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CHAPTER 65:  Community-Acquired Pneumonia, Aspir ation Pneumonia, and Noninf ectious Pulmonar y Infiltra tes      439  DIAGNOSIS Diagnosis is often clinical, especially during epidemics; however, less than 10% of patients with prolonged cough or posttussive emesis will test positive. 77 Definitive diagnosis is usually by polymerase chain reac tion of nasopharyngeal secretions or serologic detection of antibodies. Other causes of respiratory illnesses with prolonged cough include Mycoplasma, Chlamydophila, influenza virus, and other respiratory viruses. In adults, chronic cough can be associated with angiotensinconverting enzyme inhibitors, gastroesophageal reflux, or asthma.  TREATMENT Treatment of pertussis is azithromycin, 500 milligrams PO on day 1 and 250 milligrams PO on days 2 to 5. 78 Trimethoprim-sulfamethoxazole, 160 milligrams/800 milligrams twice a day for 14 days (check renal dosing), is an alternative to those allergic to, or unable to tolerate, macrolides. Treatment is best if started early, in the first week. After that, antibiotic treatment does not alter the duration of cough. Chemoprophylaxis (same regimen as for treatment) is typically given for household contacts. 78 No antitussive agent has been shown to be clearly effective in reducing the symptoms of the spasmodic (whooping) cough.79 REFERENCES The complete reference list is available online at www.TintinalliEM.com. Community-Acquired Pneumonia, Aspiration Pneumonia, and Noninfectious Pulmonary Infiltrates Eric Anderson Simone French Gerald E. Maloney  COMMUNITY-ACQUIRED PNEUMONIA INTRODUCTION AND EPIDEMIOLOGY Pneumonia is an infection of the alveolar (gas-exchanging) portion of the lung. Community-acquired pneumonia (CAP) accounts for approximately 3 million cases and 1.6 million hospitalizations per year in the United States. 1,2 One third of pneumonia cases occur in adults over age 65 years, and approximately 4 in 100 children will develop pneumonia each year. According to 2016 data, 544,000 ED visits were due to pneu monia. Pneumonia accounts for 16.1 deaths per 100,000 population, making it the eighth leading cause of death, particularly among older adults, with an age-adjusted death rate of 22%. Pneumococcal pneumonia produces typical symptoms of fever, cough, and rigors, but atypical infections, infections in compromised hosts, and infections in patients at the extremes of age may produce atypical findings, such as a change in mental status or a decline in function. Patients with healthcare–associated pneumonia are at risk for infection with resistant organisms. When predicting the causative organism and selecting treatment choices in pneumonia patients, think of the acquiring environment, especially community versus healthcare settings (Table 65-1). 3,4 CHAPTER TABLE 65-1 Acquisition Environment Classification for Pneumonia Classification Criteria Community-acquired pneumonia Acute pulmonary infection in a patient who is not hospitalized or residing in a long-term care facility ≥14 d before presentation Hospital-acquired pneumonia New infection occurring ≥48 h after hospital admission Ventilator-acquired pneumonia New infection occurring ≥48 h after endotracheal intubation Healthcare–associated pneumonia

y infection in a patient who is not hospitalized or residing in a long-term care facility ≥14 d before presentation Hospital-acquired pneumonia New infection occurring ≥48 h after hospital admission Ventilator-acquired pneumonia New infection occurring ≥48 h after endotracheal intubation Healthcare–associated pneumonia Patients hospitalized for ≥2 d within the past 90 d Nursing home/long-term care residents Patients receiving home IV antibiotic therapy Dialysis patients Patients receiving chronic wound care Patients receiving chemotherapy Immunocompromised patients PATHOPHYSIOLOGY Pathogenic organisms are inhaled or aspirated directly into the lungs, with aspiration being more common, especially in healthcare settings. Some bacteria, such as Staphylococcus aureus or Pneumococcus , may produce pneumonia by hematogenous seeding. Patients most at risk for pneumonia are those with a predisposition to aspiration, with impaired mucociliary clearance, or likely to have bacteremia (Table 65-2). Some forms of pneumonia produce an intense inflammatory response within the alveoli that leads to filling of the air space with exudate and WBCs. Organisms can distribute throughout the lung by spreading along the bronchial tree or through pores between adjacent alveoli TABLE 65-2 Risk Factors for Pneumonia Aspiration risk •  Swallowing  and esophageal motility disorders •  Stroke •  Nasogastric  tube •  Intubation •  Seizure  and syncope Bacteremia risk •  Indwelling  vascular devices •  Intrathoracic  devices (e.g., chest tube) •  Debilitation •  Alcoholism •  Extremes  of age •  Neoplasia •  Immunosuppression •  Chronic  diseases •  Diabetes •  Renal  failure •  Liver  failure •  Valvular  heart disease •  Congestive  heart failure Pulmonary disorders •  Chronic  obstructive pulmonary disease •  Chest  wall disorders •  Skeletal  muscle disorders •  Bronchial  obstruction •  Bronchoscopy •  Viral  lung infections Tintinalli_Sec08_p0425-0472.indd 439 8/1/19 2:10 PM

