Streptococcus pneumoniae, Haemo- balance in the setting of volume overload, or surgery such philus influenzae, Moroxella catorrhalis, and Mycoplasma as valve repair or cardiac transplantation) has been shown pneumoniae. Antibiotics are indicated in patients who have to improve CSA. This patient's CSA is most likely related to increased sputum purulence and either increased dyspnea use of opioid analgesics. Because initial management of CSA or increased sputum volume, as well as in patients who should target modiflable risk factors, a pain rehabilitation require invasive or noninvasive mechanical ventilation. program to help the patient curtail opioid use is appropriate. The recommended duration of antibiotic therapy is 5 days. Additionally, a more appropriate long term pain manage The antibiotic used should be based on local bacterial ment stratery is needed to improve her qualig of life. How resistance patterns; common initial treatments include ever, adherence to a pain management plan that includes amoxicillin with clavulanic acid and macrolide and opioid reduction may be difficult and failure is frequent. tetracycline antibiotics. Thus, azithromycin would be an Adaptive servo ventilation (ASV) (Option A) is a form appropriate treatment for this patient. of positive airway pressure therapy that effectively sup The methylxanthines (aminophylline and theophylline) presses CSA. Small observational studies suggest that it has are now rarely used to treat COPD. Theophylline (Option A) some efficacy in opioid-induced CSA, but controlled trials has been shown to improve functional capacity and reduce are lacking to demonstrate improvements in important out the number of exacerbations. However, it has a narrow win- comes. Although a trial of ASV may be warranted in some dow between therapeutic and toxic dosages and therefore patients with opioid related CSA, it should be preceded by is used only for patients with advanced COPD who have an attempt to reduce opioid use and to try other treatments refractory symptoms not controlled using standard therapy. with proven efficacy and safety. Consideration should also Studies of the use of either aminophylline or theophylline be given to an increased risk ofdeath associated with ASV during acute exacerbations have shown no beneflt. 158

Answers and Critiques This patient does not have a fever or an inflltrate on Erythropoietin stimulating agents (Option B) and iron chest radiograph; thus, broad-spectrum antibiotics such as supplementation are used in protocols for patients who piperacillin-tazobactam (Option B) would be inappropri- cannot receive blood. In this patier.rt, reducing blood loss ate. Potential indications for Pseudomoncs coverage with through discontinuation of routine daily blood tests is a piperacillin-tazobactam would include chronic coloniza- much more practical, safe, and economical management tion with Pseudomonas or previous documented infection approach for anemia. within the previous 12 months, very severe COPD, bron- Anemia in nonbleeding critically ill patients can be chiectasis on imaging, broad-spectrum antibiotic use in the challenging to evaluate because the inflammatory state may previous 3 months, or chronic oral glucocorticoid use. result ir.r inflammatory anentia. lron studies (Option C) can For patients with acute hypercapnic respiratory failure help diagnose inflammatory anemia. llowever, inflamma- with acidosis due to a COPD exacerbation, noninvasive ven- tory anemia usually does not result in hemoglobin concen tilation with bilevel positive airway pressure (Option C) can trations of less than 10 g/dl (l 00 g/L) and certainly not over improve symptoms and reduce intubation rates, length of 12 days, and since hemolysis has been excluded, the elevated vt (l, hospital stay, and mortality. However, this patient has ade- reticulocyte count suggests blood loss. quate ventilation (as evidenced by his normal pH and Pco, ET Guidelines recommend transfusion of erythrocytes levels) and does not require noninvasive ventilation. (Option D) in nonbleeding critically ill patients at a hemo IJ globin threshold of Z gldL (70 g/t.). In patients with acute E coronary syndrome, the threshold is unclear, but guidelines .E r Antibiotics are indicated in patients with COPD exac- recommend thresholds of 8 to 9 gldL (80 90 g/L). This t/l erbation who have increased sputum purulence and patient does not require a transfusion but rather discontin- o B either increased dyspnea or increased sputum vol- uation of routine daily blood tests. UI

This patient does not have a fever or an inflltrate on Erythropoietin stimulating agents (Option B) and iron chest radiograph; thus, broad-spectrum antibiotics such as supplementation are used in protocols for patients who piperacillin-tazobactam (Option B) would be inappropri- cannot receive blood. In this patier.rt, reducing blood loss ate. Potential indications for Pseudomoncs coverage with through discontinuation of routine daily blood tests is a piperacillin-tazobactam would include chronic coloniza- much more practical, safe, and economical management tion with Pseudomonas or previous documented infection approach for anemia. within the previous 12 months, very severe COPD, bron- Anemia in nonbleeding critically ill patients can be chiectasis on imaging, broad-spectrum antibiotic use in the challenging to evaluate because the inflammatory state may previous 3 months, or chronic oral glucocorticoid use. result ir.r inflammatory anentia. lron studies (Option C) can For patients with acute hypercapnic respiratory failure help diagnose inflammatory anemia. llowever, inflamma- with acidosis due to a COPD exacerbation, noninvasive ven- tory anemia usually does not result in hemoglobin concen tilation with bilevel positive airway pressure (Option C) can trations of less than 10 g/dl (l 00 g/L) and certainly not over improve symptoms and reduce intubation rates, length of 12 days, and since hemolysis has been excluded, the elevated vt (l, hospital stay, and mortality. However, this patient has ade- reticulocyte count suggests blood loss. quate ventilation (as evidenced by his normal pH and Pco, ET Guidelines recommend transfusion of erythrocytes levels) and does not require noninvasive ventilation. (Option D) in nonbleeding critically ill patients at a hemo IJ globin threshold of Z gldL (70 g/t.). In patients with acute E coronary syndrome, the threshold is unclear, but guidelines .E r Antibiotics are indicated in patients with COPD exac- recommend thresholds of 8 to 9 gldL (80 90 g/L). This t/l erbation who have increased sputum purulence and patient does not require a transfusion but rather discontin- o B either increased dyspnea or increased sputum vol- uation of routine daily blood tests. UI ume, as well as in patients who require invasive or noninvasive mechanical ventilation. . Commonly used antibiotics for COPD exacertations . Approximately 2Oo/o of laboratory tests obtained in hospitalized patients are not needed. include amoxicillin with clavulanic acid and macrolide and tetracycline anfibiotics. . Excessive laboratory testing in hospital2ed patients can result in iatrogenic anemia. Bibliography Dobler CC, Morrow AS, Beuschel B, et al. Pharmacologic therapies in Bibliograptry patients with exacerbation of chronic obstructive pulmonary disease: A Bindraban RS, Ten Berg MJ, Naaktgeboren CA, et al. Reducing test utilization systematic review with meta-analysis. Ann Intem Med. 2O2O ;172:413 -422. in hospital settings: A narrative review. Ann tab Med. 2O78;38:4Q2-472. IPMID : 320927 621 doi:10.7326lMl9-3007 IPMID: 297978091 doi:10.3343/alm.2018.38.5.402

ume, as well as in patients who require invasive or noninvasive mechanical ventilation. . Commonly used antibiotics for COPD exacertations . Approximately 2Oo/o of laboratory tests obtained in hospitalized patients are not needed. include amoxicillin with clavulanic acid and macrolide and tetracycline anfibiotics. . Excessive laboratory testing in hospital2ed patients can result in iatrogenic anemia. Bibliography Dobler CC, Morrow AS, Beuschel B, et al. Pharmacologic therapies in Bibliograptry patients with exacerbation of chronic obstructive pulmonary disease: A Bindraban RS, Ten Berg MJ, Naaktgeboren CA, et al. Reducing test utilization systematic review with meta-analysis. Ann Intem Med. 2O2O ;172:413 -422. in hospital settings: A narrative review. Ann tab Med. 2O78;38:4Q2-472. IPMID : 320927 621 doi:10.7326lMl9-3007 IPMID: 297978091 doi:10.3343/alm.2018.38.5.402 llem77 tr Item 76 Answer: A Ed u cati o na I O bjective : Diagnose excessive laboratory Answer: A Educational Objective: Treat preeclampsia with delivery. tr testing as the cause of anemia. The most appropriate next step in management for this The most appropriate strateS/ is discontinuation of routine patient with preeclampsia is delivery (Option A). Pre blood testing (Option A). Numerous studies in the litera- eclampsia is a disorder of pregnancy that is associated ture have documented excessive use of laboratory studies with new-onset hypertension, most often occurring after in the hospital setting in general and in the ICU in partic- 20 weeks of gestation. Although hypertension is often ular. Estimates suggest that approximately 2O'k of labora- accompanied by new-onset proteinuria, some women tory tests obtained in hospitalized patients are not needed, present with hypertension and signs or symptoms of end- resulting in waste. In addition to the flnancial impact to the organ dysfunction without proteinuria. The presence of one health care system, overutilization invariably results in false or more of the following findings of end-organ dysfunc positive test results, leading to further downstream testing. tion indicates a diagnosis of preeclampsia with severe fea- Studies show that excessive blood draws can result in iatro- tures: thrombocytopenia (<1()0,000/pL [too x t0'q/L]); liver genic anemia, as is likely the case in this patient. Efforts to enzyme levels twice the upper limit of normal; severe per- reduce unnecessary laboratory testing have the dual benefit sistent right upper quadrant or epigastric pain not accounted of improving patient safety and reducing health care expen for by alternative diagnosesl kidney injury (serum creatinine ditures. Studies have shown that a reduction in laboratory concentration >1.1 mg/dl [97.2 Umoli L] or a doubling of the testing does not lead to adverse patient outcomes, and some serum creatinine concentration in the absence of another studies suggest a decrease in hospital lengths of hospital stay kidney disease); pulmonary edema; or new onset headache and the need for transfusion. The flrst management step in unresponsive to acetaminophen and not accounted for by this patient is to discontinue daily routine laboratory testing. alternative diagnoses or visual disturbance. Patients with Laboratory testing should only be undertaken in response to preeclampsia are also at risk of developing HELLP syndrome specifi c clinical questions. (hemolysis, elevated liver enzymes, and low platelet count),

llem77 tr Item 76 Answer: A Ed u cati o na I O bjective : Diagnose excessive laboratory Answer: A Educational Objective: Treat preeclampsia with delivery. tr testing as the cause of anemia. The most appropriate next step in management for this The most appropriate strateS/ is discontinuation of routine patient with preeclampsia is delivery (Option A). Pre blood testing (Option A). Numerous studies in the litera- eclampsia is a disorder of pregnancy that is associated ture have documented excessive use of laboratory studies with new-onset hypertension, most often occurring after in the hospital setting in general and in the ICU in partic- 20 weeks of gestation. Although hypertension is often ular. Estimates suggest that approximately 2O'k of labora- accompanied by new-onset proteinuria, some women tory tests obtained in hospitalized patients are not needed, present with hypertension and signs or symptoms of end- resulting in waste. In addition to the flnancial impact to the organ dysfunction without proteinuria. The presence of one health care system, overutilization invariably results in false or more of the following findings of end-organ dysfunc positive test results, leading to further downstream testing. tion indicates a diagnosis of preeclampsia with severe fea- Studies show that excessive blood draws can result in iatro- tures: thrombocytopenia (<1()0,000/pL [too x t0'q/L]); liver genic anemia, as is likely the case in this patient. Efforts to enzyme levels twice the upper limit of normal; severe per- reduce unnecessary laboratory testing have the dual benefit sistent right upper quadrant or epigastric pain not accounted of improving patient safety and reducing health care expen for by alternative diagnosesl kidney injury (serum creatinine ditures. Studies have shown that a reduction in laboratory concentration >1.1 mg/dl [97.2 Umoli L] or a doubling of the testing does not lead to adverse patient outcomes, and some serum creatinine concentration in the absence of another studies suggest a decrease in hospital lengths of hospital stay kidney disease); pulmonary edema; or new onset headache and the need for transfusion. The flrst management step in unresponsive to acetaminophen and not accounted for by this patient is to discontinue daily routine laboratory testing. alternative diagnoses or visual disturbance. Patients with Laboratory testing should only be undertaken in response to preeclampsia are also at risk of developing HELLP syndrome specifi c clinical questions. (hemolysis, elevated liver enzymes, and low platelet count), 159

Answers and Critiques tr CONT. which has been associated with increased rates of maternal morbidity and mortality. Definitive treatment of severe pre- eclampsia in patients who are at or beyond 34 weeks' gesta patients who are evaluated for pulmonary hypertension outside of pulmonary hypertension referral centers receive an incorrect diagnosis as much as 33'2, of the time. The eval- tion includes emergent management of severe hypertension uation of PH also includes additional testing to identify an and prompt delivery. underlying cause of PH such as lung disease, left-sided heart Antenatal glucocorticoids (betamethasone or dexa failure, chronic thromboembolic pulmonary hypertension, methasone) (Option B) to promote fetal lung maturity and causes ofnocturnal hypoxemia. should be administered befbre 3,1 rveeks of gestation for a Coronary angiography (Option A) might be considered patient with nonsevere preeclampsia in whom delivery in if ischemic cardiomyopathy with left ventricular failure is the next 7 days is anticipated. Delivery should not be delayed suspected as the cause of PII. However. this patient has no fbr the administration of glucocorticoids in the late preterm symptoms or ECG or echocardiographic findings to support period. this diagnosis. Coronary angiography is not indicated. D Angiotensin converting enzyme inhibitors, including The current classification system subdivides PH into ut enalapril (Option C), are teratogenic and should be avoided flve groups, which are based on similarities in mechanisms, € (D during pregnancy. Recommended flrst line antihypertensives hemodynamics, clinical presentation. and approach to treat- Ut fbr urgent blood pressure control in pregnanry include intra ment. Group 1 includes patients with puimonary arterial o, venous labetalol, intravenous hvdralazine, and immediate hypertension (PAH), including those with idiopathic and CL release nif'edipine. heritable disease, and disease related to drugs and toxins. rl lntravenous sodium nitroprusside (Option D) is recom connective tissue diseases, ttlV inf'ection, schistosomiasis, st mended only for hypertensive emergencies resistant to flrst congenital heart disease, and portal hypertension. High dose line therapy and the presence ol end-organ damage. When calcium channel blockers, such as nifedipine (Option C), can .D UI used, it should be intused for the shortest amount of time be eflbctive treatment in a small number of group 1 patients possible because ol cyanide and thioc.yanate toxicity risk in who are "vasoreactive" by demonstrating marked improve the patient and fetus or newborn. Sodium nitroprusside can ment in mean pulmonary artery pressure with administra also be associated with increased intracranial pressure with tion olnitric oxide, epoprostenol, or adenosine during right potential worsening of cerebral edema in the patient. heart catheterization. Sildenafil (Option D), a phosphodies- terase 5 inhibitor, may be effeclive in mild to moderate PAH IEY POITT in the absence of vasoreactiviU. However, neither nifedipine . In patients who are at or beyond 34 weeks'gestation nor sildena{il is indicated fbr the treatment of PA}{ until the and who develop preeclampsia with severe features, diagnosis of PH has been confirmed and other causes of PI{ emergent management of severe hlpertension and have been excluded. prompt delivery are recommended to avoid maternal and fetal complications. IEY POITIS o Pulmonary hypertension should be suspected in Bibliography patients with progressive dyspnea, elevated central Gestational h)rpertension and preeclampsia: ACOG practice bulletin, number venous pressure, prominent venous o wave, fixed 222. Obstet Gynecol. 2020;135:e237 -e26O. [PMID: 32443079] doi:10.1097/ splitting of Sr, and the murmur of tricuspid regurgi- AOG.0000000000003891 tation. . Right heart catheterization and measurement of pul- tr Item 78 Answer: B Educational Objective: Diagnose pulmonary hyperten- monary artery pressure is the diagnostic gold standard for pulmonary hypertension. sion. Bibliography The most appropriate next step for this patient is right heart Klinger JR, Elliott CG, Levine DJ, et al. Therapy for pulmonary arterial catheterization (Option B). This patient has symptoms h)?ertension in adults: update of the CHEST guideline and expert (progressive dyspnea) and signs (elevated central venous panel report. Chest. 2019;155:565-586. IPMID: 30660783] doi:10.1016/ j.chest.2018.11.030 pressure, venous o wave, fixed splitting of Sr, tricuspid regurgitation) of pulmonary hypertension (PH). If PH is suspected, transthoracic echocardiography can estimate Item 79 pulmonary ar-tery systolic pressure. However, echocardiog raphy does not confirm the diagnosis of PH because pres- Answer: A Educational Objective: Treat severe hypothermia with tr active internal rewarming. sure estimation by echocardiography may be inaccurate. Right heart catheterization confirms the diagnosis of PI{ The most appropriate treatment is active internal rewarming and is an essential component of the diagnostic evaluation. (Option A). This patient has severe hypothermia, defined by Guidelines recommend ref'erral of patients with severe pul a core temperature of less than 28.0 "C (82.4 "F) in the set- monary hypefiension or right ventricular dysfunction to a ting of ongoing coma or cardiovascular collapse. Other flnd- pulmonary hypertension refbrral center. Data sug3est that ings in severe hyperthermia are absent reflexes, ventricular

tr CONT. which has been associated with increased rates of maternal morbidity and mortality. Definitive treatment of severe pre- eclampsia in patients who are at or beyond 34 weeks' gesta patients who are evaluated for pulmonary hypertension outside of pulmonary hypertension referral centers receive an incorrect diagnosis as much as 33'2, of the time. The eval- tion includes emergent management of severe hypertension uation of PH also includes additional testing to identify an and prompt delivery. underlying cause of PH such as lung disease, left-sided heart Antenatal glucocorticoids (betamethasone or dexa failure, chronic thromboembolic pulmonary hypertension, methasone) (Option B) to promote fetal lung maturity and causes ofnocturnal hypoxemia. should be administered befbre 3,1 rveeks of gestation for a Coronary angiography (Option A) might be considered patient with nonsevere preeclampsia in whom delivery in if ischemic cardiomyopathy with left ventricular failure is the next 7 days is anticipated. Delivery should not be delayed suspected as the cause of PII. However. this patient has no fbr the administration of glucocorticoids in the late preterm symptoms or ECG or echocardiographic findings to support period. this diagnosis. Coronary angiography is not indicated. D Angiotensin converting enzyme inhibitors, including The current classification system subdivides PH into ut enalapril (Option C), are teratogenic and should be avoided flve groups, which are based on similarities in mechanisms, € (D during pregnancy. Recommended flrst line antihypertensives hemodynamics, clinical presentation. and approach to treat- Ut fbr urgent blood pressure control in pregnanry include intra ment. Group 1 includes patients with puimonary arterial o, venous labetalol, intravenous hvdralazine, and immediate hypertension (PAH), including those with idiopathic and CL release nif'edipine. heritable disease, and disease related to drugs and toxins. rl lntravenous sodium nitroprusside (Option D) is recom connective tissue diseases, ttlV inf'ection, schistosomiasis, st mended only for hypertensive emergencies resistant to flrst congenital heart disease, and portal hypertension. High dose line therapy and the presence ol end-organ damage. When calcium channel blockers, such as nifedipine (Option C), can .D UI used, it should be intused for the shortest amount of time be eflbctive treatment in a small number of group 1 patients possible because ol cyanide and thioc.yanate toxicity risk in who are "vasoreactive" by demonstrating marked improve the patient and fetus or newborn. Sodium nitroprusside can ment in mean pulmonary artery pressure with administra also be associated with increased intracranial pressure with tion olnitric oxide, epoprostenol, or adenosine during right potential worsening of cerebral edema in the patient. heart catheterization. Sildenafil (Option D), a phosphodies- terase 5 inhibitor, may be effeclive in mild to moderate PAH IEY POITT in the absence of vasoreactiviU. However, neither nifedipine . In patients who are at or beyond 34 weeks'gestation nor sildena{il is indicated fbr the treatment of PA}{ until the and who develop preeclampsia with severe features, diagnosis of PH has been confirmed and other causes of PI{ emergent management of severe hlpertension and have been excluded. prompt delivery are recommended to avoid maternal and fetal complications. IEY POITIS o Pulmonary hypertension should be suspected in Bibliography patients with progressive dyspnea, elevated central Gestational h)rpertension and preeclampsia: ACOG practice bulletin, number venous pressure, prominent venous o wave, fixed 222. Obstet Gynecol. 2020;135:e237 -e26O. [PMID: 32443079] doi:10.1097/ splitting of Sr, and the murmur of tricuspid regurgi- AOG.0000000000003891 tation. . Right heart catheterization and measurement of pul- tr Item 78 Answer: B Educational Objective: Diagnose pulmonary hyperten- monary artery pressure is the diagnostic gold standard for pulmonary hypertension. sion. Bibliography The most appropriate next step for this patient is right heart Klinger JR, Elliott CG, Levine DJ, et al. Therapy for pulmonary arterial catheterization (Option B). This patient has symptoms h)?ertension in adults: update of the CHEST guideline and expert (progressive dyspnea) and signs (elevated central venous panel report. Chest. 2019;155:565-586. IPMID: 30660783] doi:10.1016/ j.chest.2018.11.030 pressure, venous o wave, fixed splitting of Sr, tricuspid regurgitation) of pulmonary hypertension (PH). If PH is suspected, transthoracic echocardiography can estimate Item 79 pulmonary ar-tery systolic pressure. However, echocardiog raphy does not confirm the diagnosis of PH because pres- Answer: A Educational Objective: Treat severe hypothermia with tr active internal rewarming. sure estimation by echocardiography may be inaccurate. Right heart catheterization confirms the diagnosis of PI{ The most appropriate treatment is active internal rewarming and is an essential component of the diagnostic evaluation. (Option A). This patient has severe hypothermia, defined by Guidelines recommend ref'erral of patients with severe pul a core temperature of less than 28.0 "C (82.4 "F) in the set- monary hypefiension or right ventricular dysfunction to a ting of ongoing coma or cardiovascular collapse. Other flnd- pulmonary hypertension refbrral center. Data sug3est that ings in severe hyperthermia are absent reflexes, ventricular 160

Answers and Critiques til IJ arrhl.thmia, asystole, and apnea. If a severely hypothermic exhaled nitric oxide, which :rll conflrm that his asthma is patient becomes pulseless ancl requires resuscitation. it well controlled. Measurement of the fraction of nitric oxide coNT 's reasonable to continue cardiopulmonary resuscitation in an exhaled breath sample provides a noninvasive way to fbr a prolonged period until the patient can be rewarmed. quantiSz eosinophilic airway inflammation and serves as a Methods ol internal rewarming include infusion of heated complementary tool in the diagnosis and management of intravenous crystalloid solution as well as lavage of the peri asthma. However, his cough and other symptoms suggest toneal or pleural cavities with warm fluids. During active gastroesophageal reflux disea:;e (GERD), a common asthma rewarming, core temperature should be monitored with an comorbidity At each asthma visit, clinicians should assess esophageal temperature probe, as rectal and bladder tem- patient symptom control, irLhaler technique and adher peratures will 1ag behind the rising core temperature during ence, and comorbidities such as rhinosinusitis, obesity, and the rewarming process. GERD. GERD is more common in patients with asthma than Extracorporeal support. inclttding cardiopulmonary the general population and may contribute to respiratory bypass (Option B), is recommended for severely hypother- symptoms such as cough, whr:ezing, and dyspnea. Potential vt (l, mic patients in cardiac arrest because it maximizes the mechanisms by which GERD may cause cough or wors ET rewarming rate and can provide hemodynamic support. ened asthma control include increased vagal tone, bronchial Hemodialysis (Option C) car.r be used for warming, hyperreactivity, and microaspiration of gastric contents into L IJ depending on the clinical circumstances. Acid base and the upper airways. Empiric tr:eatment of GERD in patients tE, electrolyte abnormalities are common in hypothermia. without worrisome symptomrs such as weight loss, dyspha- .g These values. along with markers of coagulopathy, will gia, or hematemesis consists of a proton pump inhibitor Ut

til IJ arrhl.thmia, asystole, and apnea. If a severely hypothermic exhaled nitric oxide, which :rll conflrm that his asthma is patient becomes pulseless ancl requires resuscitation. it well controlled. Measurement of the fraction of nitric oxide coNT 's reasonable to continue cardiopulmonary resuscitation in an exhaled breath sample provides a noninvasive way to fbr a prolonged period until the patient can be rewarmed. quantiSz eosinophilic airway inflammation and serves as a Methods ol internal rewarming include infusion of heated complementary tool in the diagnosis and management of intravenous crystalloid solution as well as lavage of the peri asthma. However, his cough and other symptoms suggest toneal or pleural cavities with warm fluids. During active gastroesophageal reflux disea:;e (GERD), a common asthma rewarming, core temperature should be monitored with an comorbidity At each asthma visit, clinicians should assess esophageal temperature probe, as rectal and bladder tem- patient symptom control, irLhaler technique and adher peratures will 1ag behind the rising core temperature during ence, and comorbidities such as rhinosinusitis, obesity, and the rewarming process. GERD. GERD is more common in patients with asthma than Extracorporeal support. inclttding cardiopulmonary the general population and may contribute to respiratory bypass (Option B), is recommended for severely hypother- symptoms such as cough, whr:ezing, and dyspnea. Potential vt (l, mic patients in cardiac arrest because it maximizes the mechanisms by which GERD may cause cough or wors ET rewarming rate and can provide hemodynamic support. ened asthma control include increased vagal tone, bronchial Hemodialysis (Option C) car.r be used for warming, hyperreactivity, and microaspiration of gastric contents into L IJ depending on the clinical circumstances. Acid base and the upper airways. Empiric tr:eatment of GERD in patients tE, electrolyte abnormalities are common in hypothermia. without worrisome symptomrs such as weight loss, dyspha- .g These values. along with markers of coagulopathy, will gia, or hematemesis consists of a proton pump inhibitor Ut improve with rewarming but should be serially measured. such as omeprazole. o -lhe patient Ut has metabolic acidosis and hyperkalemia, but Switching to a medium dose inhaled glucocorticoid = E neither is severe enough to warrant hemodialysis, and (Option B) is not needed because the patient is tolerating the rewarming can be accomplished by other means. current therapy and it is controlling his asthma symptoms. Hypothermic patients who are shivering will passively Stepping up this patient's therapy by increasing the rewarm themselves (Option D) if they are removed from strength of his inhaled glucocorticoid (Option C) mainte the cold environment and given adequate insulation to pre- nance inhaler is not necessary without signs of worsening vent heat loss. but as hypothermia progresses, shivering asthma. stops. Fbr core temperatr-rres of 28.0 'C to 35.0 'C (82.4 "F to Performing upper endoscopy (Option D) is unnecessary 95.0 'F), active external warming is usually sufficient. This in patients with uncomplicated GERD without suspicion consists olwarming blankets and forced u,arm air. Fbr tem for malignancy, erosive esophagitis, or mechanical issues peratures less than 28.0'C (82.,1 'F) and for patients who fail causing dysphagia, such as welbs, rings, or strictures. Patients to respond adequately to active external rewarming, active whose reflux symptoms do not improve should be con internal rewarming methods should be applied. sidered for further testing sur:h as endoscopy and 24-hour esophageal pH monitoring. f,EY POIl{TS . Severe hypothermia is defined by a core temperature IEY POITIS of less than 28.0 'C (82.4 "F) in the setting of ongoing o Gastrointestinal reflux disease is more common in coma or cardiovascular collapse. patients with asthma than the general population and o For temperatures less than 28.0 'C (82.4'F) and for may contribute to respiratory symptoms such as cough, patients who fail to respond adequately to active wheezing, and dyspnea. external rewarming, active internal rewarming meth- o Patients with respiratory symptoms and gastroesoph- ods, including infusion of heated intravenous crystal- ageal reflux disease shoukl be treated with an empiric loid solution and lavage ofthe peritoneal or pleural trial of a proton pump inhLibitor. cavities with warm fluids, should be applied. Bibliography Bibliography Vaezi ME Katzka D, Zerbib E Extriresophageal symptoms and diseases attributed to GERD: where is the pendulum swinging now? Clin Paal P, Brugger H, Strapazzon G. Accidental hypothermia. Handb Clin Gastroenterol Hepatol. 2018t 16 :101 8 1029. [PMID : 29 427831 doi:70.7076 I Neurol. 20i8;157:547-563. IPMID: 30459025] doi:10.1016/B978-0-444 i.cgh.2018.02.001 64074 1.OOO33-1

improve with rewarming but should be serially measured. such as omeprazole. o -lhe patient Ut has metabolic acidosis and hyperkalemia, but Switching to a medium dose inhaled glucocorticoid = E neither is severe enough to warrant hemodialysis, and (Option B) is not needed because the patient is tolerating the rewarming can be accomplished by other means. current therapy and it is controlling his asthma symptoms. Hypothermic patients who are shivering will passively Stepping up this patient's therapy by increasing the rewarm themselves (Option D) if they are removed from strength of his inhaled glucocorticoid (Option C) mainte the cold environment and given adequate insulation to pre- nance inhaler is not necessary without signs of worsening vent heat loss. but as hypothermia progresses, shivering asthma. stops. Fbr core temperatr-rres of 28.0 'C to 35.0 'C (82.4 "F to Performing upper endoscopy (Option D) is unnecessary 95.0 'F), active external warming is usually sufficient. This in patients with uncomplicated GERD without suspicion consists olwarming blankets and forced u,arm air. Fbr tem for malignancy, erosive esophagitis, or mechanical issues peratures less than 28.0'C (82.,1 'F) and for patients who fail causing dysphagia, such as welbs, rings, or strictures. Patients to respond adequately to active external rewarming, active whose reflux symptoms do not improve should be con internal rewarming methods should be applied. sidered for further testing sur:h as endoscopy and 24-hour esophageal pH monitoring. f,EY POIl{TS . Severe hypothermia is defined by a core temperature IEY POITIS of less than 28.0 'C (82.4 "F) in the setting of ongoing o Gastrointestinal reflux disease is more common in coma or cardiovascular collapse. patients with asthma than the general population and o For temperatures less than 28.0 'C (82.4'F) and for may contribute to respiratory symptoms such as cough, patients who fail to respond adequately to active wheezing, and dyspnea. external rewarming, active internal rewarming meth- o Patients with respiratory symptoms and gastroesoph- ods, including infusion of heated intravenous crystal- ageal reflux disease shoukl be treated with an empiric loid solution and lavage ofthe peritoneal or pleural trial of a proton pump inhLibitor. cavities with warm fluids, should be applied. Bibliography Bibliography Vaezi ME Katzka D, Zerbib E Extriresophageal symptoms and diseases attributed to GERD: where is the pendulum swinging now? Clin Paal P, Brugger H, Strapazzon G. Accidental hypothermia. Handb Clin Gastroenterol Hepatol. 2018t 16 :101 8 1029. [PMID : 29 427831 doi:70.7076 I Neurol. 20i8;157:547-563. IPMID: 30459025] doi:10.1016/B978-0-444 i.cgh.2018.02.001 64074 1.OOO33-1 Item 80 Answer: A Ed ucati o na I O bjective: Treat gastroesophageal refl ux Item 81 Answer: D Educational Objective: Diagnose mesothelioma. tr disease in a patient with asthma. The most appropriate diagnostic test is thoracoscclpic pleural The most appropriate management for this patient is to begin biopsy (Option D). 'lhis patient has a unilateral exudative omeprazole (Option A). The patient has a normal Asthma pleural effusion in the setting of pleural thickening and evi Control Test score, normal spirometry and normal fractional dence of asbestos exposure. 'Ihis clinical scenario strongiy

