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Pulmonary and Critical Care Medicine Solitary Pulmonary Nodule Diagnosis lymphad- An SPN is a lesion of the lung parenchyma measuring <3 cm in diameter that is not associated with other lesions or Approximately 35% of SPNs are bronchogenic carcinomas' The first step in enopathy and is not invading other structures' l evaluation is comparison with previous imaging studies. Stability over time reduces the possibility of cancer' The first step in evaluating a solid pulmonary nodule larger than B mm is to estimate the probability of malignancy; increasing age and smoking history increase risk. Solid nodules with moderate probability of malignancy should be characterized further with a PET scan. If the PET scan is negative, continued surveillance is warranted, whereas a positive PET scan result may require resection. If the probability of malignancy is initially high, obtain PET scan followed by surgical resection or chemotherapy and radiation. Solid nodules B mm or smaller are estimated for risk of malignancy. Most can be monitored with serial CT according to guidelines. STUDY TABIE: Fleischner Society Recommendations for Single Solid Pulmonary Nodule Follow-up Risk Factors for Lung Cancer? Size Recommended Follow-up No (low-risk patient) <6 mm No follow-up

Solid nodules B mm or smaller are estimated for risk of malignancy. Most can be monitored with serial CT according to guidelines. STUDY TABIE: Fleischner Society Recommendations for Single Solid Pulmonary Nodule Follow-up Risk Factors for Lung Cancer? Size Recommended Follow-up No (low-risk patient) <6 mm No follow-up 6-8 mm Cf at6-12 months, then consider CT at 18-24 months >B mm ConsiderCTat 3 months, PEf /Cf , ortissue sampling Yes (high-risk patient) <6 mm Optional Cf at12 months 6-8 mm Cf at 6-12 months, then Cf ar 18-24 months >B mm Consider CT at 3 months,PET/Cf , or tissue sampling Data from MacMahon H, Naidich DP, Goo JM, Lee KS, Leung ANC, Mayo JR, et al. Guidelines for management of incidental pulmonary nodules detected on CT images: Irom the Fleischner Society 201 7. Radiology. 201 7;284:228-243.IPMID:2824O562) doi:\ 0.1 1 48/radiol.20 1 7 1 61 659. A subsolid nodule is a focal, rounded opacity that is pure ground glass in appearance (focal density with underlying lung archi- tecture still preserved) or has a solid component (part solid) but is still more than 50'2, ground glass. Development of a solid component in a pure ground-glass nodule or enlargement of the solid component suggests malignancy.

A subsolid nodule is a focal, rounded opacity that is pure ground glass in appearance (focal density with underlying lung archi- tecture still preserved) or has a solid component (part solid) but is still more than 50'2, ground glass. Development of a solid component in a pure ground-glass nodule or enlargement of the solid component suggests malignancy. STUDY TABLE: Fleischner Society Recommendations for Follow-up of Solitary Subsolid Lung Nodule lmaging Findings Size Recommended Follow-up Pure ground glass <6 mm No follow-up >6 mm Cf at 6-12 months to confirm persistence, then CT every 2 years until 5 years Part solid nodule <6 mm No follow-up >6 mm CT at 3-6 months to confirm persistence. lf unchanged and solid component remains <6 mm, annual CT should be performed for 5 years TESTYOURSETF A 65 year-old man is incidentally found to have a 7 mm pulmonary nodule on chest x ray obtained before an elective cholecystec- tomy. On chest CT, the nodule is subsolid, and no other nodules or lymphadenopathy is evident. He has a S0-pack-year history of cigarette smoking. ANSWER: For management, choose follow-up chest CT in 1year. Pulmonary mass, defined as >3 cm in diameter, is highly suspicious for malignancy in a patient with risk factors. Either a biopsy for tissue diagnosis (in the absence of suspected metastases) or surgical resection (if no evidence of metastatic disease) is typi cally the first step in the evaluation. In patients with radiographic evidence of advanced stage disease, diagnosis and staging are best accomplished with a single invasive test at a location that will establish the diagnosis and the stage of disease. 354

Pulmonary and Critical Care Medicine DON'T BE TRICKED . Before ordering contrast CT, bronchoscopy, or pET scan, compare current image with previous image to determine stability over time. r PET scans may be falsely negative in alveolar cell carcinoma or lesions <l cm in diameter and falsely positive in various infl ammatory lesions. . A nonspecific negative result from flberoptic bronchoscopy or transthoracic needle aspiration biopsy does not reliably exclude the presence of a malignant growth. I l I Mediastinal Masses Diagnosis The mediastinum can be divided into three separate compartments, which can help narrow the differential diagnosis of a medi astinal mass. Origin of Mass lmportantAssociations Anterior Mediastinum Thymus Most common tumor of anterior mediastinum; 40% have MG Other syndromes include pure red cell aplasia and acquired hypoga m mag lobu linem ia Teratoma/germ cell Teratomas may contain fat, fluid, and bone discernable on CT imaging Ly,.n p homa Second most common anterior mediastinal tumor; Hodgkin disease is the most common lymphoma