failure •  Liver  failure •  Valvular  heart disease •  Congestive  heart failure Pulmonary disorders •  Chronic  obstructive pulmonary disease •  Chest  wall disorders •  Skeletal  muscle disorders •  Bronchial  obstruction •  Bronchoscopy •  Viral  lung infections Tintinalli_Sec08_p0425-0472.indd 439 8/1/19 2:10 PM 440 SECTION 8: Pulmonary Disorders (pores of Kohn). Bacterial pneumonia results in an intense inflamma tory response and tends to cause a productive cough. Atypical organisms do not cause an intense inflammatory response and may trigger a mild, nonproductive cough. In about half of patients with CAP , a specific pathogen is not identified. When identified, Pneumococcus is still the most common, followed by viruses and the atypical agents Mycoplasma, Chlamydia, and Legionella. Two organisms that account for the most severe CAP in otherwise healthy adults are Streptococcus pneumoniae and Legionella. The treat ment of CAP targets covering at least these two organisms. In up to 5% of cases, multiple agents exist. In special populations, including nursing home residents, chronic alcoholics, and human immunodeficiency virus (HIV)–infected patients, a different spectrum of agents causes pneumonia. CLINICAL FEATURES Patients with pneumonia frequently will present with cough (79% to 91%), fatigue (90%), fever (71% to 75%), dyspnea (67% to 75%), spu tum production (60% to 65%), and pleuritic chest pain (39% to 49%). However, the individual symptoms and physical findings vary and make clinical diagnosis and differentiation from upper respiratory tract dis ease difficult. 6,7 The classic presentation of pneumococcal pneumonia is a sudden onset of illness with fever, an episode of severe rigor, dyspnea, bloody sputum production, chest pain, tachycardia, tachypnea, and abnormal findings on lung examination; that pattern is not common. Pneumonia may be preceded by symptoms of a viral upper respiratory infection, such as coryza, low-grade fever, rhinorrhea, or nonproductive cough. Weight loss, malaise, dizziness, and weakness may also be associated with pneumonia. Some of the atypical agents trigger headache or GI illness. Occasionally, pneumonia is associated with extrapulmonary symptoms, including joint pain, hematuria, or skin rashes. The physical examination may show evidence of alveolar fluid (inspiratory rales), consolidation (bronchial breath sounds), pleural effusion (dullness and decreased breath sounds), or bronchial congestion (rhonchi and wheezing).

is associated with extrapulmonary symptoms, including joint pain, hematuria, or skin rashes. The physical examination may show evidence of alveolar fluid (inspiratory rales), consolidation (bronchial breath sounds), pleural effusion (dullness and decreased breath sounds), or bronchial congestion (rhonchi and wheezing). 6,7 Radiologic findings in pneumonia are nonspecific and do not provide a specific radiologic diagnosis; typical radiologic features are listed in TABLE 65-3 Clinical Characteristics of Common Bacterial Pneumonias Organism Symptoms Sputum Chest Radiograph Streptococcus pneumoniae Sudden onset, fever, rigors, pleuritic chest pain, productive cough, dyspnea Rust-colored; gram-positive encapsulated diplococci Lobar infiltrate, occasionally patchy, occasional pleural effusion Staphylococcus aureus Gradual onset of productive cough, fever, dyspnea, especially just after viral illness Purulent; gram-positive cocci in clusters Patchy, multilobar infiltrate; empyema, lung abscess Klebsiella pneumoniae Sudden onset, rigors, dyspnea, chest pain, bloody sputum; especially in alcoholics or nursing home patients Brown “currant jelly”; thick, short, plump, gram-negative, encapsulated, paired coccobacilli Upper lobe infiltrate, bulging fissure sign, abscess formation Pseudomonas aeruginosa Recently hospitalized, debilitated, or immunocompromised patient with fever, dyspnea, cough Gram-negative coccobacilli Patchy infiltrate with frequent abscess formation Haemophilus influenzae Gradual onset, fever, dyspnea, pleuritic chest pain; especially in elderly and COPD Short, tiny, gram-negative encapsulated coccobacilli Patchy, frequently basilar infiltrate, occasional pleural effusion Legionella pneumophila Fever, chills, headache, malaise, dry cough, dyspnea, anorexia, diarrhea, nausea, vomiting Few neutrophils and no predominant bacterial species Multiple patchy nonsegmented infiltrates, progresses to consolidation, occasional cavitation and pleural effusion Moraxella catarrhalis Indolent course of cough, fever, sputum, and chest pain; more common in COPD patients Gram-negative diplococci found in sputum Diffuse infiltrates Chlamydophila pneumoniae Gradual onset, fever, dry cough, wheezing, occasionally sinus symptoms Few neutrophils, organisms not visible Patchy subsegmental infiltrates Mycoplasma pneumoniae Upper and lower respiratory tract symptoms, nonproductive cough, bullous myringitis, headache, malaise, fever Few neutrophils, organisms not visible Interstitial infiltrates (reticulonodular pattern), patchy densities, occasional consolidation Anaerobic organisms Gradual onset, putrid sputum, especially in alcoholics Purulent; multiple neutrophils and mixed organisms Consolidation of dependent portion of lung; abscess formation Abbreviation: COPD = chronic obstructive pulmonary disease. Table 65-3. Immunocompromised hosts, such as those with acquired immunodeficiency syndrome or neutropenia, may not manifest radio graphic evidence of pneumonia despite clinical findings suggestive of pneumonia. Clinical and radiographic findings do not necessarily correspond; the patient may be improving clinically despite having a worsening appearance on their chest radiograph.  PNEUMOCOCCAL PNEUMONIA The elderly, children <2 years old, minorities, children who attend group daycare centers, and persons with underlying medical conditions (including HIV infection and sickle cell disease) are at higher risk for pneumococcal pneumonia. Patients will frequently have lobar pneumonia (Figure 65-1 ), with parapneumonic pleural effusions occurring in about 25% of patients.

hildren who attend group daycare centers, and persons with underlying medical conditions (including HIV infection and sickle cell disease) are at higher risk for pneumococcal pneumonia. Patients will frequently have lobar pneumonia (Figure 65-1 ), with parapneumonic pleural effusions occurring in about 25% of patients. Patients with functional or anatomic asplenia or those being treated with immunosuppressive drugs, such as transplant patients or inflammatory bowel disease or connective tissue disease patients, may have a very rapid progression of disease, with acute prostration and septic shock progressing to multisystem organ failure. Patients with chronic lung disease, nursing home patients, or otherwise healthy elderly patients tend to have a slower progression of pneumonia, with symptoms of malaise with minimal cough or sputum production. Laboratory findings in pneumonia include leukocytosis, elevation of the serum bilirubin or hepatic enzymes, or hyponatremia. Pneumococcal pneumonia responds to a variety of antibiotics, although there is an increased incidence of penicillin-, macrolide-, and fluoroquinolone-resistant pneumococci. 8 Penicillin resistance ranges from 5% to 80%, depending on location, with increasing resistance reported in Spain, Italy, and Eastern Europe. The risk factors for rela tive penicillin resistance include patients at the extremes of age, day care attendance, immunosuppression from alcoholism or cancer, and recent use of broad-spectrum antibiotics or travel to areas where penicillin resistance is common. Resistance is increasing to tetracycline and trimethoprim-sulfamethoxazole. Patients with intermediate penicillin-resistant pneumococci can receive routine antibiotics so long as an adequate dose is administered. 9 A typical regimen for patients admitted to the hospital with CAP has been the use of a third-generation cephalosporin and a macrolide, and outpatient treatment often starts with macrolide monotherapy. There have recently been reports of increasing macrolide Tintinalli_Sec08_p0425-0472.indd 440 8/1/19 2:10 PM