Item 80 Answer: A Ed ucati o na I O bjective: Treat gastroesophageal refl ux Item 81 Answer: D Educational Objective: Diagnose mesothelioma. tr disease in a patient with asthma. The most appropriate diagnostic test is thoracoscclpic pleural The most appropriate management for this patient is to begin biopsy (Option D). 'lhis patient has a unilateral exudative omeprazole (Option A). The patient has a normal Asthma pleural effusion in the setting of pleural thickening and evi Control Test score, normal spirometry and normal fractional dence of asbestos exposure. 'Ihis clinical scenario strongiy 161

Answers and Critiques tr CONT, suggests malignant pleural mesothelioma. N4alignant pleu- ral mesothelioma is a rare neoplasm that originates from the cetls that line the pleural cavity (mesothelium). It can in altitude with occasional pressurization to an equivalent altitude of about 3000 meters (-10,000 feet) for short dura tions, if necessary to accommodate flying conditions. Peo- present as small nodules, plaque-like masses, or confiuent ple with normal cardiopulmonary function experience very sheets that call encase the lung. [t is associated rt'ith inhala- little change in oxygenation at these altitudes. In patients tional exposure to asbestos fibers ancl has a latency of 20 to whose baseline arterial Po, is less than 95 mm Hg, however, 40 years. Tissue biopsy is required to confirm tl.re diagnosis; flying altitudes cause a much greater decrease in oxygen it can be perfbrmed with medical tl-roracoscopy or video saturation because these patients are on the steep portion assisted thoracoscopic surgery which has 90'll, sensitivity of the oxyhemoglobin dissociation curve. A patient whose fbr malignancy. Because mesothelioma can be dillicult to oxygenation as measured by pulse oximetry (Spor) is 90'1, diagnose. patients will typically present rvith advanced dis at sea leve1 may only have an Spo, of 84% at 2500 meters ease. Other conditions that rnay har,e a similar presentation (-SzOO feet), which can result in symptoms of hypoxia. include a chronic empl,ema and malignant conditions such Resting pulse oximetry is helpful in screening patients for vl as sarcomas and peripheral adenocarcinomas. in-flight hypoxemia. Patients with resting Spo, greater than € (D the sensitivity of pleural fluid cytologr tbr the diagnosis 95"/,, are unlikely to experience signiflcant hypoxemia in ta of n-resotheliorna is as lor,r, as 5'/,,: therefbre a pleural biopsl,' flight. Patients with resting Spo, between 92% and 95% q, is required to make the diagnosis. Adding a closed pleural require assessment of risk factors and may need additional IL biopsy to thoracentesis increases the sensitivity to approyi testing such as high-altitude simulation testing, if available. rl mately 36',4,. Medical or surgical tl-roracoscopy has greater than For those whose resting Spo, is less than92'/,,, supplemental 90',1, sensitivity fbr n.ralignar-rc'y. 'Iherefbre. neither a closed oxygen should be prescribed and there is no need for addi- tt biopsy (Option A) nor a repeat thoracentesis (Option C) is tional testing. Typically, ifpatients do not require oxygen at .D ut the most appropriate diagnostic test. baseline, then prescribing 2 L/min of oxygen is sufflcient. Once the diagnosis is made, fluorodeoxl,glucose PET High-altitude simulation testing (Option A) is consid- (Option B) should be perfbrmed to evaluate the extent of the ered the gold standard of clinical testing in this scenario. disease and help with staging. PE'l will not be as useful befbre However, it is not widely available and thus is not the flrst biopsy because it will not differentiate between an inf'ectious choice for testing. and an inflammatory cause of the pleural thickening. After Patients who require greater than 4 Ll min of oxygen at tissue confirmation, mesothelioma is staged according to the rest should not travel (Option B) because of the uncertain TNM system; PET is often perfbrn.red to help determine the ability to deliver sufficient oxygen during the flight to pre- extent of involvement. If there is lirnited involvement and ncr vent hypoxemia. However, this patient has not required any distant disease, some patients r,r,ill benefit fiom surgery as oxygen at baseline and should not be disqualifled preemp- well as chemotherapy ar-rd radiation. Prognosis fbr mesothe tively from flying. lioma depends on the histologic f'eatures (sarcomatoid versus Because this patient is at potential risk for in flight epithelioid) and staging at diagnosis. but overall it remains hypoxemia, no further testing (Option D) is not the best poor (median surviral, 6 9 months). management. His assessment should begin with measure ment of Spor. TEY POIlIT r For suspected mesothelioma, tissue biopsy is required IEY POIl{IS to confirm the diagnosis; biopsy can be performed o Resting pulse oximetry is helpful in screening patients with medical thoracoscopy or video-assisted thoraco for in flight hypoxemia. scopic surgery. o Patients not using baseline oxygen and with a resting Spo, less than92% should be prescribed supplemental Bibliography oxygen during air travel without additional testing. Scherpereel A. Opitz I, Berghmans T, et al. ERS/ESTSIEACTSi ESTRO guide lines Ibr the management of malignant pleural mesothelioma. Eur Respir J. 2020;55. [PMtD: 32451346] doi:10.1183i13993003.009s3-2019 Bibliography Edvardsen A, Akero A. Christensen CC, et al. Air travel and chronic obstruc tive pulmonary disease: a new algorithm for pre flight evaluation. Thorar. 2012;67 :964-9. IPMID : 22767 877] doi:10.1136/thoraxinl,2012 201855 Item 82 Answer: C Educational Objective: Screen a patient with COPD for air travel safet5L

tr CONT, suggests malignant pleural mesothelioma. N4alignant pleu- ral mesothelioma is a rare neoplasm that originates from the cetls that line the pleural cavity (mesothelium). It can in altitude with occasional pressurization to an equivalent altitude of about 3000 meters (-10,000 feet) for short dura tions, if necessary to accommodate flying conditions. Peo- present as small nodules, plaque-like masses, or confiuent ple with normal cardiopulmonary function experience very sheets that call encase the lung. [t is associated rt'ith inhala- little change in oxygenation at these altitudes. In patients tional exposure to asbestos fibers ancl has a latency of 20 to whose baseline arterial Po, is less than 95 mm Hg, however, 40 years. Tissue biopsy is required to confirm tl.re diagnosis; flying altitudes cause a much greater decrease in oxygen it can be perfbrmed with medical tl-roracoscopy or video saturation because these patients are on the steep portion assisted thoracoscopic surgery which has 90'll, sensitivity of the oxyhemoglobin dissociation curve. A patient whose fbr malignancy. Because mesothelioma can be dillicult to oxygenation as measured by pulse oximetry (Spor) is 90'1, diagnose. patients will typically present rvith advanced dis at sea leve1 may only have an Spo, of 84% at 2500 meters ease. Other conditions that rnay har,e a similar presentation (-SzOO feet), which can result in symptoms of hypoxia. include a chronic empl,ema and malignant conditions such Resting pulse oximetry is helpful in screening patients for vl as sarcomas and peripheral adenocarcinomas. in-flight hypoxemia. Patients with resting Spo, greater than € (D the sensitivity of pleural fluid cytologr tbr the diagnosis 95"/,, are unlikely to experience signiflcant hypoxemia in ta of n-resotheliorna is as lor,r, as 5'/,,: therefbre a pleural biopsl,' flight. Patients with resting Spo, between 92% and 95% q, is required to make the diagnosis. Adding a closed pleural require assessment of risk factors and may need additional IL biopsy to thoracentesis increases the sensitivity to approyi testing such as high-altitude simulation testing, if available. rl mately 36',4,. Medical or surgical tl-roracoscopy has greater than For those whose resting Spo, is less than92'/,,, supplemental 90',1, sensitivity fbr n.ralignar-rc'y. 'Iherefbre. neither a closed oxygen should be prescribed and there is no need for addi- tt biopsy (Option A) nor a repeat thoracentesis (Option C) is tional testing. Typically, ifpatients do not require oxygen at .D ut the most appropriate diagnostic test. baseline, then prescribing 2 L/min of oxygen is sufflcient. Once the diagnosis is made, fluorodeoxl,glucose PET High-altitude simulation testing (Option A) is consid- (Option B) should be perfbrmed to evaluate the extent of the ered the gold standard of clinical testing in this scenario. disease and help with staging. PE'l will not be as useful befbre However, it is not widely available and thus is not the flrst biopsy because it will not differentiate between an inf'ectious choice for testing. and an inflammatory cause of the pleural thickening. After Patients who require greater than 4 Ll min of oxygen at tissue confirmation, mesothelioma is staged according to the rest should not travel (Option B) because of the uncertain TNM system; PET is often perfbrn.red to help determine the ability to deliver sufficient oxygen during the flight to pre- extent of involvement. If there is lirnited involvement and ncr vent hypoxemia. However, this patient has not required any distant disease, some patients r,r,ill benefit fiom surgery as oxygen at baseline and should not be disqualifled preemp- well as chemotherapy ar-rd radiation. Prognosis fbr mesothe tively from flying. lioma depends on the histologic f'eatures (sarcomatoid versus Because this patient is at potential risk for in flight epithelioid) and staging at diagnosis. but overall it remains hypoxemia, no further testing (Option D) is not the best poor (median surviral, 6 9 months). management. His assessment should begin with measure ment of Spor. TEY POIlIT r For suspected mesothelioma, tissue biopsy is required IEY POIl{IS to confirm the diagnosis; biopsy can be performed o Resting pulse oximetry is helpful in screening patients with medical thoracoscopy or video-assisted thoraco for in flight hypoxemia. scopic surgery. o Patients not using baseline oxygen and with a resting Spo, less than92% should be prescribed supplemental Bibliography oxygen during air travel without additional testing. Scherpereel A. Opitz I, Berghmans T, et al. ERS/ESTSIEACTSi ESTRO guide lines Ibr the management of malignant pleural mesothelioma. Eur Respir J. 2020;55. [PMtD: 32451346] doi:10.1183i13993003.009s3-2019 Bibliography Edvardsen A, Akero A. Christensen CC, et al. Air travel and chronic obstruc tive pulmonary disease: a new algorithm for pre flight evaluation. Thorar. 2012;67 :964-9. IPMID : 22767 877] doi:10.1136/thoraxinl,2012 201855 Item 82 Answer: C Educational Objective: Screen a patient with COPD for air travel safet5L The most appropriate management is resting pulse oximetry Item 83 Answer: A Educational Objective: Diagnose connective tissue tr (Option C). Patients with underlying lung disease are at risk disease-associated interstitial lung disease. for signiflcant hypoxia during air travel as a result of the The most likely diagnosis in this patient is interstitial lung dis- decreased oxygen tension of inspired air at higher altitudes. ease (ll-D) associated with connective tissue disease (OptionA). Commercial airlines are required to pressurize cabins to ILD is common among patients with connective tissue disease the equivalent of approximately 2500 meters (-SzOO feet) and can occasionally be the first mani{bstation. In this patient,

The most appropriate management is resting pulse oximetry Item 83 Answer: A Educational Objective: Diagnose connective tissue tr (Option C). Patients with underlying lung disease are at risk disease-associated interstitial lung disease. for signiflcant hypoxia during air travel as a result of the The most likely diagnosis in this patient is interstitial lung dis- decreased oxygen tension of inspired air at higher altitudes. ease (ll-D) associated with connective tissue disease (OptionA). Commercial airlines are required to pressurize cabins to ILD is common among patients with connective tissue disease the equivalent of approximately 2500 meters (-SzOO feet) and can occasionally be the first mani{bstation. In this patient, 162

Answers and Critiques [Il systemic sclerosis is suggested by the presence of Raynaud bleeding (Option A) in this patient. A2O2O systematic review lff phenomenon. gastroesophageal reflux disease, "puf$r fingers" and network meta-analysis of 72 trials involving 12,660 LUNr'(a finding of early skin disease), and positive antitopoisomer- patients fbund that the beneflt of gastric acid suppression ase I (anti Scl 70) antibody. A patulous esophaguscan be seen to reduce the risk ofgastrointestinal bleeding in critically ill on the chest CT scan. Radiographic flndings mirror those of patients is flnely balanced against harms. There is moderate other idiopathic interstitial pneumonias, with the nonspeciflc evidence that compared with placebo, proton pump inhib interstitial pneumonia pattern characterized by ground-glass itors (PPIS) and histamine-2 receptor antagonists (H2RAS), opacities with predominance at the base of the lungs seen in but not sucralfate, reduce the incidence of gastrointestinal this patient. This radiographic pattem is present in more than bleeding, with PPIs likely to be more effective than H2RAs. 80')(, of persons with systemic sclerosis-associated ILD. In Patients at highest risk ficr gastrointestinal bleeding (risk patients with diffuse parenchymal lung disease, the presence >4%) benefited the most. Patients at highest risk were iden of an underlying connective tissue disease has prognostic tifled as those with a coagulopathy, those with chronic liver and therapeutic implications. In contrast to idiopathic disease, and those receiving mechanical ventilation but not tl(l, interstitial pneumonia, patients with connective tissue enteral nutrition. Highest risk patients also included those EF disease associated ILD are treated with immunomodulatory with two or more of the fbllowing risk factors: mechanical medications and tend to have a more lavorable prognosis. ventilation with enteral nutrition, acute kidney injury sep (J Hypersensitivity pneumonitis (Option B) results from sis, and shock. Compared with placebo, the absolute differ =, E exposure to a wide variety of antigens that provoke an ence in bleeding rates flor patients at highest risk receiving a tu exaggerated immune response in susceptible persons. PPI was 3.3'1,. This patient is at high risk for gastrointestinal ta (l, High-resolution CT imaging of the chest shows findings bleeding and use of a PPI will decrease this risk. 3 of' ground-glass opacities and centrilobular micronodules UI Both PPIs and H2RAs may increase the risk of pneumo. that are mid and upper-lung predominant. However, nia (low certainty evidence); however, the impact on risk for this patient's chest radiographic findings, lack of environ- Clostridioides dfficile remains uncertain due to the low inci mental exposures, and findings of systemic sclerosis make dence of infection overall. Although gastric acid suppression the diagnosis of hypersensitivity pneumonitis unlikely. appears likely to reduce the risk of gastrointestinal bleeding in Idiopathic pulmonary fibrosis (lPF) (Option C) is the patients at highest risk, it has no important impact on clinical most common idiopathic interstitial pneumonia. It occurs outcomes such as length of hospital stay (Option B), Iength predominantly in older persons; the diagnosis of IPF is rare of ICU stay (Option C), mortality (Option D), or duration of in those younger than 50 years of age. Gradual onset of dys- mechanical ventilation. pnea and cough over months to years is typical. Sarcoidosis (Option D) is a granulomatous disease of unknor,rrr cause that can affect multiple oryan systems, includ- o Stress ulcer prophylaxis reduces the risk of gastroin- ing the lungs. Frequent radiographic findings of sarcoidosis testinal bleeding in high-risk critically ill patients but include lymphadenopathy and the presence of nodules along has no discemable impact on mortality or ICU or hos- bronchovascular bundles.'lhis patient's radiographic findings pital lengths ofstay. are not consistent with sarcoidosis. Bibliography Wang Y Ye Z, Ge L. et al. lifficacy and safety of gastrointestinal bleeding o Interstitial lung disease is common among patients prophylaxis in cdtically ill patients: systematic review and netlvork meta analysis. BNI J. 2020 ;368 1674 4. IPMID : 319 07 16 6l doi: 10. 1136 /bmj. :

[Il systemic sclerosis is suggested by the presence of Raynaud bleeding (Option A) in this patient. A2O2O systematic review lff phenomenon. gastroesophageal reflux disease, "puf$r fingers" and network meta-analysis of 72 trials involving 12,660 LUNr'(a finding of early skin disease), and positive antitopoisomer- patients fbund that the beneflt of gastric acid suppression ase I (anti Scl 70) antibody. A patulous esophaguscan be seen to reduce the risk ofgastrointestinal bleeding in critically ill on the chest CT scan. Radiographic flndings mirror those of patients is flnely balanced against harms. There is moderate other idiopathic interstitial pneumonias, with the nonspeciflc evidence that compared with placebo, proton pump inhib interstitial pneumonia pattern characterized by ground-glass itors (PPIS) and histamine-2 receptor antagonists (H2RAS), opacities with predominance at the base of the lungs seen in but not sucralfate, reduce the incidence of gastrointestinal this patient. This radiographic pattem is present in more than bleeding, with PPIs likely to be more effective than H2RAs. 80')(, of persons with systemic sclerosis-associated ILD. In Patients at highest risk ficr gastrointestinal bleeding (risk patients with diffuse parenchymal lung disease, the presence >4%) benefited the most. Patients at highest risk were iden of an underlying connective tissue disease has prognostic tifled as those with a coagulopathy, those with chronic liver and therapeutic implications. In contrast to idiopathic disease, and those receiving mechanical ventilation but not tl(l, interstitial pneumonia, patients with connective tissue enteral nutrition. Highest risk patients also included those EF disease associated ILD are treated with immunomodulatory with two or more of the fbllowing risk factors: mechanical medications and tend to have a more lavorable prognosis. ventilation with enteral nutrition, acute kidney injury sep (J Hypersensitivity pneumonitis (Option B) results from sis, and shock. Compared with placebo, the absolute differ =, E exposure to a wide variety of antigens that provoke an ence in bleeding rates flor patients at highest risk receiving a tu exaggerated immune response in susceptible persons. PPI was 3.3'1,. This patient is at high risk for gastrointestinal ta (l, High-resolution CT imaging of the chest shows findings bleeding and use of a PPI will decrease this risk. 3 of' ground-glass opacities and centrilobular micronodules UI Both PPIs and H2RAs may increase the risk of pneumo. that are mid and upper-lung predominant. However, nia (low certainty evidence); however, the impact on risk for this patient's chest radiographic findings, lack of environ- Clostridioides dfficile remains uncertain due to the low inci mental exposures, and findings of systemic sclerosis make dence of infection overall. Although gastric acid suppression the diagnosis of hypersensitivity pneumonitis unlikely. appears likely to reduce the risk of gastrointestinal bleeding in Idiopathic pulmonary fibrosis (lPF) (Option C) is the patients at highest risk, it has no important impact on clinical most common idiopathic interstitial pneumonia. It occurs outcomes such as length of hospital stay (Option B), Iength predominantly in older persons; the diagnosis of IPF is rare of ICU stay (Option C), mortality (Option D), or duration of in those younger than 50 years of age. Gradual onset of dys- mechanical ventilation. pnea and cough over months to years is typical. Sarcoidosis (Option D) is a granulomatous disease of unknor,rrr cause that can affect multiple oryan systems, includ- o Stress ulcer prophylaxis reduces the risk of gastroin- ing the lungs. Frequent radiographic findings of sarcoidosis testinal bleeding in high-risk critically ill patients but include lymphadenopathy and the presence of nodules along has no discemable impact on mortality or ICU or hos- bronchovascular bundles.'lhis patient's radiographic findings pital lengths ofstay. are not consistent with sarcoidosis. Bibliography Wang Y Ye Z, Ge L. et al. lifficacy and safety of gastrointestinal bleeding o Interstitial lung disease is common among patients prophylaxis in cdtically ill patients: systematic review and netlvork meta analysis. BNI J. 2020 ;368 1674 4. IPMID : 319 07 16 6l doi: 10. 1136 /bmj. : with connective tissue disease and can occasionally 16744 be the first manifestation. . Most patients with systemic sclerosis-related lung Item 85 Answer: A disease have a nonspecific interstitial pneumonia pat- Educational Objective: Assess asthma symptom control tern characterized by ground-glass opacities with pre- using a standardized. validated questionnaire. dominance at the base of the lungs. The most appropriate rlext step in management is to adminis-

with connective tissue disease and can occasionally 16744 be the first manifestation. . Most patients with systemic sclerosis-related lung Item 85 Answer: A disease have a nonspecific interstitial pneumonia pat- Educational Objective: Assess asthma symptom control tern characterized by ground-glass opacities with pre- using a standardized. validated questionnaire. dominance at the base of the lungs. The most appropriate rlext step in management is to adminis- Bibliography ter a standardized. valiclated questionnaire such as the Asthma Perelas A, Silver RM, Arrossi AV et al. Systemic sclerosis-associated intersti- Control Test (Option :\) to assess symptom control. Assess- tial lung disease. Lancet Respir Med. 2020;8:304-320. [PMID: 32U3575] ment of symptonr control and risk is an essential component doi:10.1016/S2213-2600(19)30480-1 in the management r.rf asthma and should be performed at each medical touchpoint. The Asthma Control Test and the Item 84 Asthma Control Questionnaire are standardized, validated tr Answer: A Educational Objective: Prevent stress ulcers in a critically questionnaires tiiat cir n discriminate between well-controlled and inadequatell' controlled asthma based on patient symp- ill patient. toms. These synrptonl control tools provide scores and cut A strategr of gastric acid suppression with a proton pump points to distinguish dillerent levels of control and to assess inhibitor is most likely to reduce the risk of gastrointestinal the patient's progrcsr.. When diflerent systems are used to

Bibliography ter a standardized. valiclated questionnaire such as the Asthma Perelas A, Silver RM, Arrossi AV et al. Systemic sclerosis-associated intersti- Control Test (Option :\) to assess symptom control. Assess- tial lung disease. Lancet Respir Med. 2020;8:304-320. [PMID: 32U3575] ment of symptonr control and risk is an essential component doi:10.1016/S2213-2600(19)30480-1 in the management r.rf asthma and should be performed at each medical touchpoint. The Asthma Control Test and the Item 84 Asthma Control Questionnaire are standardized, validated tr Answer: A Educational Objective: Prevent stress ulcers in a critically questionnaires tiiat cir n discriminate between well-controlled and inadequatell' controlled asthma based on patient symp- ill patient. toms. These synrptonl control tools provide scores and cut A strategr of gastric acid suppression with a proton pump points to distinguish dillerent levels of control and to assess inhibitor is most likely to reduce the risk of gastrointestinal the patient's progrcsr.. When diflerent systems are used to 163