Origin of Mass lmportantAssociations Anterior Mediastinum Thymus Most common tumor of anterior mediastinum; 40% have MG Other syndromes include pure red cell aplasia and acquired hypoga m mag lobu linem ia Teratoma/germ cell Teratomas may contain fat, fluid, and bone discernable on CT imaging Ly,.n p homa Second most common anterior mediastinal tumor; Hodgkin disease is the most common lymphoma Thv roid Often causes compressive symptoms (dyspnea, dysph Middle Mediastinum Lymph nodes Lymphadenopathy is the most common cause of middle mediastinal masses Cysts lncludes benign pericardial, bronchogenic, and esophageal cysts Mediastinum: A lateral chest x'ray demonstrales the anterior (red), Posterior Mediastinum middle (yel/ow), and posterior (biue) mediastinal compartments. Neurogenic tumors Schwannomas are most common in adults Obstructive Sleep Apnea Diagnosis Characteristic findings of OSA include snoring, apnea, excessive daytime sleepiness, and obesity (risk determined by either BMI >30 or neck circumference >17 in) and an enlarged and elongated soft palate (crowded pharynx). Occasionally, OSA first presents following a surgical procedure involving general anesthesia and/or narcotic analgesia' The STOP-Bang is used to identiff OSA during preanesthesia evaluation. 355

l i 1 i Pulmonary and Critical Care Medicine 1 J '1 I In-laboratory polysomnography is the gold standard test for: 'l 1 o mission critical workers (truck drivers, pilots) o complicated OSA I J . patients with HF, neuromuscular disease, or advanced pulmonary disease 1 I Home sleep apnea testing is sensitive in diagnosing OSA in those with a pretest likelihood of moderate to severe disease and no l indications for in-laboratory polysomnography. The severity of OSA can be classified by the AHI' Diagnose OSA in patients with 't I an AHI of>Sih during a sleep study. I I DOil'T BETRICKED I . Do not confuse obesity-hypoventilation syndrome with OSA. Obesity-hypoventilation syndrome is usually associated with COPD and always with elevated arterial Pco, Ievels when awake. . Obesity-hypoventilation syndrome may coexist with OSA. . Overnight oximetry has not been validated as a screening tool for OSA.

DOil'T BETRICKED I . Do not confuse obesity-hypoventilation syndrome with OSA. Obesity-hypoventilation syndrome is usually associated with COPD and always with elevated arterial Pco, Ievels when awake. . Obesity-hypoventilation syndrome may coexist with OSA. . Overnight oximetry has not been validated as a screening tool for OSA. Treatment Lifestyle changes: . weight loss . avoiding alcohol/sedatives/opioids before bedtime . sleeping in the lateral position CPAP is the initial treatment of choice for OSA and has been shown to improve quality of life, cognitive function, and symptoms of daytime sleepiness. Oral appliances are an alternative to CPAP therapy for mild to moderate OSA. Oral appliances are not as effective as CPAP in reducing AHI. Maxillomandibular advancement surgery improves the AHI and can be considered for patients who do not benefit from or toler ate positive airway pressure therapy. DOil'T BE TRICKED . Supplemental oxygen is not recommended as a primary therapy for OSA. . Upper airway surgery is not recommended as initial therapy. . Uvulopalatopharyngoplasty is a recommended surgical option in patients requiring surgery Obesity- Hypoventi lation Synd rome Diagnosis The hallmark is daytime hypercapnia, defined as a pco, >45 mm Hg. OSA is usually but not always superimposed. HF, pH, and volume overload are common. Treatment Weight loss, including bariatric surgery and bilevel positive airway pressure ventilation are recommended. CpAp can be considered if severe OSA is also present. Supplemental oxygen may be needed. 356