istered. 9 A typical regimen for patients admitted to the hospital with CAP has been the use of a third-generation cephalosporin and a macrolide, and outpatient treatment often starts with macrolide monotherapy. There have recently been reports of increasing macrolide Tintinalli_Sec08_p0425-0472.indd 440 8/1/19 2:10 PM CHAPTER 65:  Community-Acquired Pneumonia, Aspir ation Pneumonia, and Noninf ectious Pulmonar y Infiltra tes      441 FIGURE 65-1. Lobar pneumonia. resistance among pneumococcus, with respiratory quinolones becoming the preferred regimen in some regions.  OTHER BACTERIAL PNEUMONIAS S. aureus is a consideration in patients with chronic lung disease, patients with laryngeal cancer, immunosuppressed patients, nursing home patients, or others at risk for aspiration pneumonia. S. aureus pneumonia may occur in otherwise healthy patients after viral illness, such as during an influenza epidemic, although pneumococcal pneumonia is still more common. Patients with staphylococcal pneumonia typically have an insidious onset of disease with low-grade fever, sputum production, and dyspnea. The chest radiograph usually demonstrates extensive disease with empyema, pleural effusions, and multiple areas of infiltrate (Figure 65-2). Patients with healthcare-acquired pneumonia are at risk for infection with methicillin-resistant S. aureus. 4,10 The rare methicillinresistant S. aureus–associated Panton-Valentine leukocidin mutation infection creates severe, necrotizing infection due to a cytotoxin; unless it is recognized and treated before toxin is entrenched, outcomes are poor. Klebsiella pneumonia often occurs in compromised patients: patients at risk of aspiration, alcoholics, the elderly, and other patients with chronic lung disease. In contrast to S. aureus, patients with Klebsiella have acute onset of severe disease with fever, rigors, and chest pain. Herpes labialis is occasionally associated with Klebsiella pneumonia. Patients with Klebsiella may develop abscesses, although more com monly they have a lobar infiltrate. The classic currant jelly sputum is not common in routine clinical practice. Pseudomonas causes a severe pneumonia with cyanosis, confusion, and other signs of systemic illness. The chest radiograph may show bilateral lower lobe infiltrates, occasionally associated with empyema. Pseudomonas is not a typical cause of CAP , but may develop in patients with a prolonged hospitalization or patients who have received broadspectrum antibiotics or high-dose steroid therapy, who have structural lung disease, or who are nursing home residents. Haemophilus influenzae pneumonia occurs in the elderly and should be considered in patients with chronic lung disease, sickle cell disease, or immunocompromised disorders and in alcoholics and diabetics; its frequency in the young (and even adults) is markedly diminished now with vaccination. Patients may either have a gradual progression of disease with low-grade fever and sputum production or occasionally have the sudden onset of chest pain, dyspnea, and sputum production. Bacteremia may be seen in older adults. Pleural effusions and multilobar infiltrates are common findings in H. influ enzae pneumonia. Moraxella catarrhalis pneumonia has clinical features similar in spectrum to those of H. influenzae. Typically, patients with M. catarrhalis have an indolent course of cough and sputum production. Fever and pleuritic chest pain are common clinical symptoms. The chest radio graph usually shows diffuse infiltrates.  PNEUMONIA FROM ATYPICAL AGENTS Atypical agents are a cause of pneumonia in older children, in young adults, and in the elderly. The atypical agents are Legionella, Chlamydia, Mycoplasma, and viruses.

Fever and pleuritic chest pain are common clinical symptoms. The chest radio graph usually shows diffuse infiltrates.  PNEUMONIA FROM ATYPICAL AGENTS Atypical agents are a cause of pneumonia in older children, in young adults, and in the elderly. The atypical agents are Legionella, Chlamydia, Mycoplasma, and viruses. Because these agents lack a cell wall, they do not respond to β-lactam antibiotics but are treated with macrolides or a respiratory fluoroquinolone. Legionella can cause a range of illness from benign self-limited disease to multisystem organ failure with acute respiratory distress syndrome. Patients at higher risk include cigarette smokers, patients with chronic lung disease, transplant patients, and the immunosuppressed. There is no seasonality to Legionella pneumonia, making it a more prominent cause of pneumonia in the summer when other pathogens decline in frequency. Legionella pneumonia is commonly complicated by GI symptoms, including abdominal pain, vomiting, and diarrhea. In addition, Legionella can affect other organ systems, causing sinusitis, pancreatitis, myocarditis, and pyelonephritis. The chest radiograph frequently shows a patchy infiltrate, with the occasional appearance of hilar adenopathy and pleural effusions ( Figure 65-3). Use of urinary Legionella antigen testing in patients with appropriate clinical suspicion can confirm the diagnosis. Chlamydia pneumonia is a common cause of respiratory infection, with about half of the population demonstrating antibodies by the age of 15 years old. Infection with Chlamydia usually causes a mild sub acute illness with sore throat, mild fever, and nonproductive cough, although occasionally patients have a more severe course. Patients with chlamydial pneumonia frequently have abnormal physical examination findings with rales or rhonchi. The chest radiograph usually shows a patchy subsegmental infiltrate. Chlamydial infection may be linked to adult-onset asthma. Mycoplasma pneumonia also occurs year-round, although it tends to cluster in epidemics every 4 to 8 years. Mycoplasma may cause a subacute respiratory illness with cough, sore throat, and headache. Myco plasma pneumonia is also frequently associated with retrosternal chest pain. Unlike Legionella, Mycoplasma usually is not associated with GI symptoms. The chest radiograph shows patchy infiltrates, with the common occurrence of hilar adenopathy and pleural effusions. Mycoplasma occasionally causes extrapulmonary symptoms, including bullous myr ingitis, rash, neurologic symptoms, arthritis and arthralgia, hematologic abnormalities, and, rarely, renal failure. FIGURE 65-2. Staphylococcal  pneumonia  with  extensive  infiltration  and  effusion  or empyema. Tintinalli_Sec08_p0425-0472.indd 441 8/1/19 2:10 PM