Answers and Critiques assess asthma control, the results broadly correlate but are (Option D). HFNC mixes and hun.ridifles high-flon' air not identical and using the same tool for each patient is most and or1'gen (30 L/min or more) to deliver a consistent FIo, reasonable. Numerical asthma control tools are more sensitive (0.21 1.00) through a nasal cannula. The high {lou'creates to change in symptom control than categorical tools. In the positir-e ainrav pressurer the amount depends on the flon' Asthma Control Test, scores range from 5 to 25, with a higher rate and cannot be measured or monitored consistentll: score indicating better asthma control. Scores that correspond A systematic review of oxygen delivered b1' HFNC versus to other than well-controlled asthma suggest the need to standard ox),gen therapy fbr hypoxemic respiratory failure review asthma risk factors, exposures, adherence, and inhaler shou'ed that HFNC may clecrease rates of endotracheal intu technique, and the need for step-up therapy. bation and has no demor.tstrated efl'ect on mortalit-\: At present, fractional exhaled nitric oxide measurement Intubation and mechanical ventilation (Option A) are (FeNO) (Option B) is not recommended to guide asthma acceptable intenentions to manage hl,poxemic respiratory treatment in the general population. Studies have demon- failure. Hou'ever. altern:rtive options such as HF\C and non strated that FeNO-guided treatment reduces exacerbation ir.rvasire ventilation ma1, be preferable because thel'are less UI rates compared with guideline-based treatment, but further ir.rrasire irnd less prone to complications of therapf il mon E studies are needed to identi8/ the populations of patients itored correctly This patient can maintain gas exchange. .D la most likely to beneflt from FeNO guided care and the opti has acceptable breathing efibrt (she is calm and is not using q, mal frequency of FeNO monitoring. For example, the 2020 :rccessory muscles to breathe). and can communicate and CL Asthma Guideline Update from the National Asthma Edu cooperate. Thus, IIFNC sl.tould be pursued first instead of' rr cation and Prevention Program conditionally recommends intubation and mechanical ventilation. FeNO monitoring in patients with persistent allergic asthma, lV{anagement ol h1,'poxemic respiraton' lailure centers tt for whom there is uncertainty in choosing, monitoring, on administration of supplemental ox)€en \rith the low .D UI or adjusting anti-inflammatory therapies based on his- est possible FIo, necessary to meet orl,genation goals. A tory clinical flndings, and spirometry as part of an ongoing therapeutic target for peripheral arterial saturation (Spo.) asthma monitoring and management strates/. This patient is betueen 90')1, and 96'1i,. if feasible. This patient requires does not need FeNO measurement. additional m:rnagement to reach that therapeutic target: Although a chest radiograph (Option C) is helpful in therefbre. no change in hl,poxenria management (Option B) the initial evaluation of signiflcant respiratory symptoms, is inappmpriate. it would not be indicated as routine care in a patient with Evidence favors the use of nonir.rvasire positire pressure controlled asthma symptoms. ventilation (NPPV) (Option C) in patients rvith COPD eracer The 6 minute walk test (Option D) provides avalid and reli- bations. cardiogenic pulmonary edema. neuronluscuiar dis able measure of exercise capacity in patients with lung disease. ease, and obesit_v hypoventilation s1'ndrome ancl in patients Patients walk at their onn pace along a course for 6 minutes, u'ho have been exlubatecl. n'hich places them at high risk ol and the total distance walked is recorded. The test can be used to morbidiq: assess response to therapy in patients with chronic respiratory TEY POI]IIS disorders, especially pulmonary arterial hypertension, but there is no indication for this test in routine asthma care. . In patients with hypoxemic respiratory failure, a ther- apeutic target for peripheral arterial saturation (Spor) TEY POIilTS is between 90% and 96%, if feasible. o Assessment of sy.rnptom control is an essential compo- . In patients with hypoxemic respiratory failure, high- nent in the management of asthma and should be per- flow nasal cannula may decrease rates ofendotracheal formed using a standardized, validated questionnaire. intubation and does not affect mortality. . At present, fractional exhaled nitric oxide measurement (FeNO) is not recommended to guide asthma treatment Bibliography in the general population. Rochwerg B, Einav S, Chaudhuri D, et al. The role for high flow nasal cannula as a respiratory support stratery in adults: a clinical practice guideline. Intensive Care Med. 202O :4 6 :2226 - 2237. [PMID: 33201321 ] doi: 10. 10O7 r Bibliography s00134 020 06312 y Cloutier MM, Dixon AE, Krishnan JA, et al. Managing asthma in adolescents and adults, 2020 asthma guideline update from the National Asthma Education and Prevention Program. I AM A. 2020 ;324 :2301 -2317. [PMID : 332700951 doi:10.1001/jama.2O2O.21974 Item 87 Answer: D Educational Obiective: Treat COPD with smoking cessation.

assess asthma control, the results broadly correlate but are (Option D). HFNC mixes and hun.ridifles high-flon' air not identical and using the same tool for each patient is most and or1'gen (30 L/min or more) to deliver a consistent FIo, reasonable. Numerical asthma control tools are more sensitive (0.21 1.00) through a nasal cannula. The high {lou'creates to change in symptom control than categorical tools. In the positir-e ainrav pressurer the amount depends on the flon' Asthma Control Test, scores range from 5 to 25, with a higher rate and cannot be measured or monitored consistentll: score indicating better asthma control. Scores that correspond A systematic review of oxygen delivered b1' HFNC versus to other than well-controlled asthma suggest the need to standard ox),gen therapy fbr hypoxemic respiratory failure review asthma risk factors, exposures, adherence, and inhaler shou'ed that HFNC may clecrease rates of endotracheal intu technique, and the need for step-up therapy. bation and has no demor.tstrated efl'ect on mortalit-\: At present, fractional exhaled nitric oxide measurement Intubation and mechanical ventilation (Option A) are (FeNO) (Option B) is not recommended to guide asthma acceptable intenentions to manage hl,poxemic respiratory treatment in the general population. Studies have demon- failure. Hou'ever. altern:rtive options such as HF\C and non strated that FeNO-guided treatment reduces exacerbation ir.rvasire ventilation ma1, be preferable because thel'are less UI rates compared with guideline-based treatment, but further ir.rrasire irnd less prone to complications of therapf il mon E studies are needed to identi8/ the populations of patients itored correctly This patient can maintain gas exchange. .D la most likely to beneflt from FeNO guided care and the opti has acceptable breathing efibrt (she is calm and is not using q, mal frequency of FeNO monitoring. For example, the 2020 :rccessory muscles to breathe). and can communicate and CL Asthma Guideline Update from the National Asthma Edu cooperate. Thus, IIFNC sl.tould be pursued first instead of' rr cation and Prevention Program conditionally recommends intubation and mechanical ventilation. FeNO monitoring in patients with persistent allergic asthma, lV{anagement ol h1,'poxemic respiraton' lailure centers tt for whom there is uncertainty in choosing, monitoring, on administration of supplemental ox)€en \rith the low .D UI or adjusting anti-inflammatory therapies based on his- est possible FIo, necessary to meet orl,genation goals. A tory clinical flndings, and spirometry as part of an ongoing therapeutic target for peripheral arterial saturation (Spo.) asthma monitoring and management strates/. This patient is betueen 90')1, and 96'1i,. if feasible. This patient requires does not need FeNO measurement. additional m:rnagement to reach that therapeutic target: Although a chest radiograph (Option C) is helpful in therefbre. no change in hl,poxenria management (Option B) the initial evaluation of signiflcant respiratory symptoms, is inappmpriate. it would not be indicated as routine care in a patient with Evidence favors the use of nonir.rvasire positire pressure controlled asthma symptoms. ventilation (NPPV) (Option C) in patients rvith COPD eracer The 6 minute walk test (Option D) provides avalid and reli- bations. cardiogenic pulmonary edema. neuronluscuiar dis able measure of exercise capacity in patients with lung disease. ease, and obesit_v hypoventilation s1'ndrome ancl in patients Patients walk at their onn pace along a course for 6 minutes, u'ho have been exlubatecl. n'hich places them at high risk ol and the total distance walked is recorded. The test can be used to morbidiq: assess response to therapy in patients with chronic respiratory TEY POI]IIS disorders, especially pulmonary arterial hypertension, but there is no indication for this test in routine asthma care. . In patients with hypoxemic respiratory failure, a ther- apeutic target for peripheral arterial saturation (Spor) TEY POIilTS is between 90% and 96%, if feasible. o Assessment of sy.rnptom control is an essential compo- . In patients with hypoxemic respiratory failure, high- nent in the management of asthma and should be per- flow nasal cannula may decrease rates ofendotracheal formed using a standardized, validated questionnaire. intubation and does not affect mortality. . At present, fractional exhaled nitric oxide measurement (FeNO) is not recommended to guide asthma treatment Bibliography in the general population. Rochwerg B, Einav S, Chaudhuri D, et al. The role for high flow nasal cannula as a respiratory support stratery in adults: a clinical practice guideline. Intensive Care Med. 202O :4 6 :2226 - 2237. [PMID: 33201321 ] doi: 10. 10O7 r Bibliography s00134 020 06312 y Cloutier MM, Dixon AE, Krishnan JA, et al. Managing asthma in adolescents and adults, 2020 asthma guideline update from the National Asthma Education and Prevention Program. I AM A. 2020 ;324 :2301 -2317. [PMID : 332700951 doi:10.1001/jama.2O2O.21974 Item 87 Answer: D Educational Obiective: Treat COPD with smoking cessation. tr Item 86 Answer: D Educational Objective: 1'reat hypoxemic respiratory Smoking cessation is the most appropriate additional ther- apy (Option D). Smoking cessation is essential in the man failure with oxygen by high-flow nasal cannula. agement of COPD because it can slow the decline of FEV, and lhe most appropriate next step in ntiutaging this patient's decrease mortality from COPD. The U.S. Preventive Services hvpoxemia is oxlgen by high Ilor,r' nasal cannula (tlFNC) Task Force recommends that clinicians ask all adults about

tr Item 86 Answer: D Educational Objective: 1'reat hypoxemic respiratory Smoking cessation is the most appropriate additional ther- apy (Option D). Smoking cessation is essential in the man failure with oxygen by high-flow nasal cannula. agement of COPD because it can slow the decline of FEV, and lhe most appropriate next step in ntiutaging this patient's decrease mortality from COPD. The U.S. Preventive Services hvpoxemia is oxlgen by high Ilor,r' nasal cannula (tlFNC) Task Force recommends that clinicians ask all adults about 164

Answers and Critiques tobacco use, advise them to stop using tobacco, and provide Bibliography behavioral interventions and approved pharmacotherapy Iabaki WW, Rosenberg SR. Chronic obstructive pulmonary disease. Ann Intem Med. 2020;173:lTC77 lTC32. IPMID: 32745458] doi:10.7326|AITC202008040 to adult tobacco users. Combining behavioral counseling with pharmacotherapy is more eflective than either modal- ity alone. Effective counseling and behavioral resources Item 88 Answer: B include problem-solving guidance (e.g., developing a plan to quit and overcoming barriers), motivational interviewing, Educational Objective: Diagnose the cause of social support, and telephone quit lines. There is a dose bronchiectasis. response relationship between the intensity and frequency The most appropriate diagnostic test to perform next is of counseling and quit rates, which seems to plateau after immunoglobulin measurement (Option B). This patient 90 minutes of total counseling. All smokers without con has symptoms and imaging findings consistent with traindications should additionally receive at least one of bronchiectasis. Bronchiectasis is a chronic obstructive the FDA-approved treatments for smoking cessation, which Iung disease that results from enlargement of the air U! c, include nicotine replacement medications, bupropion, and ways, which leads to chronic inflammation, recurrent E varenicline. Varenicline is superior to single forms of nic- infection, and ineffective airway clearance. Bronchiec otine replacement therapy and bupropion. Moderate- and tasis should be considered in the differential diagnosis (., high dose preparations ofnicotine replacement therapy are of any patient with a chronic cough and mucopurulent 'E more effective than lower dose ones, and combining more E sputum production. Other possible symptoms include .E than one type of nicotine replacement therapy (short-acting UI hemoptysis, wheezing, and chest pain. Initial evaluation (l, and long acting) is more effective than monotherapy. Ini- of patients with bronchiectasis should include testing tiation of nicotine replacement therapy before smoking is for common causes, including abnormal immune func = UI g stopped may also increase quitting success rates. tion (by measuring immunoglobulin levels) and con Macrolide antibiotics have anti-inflammatory and anti nective tissue disease. Patients should also be evaluated microbial effects. Long term macrolide therapy may reduce for other causes of bronchiectasis depending on their the frequency ofexacerbations when prescribed to patients presentation, including cystic fibrosis, ciliary dysfunc with severe COPD and a history of frequent exacerbations tion, cx,r-antitrypsin deficiency, aspiration, and allergic but do not result in slowing the decline in Iung function or bronchopulmonary aspergillosis. All patients who can reduce the risk of death. Indication for macrolide use is in expectorate sputum should also be tested for chronic patients with COPD treated with combination long-acting bacterial and mycobacterial infections to target for eradi p, agonist, long-acting muscarinic antagonist, and inhaled cation or treatment during exacerbations. More than half glucocorticoid who continue to have exacerbations, espe of cases of bronchiectasis are considered idiopathic after cially in those who are not current smokers. This patient a thorough evaluation. does not have an indication for azithromycin (Option A) as Some patients with bronchiectasis require bronchos he does not have frequent exacerbations. copy with bronchoalveolar lavage (Option A) to test for Oral glucocorticoids (Option B) are recommended for chronic infections that may be missed in sputum cultures short-duration treatment of acute exacerbations of COPD. (including mycobacterial infections) or in patients who can However, long term use of oral glucocorticoids does not not expectorate. Bronchoscopy is not included in the initial slow the decline in lung function or reduce risk ofdeath and diagnostic evaluation of bronchiectasis. should be avoided due to the risk of signiflcant side effects, Common variable immunodeflciency is a heterogenous including diabetes and osteoporosis. syndrome associated with decreased quantitative immuno In patients with COPD, pulmonary rehabilitation globulin levels and impaired humoral response to antigens. (Option C) improves symptoms and quality of life and Impaired humoral response can be tested by measuring decreases frequency of hospitalizations, but it does not speciflc antibody production befbre and after immunization slow the decline in lung function or decrease mortality. with tetanus and pneumococcal polysaccharide vaccines It is recommended for patients with moderate to severe (Option C). Such testing is indicated in patients suspected of symptoms and for patients with at least one exacerbation per having a primary immunodeflciency disorder. However, the year. This patient does not have an indication for pulmonary flrst step in this evaluation is documentation of low immu rehabilitation. noglobulin levels. Primary ciliary dyskinesia is an autosomal recessive I(EY POITIS genetic disorder that causes ineflective ciliary action in . Smoking cessation is essential in the management of the respiratory tract, fallopian tube, and sperm cells. COPD because it is the only therapy that can slow the It can be diagnosed through genetic testing and nasal decline of FEV, and decrease mortality from COPD. ciliary biopsy (Option D); a Iow nasal nitric oxide mea- o All smokers without contraindications should receive surement can also support the diagnosis. Although nasal at least one of seven FDA-approved treatments for ciliary biopsy may be indicated for some patients, it would not be included in the initial diagnostic evaluation smoking cessation. of bronchiectasis.

tobacco use, advise them to stop using tobacco, and provide Bibliography behavioral interventions and approved pharmacotherapy Iabaki WW, Rosenberg SR. Chronic obstructive pulmonary disease. Ann Intem Med. 2020;173:lTC77 lTC32. IPMID: 32745458] doi:10.7326|AITC202008040 to adult tobacco users. Combining behavioral counseling with pharmacotherapy is more eflective than either modal- ity alone. Effective counseling and behavioral resources Item 88 Answer: B include problem-solving guidance (e.g., developing a plan to quit and overcoming barriers), motivational interviewing, Educational Objective: Diagnose the cause of social support, and telephone quit lines. There is a dose bronchiectasis. response relationship between the intensity and frequency The most appropriate diagnostic test to perform next is of counseling and quit rates, which seems to plateau after immunoglobulin measurement (Option B). This patient 90 minutes of total counseling. All smokers without con has symptoms and imaging findings consistent with traindications should additionally receive at least one of bronchiectasis. Bronchiectasis is a chronic obstructive the FDA-approved treatments for smoking cessation, which Iung disease that results from enlargement of the air U! c, include nicotine replacement medications, bupropion, and ways, which leads to chronic inflammation, recurrent E varenicline. Varenicline is superior to single forms of nic- infection, and ineffective airway clearance. Bronchiec otine replacement therapy and bupropion. Moderate- and tasis should be considered in the differential diagnosis (., high dose preparations ofnicotine replacement therapy are of any patient with a chronic cough and mucopurulent 'E more effective than lower dose ones, and combining more E sputum production. Other possible symptoms include .E than one type of nicotine replacement therapy (short-acting UI hemoptysis, wheezing, and chest pain. Initial evaluation (l, and long acting) is more effective than monotherapy. Ini- of patients with bronchiectasis should include testing tiation of nicotine replacement therapy before smoking is for common causes, including abnormal immune func = UI g stopped may also increase quitting success rates. tion (by measuring immunoglobulin levels) and con Macrolide antibiotics have anti-inflammatory and anti nective tissue disease. Patients should also be evaluated microbial effects. Long term macrolide therapy may reduce for other causes of bronchiectasis depending on their the frequency ofexacerbations when prescribed to patients presentation, including cystic fibrosis, ciliary dysfunc with severe COPD and a history of frequent exacerbations tion, cx,r-antitrypsin deficiency, aspiration, and allergic but do not result in slowing the decline in Iung function or bronchopulmonary aspergillosis. All patients who can reduce the risk of death. Indication for macrolide use is in expectorate sputum should also be tested for chronic patients with COPD treated with combination long-acting bacterial and mycobacterial infections to target for eradi p, agonist, long-acting muscarinic antagonist, and inhaled cation or treatment during exacerbations. More than half glucocorticoid who continue to have exacerbations, espe of cases of bronchiectasis are considered idiopathic after cially in those who are not current smokers. This patient a thorough evaluation. does not have an indication for azithromycin (Option A) as Some patients with bronchiectasis require bronchos he does not have frequent exacerbations. copy with bronchoalveolar lavage (Option A) to test for Oral glucocorticoids (Option B) are recommended for chronic infections that may be missed in sputum cultures short-duration treatment of acute exacerbations of COPD. (including mycobacterial infections) or in patients who can However, long term use of oral glucocorticoids does not not expectorate. Bronchoscopy is not included in the initial slow the decline in lung function or reduce risk ofdeath and diagnostic evaluation of bronchiectasis. should be avoided due to the risk of signiflcant side effects, Common variable immunodeflciency is a heterogenous including diabetes and osteoporosis. syndrome associated with decreased quantitative immuno In patients with COPD, pulmonary rehabilitation globulin levels and impaired humoral response to antigens. (Option C) improves symptoms and quality of life and Impaired humoral response can be tested by measuring decreases frequency of hospitalizations, but it does not speciflc antibody production befbre and after immunization slow the decline in lung function or decrease mortality. with tetanus and pneumococcal polysaccharide vaccines It is recommended for patients with moderate to severe (Option C). Such testing is indicated in patients suspected of symptoms and for patients with at least one exacerbation per having a primary immunodeflciency disorder. However, the year. This patient does not have an indication for pulmonary flrst step in this evaluation is documentation of low immu rehabilitation. noglobulin levels. Primary ciliary dyskinesia is an autosomal recessive I(EY POITIS genetic disorder that causes ineflective ciliary action in . Smoking cessation is essential in the management of the respiratory tract, fallopian tube, and sperm cells. COPD because it is the only therapy that can slow the It can be diagnosed through genetic testing and nasal decline of FEV, and decrease mortality from COPD. ciliary biopsy (Option D); a Iow nasal nitric oxide mea- o All smokers without contraindications should receive surement can also support the diagnosis. Although nasal at least one of seven FDA-approved treatments for ciliary biopsy may be indicated for some patients, it would not be included in the initial diagnostic evaluation smoking cessation. of bronchiectasis. 165

Answers and Critiques XEY POITTS treatment of hypersensitivity pneumonitis. Elimination of o Bronchiectasis should be considered in the differential the oflending antigen reduces the risk of exacerbation as well as disease progression. diagnosis of any patient with a chronic cough, especially Early referral for lung transplant (Option A) is pru ifthe patient has a history offrequent respiratory infec- dent in patients with idiopathic pulmonary flbrosis because tions or ifthe cough is productive. the disease has a progressive course as well as potential o Initial evaluation of patients with bronchiectasis for unpredictable and sudden decline. For hlpersensitivity should include testing for common causes, including pneumonitis, lung transplant is an option for hypoxemic abnormal immune function (by measuring immuno- patients with severe disease that is refractory to conservative globulin levels) and connective tissue disease. management strategies. Referral for lung transplant should not precede the removal ofthe offending antigen. Bibliography Nintedanib (Option B), a tyrosine kinase inhibitor, is an Hill AT, Sullivan AL, Chalmers JD, et al. British thoracic society guideline antiflbrotic agent approved for the treatment of idiopathic IA for bronchiectasis in adults. Thorax. 2019;74:1-69. [PMID: 305,15985] pulmonary flbrosis. Although the flbrotic stage of hyper € doi:10.l136,rthoraxjnl 2018 212463 (D sensitivity pneumonitis can mimic idiopathic pulmonary (a fibrosis radiologically, nintedanib does not have a current g, Item 89 Answer: C therapeutic indication for the management of hypersensi CL tivity pneumonitis. n Ed ucatio na I O biective : Treat hypersensitivity Surgical or transbronchial lung biopsy (Option D) may pneumonitis. lt be required if the diagnosis remains uncertain. Typical histo- The most appropriate management for this patient is to pathologic flndings in early stages of hypersensitivity pneu rD UI remove the pet parakeet from the environment (Option C). monitis include lymphocytic cellular inflltration with poorly The patient's clinical and radiographic picture is consistent formed granulomas. Once flbrosis develops, the pattern may with a diagnosis of subacute hypersensitivity pneumonitis. be histologically indistinguishable from the usual interstitial The symptoms started soon after he acquired the pet para- pattem seen in idiopathic pulmonary fibrosis. In this patient, keet. A comprehensive clinical history eliciting the temporal the temporal relationship between antigen exposure and association of a speciflc exposure (avian antigen in this development of symptoms plus supportive imaging flndings case) with symptom development suggests the diagnosis. strongly suggest the diagnosis of hlpersensitivity pneumonitis. The radiographic flndings of micronodular opacities in the mid and upper-lung zones are consistent with the diag- TEY POI]ITS nosis of subacute hypersensitivity pneumonitis. High o The temporal association of a specific exposure with resolution CT scan ofthe chest typically reveals ground-glass symptom development and ground-glass or centrilob- opacities (faint opaciflcation of the lung, as indicated by ular nodular opacities on high-resolution chest CT yellow arrows in the left panel below) and diffuse centrilob scan supports the diagnosis of hypersensitivity pneu- ular micronodules (examples indicated by red arrows in the monitis. right panel below). Untreated, the disease can progress to a o An essential and critical first step in the treatment of chronic form with the development of traction bronchiecta- hypersensitivity pneumonitis is identification and sis and honeycomb changes. Removal ofthe offending anti removal of the offending antigen. gen, if identified, is an essential and critical flrst step in the

XEY POITTS treatment of hypersensitivity pneumonitis. Elimination of o Bronchiectasis should be considered in the differential the oflending antigen reduces the risk of exacerbation as well as disease progression. diagnosis of any patient with a chronic cough, especially Early referral for lung transplant (Option A) is pru ifthe patient has a history offrequent respiratory infec- dent in patients with idiopathic pulmonary flbrosis because tions or ifthe cough is productive. the disease has a progressive course as well as potential o Initial evaluation of patients with bronchiectasis for unpredictable and sudden decline. For hlpersensitivity should include testing for common causes, including pneumonitis, lung transplant is an option for hypoxemic abnormal immune function (by measuring immuno- patients with severe disease that is refractory to conservative globulin levels) and connective tissue disease. management strategies. Referral for lung transplant should not precede the removal ofthe offending antigen. Bibliography Nintedanib (Option B), a tyrosine kinase inhibitor, is an Hill AT, Sullivan AL, Chalmers JD, et al. British thoracic society guideline antiflbrotic agent approved for the treatment of idiopathic IA for bronchiectasis in adults. Thorax. 2019;74:1-69. [PMID: 305,15985] pulmonary flbrosis. Although the flbrotic stage of hyper € doi:10.l136,rthoraxjnl 2018 212463 (D sensitivity pneumonitis can mimic idiopathic pulmonary (a fibrosis radiologically, nintedanib does not have a current g, Item 89 Answer: C therapeutic indication for the management of hypersensi CL tivity pneumonitis. n Ed ucatio na I O biective : Treat hypersensitivity Surgical or transbronchial lung biopsy (Option D) may pneumonitis. lt be required if the diagnosis remains uncertain. Typical histo- The most appropriate management for this patient is to pathologic flndings in early stages of hypersensitivity pneu rD UI remove the pet parakeet from the environment (Option C). monitis include lymphocytic cellular inflltration with poorly The patient's clinical and radiographic picture is consistent formed granulomas. Once flbrosis develops, the pattern may with a diagnosis of subacute hypersensitivity pneumonitis. be histologically indistinguishable from the usual interstitial The symptoms started soon after he acquired the pet para- pattem seen in idiopathic pulmonary fibrosis. In this patient, keet. A comprehensive clinical history eliciting the temporal the temporal relationship between antigen exposure and association of a speciflc exposure (avian antigen in this development of symptoms plus supportive imaging flndings case) with symptom development suggests the diagnosis. strongly suggest the diagnosis of hlpersensitivity pneumonitis. The radiographic flndings of micronodular opacities in the mid and upper-lung zones are consistent with the diag- TEY POI]ITS nosis of subacute hypersensitivity pneumonitis. High o The temporal association of a specific exposure with resolution CT scan ofthe chest typically reveals ground-glass symptom development and ground-glass or centrilob- opacities (faint opaciflcation of the lung, as indicated by ular nodular opacities on high-resolution chest CT yellow arrows in the left panel below) and diffuse centrilob scan supports the diagnosis of hypersensitivity pneu- ular micronodules (examples indicated by red arrows in the monitis. right panel below). Untreated, the disease can progress to a o An essential and critical first step in the treatment of chronic form with the development of traction bronchiecta- hypersensitivity pneumonitis is identification and sis and honeycomb changes. Removal ofthe offending anti removal of the offending antigen. gen, if identified, is an essential and critical flrst step in the 7 \l

XEY POITTS treatment of hypersensitivity pneumonitis. Elimination of o Bronchiectasis should be considered in the differential the oflending antigen reduces the risk of exacerbation as well as disease progression. diagnosis of any patient with a chronic cough, especially Early referral for lung transplant (Option A) is pru ifthe patient has a history offrequent respiratory infec- dent in patients with idiopathic pulmonary flbrosis because tions or ifthe cough is productive. the disease has a progressive course as well as potential o Initial evaluation of patients with bronchiectasis for unpredictable and sudden decline. For hlpersensitivity should include testing for common causes, including pneumonitis, lung transplant is an option for hypoxemic abnormal immune function (by measuring immuno- patients with severe disease that is refractory to conservative globulin levels) and connective tissue disease. management strategies. Referral for lung transplant should not precede the removal ofthe offending antigen. Bibliography Nintedanib (Option B), a tyrosine kinase inhibitor, is an Hill AT, Sullivan AL, Chalmers JD, et al. British thoracic society guideline antiflbrotic agent approved for the treatment of idiopathic IA for bronchiectasis in adults. Thorax. 2019;74:1-69. [PMID: 305,15985] pulmonary flbrosis. Although the flbrotic stage of hyper € doi:10.l136,rthoraxjnl 2018 212463 (D sensitivity pneumonitis can mimic idiopathic pulmonary (a fibrosis radiologically, nintedanib does not have a current g, Item 89 Answer: C therapeutic indication for the management of hypersensi CL tivity pneumonitis. n Ed ucatio na I O biective : Treat hypersensitivity Surgical or transbronchial lung biopsy (Option D) may pneumonitis. lt be required if the diagnosis remains uncertain. Typical histo- The most appropriate management for this patient is to pathologic flndings in early stages of hypersensitivity pneu rD UI remove the pet parakeet from the environment (Option C). monitis include lymphocytic cellular inflltration with poorly The patient's clinical and radiographic picture is consistent formed granulomas. Once flbrosis develops, the pattern may with a diagnosis of subacute hypersensitivity pneumonitis. be histologically indistinguishable from the usual interstitial The symptoms started soon after he acquired the pet para- pattem seen in idiopathic pulmonary fibrosis. In this patient, keet. A comprehensive clinical history eliciting the temporal the temporal relationship between antigen exposure and association of a speciflc exposure (avian antigen in this development of symptoms plus supportive imaging flndings case) with symptom development suggests the diagnosis. strongly suggest the diagnosis of hlpersensitivity pneumonitis. The radiographic flndings of micronodular opacities in the mid and upper-lung zones are consistent with the diag- TEY POI]ITS nosis of subacute hypersensitivity pneumonitis. High o The temporal association of a specific exposure with resolution CT scan ofthe chest typically reveals ground-glass symptom development and ground-glass or centrilob- opacities (faint opaciflcation of the lung, as indicated by ular nodular opacities on high-resolution chest CT yellow arrows in the left panel below) and diffuse centrilob scan supports the diagnosis of hypersensitivity pneu- ular micronodules (examples indicated by red arrows in the monitis. right panel below). Untreated, the disease can progress to a o An essential and critical first step in the treatment of chronic form with the development of traction bronchiecta- hypersensitivity pneumonitis is identification and sis and honeycomb changes. Removal ofthe offending anti removal of the offending antigen. gen, if identified, is an essential and critical flrst step in the 7 \l ITEM 89