Pulmonary and Critical Care Medicine Hypercapnic Respiratory (Ventitatory) Failure : Diagnosis Hypercapnic respiratory (ventilatory) failure occurs when alveolar ventilation is inadequate and the level of CO, increases in the blood. Because oxygenation also depends on ventilation, patients are often hypoxic as well. Howeveq hypoxia will often improve t with supplemental oxygen. Chronic hypercapnic respiratory f'ailure occurs most often in patients with: I t o COPD and asthma I I I . neuromuscular disease (MG, ALS, MS) I . restrictive lung diseases (chest wall skeletal disorders, obesity) . depressed respiratory drive (opioids and sedatives) Testing All patients suspected of having hypercapnic respiratory failure should have arterial blood gas analysis even if hypoxemia resolves with oxygen administration. In patients with neuromuscular disease, PFTs show restriction on spirometry and lung volume measurement but normal dif fusing capacity. STUDY TABLE: Pulmonary Function Values Suggestive of Neuromuscular Weakness Function Value FVC >20% decrement in FVC while supine compared with upright position Maximal inspiratory pressure (MlP) Less than -60 cm H2O or 50% of predicted Maximal expiratory pressure (MEP) Less than +60 cm H2O or 50% of predicted Patients with respiratory muscle weakness, obesity-hypoventilation syndrome, and disorders ol ventilatory control first hypoventilate during REM sleep. Order polysomnography if nocturnal hypoventilation is suspected (da,.time sleepiness, noc- turnal awakenings, morning headaches). TESTVOURSETF A 36 year old man with myotonic dystrophy awakens at night gasping for air and experiences increasing fatigue. Cardiopulmonary examination is normal. Neurologic examination shows 4+/5 strength in all muscle groups. ANSWER: For diagnosis, choose nocturnal hypercapnic respiratory failure. For management, elect polysomnography.

TESTVOURSETF A 36 year old man with myotonic dystrophy awakens at night gasping for air and experiences increasing fatigue. Cardiopulmonary examination is normal. Neurologic examination shows 4+/5 strength in all muscle groups. ANSWER: For diagnosis, choose nocturnal hypercapnic respiratory failure. For management, elect polysomnography. Hypoxemic Respiratory Failure Hypoxemic respiratory failure is caused by inadequate oxygenation of hemoglobin. 'l'he most common causes of hypoxic res- piratory failure in the ICU are V/Q mismatch (or shunt, when V/Q = 0), which occurs when perfused areas of the lung are not ventilated. Acute Respiratory Distress Syndrome ARDS is a syndrome of hypoxemic respiratory failure presenting as noncardiogenic pulmonary edema. Precipitating causes of ARDS include pulmonary infection, hemorrhagic shock, pancreatitis, trauma, transfusions, and sepsis. 357

Pulmonary and Critical Care Medicine STUDY TABLE: Diagnosing and Classi{ying ARDS Classification Features 1 Common to all Acute onset (<1 week), known clinical insults (ARDS risk factors) I cases of ARDS l Bilateral lung opacities on imaging not fully explained by effusions, lobar/lung collapse or nodules \l Respiratory failure not explained by HF orvolume overload (although ARDS can coexist with HF orfluid overload states) ''t MiId ARDS Arterial Po2lFro 2ratio ol 201-300 mm Hg, measured with PEEP >5 cm H2O l Moderate ARDS Arterial Po2lFro2 ratio of 100-200 mm Hg, measured with PEEP >5 cm H2O l Severe ARDS Arterial Po2lFro2 ratio <1 00 mm Hg, measured with PEEP >5 cm H2O 1 I

Moderate ARDS Arterial Po2lFro2 ratio of 100-200 mm Hg, measured with PEEP >5 cm H2O l Severe ARDS Arterial Po2lFro2 ratio <1 00 mm Hg, measured with PEEP >5 cm H2O 1 I STUDY TABLE: Mimics of ARDS I l Disease Characteristics Cardiogenic pulmonary edema History of cardiac disease, enlarged heart, 53, chest x-ray showing an enlarged cardiac silhouette, pleural effusions, and Kerley B lines Rapid improvement with diuresis or afterload reduction Diffuse alveolar hemorrhage High Drco by pulmonary function testing AKI with microscopic or gross hematuria or other evidence of vasculitis present Associated with stem cell transplantation Hemosiderin-laden macrophages in bronchoalveolar lavage fluid Acute eosinophilic pneumonia Cough, fever, pleuritic chest pain, and myalgia; may be precipitated by initiation of smoking >1 5% eosinophils in bronchoalveolar lavage fluid Hypersensitivity pneumonitis Typically slower onset than ARDS (over weeks) with progressive course; however, may present acutely, mimicking ARDS Positive exposure history (e.g., farmers, bird fanciers, hot tub exposure) Acute interstitial pneumonia May be impossible to distinguish from ARDS Absence of typical inciting factors for ARDS May respond to glucocorticoid administration Treatment Optimal mechanical ventilation associated with the prevention of ventilator associated lung injury includes:

Hypersensitivity pneumonitis Typically slower onset than ARDS (over weeks) with progressive course; however, may present acutely, mimicking ARDS Positive exposure history (e.g., farmers, bird fanciers, hot tub exposure) Acute interstitial pneumonia May be impossible to distinguish from ARDS Absence of typical inciting factors for ARDS May respond to glucocorticoid administration Treatment Optimal mechanical ventilation associated with the prevention of ventilator associated lung injury includes: o lung protective ventilation using volume controlled ventilation with a tidal volume of 4 to B ml/kg of ideal body weight (low tidal volume) o plateau (end inspiratory) pressure <30 cm HrO (even if this results in .,permissive,' hypercapnia and acidosis) o PEEP Limiting IV fluids and using diuretics to keep CVp at lower targets has been associated with a more rapid improvement in lung function but no effect on mortality. Use of prone positioning in severe ARDS has a mortality benefit. DOil'T BE TRICKED . Glucocorticoids are not indicated for the acute treatment of ARDS. TESTYOURSELF A S5-year-old woman with acute pancreatitis has increasingly severe shortness ofbreath for 12 hours. She has no history ofcardiac disease. Pulse rate is 116/min, respiration rate is 40/min, and arterial O, saturation is 86%, (on supplemental oxygen). Diffuse bilat eral crackles are heard. Chest x ray shows diffuse airspace disease. She is intubated and mechanically ventilated. With an Fro, of. 1.0, her arterial Po, is 150 mm Hg. ANSWER: For diagnosis, choose moderate ARDS. For management, select a tidal volume of 4 to g ml/kg of ideal body weight. 358

Pulmonary and Critical Care Medicine Noninvasive Positive-pressure Ventilation lndications in Critically lll patients NPPV is the use of positive-pressure ventilation without the need for an invasive airway. NppV may be used as the ventilatory mode of first choice in these conditions: t . COPD exacerbations (not stable COPD) i . cardiogenic pulmonary edema I o neuromuscular disease . prevention of recurrent respiratory failure in recently extubated high_risk patients r obesity-hypoventilation syndrome The most common contraindications to NppV include: . respiratory arrest r medical instability . inability to protect airway and/or excessive secretions or nausea and vomiting o uncooperative or agitated patient Improvements in blood gas values and clinical condition should occur within 2 hours of starting NppV Ilnot, intubation should be considered to avoid undue delay and prevent respiratory arrest. I nvasive Mechanical Ventilation lndications Patients may require invasive mechanical ventilatory support fbr hypoxemic respiratory failure (low arterial Po2) or hypercapnic ventilatory failure (increased arterial Pcor). The indications for invasive mechanical ventilation are hypoxemic or hypercapnic respiratory failure, contraindication to NPPV and inabiliry to protect the airway.

I nvasive Mechanical Ventilation lndications Patients may require invasive mechanical ventilatory support fbr hypoxemic respiratory failure (low arterial Po2) or hypercapnic ventilatory failure (increased arterial Pcor). The indications for invasive mechanical ventilation are hypoxemic or hypercapnic respiratory failure, contraindication to NPPV and inabiliry to protect the airway. STUDY TABLE: Ventilator Management lf you would ...the intermediate ...make the ventilator Notes: like to... step is... do this by: lmprove J Arterial Pco2 lncreasing respiratory rate Watch {or auto-PEEP at high respiratory rates, which respiratory can cause hypotension by reducing preload lncreasing tidal volume: acidosis ln volume control mode, Don't be tricked: lf the patient has ARDS, respiratory directly choose the tidal acidosis (pH -7.2)should generally be tolerated volume; in pressure control rather than raising the tidal volume >4-8 mUkg mode, increase the inspiratory support pressure to increase tidal volume lmprove 'l Arterial Pco2 Decreasing respi ratory rate lfthe patient is breathing fasterthan the set respiratory ventilator rate, this strategy won't work Decreasing tidal volume alkalosis Determine why respiratory alkalosis is present (sepsis, PE, liver disease, pain)

STUDY TABLE: Ventilator Management lf you would ...the intermediate ...make the ventilator Notes: like to... step is... do this by: lmprove J Arterial Pco2 lncreasing respiratory rate Watch {or auto-PEEP at high respiratory rates, which respiratory can cause hypotension by reducing preload lncreasing tidal volume: acidosis ln volume control mode, Don't be tricked: lf the patient has ARDS, respiratory directly choose the tidal acidosis (pH -7.2)should generally be tolerated volume; in pressure control rather than raising the tidal volume >4-8 mUkg mode, increase the inspiratory support pressure to increase tidal volume lmprove 'l Arterial Pco2 Decreasing respi ratory rate lfthe patient is breathing fasterthan the set respiratory ventilator rate, this strategy won't work Decreasing tidal volume alkalosis Determine why respiratory alkalosis is present (sepsis, PE, liver disease, pain) Alleviate I 02 saturation, lncreasing Fto2 Occasionally, increasing PEEP will lower cardiac hypoxemia arterial Po2 output by reducing preload;this can worsen oxygen lncreasing PEEP delivery to tissues lf no contraindications, attempt to increase preload with lVfluids

Alleviate I 02 saturation, lncreasing Fto2 Occasionally, increasing PEEP will lower cardiac hypoxemia arterial Po2 output by reducing preload;this can worsen oxygen lncreasing PEEP delivery to tissues lf no contraindications, attempt to increase preload with lVfluids 359