causes extrapulmonary symptoms, including bullous myr ingitis, rash, neurologic symptoms, arthritis and arthralgia, hematologic abnormalities, and, rarely, renal failure. FIGURE 65-2. Staphylococcal  pneumonia  with  extensive  infiltration  and  effusion  or empyema. Tintinalli_Sec08_p0425-0472.indd 441 8/1/19 2:10 PM 442 SECTION 8: Pulmonary Disorders Q fever is an uncommon cause of pneumonia in the United States, although there have been outbreaks in Southwest Asia. The causative organism is Coxiella burnetii, transmitted via infected animals through dried urine that is inhaled or unpasteurized milk. It can cause an acute infection with lobar infiltrates and pleural effusions or a more indolent infection with multisystem involvement including endocarditis and hepatitis. The chronic form of Q fever has a higher mortality than the acute form, with nearly 100% of Q fever patients with endocarditis dying without treatment. Doxycycline or a respiratory quinolone are first-line treatment. Human-to-human Q fever transmission is rare, and isolation of an infected person is unnecessary. Viruses can cause severe pneumonia. The outbreak of severe acute respiratory syndrome in 2003, associated with group 2 coronavirus, is one example of a virus causing rapid worldwide involvement. 11 The emergence of pandemic influenza is an ongoing pressing public health issue. The 2017 to 2018 influenza season had >30,000 U.S. hospital izations for influenza, with pneumonia, from either primary viral or secondary bacterial infection, being the most common reason for admission. The most recent pandemic viral infections have been H1N1 and H5N1 influenza over the past years. 12 Pregnant women are particularly susceptible to developing severe influenza-associated pneumonia, and use of antivirals is recommended for pregnant women with an influenza-like illness. Varicella, typically benign in most childhood infections, can likewise lead to a virulent pneumonia in pregnant patients. Antiviral agents are recommended in pregnancy, but are not currently recommended for varicella or influenza pneumonia in children and nonpregnant immunocompetent adults. DIAGNOSIS Pneumonia is a clinical diagnosis based on a constellation of symptoms and signs; any individual symptom and clinical finding may lack accu racy for precise diagnosis. Physician judgment for chest radiographs or treating pneumonia (with or without a chest radiograph) is more sensitive than scoring systems to predict the need for chest radiography to diagnose pneumonia. 14 Diagnosis is based on fever, cough, and the presence of rales or rhonchi on lung examination with radiographic infiltrate confirmation. 15 Other findings, such as egophony or pecto riloquy, are specific for pneumonia but infrequently encountered in physical exam. The Infectious Diseases Society of America revised its CAP guidelines in 2017; it emphasizes clinical judgment by the provider and shared decision making with the patient regarding decisions on admission and testing and treatment options. No single set of recommendations for diagnostic testing can apply to all patients, and additional ancillary studies are used based on clinical judgment. In otherwise healthy, mildly ill, ambulatory patients, no further ancillary testing may be necessary. If a patient requires admission, additional tests may be necessary, including CBC and determination of serum electrolyte, BUN, creatinine, and glucose levels. Evaluation of arterial blood gas aids if patients are markedly desaturated or have severe respiratory distress. The usefulness of blood or sputum cultures depends on the degree of illness severity and the likelihood of hospital admission.

CBC and determination of serum electrolyte, BUN, creatinine, and glucose levels. Evaluation of arterial blood gas aids if patients are markedly desaturated or have severe respiratory distress. The usefulness of blood or sputum cultures depends on the degree of illness severity and the likelihood of hospital admission. Most patients do not require identification of a specific organism through blood or sputum analysis to direct antibiotic treatment. The incidence of positive blood cultures in nonhospitalized patients with CAP is low, pathogen identification usually does not alter treatment, and the overwhelming majority of patients respond to empiric antibiotic treatment. The value of sputum culture is similar to the value of blood cultures in these circumstances. In patients with fever, cough, and radiographic abnormalities, or in whom bacteremia is suspected, the etiology of the infection can be confirmed, but >80% of the time, no added information is possible, often because of poor sampling (sputum) or infrequent growth (blood). Detecting atypical agents usually requires titers from acute and conva lescent sera or direct fluorescent antibody testing. In patients with CAP who are hospitalized, the incidence of positive blood cultures increases with increasing disease severity. 16 Blood cultures are recommended for selected patients, including those admitted to the intensive care unit (ICU) and those with leukopenia, cavitary lesions, severe liver disease, alcohol abuse, asplenia, or pleural effusions (moderate level of evidence). 15 Regarding the usefulness of sputum cultures, many patients are unable to produce adequate sputum, the Gram stain is frequently negative, and results rarely change therapy. 17 Send sputum culture and Gram stain only when a good-quality specimen exists. Obtain a Legionella urine antigen test in ICU patients, alcoholics, or patients with a recent (within the past 2 weeks) travel history. The differential diagnosis of patients with cough and radiographic abnormality includes lung cancer, tuberculosis, pulmonary embolism, chemical or hypersensitivity pneumonitis, connective tissue disorders, granulomatous disease, and fungal infections. Because radiographic signs of pneumonia vary, it is difficult to predict the causative micro organism by its radiographic appearance. In general, patients with bacterial pneumonia are more likely to have unilobar or focal infiltrates than patients with viral or atypical pneumonia. Hilar adenopathy is more common in patients with atypical pneumonia. Pleural effusions can accompany bacterial, viral, or atypical pneumonia. Cavitary lesions occur in patients with bacterial pneumonia or tuberculosis. Lung abscesses are rare complications of pneumonia in the antibiotic era, but they sometimes occur due to S. aureus or Klebsiella . Pneumonia may mimic the appearance of lung masses, particularly when the cause is pneumococcal (“round pneumonia”) or staphylococcal. Q fever and tularemia may appear radiographically as discrete masses. PNEUMONIA IN SPECIAL POPULATIONS  PNEUMONIA IN ALCOHOLICS Alcoholics have a higher risk than the normal population for many lung diseases, including pneumonia, tuberculosis, pleurisy, bronchitis, empyema, and chronic obstructive pulmonary disease. Alcoholics often are undernourished, aspirate, have poor dentition, are smokers, and have concomitant liver disease. Compared with the nonalcoholic, the alcoholic has greater oropharyngeal colonization with gram-negative bacteria and is more likely to have pulmonary function abnormali ties, including reduced long volumes, increased airway resistance, and decreased diffusion capacity. In addition, alcohol depresses granulocyte FIGURE 65-3. Pneumonia suggesting Legionella. Tintinalli_Sec08_p0425-0472.indd 442 8/1/19 2:10 PM