XEY POITTS treatment of hypersensitivity pneumonitis. Elimination of o Bronchiectasis should be considered in the differential the oflending antigen reduces the risk of exacerbation as well as disease progression. diagnosis of any patient with a chronic cough, especially Early referral for lung transplant (Option A) is pru ifthe patient has a history offrequent respiratory infec- dent in patients with idiopathic pulmonary flbrosis because tions or ifthe cough is productive. the disease has a progressive course as well as potential o Initial evaluation of patients with bronchiectasis for unpredictable and sudden decline. For hlpersensitivity should include testing for common causes, including pneumonitis, lung transplant is an option for hypoxemic abnormal immune function (by measuring immuno- patients with severe disease that is refractory to conservative globulin levels) and connective tissue disease. management strategies. Referral for lung transplant should not precede the removal ofthe offending antigen. Bibliography Nintedanib (Option B), a tyrosine kinase inhibitor, is an Hill AT, Sullivan AL, Chalmers JD, et al. British thoracic society guideline antiflbrotic agent approved for the treatment of idiopathic IA for bronchiectasis in adults. Thorax. 2019;74:1-69. [PMID: 305,15985] pulmonary flbrosis. Although the flbrotic stage of hyper € doi:10.l136,rthoraxjnl 2018 212463 (D sensitivity pneumonitis can mimic idiopathic pulmonary (a fibrosis radiologically, nintedanib does not have a current g, Item 89 Answer: C therapeutic indication for the management of hypersensi CL tivity pneumonitis. n Ed ucatio na I O biective : Treat hypersensitivity Surgical or transbronchial lung biopsy (Option D) may pneumonitis. lt be required if the diagnosis remains uncertain. Typical histo- The most appropriate management for this patient is to pathologic flndings in early stages of hypersensitivity pneu rD UI remove the pet parakeet from the environment (Option C). monitis include lymphocytic cellular inflltration with poorly The patient's clinical and radiographic picture is consistent formed granulomas. Once flbrosis develops, the pattern may with a diagnosis of subacute hypersensitivity pneumonitis. be histologically indistinguishable from the usual interstitial The symptoms started soon after he acquired the pet para- pattem seen in idiopathic pulmonary fibrosis. In this patient, keet. A comprehensive clinical history eliciting the temporal the temporal relationship between antigen exposure and association of a speciflc exposure (avian antigen in this development of symptoms plus supportive imaging flndings case) with symptom development suggests the diagnosis. strongly suggest the diagnosis of hlpersensitivity pneumonitis. The radiographic flndings of micronodular opacities in the mid and upper-lung zones are consistent with the diag- TEY POI]ITS nosis of subacute hypersensitivity pneumonitis. High o The temporal association of a specific exposure with resolution CT scan ofthe chest typically reveals ground-glass symptom development and ground-glass or centrilob- opacities (faint opaciflcation of the lung, as indicated by ular nodular opacities on high-resolution chest CT yellow arrows in the left panel below) and diffuse centrilob scan supports the diagnosis of hypersensitivity pneu- ular micronodules (examples indicated by red arrows in the monitis. right panel below). Untreated, the disease can progress to a o An essential and critical first step in the treatment of chronic form with the development of traction bronchiecta- hypersensitivity pneumonitis is identification and sis and honeycomb changes. Removal ofthe offending anti removal of the offending antigen. gen, if identified, is an essential and critical flrst step in the 7 \l ITEM 89 165

Answers and Critiques Bibtiography e'thylene glycol poisoning. However, hemodialysis is invasive Fernrndez Perez ER, Koelsch TL, Leone PM, et al. Clinical decision-making ancl resource intensire and is generally not necessary for in hypersensitivity pneumonitis: diagnosis and management. Semin Respir Crit Care Med. 2020;41:214 228. [PMID: 322792921 doi:10.i055/ cthanol or isopropyl alcohol ingestion. s OO40 17012.50 I(EY POIlITS o Ethanol and isopropyl alcohol intoxication are managed with supportive care. tr Item 90 Answer: E Ed ucationa I Objective: Treat alcohol intoxication. . Patients with underlying chronic alcoholism and acute ethanol or isopropyl alcohol toxicity should be The most appropriate ntanagcment is supportive care monitored for signs of alcohol withdrawal. (Option E) and monitoring firr signs of alcohol rn,ithdrawal. The patient is intoxicated by thc high alcohol concen Bibliography trations firund in hand sanitizer. Most sanitizers contain t,! Gallagher N, Edwards FJ. The diagnosis and management of toxic alcohol o ethanol or isopropyl alcohol in concentrations generally poisoning in the emergency department: A review article. Adv J Emerg Med. 2019;3:e28. IPMID: 31410405] doi:10.22114lajem.v0i0.153 ET above 60')1,. Irthanol and other ingested alcohols lctivate the y-aminobutyric acid receptor, which is the primary central (J nervous system inhibitor; this in turn leads to cenlral ner vous system depression, including loss of consciousness and supprcssion of respiratory drive at high closes, which Item 91 Answer: D Educational Objective: Diagnose a malignant pleural tr "!E E .g vt effusion. (l, can lead to respiratory failurc or aspiration events. Alco U! hol intoxication due to ethar.rol and isopropyl alcohol is Thc most likely cliagnosis is malignant pleural ellusion = managed with supportive care. 'lhe patient has a history (Option D). The patient presented r.r,ith increasing dys of chronic alcoholism, and once the acute intoxication pnea in the setting of a new unilatcrul pleural eflusion. subsides, he should be monitorcd for signs olalcohol with 'lhe presence of heart failure, hepatomegaly and possible drawal. Withdrawal can begin within hours to days of the ascites, her occupational history, and her history of brcast last ingestion and can be fatal. cancer broaden the differential diagnosis. Given the diag Ethanol (Option A) has been used historically as a nostic uncertainty of the cause ol the effusion, it shoulcl competitive inhibitor of alcohol dehydrogenase in the set bc sanrpled. The eflusion was bloody in appearance and ting of methanol or ethylenc glycol poisoning. lt should cxudative by all threc of Light's criteria (ratio of pleural not be givcn in the setting ol' ethanol toxicity and aiso fluid protein to serum protein >0.5, ratio of pleural fluid has no role in isopropyl alcohol ingestion. When either lactate dehydrogcnase [LDH] to serum LDH greater than methanol or ethylene glycol has been ingested. there is 0.6, and pleural fluid LDII greater than trno thirds of the an increascd anion gap metabolic acidosis as well as an upper limit of normal fbr serum I-DH). There are many increased osmolal gap that provides an important ciue causes of exudative eflusions. but the most com[ron ilrc to the correct diagnosis. In this case the presence of an inf'ection and malignancy. Given her history of breast cxn osmolal gap and normal anion gap support the diagnosis of cer, the bloody appcarance and exudative characteristic isopropvl alcohol poisoning. of the effusion make it highly suspicious for malignancy. Flumazenil (Option B), a y aminobutyric acid receptor While pleural fluicl cytology is pending, it may not be very antagonist. is the antidote fbr benzodiazepine toxicity It helpful. The sensitivity of pleural fluid cytology is lppr<-rri rtould not be expected to have any effect on outcomes in mately 60'/". and some estimates suggest that it might evcn ethanol or isopropyl alcohol intoxication. 'lhere is reluc be lower (+6'l,,) when all types of malignancy are included. tance to usc flumazenil even in benzodiazepine overdose. 'lhe sensitivity is highest fbr adenocarcinomas (79')1,) and Administration of flumazenil fbr suspected benzodiazepine lowest tbr mesothelioma (rt'1,). Givcn the high suspicion overdose can reverse the efl'ect ofbenzodiazepines leading to of malignancy in this patient, additional testing should be life-threatening central nervous system activation. including pursued consisting ola repeat thor:rccntesis rtith cytology seizures. which are most likely in patients taking benzodiaz (if the first sample is negative) or thoracoscopic pleurirl epines chronically. biopsy. Fomepizole (Option C), an inhibitor of alcohol dehy- Benign asbestos pleural eflusions (Option A) can be drogenase, is used to slow the fbrmation of toxic nretabolites bloody and are typically exudative, and they are seett in when methanol or ethylene glycol is ingested. lt is the first thc context of asbestos exposure. I lowcver, benign asbes line agent fbr rnethanol or ethylene glycol ingestion. Intra tos pleural ellusions are typically associated with pleural \,enous ethanol is second line trcatment and also reduces plaques not seen on this patient's radiograph. toxic metabolite fbrmation. Neither methanol nor ethylene Both heart failure (typically bilateral effusions) glycol ingestir)n is suspected in this patient, so fi)mepizole is (Option B) ancl lrepatic hydrothorax (Option C) (rnore not appropriate. olten right sided) are serous effusions that are trunsLl Hemodialysis (Option D) can remove alcohols from the dates and as such are excluded fiont this patient's dilfer blood; it is usually indicated in the setting clf methanol or ential diagnosis.

Bibtiography e'thylene glycol poisoning. However, hemodialysis is invasive Fernrndez Perez ER, Koelsch TL, Leone PM, et al. Clinical decision-making ancl resource intensire and is generally not necessary for in hypersensitivity pneumonitis: diagnosis and management. Semin Respir Crit Care Med. 2020;41:214 228. [PMID: 322792921 doi:10.i055/ cthanol or isopropyl alcohol ingestion. s OO40 17012.50 I(EY POIlITS o Ethanol and isopropyl alcohol intoxication are managed with supportive care. tr Item 90 Answer: E Ed ucationa I Objective: Treat alcohol intoxication. . Patients with underlying chronic alcoholism and acute ethanol or isopropyl alcohol toxicity should be The most appropriate ntanagcment is supportive care monitored for signs of alcohol withdrawal. (Option E) and monitoring firr signs of alcohol rn,ithdrawal. The patient is intoxicated by thc high alcohol concen Bibliography trations firund in hand sanitizer. Most sanitizers contain t,! Gallagher N, Edwards FJ. The diagnosis and management of toxic alcohol o ethanol or isopropyl alcohol in concentrations generally poisoning in the emergency department: A review article. Adv J Emerg Med. 2019;3:e28. IPMID: 31410405] doi:10.22114lajem.v0i0.153 ET above 60')1,. Irthanol and other ingested alcohols lctivate the y-aminobutyric acid receptor, which is the primary central (J nervous system inhibitor; this in turn leads to cenlral ner vous system depression, including loss of consciousness and supprcssion of respiratory drive at high closes, which Item 91 Answer: D Educational Objective: Diagnose a malignant pleural tr "!E E .g vt effusion. (l, can lead to respiratory failurc or aspiration events. Alco U! hol intoxication due to ethar.rol and isopropyl alcohol is Thc most likely cliagnosis is malignant pleural ellusion = managed with supportive care. 'lhe patient has a history (Option D). The patient presented r.r,ith increasing dys of chronic alcoholism, and once the acute intoxication pnea in the setting of a new unilatcrul pleural eflusion. subsides, he should be monitorcd for signs olalcohol with 'lhe presence of heart failure, hepatomegaly and possible drawal. Withdrawal can begin within hours to days of the ascites, her occupational history, and her history of brcast last ingestion and can be fatal. cancer broaden the differential diagnosis. Given the diag Ethanol (Option A) has been used historically as a nostic uncertainty of the cause ol the effusion, it shoulcl competitive inhibitor of alcohol dehydrogenase in the set bc sanrpled. The eflusion was bloody in appearance and ting of methanol or ethylenc glycol poisoning. lt should cxudative by all threc of Light's criteria (ratio of pleural not be givcn in the setting ol' ethanol toxicity and aiso fluid protein to serum protein >0.5, ratio of pleural fluid has no role in isopropyl alcohol ingestion. When either lactate dehydrogcnase [LDH] to serum LDH greater than methanol or ethylene glycol has been ingested. there is 0.6, and pleural fluid LDII greater than trno thirds of the an increascd anion gap metabolic acidosis as well as an upper limit of normal fbr serum I-DH). There are many increased osmolal gap that provides an important ciue causes of exudative eflusions. but the most com[ron ilrc to the correct diagnosis. In this case the presence of an inf'ection and malignancy. Given her history of breast cxn osmolal gap and normal anion gap support the diagnosis of cer, the bloody appcarance and exudative characteristic isopropvl alcohol poisoning. of the effusion make it highly suspicious for malignancy. Flumazenil (Option B), a y aminobutyric acid receptor While pleural fluicl cytology is pending, it may not be very antagonist. is the antidote fbr benzodiazepine toxicity It helpful. The sensitivity of pleural fluid cytology is lppr<-rri rtould not be expected to have any effect on outcomes in mately 60'/". and some estimates suggest that it might evcn ethanol or isopropyl alcohol intoxication. 'lhere is reluc be lower (+6'l,,) when all types of malignancy are included. tance to usc flumazenil even in benzodiazepine overdose. 'lhe sensitivity is highest fbr adenocarcinomas (79')1,) and Administration of flumazenil fbr suspected benzodiazepine lowest tbr mesothelioma (rt'1,). Givcn the high suspicion overdose can reverse the efl'ect ofbenzodiazepines leading to of malignancy in this patient, additional testing should be life-threatening central nervous system activation. including pursued consisting ola repeat thor:rccntesis rtith cytology seizures. which are most likely in patients taking benzodiaz (if the first sample is negative) or thoracoscopic pleurirl epines chronically. biopsy. Fomepizole (Option C), an inhibitor of alcohol dehy- Benign asbestos pleural eflusions (Option A) can be drogenase, is used to slow the fbrmation of toxic nretabolites bloody and are typically exudative, and they are seett in when methanol or ethylene glycol is ingested. lt is the first thc context of asbestos exposure. I lowcver, benign asbes line agent fbr rnethanol or ethylene glycol ingestion. Intra tos pleural ellusions are typically associated with pleural \,enous ethanol is second line trcatment and also reduces plaques not seen on this patient's radiograph. toxic metabolite fbrmation. Neither methanol nor ethylene Both heart failure (typically bilateral effusions) glycol ingestir)n is suspected in this patient, so fi)mepizole is (Option B) ancl lrepatic hydrothorax (Option C) (rnore not appropriate. olten right sided) are serous effusions that are trunsLl Hemodialysis (Option D) can remove alcohols from the dates and as such are excluded fiont this patient's dilfer blood; it is usually indicated in the setting clf methanol or ential diagnosis. 167

Answers and Critiques f,EY POIf,TI f,EY POITT . The presence of one or more of Light's criteria is very r Guidelines recommend that caloric and protein needs sensitive in the diagnosis of an exudative effusion. of critically ill patients at risk for refeeding syndrome o The most common causes of exudative effusions are should be gradually increased to their goal over the infection and malignancy. course of 3 to 7 days. Bibliography Bibliography Ftller-Kopman D, Light R. Pleural disease. N Engl I Med. 2018;378:740 751. Singer P Blaser AR, Berger MM, et al. ESPEN guideline on clinical nutrition IPMID: 294661461 doi:10.1056,'NEJMra1403503 in the intensive care unit. Clin Nutr. 2019138:48-79. [PMID: 30348a63] doi: 10.1016ij.clnu.2018.08.037

Bibliography Bibliography Ftller-Kopman D, Light R. Pleural disease. N Engl I Med. 2018;378:740 751. Singer P Blaser AR, Berger MM, et al. ESPEN guideline on clinical nutrition IPMID: 294661461 doi:10.1056,'NEJMra1403503 in the intensive care unit. Clin Nutr. 2019138:48-79. [PMID: 30348a63] doi: 10.1016ij.clnu.2018.08.037 Item 92 Answer: C Item 93 Answer: C vt Educational Objective: Manage the progression of Educational Objective: Diagnose glucocorticoid- E enteral feeding in a malnourished patient. responsive asthma with fractional exhaled nitric oxide (D 'lhe most appropriate enterirl f'ccdir-rg strategy fbr this testing. UI o, patier-rt is incrementalll, increasing to 1.,160 calories daily Fractional exhaled nitric oxide (FeNO) (Option C) will help EL a.l over 3 to 7 days (Option C). Patier.rts r,vith critical ill predict this patient's responsiveness to inhaled glucocor- ncss should receive early oral feeding vvl-ren possible ar.rd ticoids. Although FeNO should not be used as a diagnostic lt shoulcl be considered at risk fbr r.nalnutrition u'hen thel' tool for asthma, it can be used to support this diagnosis in .D har.'e not received nutrition fbr more thar.r 48 hours. If situations in which additional objective evidence is needed. vt oral nutrition is r-rot feasible, early, cnteral nutrition is FeNO may be useful if there is uncertainty in choosing, indicated to minimize irrf'ectious complications associated monitoring, or adjusting anti-inflammatory therapies based rt,ith delayed enteral nutrition. 51qu, guidelines suggest on history clinical flndings, and spirometry as part of an tl.rat. in malnourished patielrts, caloric and protein needs ongoing asthma monitoring and management strateSi. In should be increased gradually to their gotrl over the course adults with respiratory symptoms, FeNO levels above 50 ppb ot ll h 7 da1,5 1o arroid risks irssrlciatecl lyith early refeeding correlate with eosinophilic airway inflammation and pre syndrome. When patients arc chronicirllv malnourished or dict response to inhaled glucocorticoids. FeNO levels below cr.tdure prolonged stan'ation. thc bodl, shifts frorn metabtr 25 ppb indicate that eosinophilic airvvay inflammation and lizing carbohl'drates to rnetabolizing protein and lat irs the glucocorticoid responsiveness are less likely; values between rnirin source of adenosine tripl.rosphate production. I11 the 25 and 50 ppb should be interpreted cautiously. In patients l)rocess. intracelL-rlar depletion of kel electrol).tes such as with asthma that is being treated with inhaled glucocor potassiurn. pl-rosphorous. ancl nragnesium begins to occur. ticoids, serial measurement of FeNO may help to monitor When carbohydrates or other simple sugars are reintro patient response to glucocorticoid therapy. ducccl lo the diet or given intravenously. production of Bronchial challenge testing (Option A) is used to iden- ir.rsulin causes rapid intracellular r-rptake and a rapicl drop tiff bronchial hyperresponsiveness, a diagnostic feature in extracellular concentrations of'electrolytes. These shifts of asthma. This is particularly helpful in patients whose have potentially life threatening conseqllences. ir-rclud symptoms are suggestive of asthma but for whom other ing cliaphragmatic r,reakness and rcspiratory impairment. pulmonary function test results are normal. Patients inhale tissue hyporia, fat:rl arrhvthlnias. and cardiomyopathies. increasing doses of a substance known to induce broncho- Guidclines suggest that entcrll intake should be increased spasm, such as methacholine or histamine, in a stepwise slou'11, oygl a period ol3 to 7 clavs. Sl.rould electroll'te levels fashion. This is followed by repeated measurements of FEV,; nrarkedll' decrease from their baselir.re. suggesting refeecl if FEV, falls by 2O% or more from the baseline value, the test ing s1'ndrome. these abnorntalities should be correctecl is considered positive. and the number of calories the patient is receivir-rg shoulcl Diffusing capacity for carbon monoxide (Dr-co) mea be either reduced or l-relcl stcacly. surement (Option B) estimates the amount of gas transfer this patient should not rcceive either 1460 calories through the alveolar/capillary unit and is proportional to or 2000 calories daily (Options A, B) on the first day o1 the surface area of a functional lung. Dr-co is measured by nutritional supplemenfati0n as it n'ral precipitate ref'eecling inhalation of a gas mixture containing carbon monoxide sYnclrome. and helium; the resulting value is corrected for hemoglobin Cuidelines indicate thirt lull targeted medical nutri level. Dlco is reduced in conditions in which functioning tion therapf is considerecl to achieve more than 70'11, ol the alveolar capillary units are destroyed, inflltrated, removed, l-esting energt'erpenditure. but rlot ntorc than 100')i. to pre or their function is compromised. Conditions that increase r,ent overfeeding. Acln.rinistcring 2000 calories to this patient pulmonary capillary blood volume, such as pulmonary alve r,rould rcpresent overleecling rr,hether aclministered on thc olar hemorrhage, left to right shunt, or asthma, can cause first clay ol f'eeding or over ll 1<l 7 days (Option D): therefbre. an elevation in Dlco. Dlco measurements do not predict it is no1 indicated. responsiveness to glucocorticoids.

Item 92 Answer: C Item 93 Answer: C vt Educational Objective: Manage the progression of Educational Objective: Diagnose glucocorticoid- E enteral feeding in a malnourished patient. responsive asthma with fractional exhaled nitric oxide (D 'lhe most appropriate enterirl f'ccdir-rg strategy fbr this testing. UI o, patier-rt is incrementalll, increasing to 1.,160 calories daily Fractional exhaled nitric oxide (FeNO) (Option C) will help EL a.l over 3 to 7 days (Option C). Patier.rts r,vith critical ill predict this patient's responsiveness to inhaled glucocor- ncss should receive early oral feeding vvl-ren possible ar.rd ticoids. Although FeNO should not be used as a diagnostic lt shoulcl be considered at risk fbr r.nalnutrition u'hen thel' tool for asthma, it can be used to support this diagnosis in .D har.'e not received nutrition fbr more thar.r 48 hours. If situations in which additional objective evidence is needed. vt oral nutrition is r-rot feasible, early, cnteral nutrition is FeNO may be useful if there is uncertainty in choosing, indicated to minimize irrf'ectious complications associated monitoring, or adjusting anti-inflammatory therapies based rt,ith delayed enteral nutrition. 51qu, guidelines suggest on history clinical flndings, and spirometry as part of an tl.rat. in malnourished patielrts, caloric and protein needs ongoing asthma monitoring and management strateSi. In should be increased gradually to their gotrl over the course adults with respiratory symptoms, FeNO levels above 50 ppb ot ll h 7 da1,5 1o arroid risks irssrlciatecl lyith early refeeding correlate with eosinophilic airway inflammation and pre syndrome. When patients arc chronicirllv malnourished or dict response to inhaled glucocorticoids. FeNO levels below cr.tdure prolonged stan'ation. thc bodl, shifts frorn metabtr 25 ppb indicate that eosinophilic airvvay inflammation and lizing carbohl'drates to rnetabolizing protein and lat irs the glucocorticoid responsiveness are less likely; values between rnirin source of adenosine tripl.rosphate production. I11 the 25 and 50 ppb should be interpreted cautiously. In patients l)rocess. intracelL-rlar depletion of kel electrol).tes such as with asthma that is being treated with inhaled glucocor potassiurn. pl-rosphorous. ancl nragnesium begins to occur. ticoids, serial measurement of FeNO may help to monitor When carbohydrates or other simple sugars are reintro patient response to glucocorticoid therapy. ducccl lo the diet or given intravenously. production of Bronchial challenge testing (Option A) is used to iden- ir.rsulin causes rapid intracellular r-rptake and a rapicl drop tiff bronchial hyperresponsiveness, a diagnostic feature in extracellular concentrations of'electrolytes. These shifts of asthma. This is particularly helpful in patients whose have potentially life threatening conseqllences. ir-rclud symptoms are suggestive of asthma but for whom other ing cliaphragmatic r,reakness and rcspiratory impairment. pulmonary function test results are normal. Patients inhale tissue hyporia, fat:rl arrhvthlnias. and cardiomyopathies. increasing doses of a substance known to induce broncho- Guidclines suggest that entcrll intake should be increased spasm, such as methacholine or histamine, in a stepwise slou'11, oygl a period ol3 to 7 clavs. Sl.rould electroll'te levels fashion. This is followed by repeated measurements of FEV,; nrarkedll' decrease from their baselir.re. suggesting refeecl if FEV, falls by 2O% or more from the baseline value, the test ing s1'ndrome. these abnorntalities should be correctecl is considered positive. and the number of calories the patient is receivir-rg shoulcl Diffusing capacity for carbon monoxide (Dr-co) mea be either reduced or l-relcl stcacly. surement (Option B) estimates the amount of gas transfer this patient should not rcceive either 1460 calories through the alveolar/capillary unit and is proportional to or 2000 calories daily (Options A, B) on the first day o1 the surface area of a functional lung. Dr-co is measured by nutritional supplemenfati0n as it n'ral precipitate ref'eecling inhalation of a gas mixture containing carbon monoxide sYnclrome. and helium; the resulting value is corrected for hemoglobin Cuidelines indicate thirt lull targeted medical nutri level. Dlco is reduced in conditions in which functioning tion therapf is considerecl to achieve more than 70'11, ol the alveolar capillary units are destroyed, inflltrated, removed, l-esting energt'erpenditure. but rlot ntorc than 100')i. to pre or their function is compromised. Conditions that increase r,ent overfeeding. Acln.rinistcring 2000 calories to this patient pulmonary capillary blood volume, such as pulmonary alve r,rould rcpresent overleecling rr,hether aclministered on thc olar hemorrhage, left to right shunt, or asthma, can cause first clay ol f'eeding or over ll 1<l 7 days (Option D): therefbre. an elevation in Dlco. Dlco measurements do not predict it is no1 indicated. responsiveness to glucocorticoids. 168

Answers and Criti gues Pulse oximetry (Option D) provides a readily available Although N-acetylcysteine (Option C) is frequently noninvasive measurement of oxygen-bound hemoglobin in tused, lor,r' quality evidence Iiom clinical trials has firiled the circulation. A normal hemoglobin saturation measured to (lernonstrate that either oml rtr ir.rhaled N,acetylcysteine by pulse oximetry is 95% to 1007,, and values below 907, prevellts or improves postoperative atelectasis; thus, it is not indicate hypoxemia. Pulse oximetry cannot predict respon recommended. siveness to glucocorticoids. f,EY POtiltt xrY Potf,t3 o Postoperative atelectasis is associated with increased o In adults with respiratory symptoms, fractional morbidity, including hypoxemia, retained secretions, exhaled nitric oxide levels above 50 ppb correlate and pneumonia, and may trigger the development of with eosinophilic airway inflammation and predict acute lung injury. response to inhaled glucocorticoids. o In patients with postoperative atelectasis caused by r Serial measurement of fractional exhaled nitric oxide pain, improved pain management should lead to vt o may be helpful to monitor patient response to inhaled decreased pain and increased chest expansion and =T E glucocorticoid therapy. may result in resolution of the atelectasis. (, Bibliography Bibliography t, Jeppegaard M, Veidal S, Sverrild A, et al. Validation of ATS clinical practice Odor PM, Bampoe S, Gilhooly D, et al. Perioperative interventions for pre- IE i guideline cut-points for FeNO in asthma. Respir Med. 2018.144:22-29. vention of postoperative pulmonary complications: systematic review vt IPMID: 30366580] doi:10.1016/j.rmed.2018.09.014 and meta analysis. BMl. 2020;368:m540. [PMID: 32161042] doi:10.1136/ (l, bmj.ms40 tl=