gram-negative bacteria and is more likely to have pulmonary function abnormali ties, including reduced long volumes, increased airway resistance, and decreased diffusion capacity. In addition, alcohol depresses granulocyte FIGURE 65-3. Pneumonia suggesting Legionella. Tintinalli_Sec08_p0425-0472.indd 442 8/1/19 2:10 PM CHAPTER 65:  Community-Acquired Pneumonia, Aspir ation Pneumonia, and Noninf ectious Pulmonar y Infiltra tes      443 and lymphocyte counts and impairs delivery of neutrophils to sites of infection. S. pneumoniae is still the most common pathogen causing pneumonia in alcoholics, but Klebsiella species and Haemophilus species are also important agents of infection. In general, rates of pneumonia and death from pneumonia are higher in alcoholics compared with nonalcoholic patients.  PNEUMONIA IN DIABETICS Diabetes mellitus is an independent risk factor for pneumonia. Diabetic patients between the ages of 25 and 64 years old are four times more likely to have pneumonia and influenza, and diabetics are two to three times more likely than nondiabetics to die with pneumonia and influenza as an underlying cause of death. Pathogens that occur with increased frequency in diabetic patients include S. aureus, gram-negative bacteria, mucormycosis, and Mycobacterium tuberculosis. Infections due to S. pneumoniae and influenza are associated with increased morbidity and mortality in diabetic patients.  PNEUMONIA IN PREGNANT WOMEN CAP in pregnancy is one of the most serious nonobstetric infections complicating pregnancy. Maternal mortality from antepartum pneumonia is approximately 3%. Pregnancy does not seem to alter the course of bacterial pneumonia, but the prognosis of viral pneumonia during pregnancy is more serious than in the nonpregnant patient. Pregnant women who develop varicella pneumonia are five times more likely to be smokers and approximately 16 times more likely to have skin lesions suggestive of the disease. Do chest radiography in pregnant patients with symptoms of respiratory tract infection and varicella exposure. Pulse oximetry or arterial blood gas analysis helps identify patients with early respiratory compromise. IV acyclovir is often started in the ED, although there is little evidence that the timing of administration affects outcome. Influenza, particularly the H1N1 influenza strain, triggers severe viral pneumonia in pregnant women. Death from H1N1-associated pneumonia in pregnant women was higher among women who have underlying medical conditions (asthma, diabetes, hypertension, malignancy, rheumatologic, renal and cardiovascular disease). The death rate did not stratify out by age, trimester, or ethnicity. Of note, the death rate was lower in women treated with a neuraminidase inhibitor and directly correlated to time from onset of symptoms to initiation of treatment with a neuraminidase inhibitor. Therefore, initiate treatment as soon as possible when a pregnant or postpartum patient presents with an influenza-like illness. Pneumocystis jirovecii pneumonia (still called PCP for pneumocystis pneumonia) is the most common cause of acquired immuno deficiency syndrome–related death in pregnant women in the United States, with a mortality rate of approximately 50%. Respiratory failure requiring mechanical ventilation occurs in over half of these patients. Combination treatment with pentamidine, steroids, and eflornithine improves survival compared with patients treated with trimethoprimsulfamethoxazole alone.  PNEUMONIA IN THE ELDERLY Pneumonia is the most common infection in the elderly and represents the fifth leading cause of death among the elderly. 18 The incidence of lower respiratory tract infection in the elderly ranges from 25 to 44 cases per 1000 in the general population, with a mortality rate approaching 40%.

.  PNEUMONIA IN THE ELDERLY Pneumonia is the most common infection in the elderly and represents the fifth leading cause of death among the elderly. 18 The incidence of lower respiratory tract infection in the elderly ranges from 25 to 44 cases per 1000 in the general population, with a mortality rate approaching 40%. Chronic obstructive pulmonary disease, congestive heart failure, cardiovascular and cerebrovascular disease, lung cancer, dementia, diminished gag reflex, and other disorders that predispose the elderly to aspiration make them more susceptible to infection. The elderly are three times more likely to have pneumococcal bacteremia than younger patients. The mortality from pneumococcal pneumonia is three to five times greater in the elderly (up to 40%) than in those younger than age 65 years old. Atypical pathogens, such as Mycoplasma, are still more common in younger populations, but they do occur in the elderly. Influenza is the most common serious viral infection in the elderly. Postinfluenza bacterial pneumonia is most commonly caused by S. pneumoniae, S. aureus, or H. influenzae. This usually presents as a worsening of respiratory symptoms after several days of improvement. Elderly patients with pneumonia may present with falls, weakness, tremulousness, functional decline, GI symptoms, and delirium or confusion. Elderly patients are more likely to be afebrile on presentation, but are more likely than younger adults to have a serious bacterial infection when the temperature is higher than 38.3°C (100.9°F). Up to one third of elderly patients with CAP will not manifest leukocytosis. Poor prognostic indicators for pneumonia in the elderly include hypothermia or a temperature >38.3°C (100.9°F), leukopenia, immunosuppression, gram-negative or staphylococcal infection, cardiac disease, bilateral infiltrates, and extrapulmonary disease. Elderly patients with pneumonia frequently require hospitalization, and about 10% may require intensive care.  PNEUMONIA IN NURSING HOME PATIENTS Pneumonia is a major cause of morbidity, mortality, and hospitalization among nursing home residents.18,19 Nursing home–acquired pneumonia affects the oldest patients and those who have cerebrovascular disease, and is associated with high mortality risk scores at ED presentation. Nursing home patients are less likely than those living independently to have a productive cough or pleuritic chest pain, but more likely to be confused and have poorer functional status and more severe disease. 19 Eight variables are significant independent predictors of pneumonia in nursing home patients: increased pulse rate, respiratory rate ≥30 breaths/min, temperature ≥38°C (100.4°F), somnolence or decreased alertness, presence of acute confusion, lung crackles on auscultation, the absence of wheezes, and an increased leukocyte count. 20 A patient with one of these variables has a 33% chance of having pneumonia, whereas three or more variables suggest a 50% likelihood of pneumonia.20 Fewer than 10% of nursing home patients with pneumonia will have no respiratory symptoms. Fever, although nonspecific, is present in approximately 40% of cases of nurs ing home–acquired pneumonia. The most frequently reported pathogens among patients with nurs ing home–acquired pneumonia are S. pneumoniae , gram-negative bacilli, and H. influenzae. Because nursing home patients live in close proximity to each other, residents are subject to outbreaks of influenza. Unfortunately, vaccination against influenza is only approximately 33% to 55% effective in preventing postinfluenzal pneumonia in nursing home patients. M. pneumoniae and Legionella are uncommon causes of pneumonia in nursing home patients.

close proximity to each other, residents are subject to outbreaks of influenza. Unfortunately, vaccination against influenza is only approximately 33% to 55% effective in preventing postinfluenzal pneumonia in nursing home patients. M. pneumoniae and Legionella are uncommon causes of pneumonia in nursing home patients. Those with nursing home–acquired pneumonia are often admitted to the hospital for care, although some studies have suggested that patients can be treated in nursing homes with either IM or PO antibiotics. Nursing home patients are at risk for the organisms linked to healthcare– associated pneumonia, and treatment for methicillin-resistant S. aureus is recommended.  PNEUMONIA IN HUMAN IMMUNODEFICIENCY VIRUS PATIENTS Among HIV-seropositive individuals, the incidence of bacterial pneu monia is 5.5 per 100 person-years, an incidence higher than pneumocystis pneumonia in this population. 22 Among hospitalized patients with HIV , the incidence of bacterial pneumonia is as high as 12.5 per 100 person-years. CAP accounts for three fourths of bacterial pneumo nia diagnosed in patients hospitalized with HIV infection. Compared with HIV-seropositive patients hospitalized without pneumonia, those admitted with pneumonia generally have a lower CD4+ T-cell count, a higher Acute Physiology and Chronic Health Evaluation II score, a longer length of hospital stay, a greater chance of ICU admission, and a higher case fatality rate. S. pneumoniae is the most common cause of bacterial pneumonia in patients with HIV , recovered on blood culture in 60% of patients with HIV compared with 15% to 30% of patients without HIV infection who have pneumococcal pneumonia. Pseudomonas aeruginosa is a common cause of bacterial pneumonia in HIV-positive patients. HIV-positive patients with P . aeruginosa pneumonia are more likely to have a lower leukocyte and CD4+ T-cell count and a longer hospital stay, but similar case fatality rate. Tintinalli_Sec08_p0425-0472.indd 443 8/1/19 2:10 PM

a. Pseudomonas aeruginosa is a common cause of bacterial pneumonia in HIV-positive patients. HIV-positive patients with P . aeruginosa pneumonia are more likely to have a lower leukocyte and CD4+ T-cell count and a longer hospital stay, but similar case fatality rate. Tintinalli_Sec08_p0425-0472.indd 443 8/1/19 2:10 PM 444 SECTION 8: Pulmonary Disorders Opportunistic infections are more likely to occur with a lower CD4+ count. Bacterial infections are more likely to cause pneumonia when the CD4+ count is >800 cells/mm 3. Between 250 and 500 cells/mm 3, infection from M. tuberculosis, Cryptococcus neoformans, or Histoplasma capsulatum poses a greater risk. The risk of pneumocystis pneumonia is more likely when the CD4+ count is <200 cells/mm3. Bacterial pneumonia produces a pleural effusion in up to about 60% of patients with acquired immunodeficiency syndrome, most commonly due to S. pneumoniae and S. aureus. Non-Hodgkin’s lymphoma, Kaposi’s sarcoma, and adenocarcinoma of the lung are the three leading nonin fectious causes of pleural effusion in HIV patients. Patients with Kaposi’s sarcoma, cytomegalovirus pneumonia, and hydrostatic pulmonary edema may present with alveolar hemorrhage as seen by bloody fluid on bronchoalveolar lavage or frank hemoptysis. Pulmonary nodules in the HIV patient are often caused by opportunistic infection, bacterial pneumonia, and tuberculosis. Fever, cough, and a nodule size of <1 cm are independent predictors of an opportunistic infection. Miliary pneumonia on CT scan or chest radiograph may represent varicella pneumonia.  PNEUMONIA IN TRANSPLANT PATIENTS Bacterial pneumonia is less common after renal transplantation, but more common in patients receiving liver, heart, or lung transplants during the first 3 months after surgery, compared with other surgical patients. Gram-negative bacilli (especially P . aeruginosa associated with mechanical ventilation), S. aureus, and Legionella predominate in the first 3 months after transplantation. Klebsiella pneumoniae, Escherichia coli, and fungi may also cause pneumonia in this time period. These early-onset nosocomial bacterial pneumonias have a high mortality rate, approximately 33%. Cytomegalovirus, P . jirovecii , and fungal infections, especially Aspergillus species, are opportunistic infections and may be seen in the first 6 months after surgery. After 6 months posttransplant, bacteria more typical of CAP ( S. pneumoniae, H. influenzae) are the most likely pathogens and portend less mortality (see Chapter 297, “The Transplant Patient”). TREATMENT Emergency physicians play a prominent role in the initiation of treat ment for pneumonia. The timing of antibiotics for CAP has been a source of controversy. The previous 4-hour guideline has been largely discredited, and The Joint Commission (formerly the Joint Commission on Accreditation of Healthcare Organizations) is no longer assessing this measure. Patients should receive antibiotics promptly after diagnosis, although it is difficult to ascribe a particular time frame within which this should be accomplished. Many different specialty societies and task forces have developed guidelines for the treatment of adults with CAP , and these guidelines undergo periodic revision. These guidelines are interpreted and imple mented based on local practices, hospital formularies, and the particular characteristics of individual patients. The Infectious Diseases Society of America revised its guidelines in 2017, and a joint Infectious Diseases Society of America/American Thoracic Society guideline is due out in 2018. The drugs listed in Tables 65-4 through 65-9 are representative of recommended treatments 3,15,23 based on site acquisition and/or comor bidities, but are not meant to be a comprehensive list.