Pulse oximetry (Option D) provides a readily available Although N-acetylcysteine (Option C) is frequently noninvasive measurement of oxygen-bound hemoglobin in tused, lor,r' quality evidence Iiom clinical trials has firiled the circulation. A normal hemoglobin saturation measured to (lernonstrate that either oml rtr ir.rhaled N,acetylcysteine by pulse oximetry is 95% to 1007,, and values below 907, prevellts or improves postoperative atelectasis; thus, it is not indicate hypoxemia. Pulse oximetry cannot predict respon recommended. siveness to glucocorticoids. f,EY POtiltt xrY Potf,t3 o Postoperative atelectasis is associated with increased o In adults with respiratory symptoms, fractional morbidity, including hypoxemia, retained secretions, exhaled nitric oxide levels above 50 ppb correlate and pneumonia, and may trigger the development of with eosinophilic airway inflammation and predict acute lung injury. response to inhaled glucocorticoids. o In patients with postoperative atelectasis caused by r Serial measurement of fractional exhaled nitric oxide pain, improved pain management should lead to vt o may be helpful to monitor patient response to inhaled decreased pain and increased chest expansion and =T E glucocorticoid therapy. may result in resolution of the atelectasis. (, Bibliography Bibliography t, Jeppegaard M, Veidal S, Sverrild A, et al. Validation of ATS clinical practice Odor PM, Bampoe S, Gilhooly D, et al. Perioperative interventions for pre- IE i guideline cut-points for FeNO in asthma. Respir Med. 2018.144:22-29. vention of postoperative pulmonary complications: systematic review vt IPMID: 30366580] doi:10.1016/j.rmed.2018.09.014 and meta analysis. BMl. 2020;368:m540. [PMID: 32161042] doi:10.1136/ (l, bmj.ms40 tl= tr Item 94 Answer: D Educational Objective: Treat postoperative atelectasis Item 95 Answer: C with pain management. Educational Objective: Diagnose neuromuscular weak- ness as the cause ofrespiratory failure. Pain control is the most appropriate nlanagement (Option D) L fbr this patient's atelectasis. 'lhe patient has postmastec 'Ihe most likely cause o{'this paticnt's respiratory failure is : tomy pain that is impairing chest wall expansion, and she neuromuscular weakness (Option C) due to Guillain Barre has developed atelectasis. Atelectasis is reported to occur syndrome (GBS). Patients r,rritl.r GIIS generally present '"vith in up to 90'){, of all anesthetizecl subjects, and it may persist rapid onset ofascending. synlnletric paralysis. and areflexia : tbr several days follorving surgery. Atelectasis can be the occurring over the course of 2 to .1 lvceks, which may lcad result of irnpaired respiratory mechanics atter thoracic and to respirator"y failure. Specific components of pulmor-rar.'r abdominal surgeries resulting in sh:rllow breathing pat, firnction testing can be helpfirl in the diirgnosis of respiratory terns and avoidance of coughing. Atelectasis is associated failure due to neuromuscular rteakness. A greater than 20'X, with increased morbidity, inclucling hypoxemia, retained clecrement in fbrced vital capacity fiom the sitting to the secretions, and pneumonia. The rnanagement of atelectasis sLlpine position and maximal inspiratory and/or expiratory starts with focusing on the cause, ir.r this case, pain. T1-re fbrce less than 50'2, of predictecl support the diagnosis of' patient is receiving inadequate pain controlr the addition neLrnrrnuscular weakness . associatecl respiratory failure. of rnultimodal pain control. which nray include increasecl l)ecreased respiratorrrr drive (Option A) leads to climin dosage ol rnorphine, NSAIDs, acetaminophen, gabapen ished alveolar CO, clearance. Pltients olten present witl.r tin. or nene blocks, r,r,ill improvc pain control and chest somnolence and diflicultl' protectillg their aim,,a1i Sedating expansion and may resolve the atelectasis. In addition to drugs (illicit or prescribecl). anesthetics. and severe alcohol plin control, the application of chest physiotherapy is one intoxicirtior.r can lead to depressed central respiratory drive. of the first steps in managenlerlt of atelectasis, if it can be Although this patient has hypercapnia. she is alert and coop tolerated by the patient. erative and has no evidence of decreased respiratory clrive. For patients with atelectasis who fail to respond to llypoxemic respiratory failure (Option B) is caused pain controi and chest physiotherapy, srlctioning and bron- by inadequate orygenation of hemoglobin. The most com choscopy (Option A) may be of some value, particularly if nlon cuuses of hypoxemic respiratory tailure in the ICU are secretions are tenacious and abundant. Bronchoscopy is ventilationi'perfusion mismatch ancl shunt, which occur not indicated in this patient who has yet to recei\,e the most when perlused areas of tl.re lung are not ventilated, r,vhether basic treatments. bccause of alrreolar collapse (atelectasis) or tillir-rg of alveoli There is no evidence that inhalation of aerosolized lvith blood. pus. protein, or water. An increased alveolar bronchodilators such as aibuterol (Option B). salmeterol, or arterial ox],gen gradient is the key feature of rentilatior-r, ipratropium are helpful in the resolution of atelectasis in a pertusion rnismatch and shunt but is normal in this patient. patient lvithout airway disease. ln addition, there is the pos Pulrnonary ernbolisnr (Option D) causes respiratory sibility of adverse efl'ects, drug interactions. and increased fiii lure, primarily through ventilation iperfusion mismatcl.t cost without evidence of benefit. and to a less common extent through shunting or low

tr Item 94 Answer: D Educational Objective: Treat postoperative atelectasis Item 95 Answer: C with pain management. Educational Objective: Diagnose neuromuscular weak- ness as the cause ofrespiratory failure. Pain control is the most appropriate nlanagement (Option D) L fbr this patient's atelectasis. 'lhe patient has postmastec 'Ihe most likely cause o{'this paticnt's respiratory failure is : tomy pain that is impairing chest wall expansion, and she neuromuscular weakness (Option C) due to Guillain Barre has developed atelectasis. Atelectasis is reported to occur syndrome (GBS). Patients r,rritl.r GIIS generally present '"vith in up to 90'){, of all anesthetizecl subjects, and it may persist rapid onset ofascending. synlnletric paralysis. and areflexia : tbr several days follorving surgery. Atelectasis can be the occurring over the course of 2 to .1 lvceks, which may lcad result of irnpaired respiratory mechanics atter thoracic and to respirator"y failure. Specific components of pulmor-rar.'r abdominal surgeries resulting in sh:rllow breathing pat, firnction testing can be helpfirl in the diirgnosis of respiratory terns and avoidance of coughing. Atelectasis is associated failure due to neuromuscular rteakness. A greater than 20'X, with increased morbidity, inclucling hypoxemia, retained clecrement in fbrced vital capacity fiom the sitting to the secretions, and pneumonia. The rnanagement of atelectasis sLlpine position and maximal inspiratory and/or expiratory starts with focusing on the cause, ir.r this case, pain. T1-re fbrce less than 50'2, of predictecl support the diagnosis of' patient is receiving inadequate pain controlr the addition neLrnrrnuscular weakness . associatecl respiratory failure. of rnultimodal pain control. which nray include increasecl l)ecreased respiratorrrr drive (Option A) leads to climin dosage ol rnorphine, NSAIDs, acetaminophen, gabapen ished alveolar CO, clearance. Pltients olten present witl.r tin. or nene blocks, r,r,ill improvc pain control and chest somnolence and diflicultl' protectillg their aim,,a1i Sedating expansion and may resolve the atelectasis. In addition to drugs (illicit or prescribecl). anesthetics. and severe alcohol plin control, the application of chest physiotherapy is one intoxicirtior.r can lead to depressed central respiratory drive. of the first steps in managenlerlt of atelectasis, if it can be Although this patient has hypercapnia. she is alert and coop tolerated by the patient. erative and has no evidence of decreased respiratory clrive. For patients with atelectasis who fail to respond to llypoxemic respiratory failure (Option B) is caused pain controi and chest physiotherapy, srlctioning and bron- by inadequate orygenation of hemoglobin. The most com choscopy (Option A) may be of some value, particularly if nlon cuuses of hypoxemic respiratory tailure in the ICU are secretions are tenacious and abundant. Bronchoscopy is ventilationi'perfusion mismatch ancl shunt, which occur not indicated in this patient who has yet to recei\,e the most when perlused areas of tl.re lung are not ventilated, r,vhether basic treatments. bccause of alrreolar collapse (atelectasis) or tillir-rg of alveoli There is no evidence that inhalation of aerosolized lvith blood. pus. protein, or water. An increased alveolar bronchodilators such as aibuterol (Option B). salmeterol, or arterial ox],gen gradient is the key feature of rentilatior-r, ipratropium are helpful in the resolution of atelectasis in a pertusion rnismatch and shunt but is normal in this patient. patient lvithout airway disease. ln addition, there is the pos Pulrnonary ernbolisnr (Option D) causes respiratory sibility of adverse efl'ects, drug interactions. and increased fiii lure, primarily through ventilation iperfusion mismatcl.t cost without evidence of benefit. and to a less common extent through shunting or low 169

Answers and Critiques fFl nrixerl venous ox-\'gen satllration. \\rith shuntir-rg significant Bibliography El s,.,nug1, to cause h1'poxentiir. the iilveolar arterial gradient Rhodes A, Evans LE, Alhazzani W et al. Surviving Sepsis Campaign: inter coNr national guidelines for management of sepsis and septic shock: 2016 \ ,'ll be abnormal. Cot.rsidering this patient's rapidly ascend Crit Care Med. 2017;45:486 552. [PMID: 28098591] doi:10.1097iCCM. ing paralysis, abnormal spironretry nleasures, and normal oooooo0000002255 alv'eolar arlerial oxlrgen gradient. tteu romuscularuveakness is a rnore likell, cause ol her respiratory lailure.

fFl nrixerl venous ox-\'gen satllration. \\rith shuntir-rg significant Bibliography El s,.,nug1, to cause h1'poxentiir. the iilveolar arterial gradient Rhodes A, Evans LE, Alhazzani W et al. Surviving Sepsis Campaign: inter coNr national guidelines for management of sepsis and septic shock: 2016 \ ,'ll be abnormal. Cot.rsidering this patient's rapidly ascend Crit Care Med. 2017;45:486 552. [PMID: 28098591] doi:10.1097iCCM. ing paralysis, abnormal spironretry nleasures, and normal oooooo0000002255 alv'eolar arlerial oxlrgen gradient. tteu romuscularuveakness is a rnore likell, cause ol her respiratory lailure. I(EY POITI Item 97 Answer: C . A greater than2Ook decrement in fbrced vital capacity Educational Objective: Diagrose COPD with spirometry. from the sitting to the supine position and maximal This patient has COPD (Option C). The diagnosis is sup inspiratory and/or expiratory forcc less than 507o of ported by his signiflcant smoking history combined with his predicted support the diagnosis o{ nettromuscular symptoms, imaging, and spirometry flndings. The possibility D weakness-associated respiratory lailure. of COPD should be considered and spirometry should be UI performed in patients 40 years of age or older with progres- E (D Bibliography sive dyspnea, chronic cough, or chronic sputum production, UT Newitt l, Strollo P Breathing problems in Ndults with tt:uromuscular weak particularly in the presence of known risk factors such as o, ness. Am J Respir Crit Care Med. 2O2O2O2:1'j31 P32. IPMID: 33258682] doi: 10.116,1,1rccm.20211P31 smoking. EL COPD is a common disorder and is associated with a.l high morbidity and mortality. However, the role of screen Item 96 .Et E .D UI tr Answer: D Educational Objective: Manage the discontinuation of ing spirometry in asymptomatic persons with risk factors is controversial. The U.S. Preventive Services Task Force guide- antibiotic therapy in a patient with aspiration pneumonitis. line and other guidelines recommend against screening for COPD in asymptomatic adults, whereas the Global Initiative lhe nrost appropriate manirgerrent is tri discontitlue allti for Chronic Obstructive Lung Disease (GOLD) advocates biotics (Option D). ln patielrts aclnritted to the ICU r,r,itl.t performing screening spirometry in persons with risk fac acutc respiratory failure and lorter respiratory tract infil tors for COPD. The diagnosis of COPD is made using spi trate. it is often difficult to deternrine whether the cause rometric measurement to document airflow obstruction. ol the infiltrates is a bacterial int'cction or another source COPD is conflrmed by a postbronchodilator FEV,/FVC ratio such as a viral inf'ection or aspiration pneumonitis. Ulti of less than 0.70. mately. the diagr.rosis ol irspiration pneumonitis is clinical. Asthma (Option A) is an inflammatory disorder of the Indicators include abrupt onset of rcspirator), s),nrptoms airways characterized by cough, wheezing, chest tightness, firllort'ir-rg aspiration of'gastric contents. lo'uv grade fer,er. dyspnea, and variable airflow obstruction. Conflrmation of and infiltrates on chest inraging. The 2019 community reversible airflow obstruction is a cornerstone of asthma ircquired pneumonia (CAP) guideline from the American diagnosis and can be assessed by spirometry with mea Thoracic Society and the Infectious Diseases Society of surement of forced expiratory volume in 1 second (FEVr), America recommends standard empiric treatment fbr CAP forced vital capacity (FVC), and the FEV,/FVC ratio, or by in patients with suspectecl irspiration pneumonia. Many serial measurement of peak expiratory flow rates. Airway patients rvith aspiratioll pneumollitis experience rapid obstruction that improves with bronchodilators, on subse- resolution of symptoms rvithir.r 24 to 48 hours. In these quent measurements, or after 4 weeks of anti inflammatory patients. removal olantibiotics ancl supportive care alone is treatment supports a diagnosis of asthma. For adults, a preferred. Because this patient improved clinically rvithin significant change in FEV, is an increase from baseline of 2.1 hours of admission. aspiration pneumor.ritis is likell,ancl at least 12"/,, and at least 200 mL. This patient does not have it is safe to discor-rtirrue theral.lt: evidence of reversible airflow obstruction, excluding the The 20i6 Surviving Sepsis guiclelines suggest that diagnosis of asthma. antimicrobial treatnlent duration of 7 to 10 days is ade Bronchiectasis (Option B) should be considered in the quate fbr most serious infections associated with sepsis differential diagnosis of any patient with a chronic cough, irncl septic shock but that shorter courses of antibiotics especially ifthe patient has a history offrequent respiratory are reasonable in paticnts r,rrith rlpicl resolution of symp infections or if the cough is productive of mucopurulent torns lbllor,rring sepsis ancl in pltier-rts r,r,ho initially ltere tenacious sputum. Bronchiectasis is diagnosed by high tl.rought to have sepsis but clo not. An additional 4-.7 -. or resolution chest CT. Diagnostic criteria include airway diam l0 day collrse ol ar,tibiotics (Options A-C) is not needed eter that is greater than that of its accompanying vessel and in this p:rtient. lack ofdistal airway tapering. This patient's clinical presen I(EY POIIII tation is not consistent with bronchiectasis. o Discontinuing antibiotic therapy is apprcpriate in Desquamative interstitial pneumonia (DIP) (Option D) patients who initially were thought to have sepsis but is a smoking-related dilluse parenchymal lung disease. Patients with DIP typically are symptomatic with a dry do not. cough and dyspnea. DIP typically is associated with pure

I(EY POITI Item 97 Answer: C . A greater than2Ook decrement in fbrced vital capacity Educational Objective: Diagrose COPD with spirometry. from the sitting to the supine position and maximal This patient has COPD (Option C). The diagnosis is sup inspiratory and/or expiratory forcc less than 507o of ported by his signiflcant smoking history combined with his predicted support the diagnosis o{ nettromuscular symptoms, imaging, and spirometry flndings. The possibility D weakness-associated respiratory lailure. of COPD should be considered and spirometry should be UI performed in patients 40 years of age or older with progres- E (D Bibliography sive dyspnea, chronic cough, or chronic sputum production, UT Newitt l, Strollo P Breathing problems in Ndults with tt:uromuscular weak particularly in the presence of known risk factors such as o, ness. Am J Respir Crit Care Med. 2O2O2O2:1'j31 P32. IPMID: 33258682] doi: 10.116,1,1rccm.20211P31 smoking. EL COPD is a common disorder and is associated with a.l high morbidity and mortality. However, the role of screen Item 96 .Et E .D UI tr Answer: D Educational Objective: Manage the discontinuation of ing spirometry in asymptomatic persons with risk factors is controversial. The U.S. Preventive Services Task Force guide- antibiotic therapy in a patient with aspiration pneumonitis. line and other guidelines recommend against screening for COPD in asymptomatic adults, whereas the Global Initiative lhe nrost appropriate manirgerrent is tri discontitlue allti for Chronic Obstructive Lung Disease (GOLD) advocates biotics (Option D). ln patielrts aclnritted to the ICU r,r,itl.t performing screening spirometry in persons with risk fac acutc respiratory failure and lorter respiratory tract infil tors for COPD. The diagnosis of COPD is made using spi trate. it is often difficult to deternrine whether the cause rometric measurement to document airflow obstruction. ol the infiltrates is a bacterial int'cction or another source COPD is conflrmed by a postbronchodilator FEV,/FVC ratio such as a viral inf'ection or aspiration pneumonitis. Ulti of less than 0.70. mately. the diagr.rosis ol irspiration pneumonitis is clinical. Asthma (Option A) is an inflammatory disorder of the Indicators include abrupt onset of rcspirator), s),nrptoms airways characterized by cough, wheezing, chest tightness, firllort'ir-rg aspiration of'gastric contents. lo'uv grade fer,er. dyspnea, and variable airflow obstruction. Conflrmation of and infiltrates on chest inraging. The 2019 community reversible airflow obstruction is a cornerstone of asthma ircquired pneumonia (CAP) guideline from the American diagnosis and can be assessed by spirometry with mea Thoracic Society and the Infectious Diseases Society of surement of forced expiratory volume in 1 second (FEVr), America recommends standard empiric treatment fbr CAP forced vital capacity (FVC), and the FEV,/FVC ratio, or by in patients with suspectecl irspiration pneumonia. Many serial measurement of peak expiratory flow rates. Airway patients rvith aspiratioll pneumollitis experience rapid obstruction that improves with bronchodilators, on subse- resolution of symptoms rvithir.r 24 to 48 hours. In these quent measurements, or after 4 weeks of anti inflammatory patients. removal olantibiotics ancl supportive care alone is treatment supports a diagnosis of asthma. For adults, a preferred. Because this patient improved clinically rvithin significant change in FEV, is an increase from baseline of 2.1 hours of admission. aspiration pneumor.ritis is likell,ancl at least 12"/,, and at least 200 mL. This patient does not have it is safe to discor-rtirrue theral.lt: evidence of reversible airflow obstruction, excluding the The 20i6 Surviving Sepsis guiclelines suggest that diagnosis of asthma. antimicrobial treatnlent duration of 7 to 10 days is ade Bronchiectasis (Option B) should be considered in the quate fbr most serious infections associated with sepsis differential diagnosis of any patient with a chronic cough, irncl septic shock but that shorter courses of antibiotics especially ifthe patient has a history offrequent respiratory are reasonable in paticnts r,rrith rlpicl resolution of symp infections or if the cough is productive of mucopurulent torns lbllor,rring sepsis ancl in pltier-rts r,r,ho initially ltere tenacious sputum. Bronchiectasis is diagnosed by high tl.rought to have sepsis but clo not. An additional 4-.7 -. or resolution chest CT. Diagnostic criteria include airway diam l0 day collrse ol ar,tibiotics (Options A-C) is not needed eter that is greater than that of its accompanying vessel and in this p:rtient. lack ofdistal airway tapering. This patient's clinical presen I(EY POIIII tation is not consistent with bronchiectasis. o Discontinuing antibiotic therapy is apprcpriate in Desquamative interstitial pneumonia (DIP) (Option D) patients who initially were thought to have sepsis but is a smoking-related dilluse parenchymal lung disease. Patients with DIP typically are symptomatic with a dry do not. cough and dyspnea. DIP typically is associated with pure 170

Answers and Critiques restrictive disease on spirometry. This patient's clinical pre- sentation and spirometry results are not consistent with DIP. . The diagnosis of pulmonary hypertension due to left sided heart disease can usually be made by . The possibility of COPD should be considered and physical examination, chest radiography, and spirometry should be performed in patients 40 years echocardiography. of age or older with progressive dyspnea, chronic cough, or chronic sputum production. Bibliography r The diagnosis of COPD is confirmed by an FEVr/FVC VachidryJL, Tedford RJ, Rosenkranz S, et al. Pulmonary h)pertension due to left heart disease. Eur Respir J. 2019;53. [PMID: 30545974] doi:10.1183/ ratio of less than 0.70 without a significant broncho- 13993003.01897 2018 dilator response.

restrictive disease on spirometry. This patient's clinical pre- sentation and spirometry results are not consistent with DIP. . The diagnosis of pulmonary hypertension due to left sided heart disease can usually be made by . The possibility of COPD should be considered and physical examination, chest radiography, and spirometry should be performed in patients 40 years echocardiography. of age or older with progressive dyspnea, chronic cough, or chronic sputum production. Bibliography r The diagnosis of COPD is confirmed by an FEVr/FVC VachidryJL, Tedford RJ, Rosenkranz S, et al. Pulmonary h)pertension due to left heart disease. Eur Respir J. 2019;53. [PMID: 30545974] doi:10.1183/ ratio of less than 0.70 without a significant broncho- 13993003.01897 2018 dilator response. Bibliography (,t Item 99 Answer: C (, Celli BR, Wedzicha JA. Update on clinical aspects of chronic obstructive pulmonary disease. N Engl J Med. 2O19;387:7257-t266. [PMID: 31553837] Educational Objective: Evaluate a 7-mm solitary pul- ET doi:10.1056/NEJMra1900500 monary nodule in a patient with low risk. L' The most appropriate next step in management is chest .E' Item 98 tr Answer: D Educational Objective: Diagnose pulmonary hyperten, CT in 6 months (Option C). The patient has an indeter minate lung nodule that is 7 mm in size; the first step in E tu v, (t, sion due to left-sided heart failure. evaluation is to estimate the probability of malignancy. 3 tt This can be done qualitatively or quantitatively with The most likely diagnosis is left-sided hearl failure (Option D) risk prediction calculators. Calculating the probability leading to pulmonary hypertension (PH). PH occurs when of malignancy is most useful in treating nodules that are a patient's pulmonary artery pressure is elevated. Normal B to 30 mm in diameter nand helps to determine sub- mean pulmonary artery pressure in adults is rarely greater sequent testing and diagnostic strategy. One commonly than 20 mm Hg. Accordingly, the Sixth World Symposiurn on used risk calculator is the Brock model (w.ww.brocku. Pulmonary Hypertension (WSPH) has defined PH as mean calcancerpredictionresearch). This model considers the pulmonary pressure greater than 20 mm Hg. The WSPH has following as risk factors: older age, female sex, fam further classifled PH into five groups based on the clinical, ily history of lung cancer, emphysema, larger nodule epidemiologic, and histologic profiles. PH related to left- size, Iocation of the nodule in the upper lobe, part solid sided heart disease (group 2) accounts for 65'7, to B0'1, of all nodule type, Iower nodule count (one to four nodules is PH diagnoses. This patient has several risk factors that sup associated with a higher risk of malignancy, whereas five port un<lerlying left-sided heart disease, inciuding advanced or more is associated with a lower risk of malignancy), age. history of hypertension, diabetes, and coronary artery and spiculation. A low-risk nodule measuring 6 to 8 mm disease. The presence clforlhopnea, elevated jugular venous should be monitored with serial CT, the first CT exam- pressure, an S.,, pulmonary congestion on chest radiography, ination in 6 to 12 months, and then CT at 18 to 24 months and echocardiographic evidence of' reduced ejection fraction can be considered. support the diagnosis ofPH related to left-sided hearl disease. For solitary solid noncalcifled nodules larger than 8 mm Chronic thromboembolic pulmonary hypertension in diameter, the Fleischner Society guideline recommends (CTEPH) (group 4) (Option A) is uncommon, even in patients consideration of a 3 month follow-up, work up with com with a history of venous thromboembolism. Approximately bined PET/CT, tissue sampling, or a combination thereof 2011, of patients with CTEPH repoft no previous deep venous (Options A, B); any one of these options may be appropri- thrombosis or pulmonary embolism. This patient's history ate depending on size, morphologr, comorbidif, and other physical eramination, and echocardiographic Iindings sup factors. This patient with a 7-mm low-risk nodule does port left'sided hear-t failure as the cause of PH. not require any of these interventions or surgical resection In patients with puhaonary arterial hypertension (Option D) given the low probability that the nodule is (group t) (Option B), the ]ung parenchyma usually appears malignant. normal on chest imaging. This patient has pulmonary vascu- lar congestion on chest imaging. This patient has findings of left-sided heart tailure ar-rd o For a low-risk, solitary solid pulmonary nodule meas- no clinical or radiographic findings to suggest interstitial uring 6 to B mm, repeat CT evaluation in 6 to 12 months lung disease (Option C). is recommended.