guidelines in 2017, and a joint Infectious Diseases Society of America/American Thoracic Society guideline is due out in 2018. The drugs listed in Tables 65-4 through 65-9 are representative of recommended treatments 3,15,23 based on site acquisition and/or comor bidities, but are not meant to be a comprehensive list. Treatment should take into account local resistance patterns. 15 Outpatient treatment is provided in Tables 65-4 and 65-5. Inpatient treatment is provided in Tables 65-6 through 65-9.  OUTPATIENT TREATMENT Outpatient treatment is listed in Tables 65-4 and 65-5. Recommended agents include a newer macrolide or a respiratory fluoroquinolone for a varying duration, depending on the agent. Doxycycline may also be used. Erythromycin is a very cost-effective agent for CAP but is associ ated with GI side effects in about 25% of adult patients and also causes photosensitivity. Clarithromycin has fewer GI side effects, although some patients may complain about a metallic taste. Azithromycin has the advantage of once-a-day dosing or single-dose therapy with the newer formulations. The newer fluoroquinolone agents, including moxifloxacin and levofloxacin, have extended coverage that includes both common bacterial agents and atypical agents, along with the advantage of once-a-day dosing. The Centers for Disease Control and Prevention’s Working Group recommends reserving fluoroqui nolones for patients who cannot tolerate other agents, with docu mented pneumococcal resistance, or failing other therapies. Do not give fluoroquinolones to patients with myasthenia gravis . Patients with significant comorbidities, including chronic cardiac, pulmo nary, renal, or hepatic disease; severe diabetics; chronic alcoholics; patients on immunosuppressive therapy; or patients with asplenia may require additional therapy. Patients who received broadspectrum antibiotics within the previous 3 months may be at risk for drug-resistant infection; in these patients, consider a respiratory fluoroquinolone or treatment with combination therapy using either an aminopenicillin or a third-generation cephalosporin with either a macrolide or doxycycline. TABLE 65-4 Therapy for Outpatient Treatment of Uncomplicated Patients* Class Examples Comments Macrolide

infection; in these patients, consider a respiratory fluoroquinolone or treatment with combination therapy using either an aminopenicillin or a third-generation cephalosporin with either a macrolide or doxycycline. TABLE 65-4 Therapy for Outpatient Treatment of Uncomplicated Patients* Class Examples Comments Macrolide Clarithromycin XL, 1000 milligrams PO each day for 7 d Azithromycin, 500 milligrams PO on day 1 and 250 milligrams on days 2–5 Respiratory fluoroquinolones could also be used, but the Centers for Disease Control and Prevention recommends reserving these agents for those who cannot tolerate or have failed other therapy. See Table 65-5. Tetracycline Doxycycline, 100 milligrams twice a day for 10–14 d Second-line choice. *Other drugs may also be effective. TABLE 65-5 Therapy for Outpatient Management of Patients With Significant Comorbidities* Without Criteria for Healthcare-Associated Pneumonia Class Examples Comments Fluoroquinolone Levofloxacin, 750 milligrams daily for 5 d Moxifloxacin, 400 milligrams daily for 7–14 d Other respiratory fluoroquinolones may also be used. β-Lactamase inhibitor penicillin derivative Amoxicillin-clavulanate, 2 grams twice daily A third-generation cephalosporin may be used instead of the aminopenicillin. Plus Plus Macrolide Azithromycin, 500 milligrams PO on day 1 and 250 milligrams on days 2–5 *Significant comorbidities include chronic heart, lung, liver, or renal disease; diabetes mellitus; alcoholism; malignancies; and asplenia. See text. Dosing may need adjustment for patients with renal insufficiency. Other therapies may also be effective. TABLE 65-6 Inpatient Therapy for Non–Intensive Care Unit Patients * With Community-Acquired Pneumonia Class Examples Comments Fluoroquinolone Levofloxacin, 750 milligrams IV Moxifloxacin, 400 milligrams IV Other respiratory fluoroquinolones may also be used. Cephalosporin Ceftriaxone, 1 gram IV Other third-generation cephalosporins may also be used in combination with other macrolides or doxycycline. Plus Plus Macrolide Azithromycin, 500 milligrams IV *Other drugs may also be effective; dosing may need adjustment for patients with renal insufficiency. Oral therapy with selected drugs may be acceptable for non–intensive care unit patients. Tintinalli_Sec08_p0425-0472.indd 444 8/1/19 2:10 PM