Bibliography (,t Item 99 Answer: C (, Celli BR, Wedzicha JA. Update on clinical aspects of chronic obstructive pulmonary disease. N Engl J Med. 2O19;387:7257-t266. [PMID: 31553837] Educational Objective: Evaluate a 7-mm solitary pul- ET doi:10.1056/NEJMra1900500 monary nodule in a patient with low risk. L' The most appropriate next step in management is chest .E' Item 98 tr Answer: D Educational Objective: Diagnose pulmonary hyperten, CT in 6 months (Option C). The patient has an indeter minate lung nodule that is 7 mm in size; the first step in E tu v, (t, sion due to left-sided heart failure. evaluation is to estimate the probability of malignancy. 3 tt This can be done qualitatively or quantitatively with The most likely diagnosis is left-sided hearl failure (Option D) risk prediction calculators. Calculating the probability leading to pulmonary hypertension (PH). PH occurs when of malignancy is most useful in treating nodules that are a patient's pulmonary artery pressure is elevated. Normal B to 30 mm in diameter nand helps to determine sub- mean pulmonary artery pressure in adults is rarely greater sequent testing and diagnostic strategy. One commonly than 20 mm Hg. Accordingly, the Sixth World Symposiurn on used risk calculator is the Brock model (w.ww.brocku. Pulmonary Hypertension (WSPH) has defined PH as mean calcancerpredictionresearch). This model considers the pulmonary pressure greater than 20 mm Hg. The WSPH has following as risk factors: older age, female sex, fam further classifled PH into five groups based on the clinical, ily history of lung cancer, emphysema, larger nodule epidemiologic, and histologic profiles. PH related to left- size, Iocation of the nodule in the upper lobe, part solid sided heart disease (group 2) accounts for 65'7, to B0'1, of all nodule type, Iower nodule count (one to four nodules is PH diagnoses. This patient has several risk factors that sup associated with a higher risk of malignancy, whereas five port un<lerlying left-sided heart disease, inciuding advanced or more is associated with a lower risk of malignancy), age. history of hypertension, diabetes, and coronary artery and spiculation. A low-risk nodule measuring 6 to 8 mm disease. The presence clforlhopnea, elevated jugular venous should be monitored with serial CT, the first CT exam- pressure, an S.,, pulmonary congestion on chest radiography, ination in 6 to 12 months, and then CT at 18 to 24 months and echocardiographic evidence of' reduced ejection fraction can be considered. support the diagnosis ofPH related to left-sided hearl disease. For solitary solid noncalcifled nodules larger than 8 mm Chronic thromboembolic pulmonary hypertension in diameter, the Fleischner Society guideline recommends (CTEPH) (group 4) (Option A) is uncommon, even in patients consideration of a 3 month follow-up, work up with com with a history of venous thromboembolism. Approximately bined PET/CT, tissue sampling, or a combination thereof 2011, of patients with CTEPH repoft no previous deep venous (Options A, B); any one of these options may be appropri- thrombosis or pulmonary embolism. This patient's history ate depending on size, morphologr, comorbidif, and other physical eramination, and echocardiographic Iindings sup factors. This patient with a 7-mm low-risk nodule does port left'sided hear-t failure as the cause of PH. not require any of these interventions or surgical resection In patients with puhaonary arterial hypertension (Option D) given the low probability that the nodule is (group t) (Option B), the ]ung parenchyma usually appears malignant. normal on chest imaging. This patient has pulmonary vascu- lar congestion on chest imaging. This patient has findings of left-sided heart tailure ar-rd o For a low-risk, solitary solid pulmonary nodule meas- no clinical or radiographic findings to suggest interstitial uring 6 to B mm, repeat CT evaluation in 6 to 12 months lung disease (Option C). is recommended. . Pulmonary hypertension (PH) related to left-sided heart Bibliography MacMahon H, Naidich DB Goo lM, et al. Guidelines for management of disease accounts for 65% to 80% ofall PH diagnoses. incidental pulmonary nodules detected on CT images: from the (Continued) Fleischner Society 2017. Radiolos/. 2ol7;2a4:228 243. [PMID: 28240562] doi: 10. 1148/radiol.2017767659

. Pulmonary hypertension (PH) related to left-sided heart Bibliography MacMahon H, Naidich DB Goo lM, et al. Guidelines for management of disease accounts for 65% to 80% ofall PH diagnoses. incidental pulmonary nodules detected on CT images: from the (Continued) Fleischner Society 2017. Radiolos/. 2ol7;2a4:228 243. [PMID: 28240562] doi: 10. 1148/radiol.2017767659 171

Answers and Critiques Item 100 Answer: B Bibliography Newbigin K, Souza CA, Torres C, et al' Fat embolism syndrome: State-of-the Educational Objective: Diagnose fat embolism art ieview focused on pulmonary imaging findings. Respir Med. 2016; syndrome. 113:93-100. [PMID: 26895808] doi:10.1016/i.rmed.2016.01.018

Item 100 Answer: B Bibliography Newbigin K, Souza CA, Torres C, et al' Fat embolism syndrome: State-of-the Educational Objective: Diagnose fat embolism art ieview focused on pulmonary imaging findings. Respir Med. 2016; syndrome. 113:93-100. [PMID: 26895808] doi:10.1016/i.rmed.2016.01.018 The most likeiy diagnosis is fat embolism syndrome (Option B). a rare but potentially lethal complication resulting from systemic manifestations of fat emboli. Most commonly associated u/ith lollg bot're and pelvic fractures, Item 101 Answer: C Ed ucationa I Obiective: Treat chronic thromboembolic tr pulmonary hypertension. lat en.rbolism svndrome can also be associated with non traumatic conditions such as par.rcreatitis. osteoml'elitis. The most appropriate treatment for this patient rvith chronic and lipid infusion. lt is a clinical diagnosis centered on thromboembolic pulmonary hypertension (CTEPH) is referral the triad of respiratory insufficiencl'. neurologic dysfunc fbr surgical thromboendarterectomy evaluation (Option C). tion, and petechial rash in an appropriate clinical setting. CTEPH consists of organized. chronic thrombi within the v! Although r-rot always present. the petechial rash is charac pulmor-rary arterial system. Patients witl-r CTEPH demon- (D teristically located on nondependent parts ofthe body such strate both mechanical obstruction of pulmonary afieries = as the neck and chest. Onset of fat entbolism syndrome and features ol disordered pulntonary angiogenesis, fibri vt A' typicirlly occurs betr,r,een 24 itnd 72 hours after a fracture nolysis, :rnd vascular rentodeling. These cl-ranges manifest in CL but may occur as early as 12 hours after. Chest radiographs increased pulmonary vascullr resistance and elevated mean a't may be normal. Chest C'l findings are nonspecific and pulmonary artery pressure. Untreated, CTEPH can lead to primarily parenclrymal; bilateral,ur,ell demarcated ground right sided heart failure ancl death. Lii'elong anticoagulation l! glass opacities or ill defined centrilobular nodules may to help prevent furtl-rer throntboen.rbolism and consicler (D UI be noted. Fat has lort,atter.ruation. and it is uncommoll to ation ol thromboendarterectolny are indicated for C'lEPIj. find filling defects on CT angiographlr. Jlgslrent is sup The only potentially curative therapy fbr CTEPH is pulmo portive. and most patients with tat embolism syndrome nary thromboendarterectomy. Because the disease is usually fully recover. although estimates of mortality range lrom progressive, surgical evaluation at an experienced center is 5"/, It't 2O"/,,. warranted in all patients with CTEPH, regardless of disease Air embolism (Option A). a potentially lethal illness. severity. Approximately hali of patients with CTEPU will results from the introduction clfair into the vasculature. Air be eligible for surgery. Puhnonary thromboendarterectomy embolism can also have respiratory and neurologic mani can result in normalization of pulmonary hemodynamics in festations: hou,ever, a rasl-r is unusual. Additionally: symp about one third ofpatients rvho undergo surgery torns olair embolism develop immediately'after the inciting For patients who are not candidates for surgical inter event. A rariety of mechanisms are responsible for air embo verltion or r,r,ho choose not to pursue this path. medical ther lisn.r. ir.rcluding neurosurgical and otolaryngologic surgical apy is indicated. Currentlyl the only medication approved for procedures, penetrating leg r,r,ounds or blur-rt chest trauma, treating CTEPH is riociguat (Option A), a stimulator olsolu- insertion of vascular catheters. and barotrauma associated ble guanylate cyclase, tl.re primary receptor for nitric oxide. with positive pressure ven tilation. Bailoon pulmonary angioplasty (Option B) may be Hospital acquired pnenrnonia (llAP) (Option C). by appropriate for some nonoperative patients. Balloon pulmo clefinition, develops more than 48 hours alter admission and nary angioplasty is an emerging field. A catheter-directed is not the correct diagnosis in this patient with symptoms balkron is inserted irrto tl.re pulmonary aftery and inflated irnd pnlmonary inflltrates lr,ithin 24 hours of admission. to inlprove blood flow and reduce vascular resistance u,ithin Additionalll,; HAP cannot account fbr the petechial rash. the pulmonary circulation. Neither riociguat nor balloon Puhnonary embolism (Option D) n.ranifests rvith tachy pulmonary angioplasf_v- should be oft'ered before considering pnea. respiratory distress. and hypoxia. Hor'relet neurologic surgical intervention. In patients \,vith inoperable CTEPH and symptoms and rash are not seen in patients r,rrith puln-ronary those lvho hare persistent pulmonary hypertension fbllolv enrbolism. CT angiography in pulmonary embolism reveals ing thrclmboendarterectomy. balloon pulmonary angioplasty i ntralum inal fl lling def'ects. or medical therapy with riociguat should be considered. No further treatment (Option D) is inappropriate for TEY POIf,It this patient. Lifelong antic<lagulant therapy is indicated in all . Fat embolism syndrome is most commonly associated patients to pre\.ent further thromboembolism, but because with long bone and pelvic fractures but can also be the disease is progressire without intervention. eraluation associated with nontraumatic conditions such as pan- fbr surgical thromboendarterectomy is impofiant. creatitis, osteomyelitis, and lipid infusion. IEY POITTS o Clinical diagnosis of fat embolism syndrome is centered r Anticoagulation and consideration of thromboendar- on the triad ofrespiratory insufhciency, neurologic dys- terectomy are indicated for all patients with chronic function, and petechial rash in the appropriate clinical thromboembolic pulmonary hypertension. context. (Continued)

The most likeiy diagnosis is fat embolism syndrome (Option B). a rare but potentially lethal complication resulting from systemic manifestations of fat emboli. Most commonly associated u/ith lollg bot're and pelvic fractures, Item 101 Answer: C Ed ucationa I Obiective: Treat chronic thromboembolic tr pulmonary hypertension. lat en.rbolism svndrome can also be associated with non traumatic conditions such as par.rcreatitis. osteoml'elitis. The most appropriate treatment for this patient rvith chronic and lipid infusion. lt is a clinical diagnosis centered on thromboembolic pulmonary hypertension (CTEPH) is referral the triad of respiratory insufficiencl'. neurologic dysfunc fbr surgical thromboendarterectomy evaluation (Option C). tion, and petechial rash in an appropriate clinical setting. CTEPH consists of organized. chronic thrombi within the v! Although r-rot always present. the petechial rash is charac pulmor-rary arterial system. Patients witl-r CTEPH demon- (D teristically located on nondependent parts ofthe body such strate both mechanical obstruction of pulmonary afieries = as the neck and chest. Onset of fat entbolism syndrome and features ol disordered pulntonary angiogenesis, fibri vt A' typicirlly occurs betr,r,een 24 itnd 72 hours after a fracture nolysis, :rnd vascular rentodeling. These cl-ranges manifest in CL but may occur as early as 12 hours after. Chest radiographs increased pulmonary vascullr resistance and elevated mean a't may be normal. Chest C'l findings are nonspecific and pulmonary artery pressure. Untreated, CTEPH can lead to primarily parenclrymal; bilateral,ur,ell demarcated ground right sided heart failure ancl death. Lii'elong anticoagulation l! glass opacities or ill defined centrilobular nodules may to help prevent furtl-rer throntboen.rbolism and consicler (D UI be noted. Fat has lort,atter.ruation. and it is uncommoll to ation ol thromboendarterectolny are indicated for C'lEPIj. find filling defects on CT angiographlr. Jlgslrent is sup The only potentially curative therapy fbr CTEPH is pulmo portive. and most patients with tat embolism syndrome nary thromboendarterectomy. Because the disease is usually fully recover. although estimates of mortality range lrom progressive, surgical evaluation at an experienced center is 5"/, It't 2O"/,,. warranted in all patients with CTEPH, regardless of disease Air embolism (Option A). a potentially lethal illness. severity. Approximately hali of patients with CTEPU will results from the introduction clfair into the vasculature. Air be eligible for surgery. Puhnonary thromboendarterectomy embolism can also have respiratory and neurologic mani can result in normalization of pulmonary hemodynamics in festations: hou,ever, a rasl-r is unusual. Additionally: symp about one third ofpatients rvho undergo surgery torns olair embolism develop immediately'after the inciting For patients who are not candidates for surgical inter event. A rariety of mechanisms are responsible for air embo verltion or r,r,ho choose not to pursue this path. medical ther lisn.r. ir.rcluding neurosurgical and otolaryngologic surgical apy is indicated. Currentlyl the only medication approved for procedures, penetrating leg r,r,ounds or blur-rt chest trauma, treating CTEPH is riociguat (Option A), a stimulator olsolu- insertion of vascular catheters. and barotrauma associated ble guanylate cyclase, tl.re primary receptor for nitric oxide. with positive pressure ven tilation. Bailoon pulmonary angioplasty (Option B) may be Hospital acquired pnenrnonia (llAP) (Option C). by appropriate for some nonoperative patients. Balloon pulmo clefinition, develops more than 48 hours alter admission and nary angioplasty is an emerging field. A catheter-directed is not the correct diagnosis in this patient with symptoms balkron is inserted irrto tl.re pulmonary aftery and inflated irnd pnlmonary inflltrates lr,ithin 24 hours of admission. to inlprove blood flow and reduce vascular resistance u,ithin Additionalll,; HAP cannot account fbr the petechial rash. the pulmonary circulation. Neither riociguat nor balloon Puhnonary embolism (Option D) n.ranifests rvith tachy pulmonary angioplasf_v- should be oft'ered before considering pnea. respiratory distress. and hypoxia. Hor'relet neurologic surgical intervention. In patients \,vith inoperable CTEPH and symptoms and rash are not seen in patients r,rrith puln-ronary those lvho hare persistent pulmonary hypertension fbllolv enrbolism. CT angiography in pulmonary embolism reveals ing thrclmboendarterectomy. balloon pulmonary angioplasty i ntralum inal fl lling def'ects. or medical therapy with riociguat should be considered. No further treatment (Option D) is inappropriate for TEY POIf,It this patient. Lifelong antic<lagulant therapy is indicated in all . Fat embolism syndrome is most commonly associated patients to pre\.ent further thromboembolism, but because with long bone and pelvic fractures but can also be the disease is progressire without intervention. eraluation associated with nontraumatic conditions such as pan- fbr surgical thromboendarterectomy is impofiant. creatitis, osteomyelitis, and lipid infusion. IEY POITTS o Clinical diagnosis of fat embolism syndrome is centered r Anticoagulation and consideration of thromboendar- on the triad ofrespiratory insufhciency, neurologic dys- terectomy are indicated for all patients with chronic function, and petechial rash in the appropriate clinical thromboembolic pulmonary hypertension. context. (Continued) 172

Answers and Critiques f,lY P0ltIl konfrnaed) The patient has already stepped up her maintenance . In patients with inoperable chronic thromboem- therapy without resolution of her symptoms; therefore, bolic pulmonary hypertension and those who have changing her therapy from budesonide to budesonide formoterol (Option E) is unlikely to be effective. persistent pulmonary hypertension following thromboendarterectomy, balloon pulmonary angio- XEY POITTS plasty or medical therapy with riociguat should be o All patients with asthma should have a written asthma considered. management plan that helps them recognize the symp- toms of an exacerbation and begin self treatment. Bibliography Sahutoglu E, Tuncay E, Aras G, et al. Chronic thromboembolic pulmonary . Patients with an asthma exacerbation who continue to hypertension in patients with persistent chest symptoms after acute have s).rnptoms after self-treatment should be treated pulmonary embolism. Anatol I Cardiol. 2O2t;25:24 29. IpMlD: 333820S2] with an oral glucocorticoid. doi:10-1,1744 /AnatolJCardiol.2020.69OS7 ra q, Bibliography ET Item 1O2 Answer: C Fergeson JE, Patel SS, Lockey RF. Acute asthma, prognosis, and treatment.

f,lY P0ltIl konfrnaed) The patient has already stepped up her maintenance . In patients with inoperable chronic thromboem- therapy without resolution of her symptoms; therefore, bolic pulmonary hypertension and those who have changing her therapy from budesonide to budesonide formoterol (Option E) is unlikely to be effective. persistent pulmonary hypertension following thromboendarterectomy, balloon pulmonary angio- XEY POITTS plasty or medical therapy with riociguat should be o All patients with asthma should have a written asthma considered. management plan that helps them recognize the symp- toms of an exacerbation and begin self treatment. Bibliography Sahutoglu E, Tuncay E, Aras G, et al. Chronic thromboembolic pulmonary . Patients with an asthma exacerbation who continue to hypertension in patients with persistent chest symptoms after acute have s).rnptoms after self-treatment should be treated pulmonary embolism. Anatol I Cardiol. 2O2t;25:24 29. IpMlD: 333820S2] with an oral glucocorticoid. doi:10-1,1744 /AnatolJCardiol.2020.69OS7 ra q, Bibliography ET Item 1O2 Answer: C Fergeson JE, Patel SS, Lockey RF. Acute asthma, prognosis, and treatment. Educational Objective: Treat an asthma exacerbation. J Allerg/ Clin Immunol. 2017;139:438-447. IPMID: 27554811] doi:l0.l0l6i j.jaci.2016.06.0s4 (, "!E' The most appropriate management for this patient with an ag vt Item 103 asthma exacerbation is to start a 5-day course ofprednisone (Option C). Asthma exacerbation is an acute worsening of symptoms or lung function from baseline that necessitates Answer: B Educational Objective: Treat exacerbation of Lrronchi tr o t, = E ectasis. a step up in therapy. Prompt recognition and treatment of asthma exacerbations are needed to relieve symptoms and 'lhc most appropriatc managenrent is ciproflur:rcin prevent hospitalizations. All patients with asthma should (Option B). ln paticnts with bronchicctasis, the presence have a written asthma management plan that helps them ol chror.ric symptoms of cough ancl spntunr productiiln typ recognize the symptoms of an exacerbation and begin ical11, indicates irr-cvcrsible ainvay dilation. Treatrnent of'the self treatment. If symptoms do not improve with self- underlf ing callse nra)' not lead to improvelnent in currcnt treatment, evaluation is appropriate. Clinicians should screen svnrploms br-rt could prevent firrthcr progression. Othcr for patient factors that contribute to an increased risk of death urisc. treatment ol'bronchiectasis firctrses on air-uvay clear from asthma and should counsel patients appropriately. ance and pre\,enting and treating exacerbalions. This patient Important risk factors include a history of near fatal asthma is experiencing a bronchiectasis e'xacerbation, rt l-tich is often attack or intubation; an emergency department or hospital characterized as a change in sputurn volunre, r,iscosit]'l or visit in the last 12 months; poor asthma medication adher- puruIcnce: increased cotigh: r,vheezing: shortness ol breath; ence or not using inhaled glucocorticoid; current or recent hcmopt-vsis: or declinc in lung function. In addition to con treatment with an oral glucocorticoid; pqychosocial stressors tinr-ring ainvay clearance therapies r,t,ith :rlbuterol and lryper or psychiatric disease; food allergz; and overuse ofa short- tonic saline nebr-rlization, exacerbations ot bronchiectirsis are acting Br-agonist. On physical examination, signs of a severe trelteci u'ith antibiotics tailored by prcvious sputum culturc asthma exacerbation that should prompt aggressive inter n-'sults. If sputunr culture resu]ts are not available. enrpiric vention and hospitalization include being unable to speak antibiotic therapf is recommendecl, oflen n'ith a fluoro in full sentencesi use of accessory muscles of respiration; cluir-rolone. to elrsure Pseudomottcis coveruge until sputurn respiration rate greater than 30/min, heart rate greater than culture results are lvailable. The stirnclarcl course ol iir-rtibi 120/min; oxygen saturation less than 90% with the patient otics fbr a bronchiectasis exacerbation is l4 days. but slrorter breathing ambient air; and agitation, confusion, or drows- cr.rurses may be used firr mild brot-tchiechsis in the abscnce of iness. This patient does not have any signs ofor risk factors l)seudolnono.s oerurgirroso. This paticnt has previousll- gror,r,n for a severe asthma exacerbation; therefore, she can be P oeruginosct ar-rd should begin tal<ing an atrtibiotic lvith safely managed as an outpatient. The best next step is to appropriate co\erage. such as ciprofloracin. begin an oral glucocorticoid such as prednisone for a period Although azithnrrnycin (Option A) is commonly used of5 to 7 days. lbr community itccluircd pneumonia and COPD exacerba Asthma exacerbations do not require antibiotics tions. it has inadetluate coverage fctr P aeruginoso. Of'note, (Option A) unless other signs suggestive of infection, such rzithromycin can bc uscd for Iong ternr tl'eatment in somc as fever, are present. patients \ rith brollchicctasis and fiequent exacerbations to Patients such as this one with low risk for a severe reduce airual,'inflarnrnation. \\'hen dcciding whether to Llsc asthma exacerbation can be treated with a 5 to 7 day course macrolide antibiotics. the physician should r,r,eigh the risk ofprednisone. A 14-day course ofprednisone (Option D) is ol' [uture exacerbatior.rs against the possibility of developing unnecessarily long, and intravenous glucocorticoids, such nracnrlide resistance. as methylprednisone, followed by a course of prednisone Inhaled clomase rrlla (Option C) is used in patients (Option B) is also excessive and unnecessary. ',r'ith cy'stic fibrosis to reduce sputum viscositl.': it itnproves

Educational Objective: Treat an asthma exacerbation. J Allerg/ Clin Immunol. 2017;139:438-447. IPMID: 27554811] doi:l0.l0l6i j.jaci.2016.06.0s4 (, "!E' The most appropriate management for this patient with an ag vt Item 103 asthma exacerbation is to start a 5-day course ofprednisone (Option C). Asthma exacerbation is an acute worsening of symptoms or lung function from baseline that necessitates Answer: B Educational Objective: Treat exacerbation of Lrronchi tr o t, = E ectasis. a step up in therapy. Prompt recognition and treatment of asthma exacerbations are needed to relieve symptoms and 'lhc most appropriatc managenrent is ciproflur:rcin prevent hospitalizations. All patients with asthma should (Option B). ln paticnts with bronchicctasis, the presence have a written asthma management plan that helps them ol chror.ric symptoms of cough ancl spntunr productiiln typ recognize the symptoms of an exacerbation and begin ical11, indicates irr-cvcrsible ainvay dilation. Treatrnent of'the self treatment. If symptoms do not improve with self- underlf ing callse nra)' not lead to improvelnent in currcnt treatment, evaluation is appropriate. Clinicians should screen svnrploms br-rt could prevent firrthcr progression. Othcr for patient factors that contribute to an increased risk of death urisc. treatment ol'bronchiectasis firctrses on air-uvay clear from asthma and should counsel patients appropriately. ance and pre\,enting and treating exacerbalions. This patient Important risk factors include a history of near fatal asthma is experiencing a bronchiectasis e'xacerbation, rt l-tich is often attack or intubation; an emergency department or hospital characterized as a change in sputurn volunre, r,iscosit]'l or visit in the last 12 months; poor asthma medication adher- puruIcnce: increased cotigh: r,vheezing: shortness ol breath; ence or not using inhaled glucocorticoid; current or recent hcmopt-vsis: or declinc in lung function. In addition to con treatment with an oral glucocorticoid; pqychosocial stressors tinr-ring ainvay clearance therapies r,t,ith :rlbuterol and lryper or psychiatric disease; food allergz; and overuse ofa short- tonic saline nebr-rlization, exacerbations ot bronchiectirsis are acting Br-agonist. On physical examination, signs of a severe trelteci u'ith antibiotics tailored by prcvious sputum culturc asthma exacerbation that should prompt aggressive inter n-'sults. If sputunr culture resu]ts are not available. enrpiric vention and hospitalization include being unable to speak antibiotic therapf is recommendecl, oflen n'ith a fluoro in full sentencesi use of accessory muscles of respiration; cluir-rolone. to elrsure Pseudomottcis coveruge until sputurn respiration rate greater than 30/min, heart rate greater than culture results are lvailable. The stirnclarcl course ol iir-rtibi 120/min; oxygen saturation less than 90% with the patient otics fbr a bronchiectasis exacerbation is l4 days. but slrorter breathing ambient air; and agitation, confusion, or drows- cr.rurses may be used firr mild brot-tchiechsis in the abscnce of iness. This patient does not have any signs ofor risk factors l)seudolnono.s oerurgirroso. This paticnt has previousll- gror,r,n for a severe asthma exacerbation; therefore, she can be P oeruginosct ar-rd should begin tal<ing an atrtibiotic lvith safely managed as an outpatient. The best next step is to appropriate co\erage. such as ciprofloracin. begin an oral glucocorticoid such as prednisone for a period Although azithnrrnycin (Option A) is commonly used of5 to 7 days. lbr community itccluircd pneumonia and COPD exacerba Asthma exacerbations do not require antibiotics tions. it has inadetluate coverage fctr P aeruginoso. Of'note, (Option A) unless other signs suggestive of infection, such rzithromycin can bc uscd for Iong ternr tl'eatment in somc as fever, are present. patients \ rith brollchicctasis and fiequent exacerbations to Patients such as this one with low risk for a severe reduce airual,'inflarnrnation. \\'hen dcciding whether to Llsc asthma exacerbation can be treated with a 5 to 7 day course macrolide antibiotics. the physician should r,r,eigh the risk ofprednisone. A 14-day course ofprednisone (Option D) is ol' [uture exacerbatior.rs against the possibility of developing unnecessarily long, and intravenous glucocorticoids, such nracnrlide resistance. as methylprednisone, followed by a course of prednisone Inhaled clomase rrlla (Option C) is used in patients (Option B) is also excessive and unnecessary. ',r'ith cy'stic fibrosis to reduce sputum viscositl.': it itnproves 173

Answers and Critiques Fll lung function and decreases the frequenry of exacerbations. Itl uo,i*.r, it is potentially harmful in patients with non- . In addition to contiflring airway elearance, bronchi- coNI rystic flbrosis bronchiectasis, as patients who were treated ectasis exacerbations are treated with antibiotics with it had more frequent exacerbations, hospitalizations, tailored by previous sputum culture results. and antibiotic and glucocorticoid courses than those who received placebo. Thus inhaled dornase alfa is not routinely o If sputum culture results are not available, empiric used for management of bronchiectasis exacerbations. antibiotic therapy is recommended, often with a fluo- Glucocorticoids (Option D) are not indicated in the roquinolone. treatment of bronchiectasis exacerbations in the absence of concomitant asthma or COPD, although they may be used in Bib[ograplry some patients with signiflcant bronchospasm. This patient Hill AT, SUIIi\xan AL, Chalmers JD, et al. British thoracic society guideline for bronchiectasis in adults. Thorax. 2019;74:l-69. [PMID: 30545985] has no indication for glucocorticoids. doi 10.1136/thoraxj il- 21la - 212463 : ut E (D UI o, n lt .D (n 174

lndex \ Note: Page numbers followed by fand t denote figure and table, respectively. or-Antitrypsin, 15 17, 20 Test questions are indicated by Q. Antitussives.20 Apnea-hypopnea index (AHl), 52-54 A Appendicitis, 87t ABCDEF Care Bundle. 60t Arformoterol for asthma, 12t Abdominal aortic aneurysm, 87t Asbestos-related pleuropulmonary disease, 341, 501, Q23 Abdominal surgical emergencies, 86 87 , 87t Ascending cholangitis, Q60 Abruptio placentae, 88t Ascites, respiratory mechanics and, 74 Acetaminophen toxicity, 86t Aspergillosis, 9, 23 Acetazolamide, 56, 57t Aspergillus spp., 9, 23 Acetylcholine receptor antibody tests, 50 Aspiration, bronchiectasis caused by, 22,231 Aclidinium, 121, 19t Aspiration pneumonitis, Q96 Active internal rewarming, Q79 Aspirin-exacerbated respiratory disease, 9 Acute cardiogenic pulmonary edema, 70 -71 Asthma, S-15 Acute fatty liver of pregnancy, 88t airway resistance and, 7 4 -7 5 Acute hypercapnic respiratory faihre, 61, 7 2 7 5, 7 2t, 7 3t bronchial challenge testing, 7-8, Q17 t Acute inhalational iniuries, 68 69 chronic,9-14 Acute interstitial pneumonia, 251, 261, 31 comorbidities, 11t Acute mountain sickness, 56-57 controller medications, l3 -14 Acute Physiologr and Chronic Health Evaluation, 58 epidemiolog/ of, 5-7 Acute respiratory distress syndrome (ARDS), 67 t, 69 -7 O, 69t exacerbations, 14, 141, Q102 acute interstitial pneumonia uersus, 31 fractional exhaled nitric oxide, Q93 amiodarone toxicity and, 28 GERD and,11, Q80 causes of, 69t management of, 9,7of,72t,14, Q6, Q13, Q85, Qr02 deflnition of 70t natural history of, 5-7 diagnosis ol Q21 pathogenesis of 7 DPLD and. 26t in pregnancy, L5 nonventilatory management in, 70 refractory 14 15 in pregnancy, 88t risk factors for, 7 radiographic flndings in, 67t symptoms o{ 7-9, Q85 treatment of, Q48 Asthma Control Test, 9, Q85 ventilatory management in, 69 70 Asthmatic triad, T Acute respiratory falfure, 67 75, 67f Atelectasis, 381,71, Q91, Q94 Acute upper airway management, 67-68 Atrial fibrillation, in PAH,43-44 Adaptive servo-ventilation, 55, 56t Atropine toxicity, 84t Adenocarcinomas, 39, 46- 47, 471 Azithromycin,22, Q14, Q50, Q75 Adenoid cystic carcinoma, 49 Adenosine deaminase, 39 B Air pollution Bakers'asthma,8, Q43 asthma risk and, 7 Bath salts, antidotes for, 85t COPD risk and, 15 Beclomethasone, 121, 191, Q6 Air travel Benfluorex,43t preflight screening, 58t Benign pleural effusions, 39-40 pulmonary disease and, 57 58, 57t Benralizumab, l2t, 13 safety for COPD patients, Q82 Benzodiazepines, 59-60, 811, 82, 851, 86t Airway edema, 68 Bilevel positive airway pressure (BPAP) Albuterol, 11, 121, 191, Q6 for cardiogenic pulmonary edema, 71 Alcohol poisoning, 82-83,831, Q90 for COPD, ss,74,Q67 Allrylating agents. PAH and. 431 effects and indications,62, 63t Allergic asthma, 8, Q24 in neuromuscular diseases, 56, 56t Allergic bronchopulmonary aspergillosis, 9. 23t for obesity hlpoventilation syndrome, 55, 73, Q49 Alveolar damage, 291, 69f for obstructive sleep apnea, 53-54 Ambrisentan for PAH, 44t Bleomycin, lung toxicity of, 29t Aminophylline, i9t,20 BODE index, 15, 16, 171, 27 Aminorex,43t Bosentan for PAH,44t Amiodarone, lung toxicity ol 28, 29t Bosutinib,43t Ammonia, inhaled exposure to, 69t Bowel distention, respiratory mechanics and, 74 Amniotic fluid emboli, 88t Bowel obstruction, 24, 87 t Analgesia in critical care patients, 59-60, 59t Bromocriptine, 8lt, 82 Anaphylaxis, 80 81, 80t, Q41 Bronchial cast formation. 68 Anaplastic lymphoma kinase receptor tyrosine kinase (ALK) Bronchial challenge testing, 1,7-8, Q17 translocation, 48 Bronchial hlperreactivity, 7-9 Anemia,35, Q76 Bronchial thermoplasty, 6t, 14 Angioedema, S0 81 Bronchial wall thickening, 23 Angiotensin, selection of, 66t Bronchiectasis, 22-24, 23f, 231, Q88, Q103 Anoxic brain injury 88-89 Bronchoconstriction, 8, 68, Q40 Antibiotics, in sepsis, 78-79, Q18, Q96 Bronchodilators, 7 , 78-20 , 181, 191, Q8 Antihistamines, toxicity of, 841, 86t Bronchoscopy, 3-5, 6t, 49, 71, Q9 Anti inflammatory agents, adverse effects of, 19t Bronchospasm, l, 9, 121, 19t, 69t Anti-Parkinson agents, toxicity ol 84t Budesonide, 11. , l2t, 79t Antisynthetase syndrome, 27 Budesonide-formoterol, 13, Q13, Q40

\ Note: Page numbers followed by fand t denote figure and table, respectively. or-Antitrypsin, 15 17, 20 Test questions are indicated by Q. Antitussives.20 Apnea-hypopnea index (AHl), 52-54 A Appendicitis, 87t ABCDEF Care Bundle. 60t Arformoterol for asthma, 12t Abdominal aortic aneurysm, 87t Asbestos-related pleuropulmonary disease, 341, 501, Q23 Abdominal surgical emergencies, 86 87 , 87t Ascending cholangitis, Q60 Abruptio placentae, 88t Ascites, respiratory mechanics and, 74 Acetaminophen toxicity, 86t Aspergillosis, 9, 23 Acetazolamide, 56, 57t Aspergillus spp., 9, 23 Acetylcholine receptor antibody tests, 50 Aspiration, bronchiectasis caused by, 22,231 Aclidinium, 121, 19t Aspiration pneumonitis, Q96 Active internal rewarming, Q79 Aspirin-exacerbated respiratory disease, 9 Acute cardiogenic pulmonary edema, 70 -71 Asthma, S-15 Acute fatty liver of pregnancy, 88t airway resistance and, 7 4 -7 5 Acute hypercapnic respiratory faihre, 61, 7 2 7 5, 7 2t, 7 3t bronchial challenge testing, 7-8, Q17 t Acute inhalational iniuries, 68 69 chronic,9-14 Acute interstitial pneumonia, 251, 261, 31 comorbidities, 11t Acute mountain sickness, 56-57 controller medications, l3 -14 Acute Physiologr and Chronic Health Evaluation, 58 epidemiolog/ of, 5-7 Acute respiratory distress syndrome (ARDS), 67 t, 69 -7 O, 69t exacerbations, 14, 141, Q102 acute interstitial pneumonia uersus, 31 fractional exhaled nitric oxide, Q93 amiodarone toxicity and, 28 GERD and,11, Q80 causes of, 69t management of, 9,7of,72t,14, Q6, Q13, Q85, Qr02 deflnition of 70t natural history of, 5-7 diagnosis ol Q21 pathogenesis of 7 DPLD and. 26t in pregnancy, L5 nonventilatory management in, 70 refractory 14 15 in pregnancy, 88t risk factors for, 7 radiographic flndings in, 67t symptoms o{ 7-9, Q85 treatment of, Q48 Asthma Control Test, 9, Q85 ventilatory management in, 69 70 Asthmatic triad, T Acute respiratory falfure, 67 75, 67f Atelectasis, 381,71, Q91, Q94 Acute upper airway management, 67-68 Atrial fibrillation, in PAH,43-44 Adaptive servo-ventilation, 55, 56t Atropine toxicity, 84t Adenocarcinomas, 39, 46- 47, 471 Azithromycin,22, Q14, Q50, Q75 Adenoid cystic carcinoma, 49 Adenosine deaminase, 39 B Air pollution Bakers'asthma,8, Q43 asthma risk and, 7 Bath salts, antidotes for, 85t COPD risk and, 15 Beclomethasone, 121, 191, Q6 Air travel Benfluorex,43t preflight screening, 58t Benign pleural effusions, 39-40 pulmonary disease and, 57 58, 57t Benralizumab, l2t, 13 safety for COPD patients, Q82 Benzodiazepines, 59-60, 811, 82, 851, 86t Airway edema, 68 Bilevel positive airway pressure (BPAP) Albuterol, 11, 121, 191, Q6 for cardiogenic pulmonary edema, 71 Alcohol poisoning, 82-83,831, Q90 for COPD, ss,74,Q67 Allrylating agents. PAH and. 431 effects and indications,62, 63t Allergic asthma, 8, Q24 in neuromuscular diseases, 56, 56t Allergic bronchopulmonary aspergillosis, 9. 23t for obesity hlpoventilation syndrome, 55, 73, Q49 Alveolar damage, 291, 69f for obstructive sleep apnea, 53-54 Ambrisentan for PAH, 44t Bleomycin, lung toxicity of, 29t Aminophylline, i9t,20 BODE index, 15, 16, 171, 27 Aminorex,43t Bosentan for PAH,44t Amiodarone, lung toxicity ol 28, 29t Bosutinib,43t Ammonia, inhaled exposure to, 69t Bowel distention, respiratory mechanics and, 74 Amniotic fluid emboli, 88t Bowel obstruction, 24, 87 t Analgesia in critical care patients, 59-60, 59t Bromocriptine, 8lt, 82 Anaphylaxis, 80 81, 80t, Q41 Bronchial cast formation. 68 Anaplastic lymphoma kinase receptor tyrosine kinase (ALK) Bronchial challenge testing, 1,7-8, Q17 translocation, 48 Bronchial hlperreactivity, 7-9 Anemia,35, Q76 Bronchial thermoplasty, 6t, 14 Angioedema, S0 81 Bronchial wall thickening, 23 Angiotensin, selection of, 66t Bronchiectasis, 22-24, 23f, 231, Q88, Q103 Anoxic brain injury 88-89 Bronchoconstriction, 8, 68, Q40 Antibiotics, in sepsis, 78-79, Q18, Q96 Bronchodilators, 7 , 78-20 , 181, 191, Q8 Antihistamines, toxicity of, 841, 86t Bronchoscopy, 3-5, 6t, 49, 71, Q9 Anti inflammatory agents, adverse effects of, 19t Bronchospasm, l, 9, 121, 19t, 69t Anti-Parkinson agents, toxicity ol 84t Budesonide, 11. , l2t, 79t Antisynthetase syndrome, 27 Budesonide-formoterol, 13, Q13, Q40 175

lndex Bum injuries, 68, 691, Q9 delirium prevention in, 60, Q1 : Busulfan, lung toxicity ol 29t early mobilization in, 60, 61, 66, Q1 hemodynamic support, 63 c hyperoxia prevention in, Q45 Caffeine toxicity, 84t intravenous access, 63-64, Q59 Calcium channel blockers, 43-44, 441,861 nutritional support in, 60, Q73 organization of 58-59 i Cancer, pleural effusions in, 39. See olso Lung cancers Cannabinoids, antidotes to, 85t patient evaluation in sepsis, Q55 Capnometry 55 pleural effusion in, Q71 Carbamate toxicity, 84t point-of-care ultrasonography, 75,77 , Q28 : Carbon monoxide poisoning, 62, 83-84 post-intensive care syndrome, 67 Carboxyhemoglobin, 83 84 principles ol 59 67 : Carcinoid tumors, 49-50 respiratory support, 6l - 62 Cardiogenic shock, 7 6 -77, 7 6t sedation in,59-61, 70, Q3l Cardiovascular disease, sleepiness and, 51 stress ulcer prophylaxis, 59, Q84 Central line associated bloodstream infections, 61t Critical illness myopatu 66, 671, 72t : Central sleep apnea (CSA) syndromes, 54-55, Q62, Q66, Q74 Critical illness neuromyopathy, 67t :

Carbon monoxide poisoning, 62, 83-84 post-intensive care syndrome, 67 Carboxyhemoglobin, 83 84 principles ol 59 67 : Carcinoid tumors, 49-50 respiratory support, 6l - 62 Cardiogenic shock, 7 6 -77, 7 6t sedation in,59-61, 70, Q3l Cardiovascular disease, sleepiness and, 51 stress ulcer prophylaxis, 59, Q84 Central line associated bloodstream infections, 61t Critical illness myopatu 66, 671, 72t : Central sleep apnea (CSA) syndromes, 54-55, Q62, Q66, Q74 Critical illness neuromyopathy, 67t : Central venous access, 65t Critical illness polyneuropathy, 66, 67t Cerebral edema, high-altitude-related, 57 Cryptogenic organizing pneumonia (COP), 31 ) Charcot triad, Q60 Crystalloid solution, sepsis treatment with, 61, 78, Q35 Chemical injuries, 68, 69t CURB 65,58 Chest radiogaphy, 4,41 Cushing syndrome,4S Cheyne-Stokes breathing, 54, 55 qenide poisoning, 84-85 Chlorine, inhaled exposure to, 69t Cystic fibrosis (CF), 231, 24 25, 40t, Qs6 Cholangitis, STt, Q6o Clstic fibrosis transmembrane conductance regulator (CFTR) gene,24, Q56 Cholerystitis, 87t Cysts, bronchial,23 Cholesterol, pleural fluid, 37, 38t Cholinesterase inhibitors, inhaled exposure to, 69t D Choosing Wisely- campaign, 61 Dantrolene, 38t,811, 82, Q65 Chronic beryllium disease (CBD), 34t Dasatinib, 381, 43t Chronic noctumal hlpoxia, 45 Dead space, increased, 72-74,72t Chronic obstructive pulmonary disease (COPD), 15 22 Decreased respiratory dive, 7 2, 72t, 73 acute exacerbations, 21 -22 Delirium,60, 601, Q1 air travel safeg for patients with, Q82 Depression, montelukast associated, Q58 airway resistance end,, 7 4 -7 5 Dermatomyositis, 28t assessment, 16-17 Desquamative interstitial pneumonia (DIP), 251, 261, 27 azithromycin for, 18t,22, Q14, Q75 Dexfenfluramine, 43t comorbid conditions, 16 Dexmedetomidine, 59, 59t diagnosis, l6 Dextromethorphan antidotes, 85t epidemiolory of, 15 Diaphragm, ultrasono$aphy ol 5 exacerbation with glucocorticoids, Q64 Diet, asthma care and, 14 heterogeneity ol 15-16 Difftrse parenchymal lung disease (DPLD), 25-33, Q20 lung volume reduction surgery in, 21, Q44 causes of, 27-31 management of 17 27,18t,191, Q8, Q87 classification of 25t oxygen therapy for hypoxemia, Q1l connective tissue diseases and, 28t pathophysiolory of, 15 CT scanning, 26-27 prevention of exacerbations, 22 diagrosis, 25 - 27, 26t, Q26 prognosis in, 17t drug-induced, 28, 29t pulmonary rehabilitation for, 20, Q63 features of occupational lung disease, 34t risk factors for, 15 ICU and,71 roflumilast for, 18t, 191, 20, 22, Q14, Q50 Digoxin toxiciry 86t severity of, 17t Distributive shock, 66t, 7 6, 7 6l sleep-related hypoventilation and, 55 Diuretics for PAH, 43-44 smoking cessation h, 17, 22, Q87 Dobutamine, 66t,78 spirometry use and, Q97 Dopamine, 661,78 Chronic thromboembolic pulmonary hlpertension (CIEPH), 44-45, Drugs ofabuse, 85 86, 85t Ql0, Ql01 Dupilumab, 121, 14 Chylothorax, 371, 39, Q32 Dust-related pneumoconiosis, 34t Ciclesonide, 12t, 19t Dysautonomia, 74, 82 Circadian rhythm disruption, 511, 52 Dyspnea scale,15, 161, 17t Clubbing, 23, 30,48f, 68, Q30, Q33 Cocaine, 431, 841, 85t E Cognitive impairment, long-term, 66 Echocardiography, 47, 42f, 75, 881, Q37, Q72 Coma,87-88,89t E cigarefte or vaping-associated lung injury (EVALI), 68-69 C-ombined pulmonary fibrosis and emphysema (CPFE), 31, 321 Qs Eclampsia,8St Common variable immunodeficiency, 23t Ectopic pregnancy, 87t Computed tomography (Cl) Edrophonium toxicity, 84t ofthe chest, types, 4-5, 4t Electromyogam testing, 66 DPLD diagnosis using, Q26, Q33 Emphysema, 16, 20, 21, 31, 321 Q5, Q44. See olso Chronic obstructive lung cancer evaluation using, Q51 pulmonary disease (COPD) pulrnonary imaging, 3 5 Empyema, 14f, 141, 381, 39 for pulmonary nodule evaluation, 4, Q99 Encephalopathy, 87-89 Confusion Assessment Methodlcu, 60 Endobronchial carcinoids, 49f Connective tissue disease (CTD),26, 27, 28t, Q83 Endobronchial ultrasonography, 5, 6t Constrictive pericarditis, 381, 76t End-organ hy,popeffusion, 75, 75f Continuous positive airway pressure (CPAP), 561, 63t Endothelin 1 antagonists, 44t Cor pulmonale, 2O, 26 Endotracheal intubation, airway protection in, Q42 Cough variant asthma, 8 Enteral nutrition, 60, 79-80, Q73, Q92 Critical care medicine. See also Intensive care units (lCUs) Eosinophilia, 3, 7 -9, 73 14, 25t, 29t blood pressure support, 65-66 Ephedrine toxiciry 84t common ICU conditions. 67-80 Epidermal growth factor receptor (EGFR) mutation,4T complications, 66-67 Epinephrine, 661, 78, 80t, Q4l

Central venous access, 65t Critical illness polyneuropathy, 66, 67t Cerebral edema, high-altitude-related, 57 Cryptogenic organizing pneumonia (COP), 31 ) Charcot triad, Q60 Crystalloid solution, sepsis treatment with, 61, 78, Q35 Chemical injuries, 68, 69t CURB 65,58 Chest radiogaphy, 4,41 Cushing syndrome,4S Cheyne-Stokes breathing, 54, 55 qenide poisoning, 84-85 Chlorine, inhaled exposure to, 69t Cystic fibrosis (CF), 231, 24 25, 40t, Qs6 Cholangitis, STt, Q6o Clstic fibrosis transmembrane conductance regulator (CFTR) gene,24, Q56 Cholerystitis, 87t Cysts, bronchial,23 Cholesterol, pleural fluid, 37, 38t Cholinesterase inhibitors, inhaled exposure to, 69t D Choosing Wisely- campaign, 61 Dantrolene, 38t,811, 82, Q65 Chronic beryllium disease (CBD), 34t Dasatinib, 381, 43t Chronic noctumal hlpoxia, 45 Dead space, increased, 72-74,72t Chronic obstructive pulmonary disease (COPD), 15 22 Decreased respiratory dive, 7 2, 72t, 73 acute exacerbations, 21 -22 Delirium,60, 601, Q1 air travel safeg for patients with, Q82 Depression, montelukast associated, Q58 airway resistance end,, 7 4 -7 5 Dermatomyositis, 28t assessment, 16-17 Desquamative interstitial pneumonia (DIP), 251, 261, 27 azithromycin for, 18t,22, Q14, Q75 Dexfenfluramine, 43t comorbid conditions, 16 Dexmedetomidine, 59, 59t diagnosis, l6 Dextromethorphan antidotes, 85t epidemiolory of, 15 Diaphragm, ultrasono$aphy ol 5 exacerbation with glucocorticoids, Q64 Diet, asthma care and, 14 heterogeneity ol 15-16 Difftrse parenchymal lung disease (DPLD), 25-33, Q20 lung volume reduction surgery in, 21, Q44 causes of, 27-31 management of 17 27,18t,191, Q8, Q87 classification of 25t oxygen therapy for hypoxemia, Q1l connective tissue diseases and, 28t pathophysiolory of, 15 CT scanning, 26-27 prevention of exacerbations, 22 diagrosis, 25 - 27, 26t, Q26 prognosis in, 17t drug-induced, 28, 29t pulmonary rehabilitation for, 20, Q63 features of occupational lung disease, 34t risk factors for, 15 ICU and,71 roflumilast for, 18t, 191, 20, 22, Q14, Q50 Digoxin toxiciry 86t severity of, 17t Distributive shock, 66t, 7 6, 7 6l sleep-related hypoventilation and, 55 Diuretics for PAH, 43-44 smoking cessation h, 17, 22, Q87 Dobutamine, 66t,78 spirometry use and, Q97 Dopamine, 661,78 Chronic thromboembolic pulmonary hlpertension (CIEPH), 44-45, Drugs ofabuse, 85 86, 85t Ql0, Ql01 Dupilumab, 121, 14 Chylothorax, 371, 39, Q32 Dust-related pneumoconiosis, 34t Ciclesonide, 12t, 19t Dysautonomia, 74, 82 Circadian rhythm disruption, 511, 52 Dyspnea scale,15, 161, 17t Clubbing, 23, 30,48f, 68, Q30, Q33 Cocaine, 431, 841, 85t E Cognitive impairment, long-term, 66 Echocardiography, 47, 42f, 75, 881, Q37, Q72 Coma,87-88,89t E cigarefte or vaping-associated lung injury (EVALI), 68-69 C-ombined pulmonary fibrosis and emphysema (CPFE), 31, 321 Qs Eclampsia,8St Common variable immunodeficiency, 23t Ectopic pregnancy, 87t Computed tomography (Cl) Edrophonium toxicity, 84t ofthe chest, types, 4-5, 4t Electromyogam testing, 66 DPLD diagnosis using, Q26, Q33 Emphysema, 16, 20, 21, 31, 321 Q5, Q44. See olso Chronic obstructive lung cancer evaluation using, Q51 pulmonary disease (COPD) pulrnonary imaging, 3 5 Empyema, 14f, 141, 381, 39 for pulmonary nodule evaluation, 4, Q99 Encephalopathy, 87-89 Confusion Assessment Methodlcu, 60 Endobronchial carcinoids, 49f Connective tissue disease (CTD),26, 27, 28t, Q83 Endobronchial ultrasonography, 5, 6t Constrictive pericarditis, 381, 76t End-organ hy,popeffusion, 75, 75f Continuous positive airway pressure (CPAP), 561, 63t Endothelin 1 antagonists, 44t Cor pulmonale, 2O, 26 Endotracheal intubation, airway protection in, Q42 Cough variant asthma, 8 Enteral nutrition, 60, 79-80, Q73, Q92 Critical care medicine. See also Intensive care units (lCUs) Eosinophilia, 3, 7 -9, 73 14, 25t, 29t blood pressure support, 65-66 Ephedrine toxiciry 84t common ICU conditions. 67-80 Epidermal growth factor receptor (EGFR) mutation,4T complications, 66-67 Epinephrine, 661, 78, 80t, Q4l 176

lndex t Epoprostenol for PAH, 44t Hypoxemia,61, Q11, Q46 Epworth Sleepiness Scale,45, 51 Hypoxemic respiratory failure, 68, 71, Q86 Ethanol,83,83t Ethylene glycol, 83, 831, Q54 I Evidence-based care protocols, 59 ICU. See Critical care medicine; Intensive care units (lCUs) Excessive daytime sleepiness, 51-52, 51t ICU care bundles, 601, 6l, 6lt Exercise ICU-acquired weakness, 66, 671, 73 6-minute walk test. 2 Idiopathic hypersomnia, 51 \ asthma care and, 14 Idiopathic pulrnonary fibrosis (lPF), 251, 261, 30, 30f, Q30, Q33 pulmonary rehabilitation, 20 Iloprost for PAH, 44t Exercise induced bronchoconstriction (EIB), 8, Q+O Immunizations for COPD patients, 20 Extubation, 62-63, 64t, 65t lmmunoglobulin measurement, Q88 Immunosuppression for NSIP, 30 31 t Inappropriate antidiuretic hormone secretion, 48 Fat embolism, 69,87, Q100 Indacaterol maleate, 121, 19t Fenoterol, adverse effects ol 19t lndirubin, PAH and,43t Fentanyl,84t, 85t Inflammatory bowel disease, 23t Fluid resuscitation, 76, 78 Inhaled agents, 69t Flumazenil, SS Inotropes, selection ol 66t Flunisolide for asthma, 12t Inspiratory squawks, 26 Ruticasone, 121, 19t, 88t Inspiratory Velcro crackles,26, 30, Q30 Fomepizole, 83, 831, Q54 Insufficient sleep syndrome, 51-52 Formoterol, l0t, 11,121,19t, Q6, Q13 Intensive Care Delirium Screening Checklist, 60 Fractional exhaled nitric oxide (FeNO), 3, 7, Q93 Intensive care units (lCUs),58-59, 67 80, Q31, Q7t. Seealso Critical care medicine G Interferons, PAH and, 43t Gastroesophageal reflux disease (GERD), 111, Q80 Interstitial lung disease (lLD), 261, 27, 30-31, Q83 Gastrointestinal bleeding, Q53 Interstitial pneumonia, 26t Germ cell tumors. 50 Intraosseous devices, 63 64 Glasgow Coma Scale,87, 89t Intrauterine infections, 88t Glucocorticoids Ipratropium, 121, 19t in asthma treatment, lof, 121, 13 15 Isopropyl alcohol, 83, 83t for COPD exacerbation, Q64 inhaled,13,20,23, Q6 J oral, 20 Jet lag,52 for refractory septic shock, Q57 Glucose intolerance, sleepiness and, 51 t Glycopyrrolate, 12t, 1 9t LABAs (long-acting p, agonists), 13, 18, 20, Q13 GOLD model, 171, 21, Q50 Lactated Ringer solution, Q35 Gottron papules, 26 LAMAs (long-acting muscarinic agents), 18, 181, 20 Guillain Barrd syndrome, 74, Q95 Large cell carcinoma, 47, 47f Leflunomide,43t H Levalbuterol, 121, 19t Haemophilus infl ue nzae, 22 Light therapy, 52 Haldane effect, 73, 74 Light's criteria, 36 Hallucinogens, antidotes for, 85t Limited cutaneous systemic sclerosis, 43 Haloperidol,82 Lithium toxicity of, 86t Hamartomas,49 Lorazepam, antidotes for, 85t Heart failure, 38t,41,70-71, Q78, Q98 Lung biopsies, 27 Heat stroke, 81,811, Q4 Lung cancers, 341,47-50, Q7, Q51, Q69 Hemodialysis, Q54 Lung sliding sign, 5 Hemorrhages, 6t, 28t, 72, 76, 881, Q53 Lung transplantation, 21 Hepatitis C antiviral therapies, 43t Lung tumors, 45-47 Heroin,84t,85t Lung ultrasonography, 5 High resolution Cl (HRCI),26 32,26t,Q26 Lung volume reduction surgery Q44 High altitude cerebral edema, 57 Lung volume reduction therapy, 21 High-altitude pulmonary edema (HAPE), 57, Q34 Lymphoma,39 High-altitude related illnesses, 56-58, 57t Lysergic acid diethylamide, 85t High-flow nasal cannulas (HFNC), 62, Q86 HIV bronchiectasis caused by, 23t M Honeycombing, 251, 30, 301 Q33 Macitentan for PAH. 44t Hospice care, decision making on, 21 Macrophages, protease release by, 15 Hour-l care bundle for sepsis, 611, Q68 Malignant hyperthermia, 8l-82, 811, Q65 Hypercapnic respiratory failure, 72 -73, 72t, 73t Malignant pleural effusion, 39, Q15, Q91 Hyperoxia, prevention in critical care, Q45 Malnutrition in critical care patients, Q73 Hypersensitivities, 23t, 27 -28 Maxillomandibular advancement, 54 Hypersensitivity pneumonitis (HP\, 27 28, 341, Q89 Mediastinal masses, 50-51 Hypertension Meigs syndrome, 38t glucocorticoids and, 121, 19t Melatonin,52 obstetric emergencies, 88t (See olso Portopulmonary hypertension; Mepolizumab, 121, 13 Pulmonary arterial hypertension (PAH); Pulmonary Mesenteric ischemia, 87t hypertension (PH)) Mesothelioma, 39, 50, Q23. Q81 Hyperthermic emergencies, 81-82, 81t Metabolic syndrome, 51 Hypertrophic pulmonary osteoarthropathy (HPOA), 48f Metal induced lung disease. 341 Hlperventilation, 54 Metaproterenol, 19t Hlpoalbuminemia, 35t, 38t Metformin toxicity, 86t Hypoglossal nerve simulator, 54 Methamphetamines, 43t, 85t Hlponatremia, paraneoplastic, 48 Methanol,83, 83t Hlpoperfusion, clinical signs of, 75f Methemoglobin, 84 Hypopneas,52 Methicillin-resistant S. oureus (MRSA), 24 Hypothermia, 82, 821, Q79 Methotrexate toxicity, 29t Hypovolemic shock. 7 6, 7 6t Methylprednisolone, 12t

t Epoprostenol for PAH, 44t Hypoxemia,61, Q11, Q46 Epworth Sleepiness Scale,45, 51 Hypoxemic respiratory failure, 68, 71, Q86 Ethanol,83,83t Ethylene glycol, 83, 831, Q54 I Evidence-based care protocols, 59 ICU. See Critical care medicine; Intensive care units (lCUs) Excessive daytime sleepiness, 51-52, 51t ICU care bundles, 601, 6l, 6lt Exercise ICU-acquired weakness, 66, 671, 73 6-minute walk test. 2 Idiopathic hypersomnia, 51 \ asthma care and, 14 Idiopathic pulrnonary fibrosis (lPF), 251, 261, 30, 30f, Q30, Q33 pulmonary rehabilitation, 20 Iloprost for PAH, 44t Exercise induced bronchoconstriction (EIB), 8, Q+O Immunizations for COPD patients, 20 Extubation, 62-63, 64t, 65t lmmunoglobulin measurement, Q88 Immunosuppression for NSIP, 30 31 t Inappropriate antidiuretic hormone secretion, 48 Fat embolism, 69,87, Q100 Indacaterol maleate, 121, 19t Fenoterol, adverse effects ol 19t lndirubin, PAH and,43t Fentanyl,84t, 85t Inflammatory bowel disease, 23t Fluid resuscitation, 76, 78 Inhaled agents, 69t Flumazenil, SS Inotropes, selection ol 66t Flunisolide for asthma, 12t Inspiratory squawks, 26 Ruticasone, 121, 19t, 88t Inspiratory Velcro crackles,26, 30, Q30 Fomepizole, 83, 831, Q54 Insufficient sleep syndrome, 51-52 Formoterol, l0t, 11,121,19t, Q6, Q13 Intensive Care Delirium Screening Checklist, 60 Fractional exhaled nitric oxide (FeNO), 3, 7, Q93 Intensive care units (lCUs),58-59, 67 80, Q31, Q7t. Seealso Critical care medicine G Interferons, PAH and, 43t Gastroesophageal reflux disease (GERD), 111, Q80 Interstitial lung disease (lLD), 261, 27, 30-31, Q83 Gastrointestinal bleeding, Q53 Interstitial pneumonia, 26t Germ cell tumors. 50 Intraosseous devices, 63 64 Glasgow Coma Scale,87, 89t Intrauterine infections, 88t Glucocorticoids Ipratropium, 121, 19t in asthma treatment, lof, 121, 13 15 Isopropyl alcohol, 83, 83t for COPD exacerbation, Q64 inhaled,13,20,23, Q6 J oral, 20 Jet lag,52 for refractory septic shock, Q57 Glucose intolerance, sleepiness and, 51 t Glycopyrrolate, 12t, 1 9t LABAs (long-acting p, agonists), 13, 18, 20, Q13 GOLD model, 171, 21, Q50 Lactated Ringer solution, Q35 Gottron papules, 26 LAMAs (long-acting muscarinic agents), 18, 181, 20 Guillain Barrd syndrome, 74, Q95 Large cell carcinoma, 47, 47f Leflunomide,43t H Levalbuterol, 121, 19t Haemophilus infl ue nzae, 22 Light therapy, 52 Haldane effect, 73, 74 Light's criteria, 36 Hallucinogens, antidotes for, 85t Limited cutaneous systemic sclerosis, 43 Haloperidol,82 Lithium toxicity of, 86t Hamartomas,49 Lorazepam, antidotes for, 85t Heart failure, 38t,41,70-71, Q78, Q98 Lung biopsies, 27 Heat stroke, 81,811, Q4 Lung cancers, 341,47-50, Q7, Q51, Q69 Hemodialysis, Q54 Lung sliding sign, 5 Hemorrhages, 6t, 28t, 72, 76, 881, Q53 Lung transplantation, 21 Hepatitis C antiviral therapies, 43t Lung tumors, 45-47 Heroin,84t,85t Lung ultrasonography, 5 High resolution Cl (HRCI),26 32,26t,Q26 Lung volume reduction surgery Q44 High altitude cerebral edema, 57 Lung volume reduction therapy, 21 High-altitude pulmonary edema (HAPE), 57, Q34 Lymphoma,39 High-altitude related illnesses, 56-58, 57t Lysergic acid diethylamide, 85t High-flow nasal cannulas (HFNC), 62, Q86 HIV bronchiectasis caused by, 23t M Honeycombing, 251, 30, 301 Q33 Macitentan for PAH. 44t Hospice care, decision making on, 21 Macrophages, protease release by, 15 Hour-l care bundle for sepsis, 611, Q68 Malignant hyperthermia, 8l-82, 811, Q65 Hypercapnic respiratory failure, 72 -73, 72t, 73t Malignant pleural effusion, 39, Q15, Q91 Hyperoxia, prevention in critical care, Q45 Malnutrition in critical care patients, Q73 Hypersensitivities, 23t, 27 -28 Maxillomandibular advancement, 54 Hypersensitivity pneumonitis (HP\, 27 28, 341, Q89 Mediastinal masses, 50-51 Hypertension Meigs syndrome, 38t glucocorticoids and, 121, 19t Melatonin,52 obstetric emergencies, 88t (See olso Portopulmonary hypertension; Mepolizumab, 121, 13 Pulmonary arterial hypertension (PAH); Pulmonary Mesenteric ischemia, 87t hypertension (PH)) Mesothelioma, 39, 50, Q23. Q81 Hyperthermic emergencies, 81-82, 81t Metabolic syndrome, 51 Hypertrophic pulmonary osteoarthropathy (HPOA), 48f Metal induced lung disease. 341 Hlperventilation, 54 Metaproterenol, 19t Hlpoalbuminemia, 35t, 38t Metformin toxicity, 86t Hypoglossal nerve simulator, 54 Methamphetamines, 43t, 85t Hlponatremia, paraneoplastic, 48 Methanol,83, 83t Hlpoperfusion, clinical signs of, 75f Methemoglobin, 84 Hypopneas,52 Methicillin-resistant S. oureus (MRSA), 24 Hypothermia, 82, 821, Q79 Methotrexate toxicity, 29t Hypovolemic shock. 7 6, 7 6t Methylprednisolone, 12t 177

lndex Methylxanthines, 20 P Mixed connective tissue disease. 28t Packed red blood cells (PRBCs), Q53 Mobilization Pain rehabilitation programs, Q74 weakness and, 66 Paralltic agents,70 Mobilization issues, 60-61, Q1 Paraneoplastic syndromes, 48 Modafinil,52 Parapneumonic efTrrsions and empyema, 39, Q39 Mometasone, 121, 19t Parenchlnnal lung disease, 291, Q20 Montelukast, l2t, 15, Q58 Parenteral nutrition. 60 Moroxella catarrhalis, 22 PEEP,69 70 Morphine toxicity, 84t Peptic ulcer perforation, 87t Mounier Kuhn syndrome, 23t Peributerol, adverse effects of, 19t Mucolytics,20 Peripartum cardiomyopathy, 88t Multiple sleep latency tests, 51 Peripheral venous access, 63 Mustard gas, inhaled exposure to, 69t Peritoneal dialysis, 38t Myasthenia gravis, 50 PET/CI, 4r, s. 46, 49, Q47 Myasthenic crisis,74 Phencyclidine. antidotes fo! 85t Mycoplasmo pneumoniae, 22 Phenylephrine, 661,78 Myxedema,38t Phenylpropanolamine, 43t Phosgene, inhaled exposure to, 69t il Phosphodiesterase 4 inhibitors, 19t Narcolepsy,5l Phosphodiesterase-5 inhibitors, 44t Nasal cannula, high-flow 62, Q86 Physostigmine toxicity, 84t Nasal end-expiratory positive airway pressure device, 54 Pirfenidone,30 Nephrotic slndrome, 38t Placenta previa, 88t Neuroleptic malignant syndrome, 811, 82, Ql9 Pleural catheters, Q15 Neuromuscular blockade, prolonged, 67t Pleuraldiseases,35 41 Neuromuscular diseases, 56 Pleural effusion.35-40 Neuromuscular weakness, 73 74, 74t, Q95 chylorax,3S-40 Neutropenic sepsis, Q18 evaluation of, 35-36 Neutrophils, protease release by, 15 exudative,3St Nicotine replacement therapy, 17 in ICU care, Q71 Nicotine toxicity, 84t imaglng, 35-36,36f Nintedanib.30 physical examination, 35-36, 35t Nitrites, 34 transudates. 38t Nitrofurantoin, toxicity ol 29t ultrasound, 36f, 37f Noninvasive positive pressure ventilation (NPPV), 21, 22, Pleural fluid analysis, 36-39, 371, 381, Q91 62-63.63t Pleurodesis for pneumothorax, Q4 Non-small cell lung cancer (NSCLC),47,49 Pneumococcal pollsaccharide laccine (PPSV23), 20 Nonspecific interstitial pneumonia (NSIP), 30-31 Pneumoconiosis, 34 Nonspecific pulmonary fibrosis (NSPF), 30-31, 30f Pneumonia Nontuberculous mycobacteria, 23t ARDS and,71 Norepinephrine, 661, 78 bronchiectasis caused by, 23t Nutritional support in critical care medicine, Q73, Q92 in pregnanry,88t ventilator-associated, 61t o Pneumonia Severity lndex, 58 Obesity, ut,51 Pneumothorax, 40, 401 401,41, 58, Q3 Obesity hypoventilation syndrome (OHS), 55-56,73, Q49 Polymyositis, 28t Obstetric emergencies. See Pregnanry Pollsomnography, 111, 45, 53-56, Q62 Obstructive lung diseases, 74-75 Portopulmonary hypertension, 43 Obstructive shock, 7 6t, 77 Positive airway pressure therapy, 53-54, 561, Q38. See olso Bilevel Obstructive sleep apnea (OSA), 52-54. See olso Sleep apnea positive ain4ay pressure (BPAP); Continuous positive asthma and, l1t airway pressure (CPAP) clinical features, 53 Post-intensive care slmdrome, 67 diagnosis ol Q46, Q62 Postpyloric feeding, 60 oral appliances, Q2 Prednisolone, 121, 191, Q64 pathophlsiolory ol 52 Prednisone. 12t risk factors, 53 Preeclampsia, S8t, Q7/ treatment, S3-54 Pregnancy Occupational asthma, 8-9, 341, Q43 asthma in. 15 Occupational lung diseases, 33-35 critically ill patients, 87, 88 evaluation oi Q25 obstetric critical care emergencies, 88t exposure histories, 33 34 PAH issues in, 43-44 features of, 34t preeclampsia in, Q7/ management of,34 35 pulmonary emboli in, Q27 screening questionnaire, 33t Primary ciliary dyskinesia, 23t spontaneous pneumothorax and, Q3 Prone positioning in ARDS, Qa8 surveillance, 35 Propofol,59 Olodaterol, 12t,19t Prostacyclin analogues, 44t Omalizumab, 72t,13,14 Prostacyclin receptor agonist, 44t Omeprazole for GERD, Q81 Pse udomonas ae ruginosa, 23, 24 Opioid related sleep apnea, Q74 Pulmonary arterial hlpertension (PAH), 41 44 Opioids, 54,85t diagnosis, 421 43 Oral appliances, 54 drugs and toxins associated with, 43t Organizing pneumonia, 261, 31 idiopathic,41f Organophosphates, 691, 84t management of, 43-44, 44t Osborne waves,82f pleural effusions and, 38t Oxidative stress,15 Pulmonary artery catheters. 63 Oximeters, function of, 3 Pulmonary disease, air travel in, 57 58, 57t Orycodone, 841, 85t Pulmonary edema, 57 ,70-71,88t Oxygen therapy, 20, 22, 62, Q11, Q86 Pulmonary embolism (PE), 72 Oxyhemoglobin, 83-84 in pregnancy, Q27 Oryhemoglobin desaturations, 52 Pulmonary Embolism Severity lndex, 58

Methylxanthines, 20 P Mixed connective tissue disease. 28t Packed red blood cells (PRBCs), Q53 Mobilization Pain rehabilitation programs, Q74 weakness and, 66 Paralltic agents,70 Mobilization issues, 60-61, Q1 Paraneoplastic syndromes, 48 Modafinil,52 Parapneumonic efTrrsions and empyema, 39, Q39 Mometasone, 121, 19t Parenchlnnal lung disease, 291, Q20 Montelukast, l2t, 15, Q58 Parenteral nutrition. 60 Moroxella catarrhalis, 22 PEEP,69 70 Morphine toxicity, 84t Peptic ulcer perforation, 87t Mounier Kuhn syndrome, 23t Peributerol, adverse effects of, 19t Mucolytics,20 Peripartum cardiomyopathy, 88t Multiple sleep latency tests, 51 Peripheral venous access, 63 Mustard gas, inhaled exposure to, 69t Peritoneal dialysis, 38t Myasthenia gravis, 50 PET/CI, 4r, s. 46, 49, Q47 Myasthenic crisis,74 Phencyclidine. antidotes fo! 85t Mycoplasmo pneumoniae, 22 Phenylephrine, 661,78 Myxedema,38t Phenylpropanolamine, 43t Phosgene, inhaled exposure to, 69t il Phosphodiesterase 4 inhibitors, 19t Narcolepsy,5l Phosphodiesterase-5 inhibitors, 44t Nasal cannula, high-flow 62, Q86 Physostigmine toxicity, 84t Nasal end-expiratory positive airway pressure device, 54 Pirfenidone,30 Nephrotic slndrome, 38t Placenta previa, 88t Neuroleptic malignant syndrome, 811, 82, Ql9 Pleural catheters, Q15 Neuromuscular blockade, prolonged, 67t Pleuraldiseases,35 41 Neuromuscular diseases, 56 Pleural effusion.35-40 Neuromuscular weakness, 73 74, 74t, Q95 chylorax,3S-40 Neutropenic sepsis, Q18 evaluation of, 35-36 Neutrophils, protease release by, 15 exudative,3St Nicotine replacement therapy, 17 in ICU care, Q71 Nicotine toxicity, 84t imaglng, 35-36,36f Nintedanib.30 physical examination, 35-36, 35t Nitrites, 34 transudates. 38t Nitrofurantoin, toxicity ol 29t ultrasound, 36f, 37f Noninvasive positive pressure ventilation (NPPV), 21, 22, Pleural fluid analysis, 36-39, 371, 381, Q91 62-63.63t Pleurodesis for pneumothorax, Q4 Non-small cell lung cancer (NSCLC),47,49 Pneumococcal pollsaccharide laccine (PPSV23), 20 Nonspecific interstitial pneumonia (NSIP), 30-31 Pneumoconiosis, 34 Nonspecific pulmonary fibrosis (NSPF), 30-31, 30f Pneumonia Nontuberculous mycobacteria, 23t ARDS and,71 Norepinephrine, 661, 78 bronchiectasis caused by, 23t Nutritional support in critical care medicine, Q73, Q92 in pregnanry,88t ventilator-associated, 61t o Pneumonia Severity lndex, 58 Obesity, ut,51 Pneumothorax, 40, 401 401,41, 58, Q3 Obesity hypoventilation syndrome (OHS), 55-56,73, Q49 Polymyositis, 28t Obstetric emergencies. See Pregnanry Pollsomnography, 111, 45, 53-56, Q62 Obstructive lung diseases, 74-75 Portopulmonary hypertension, 43 Obstructive shock, 7 6t, 77 Positive airway pressure therapy, 53-54, 561, Q38. See olso Bilevel Obstructive sleep apnea (OSA), 52-54. See olso Sleep apnea positive ain4ay pressure (BPAP); Continuous positive asthma and, l1t airway pressure (CPAP) clinical features, 53 Post-intensive care slmdrome, 67 diagnosis ol Q46, Q62 Postpyloric feeding, 60 oral appliances, Q2 Prednisolone, 121, 191, Q64 pathophlsiolory ol 52 Prednisone. 12t risk factors, 53 Preeclampsia, S8t, Q7/ treatment, S3-54 Pregnancy Occupational asthma, 8-9, 341, Q43 asthma in. 15 Occupational lung diseases, 33-35 critically ill patients, 87, 88 evaluation oi Q25 obstetric critical care emergencies, 88t exposure histories, 33 34 PAH issues in, 43-44 features of, 34t preeclampsia in, Q7/ management of,34 35 pulmonary emboli in, Q27 screening questionnaire, 33t Primary ciliary dyskinesia, 23t spontaneous pneumothorax and, Q3 Prone positioning in ARDS, Qa8 surveillance, 35 Propofol,59 Olodaterol, 12t,19t Prostacyclin analogues, 44t Omalizumab, 72t,13,14 Prostacyclin receptor agonist, 44t Omeprazole for GERD, Q81 Pse udomonas ae ruginosa, 23, 24 Opioid related sleep apnea, Q74 Pulmonary arterial hlpertension (PAH), 41 44 Opioids, 54,85t diagnosis, 421 43 Oral appliances, 54 drugs and toxins associated with, 43t Organizing pneumonia, 261, 31 idiopathic,41f Organophosphates, 691, 84t management of, 43-44, 44t Osborne waves,82f pleural effusions and, 38t Oxidative stress,15 Pulmonary artery catheters. 63 Oximeters, function of, 3 Pulmonary disease, air travel in, 57 58, 57t Orycodone, 841, 85t Pulmonary edema, 57 ,70-71,88t Oxygen therapy, 20, 22, 62, Q11, Q86 Pulmonary embolism (PE), 72 Oxyhemoglobin, 83-84 in pregnancy, Q27 Oryhemoglobin desaturations, 52 Pulmonary Embolism Severity lndex, 58 178

lndex Pulmonary fibrosis patient evaluation in. Q12 acute respimtory failure and, 67t transthoracic echocardiography in, Q72 asbestos and, 34t Short-acting P, agonist (SABA),8,11, 18 DPLD and, 25t,26t,77 Sildenafil for PAH, 44t idiopathic, 27,30 37,301 321 Q30 Simplified Acute Physiolos/ Score, 58 Pulmonary fibrosis and emphysema, combined (CPFE), 31, 32f, e5 Sinus disease, asthlna and, 11t Pulmonary function testing, 1-3, 1t, 2f 6-minute walk test. 2 Pulmonary hypertension (PH), 26, 4t 45 Sjdgren s syndrome, 231, 28t classiflcation ol 41t Sleep apnea, Q62. Q74. See olso Obstructive sleep apnea (OSA); Central sleep diagnosis of, Q78, Q98 apnea (CSA) s_!ndromes evaluation of, 42f, 45, Q37 Sleep hygiene, 51 Pulmonary imaging, 3-5, 4t Sleep medicine, 51-56 Pulmonary I-angerhans cell histiocltosis (PLCH), 27 Sleep disordered breathing, 45 Pulmonary nodules, 45-47, 46f, 46t, Q7, Q36, Q47, Q99 Sleepiness, daltime. 51 52, 51t Pulmonary rehabilitation, 20, Q63 Sleep-related hypoventilation syndromes, 55 56, 55t Pulmonary sarcoidosis, Q16 Small cell lung cancer (SCLC), 47, 48f, Q29 Pulmonary vascular disease, 41 45 Smoking Pulse oximetry 3 asthma and, 14. 15 abnormal readings, Q52 cessation o{ 17, Q87 in airway obstruction, 68 DPLD and. 27 in carbon monoxide poisoning, 83-84 lung cancer and, 48 in ICU,67 parenchymal lung disease and, Q20 overnight,53 Smoking-related interstitial fibrosis (SRIF), 27 oxygen saturation and' 20, 22 Sodium thiosulfate, 84 preflight screening, 58t Spinal cord injuries, 74 at rest, 16, 26 Spirometry 1,7,Q97 Pure red cell aplasia, 50 Spontaneous breathing trials, 65t Spontaneous pneumothorax, 40, 40t, Q3 o Squamous cell carcinomil, 39, 47,47f qSOFA scores, 77, 77t St. lohn's wort, 43t Q/V mismatch, T2t Status asthmaticus. E8t Steam inhalation, 68 R Streptococcus onginosu.s. 39 Radiation pneumonitis, 28-29, Q70 Streptococcus oureus, 24. 39 Rapeseed oil, 43t St reptococcus pneumon ioe, 22, 39 Rapid response teams, 58 Streptococcus pa oge nes, 39 Reactive always dysfunction slrrdrome, 9 Stress ulcer prophylaxis. 59, Q84 Refractory septic shock, Q57 Succinylcholine, Q65 Residual volume (RV), 3t Sulfonylurea toxicity, 86t Reslizumab, 121, 13 Surviving Sepsis Campaign, TS 80 Respiratory bronchiolitis, 26t Sympathomimetics, 85t Respiratory bronchiolitis associated interstitial lung disease (RBILD), 27 Systemic lupus erlthematosus (SLE), 28t Respiratory drive. decreased, 73 Systemic sclerosis, 28t, lrl Respiratory failure, radiogaphic findings, 67t Restrictive chest wall disease, 74 T Reynolds pentad, Q60 Tadalafil for PAH, 44t Rheumatoid arthritis, 231, 28t Talc, pleural space obliteration with, 39-40 Riociguat for PAH, 441, 45 Teratomas, S0 Risperidone, discontinuation of, Q19 Terbutaline, adverse effects of 19t Roflumilast, 181,191, 20, 22, Q50 "Terrible T's," 50 ROS proto-oncogene 1 receptor tyrosine kinase (ROSI) translocation, 48 Theophylline, l2t, 20 ROX index, 62 Thermal injuries, 68, Q9 Thoracentesis, 4t, 5, 35. 36,39 s Thoracoscopy, 39, 50, Q81 Safety Data Sheets, 331, Q25 Thoracostomy, Q4 Salicylate toxicity, 86t Thrombolytic therapy, zz Salmeterol, 121, 19t Thymomas,50 Sarcoidosis, 261, 31-33, 321 321, 331, Q16 Thyroid tumors, 50 Scopolamine toxicity, 84t Tidal volume, decreased. 73 74 Sedation Tiotropium, 12t, 13, 191. Q8 in critical care patients, 59-60, 59t, Q31 Tocolltic therapy, 881 decreased respiratory drive and, 73 Tongue, angioedema of. 80f Seizures, obstetric emergencies, 88t Tonsillectomy, 54 Selexipag,44t Total lung capacity (TLC), 7,3t,27,74 Sepsis, 61t, 75-80 Toxic megacolon, 87t adiunctive therapies, 79 80 Toxicolos/, 82-86 epidemiolory of 78 Tracheotomy,54 glucose control in, 79 80 Transthoracic echoealdiography, 41,77 , Q72 hour-1 care bundle for, Q68 Treprostinil for PAFI. l ll management of, 78 80 Tricyclic antidepressdnls, toxicity ol 84t, 86t neutropenic, Q18 Triglycerides, pleulal ellusions and, 39 patient evaluation in, Q55 L-tryptophan,43t presentation of, 77 Tuberculosis, 23t, 39 treatment of Q35 Septic shock, 79 80, Q57, Q71 U Sequential Organ Failurc Assessment (SOFA), 58,77,77t Ultrasonography Serotonin syndrome, 811, 82, Q61 lung, 5 Shift work sleep disorder, 52, Q22 point-of care. Q28 Shock.75 77 point-of-care i;r sho. k, 75, 77, Q12 causes ol 76t pulmonary in)rgiIlB. 4t clinical flndings, 75t thoracic,35 36 IV access in, Q59 Umeclidinium, 121. 13. 19t

Pulmonary fibrosis patient evaluation in. Q12 acute respimtory failure and, 67t transthoracic echocardiography in, Q72 asbestos and, 34t Short-acting P, agonist (SABA),8,11, 18 DPLD and, 25t,26t,77 Sildenafil for PAH, 44t idiopathic, 27,30 37,301 321 Q30 Simplified Acute Physiolos/ Score, 58 Pulmonary fibrosis and emphysema, combined (CPFE), 31, 32f, e5 Sinus disease, asthlna and, 11t Pulmonary function testing, 1-3, 1t, 2f 6-minute walk test. 2 Pulmonary hypertension (PH), 26, 4t 45 Sjdgren s syndrome, 231, 28t classiflcation ol 41t Sleep apnea, Q62. Q74. See olso Obstructive sleep apnea (OSA); Central sleep diagnosis of, Q78, Q98 apnea (CSA) s_!ndromes evaluation of, 42f, 45, Q37 Sleep hygiene, 51 Pulmonary imaging, 3-5, 4t Sleep medicine, 51-56 Pulmonary I-angerhans cell histiocltosis (PLCH), 27 Sleep disordered breathing, 45 Pulmonary nodules, 45-47, 46f, 46t, Q7, Q36, Q47, Q99 Sleepiness, daltime. 51 52, 51t Pulmonary rehabilitation, 20, Q63 Sleep-related hypoventilation syndromes, 55 56, 55t Pulmonary sarcoidosis, Q16 Small cell lung cancer (SCLC), 47, 48f, Q29 Pulmonary vascular disease, 41 45 Smoking Pulse oximetry 3 asthma and, 14. 15 abnormal readings, Q52 cessation o{ 17, Q87 in airway obstruction, 68 DPLD and. 27 in carbon monoxide poisoning, 83-84 lung cancer and, 48 in ICU,67 parenchymal lung disease and, Q20 overnight,53 Smoking-related interstitial fibrosis (SRIF), 27 oxygen saturation and' 20, 22 Sodium thiosulfate, 84 preflight screening, 58t Spinal cord injuries, 74 at rest, 16, 26 Spirometry 1,7,Q97 Pure red cell aplasia, 50 Spontaneous breathing trials, 65t Spontaneous pneumothorax, 40, 40t, Q3 o Squamous cell carcinomil, 39, 47,47f qSOFA scores, 77, 77t St. lohn's wort, 43t Q/V mismatch, T2t Status asthmaticus. E8t Steam inhalation, 68 R Streptococcus onginosu.s. 39 Radiation pneumonitis, 28-29, Q70 Streptococcus oureus, 24. 39 Rapeseed oil, 43t St reptococcus pneumon ioe, 22, 39 Rapid response teams, 58 Streptococcus pa oge nes, 39 Reactive always dysfunction slrrdrome, 9 Stress ulcer prophylaxis. 59, Q84 Refractory septic shock, Q57 Succinylcholine, Q65 Residual volume (RV), 3t Sulfonylurea toxicity, 86t Reslizumab, 121, 13 Surviving Sepsis Campaign, TS 80 Respiratory bronchiolitis, 26t Sympathomimetics, 85t Respiratory bronchiolitis associated interstitial lung disease (RBILD), 27 Systemic lupus erlthematosus (SLE), 28t Respiratory drive. decreased, 73 Systemic sclerosis, 28t, lrl Respiratory failure, radiogaphic findings, 67t Restrictive chest wall disease, 74 T Reynolds pentad, Q60 Tadalafil for PAH, 44t Rheumatoid arthritis, 231, 28t Talc, pleural space obliteration with, 39-40 Riociguat for PAH, 441, 45 Teratomas, S0 Risperidone, discontinuation of, Q19 Terbutaline, adverse effects of 19t Roflumilast, 181,191, 20, 22, Q50 "Terrible T's," 50 ROS proto-oncogene 1 receptor tyrosine kinase (ROSI) translocation, 48 Theophylline, l2t, 20 ROX index, 62 Thermal injuries, 68, Q9 Thoracentesis, 4t, 5, 35. 36,39 s Thoracoscopy, 39, 50, Q81 Safety Data Sheets, 331, Q25 Thoracostomy, Q4 Salicylate toxicity, 86t Thrombolytic therapy, zz Salmeterol, 121, 19t Thymomas,50 Sarcoidosis, 261, 31-33, 321 321, 331, Q16 Thyroid tumors, 50 Scopolamine toxicity, 84t Tidal volume, decreased. 73 74 Sedation Tiotropium, 12t, 13, 191. Q8 in critical care patients, 59-60, 59t, Q31 Tocolltic therapy, 881 decreased respiratory drive and, 73 Tongue, angioedema of. 80f Seizures, obstetric emergencies, 88t Tonsillectomy, 54 Selexipag,44t Total lung capacity (TLC), 7,3t,27,74 Sepsis, 61t, 75-80 Toxic megacolon, 87t adiunctive therapies, 79 80 Toxicolos/, 82-86 epidemiolory of 78 Tracheotomy,54 glucose control in, 79 80 Transthoracic echoealdiography, 41,77 , Q72 hour-1 care bundle for, Q68 Treprostinil for PAFI. l ll management of, 78 80 Tricyclic antidepressdnls, toxicity ol 84t, 86t neutropenic, Q18 Triglycerides, pleulal ellusions and, 39 patient evaluation in, Q55 L-tryptophan,43t presentation of, 77 Tuberculosis, 23t, 39 treatment of Q35 Septic shock, 79 80, Q57, Q71 U Sequential Organ Failurc Assessment (SOFA), 58,77,77t Ultrasonography Serotonin syndrome, 811, 82, Q61 lung, 5 Shift work sleep disorder, 52, Q22 point-of care. Q28 Shock.75 77 point-of-care i;r sho. k, 75, 77, Q12 causes ol 76t pulmonary in)rgiIlB. 4t clinical flndings, 75t thoracic,35 36 IV access in, Q59 Umeclidinium, 121. 13. 19t 179

lndcx I Un€xpandablelun& 38t \hrdlator-assodahd prEumonia, 61t Um€r ainvay petency, 52, 55t ldlaory htlut, 6f . See abo Hypercapnic rcsplratory frtlurt Urlnothora& 38t ldlatory oErsttoot, tl, 57 Ut€rine atony, 88t Vtlantercl,Ilt, l9t Utertrc ruptur€, 88t Vttamin E ecetate, 68 Ltuulqalatopharf8oplesty, il \bcal cod dnfimction (VCD), 8, 9, Ut tbhmeoverlo47I) U \,bhrtreuma" 53.69 Vacrinadons,20 v/Q mismatctl 68, 70, 72-74, QIO \hping,68-59 \hsopresstl 66t,78 T thsoEessors, 66t, 78, 79 \Ibrlcs'compemadon, 34-35 ry'srous acless ln shoclg 63-64, 65t Q59 Wrist actigraph, 51 lftnous thrcmboemboli, 88t rrtndlaflon, mechanical, 62-63. See also Nonimastve pmltlrrE prcssuevenflladon (NPPD exhrbadon, 62-63, 54t, 6St lforr8syndrome,23t general prlnctples, 62-63 modes,54t l sedaflon an4 59-60, 59t ZafrtukasG f2t 15 rmning ftom, 61,63,65t akubn, l2t t t 180