acrolides or doxycycline. Plus Plus Macrolide Azithromycin, 500 milligrams IV *Other drugs may also be effective; dosing may need adjustment for patients with renal insufficiency. Oral therapy with selected drugs may be acceptable for non–intensive care unit patients. Tintinalli_Sec08_p0425-0472.indd 444 8/1/19 2:10 PM CHAPTER 65:  Community-Acquired Pneumonia, Aspir ation Pneumonia, and Noninf ectious Pulmonar y Infiltra tes      445 TABLE 65-7 Empiric Therapy for Patients With Suspected Healthcare-Associated Pneumonia Three-Drug Regimen Recommended Class Examples Comments Antipseudomonal cephalosporin

acrolides or doxycycline. Plus Plus Macrolide Azithromycin, 500 milligrams IV *Other drugs may also be effective; dosing may need adjustment for patients with renal insufficiency. Oral therapy with selected drugs may be acceptable for non–intensive care unit patients. Tintinalli_Sec08_p0425-0472.indd 444 8/1/19 2:10 PM CHAPTER 65:  Community-Acquired Pneumonia, Aspir ation Pneumonia, and Noninf ectious Pulmonar y Infiltra tes      445 TABLE 65-7 Empiric Therapy for Patients With Suspected Healthcare-Associated Pneumonia Three-Drug Regimen Recommended Class Examples Comments Antipseudomonal cephalosporin Cefepime, 1–2 grams every 8–12 h Ceftazidime, 2 grams every 8 h An aminoglycoside may be substituted in place of the fluoroquinolone. Levofloxacin, 750 milligrams every 8 h, may be substituted for ciprofloxacin. Linezolid, 600 milligrams every 12 h, may be substituted for vancomycin. Plus Plus Fluoroquinolone Ciprofloxacin, 400 milligrams every 8 h* Plus Plus Anti-MRSA drug Vancomycin, 15 milligrams/kg every 12 h Antipseudomonal carbapenem Imipenem, 500 milligrams every 6 h Meropenem, 1 gram every 8 h An aminoglycoside may be substituted in place of the fluoroquinolone. Levofloxacin, 750 milligrams every 8 h, may be substituted for ciprofloxacin. Linezolid, 600 milligrams every 12 h, may be substituted for vancomycin. Plus Plus Fluoroquinolone Ciprofloxacin, 400 milligrams every 8 h* Plus Plus Anti-MRSA drug Vancomycin, 15 milligrams/kg every 12 h β-Lactam/β-lactamase inhibitor Piperacillin-tazobactam, 4.5 grams every 6 h An aminoglycoside may be substituted in place of the fluoroquinolone. Levofloxacin, 750 milligrams every 8 h, may be substituted for ciprofloxacin. Linezolid, 600 milligrams every 12 h, may be substituted for vancomycin. Plus Plus Antipseudomonal fluoroquinolone Ciprofloxacin, 400 milligrams every 8 h* Plus Plus Anti-MRSA drug Vancomycin, 15 mg/kg every 12 h Note: Healthcare-associated pneumonia risks include (1) patients hospitalized for 2 or more days within the past 90 days, (2) nursing home/long-term care residents, (3) patients receiving home IV antibiotic therapy, (4) dialysis patients, (5) patients receiving chronic wound care, (6) patients receiving chemotherapy, and (7) immunocompromised patients. Abbreviation: MRSA = methicillin-resistant Staphylococcus aureus. *See text. Dosing may need adjustment for patients with renal insufficiency. TABLE 65-8 Inpatient Therapy for Intensive Care Unit Patients* Class Example Comments Cephalosporin Ceftriaxone, 1 gram IV Other β-lactams may also be used in place of ceftriaxone. See Table 65-9 for additional recommendations. Plus Plus Macrolide Azithromycin, 500 milligrams IV Cephalosporin Ceftriaxone, 1 gram Other β-lactams may also be used in place of ceftriaxone. See Table 65-9 for additional recommendations. Plus Plus Fluoroquinolone Either moxifloxacin, 400 milligrams IV Levofloxacin, 750 milligrams IV Fluoroquinolone Moxifloxacin, 400 milligrams IV Aztreonam is generally well tolerated in penicillin-allergic patients.Plus or Either a monobactam Levofloxacin, 750 milligrams IV or Plus A lincosamide Either aztreonam, 1–2 grams IV Clindamycin, 600 milligrams IV Anti-MRSA drug (add if HCAP or MRSA risk) Vancomycin, 10–15 milligrams/kg IV Linezolid, 600 milligrams IV To be added to one of the above regimens for patients with MRSA or HCAP risk. Abbreviations: HCAP = healthcare-associated pneumonia; MRSA = methicillin-resistant Staphylococcus aureus. *Other combinations may also be used. Dosing may need adjustment for patients with renal insufficiency. TABLE 65-9 Inpatient Therapy for Patients With Pseudomonas Risk* Class Example Comments β-Lactam/β-lactamase inhibitor Piperacillin-tazobactam, 3.375 milligrams IV Other antipseudomonal cephalosporins or quinolones may be used. Carbapenems are also appropriate. Consider adding an aminoglycoside if substituting a macrolide. Plus Plus Fluoroquinolone Ciprofloxacin, 400 milligrams IV Monobactam Aztreonam, 1 gram IV May be used for patients with penicillin allergy. Carbapenems and aminoglycosides may also be appropriate.

r quinolones may be used. Carbapenems are also appropriate. Consider adding an aminoglycoside if substituting a macrolide. Plus Plus Fluoroquinolone Ciprofloxacin, 400 milligrams IV Monobactam Aztreonam, 1 gram IV May be used for patients with penicillin allergy. Carbapenems and aminoglycosides may also be appropriate. Plus Plus Fluoroquinolone Either moxifloxacin, 400 milligrams IV Levofloxacin, 750 milligrams IV Anti-MRSA drug (add if HCAP or MRSA risk) Vancomycin, 10–15 milligrams/kg IV Linezolid, 600 milligrams IV To be added to one of the above regimens for patients with MRSA or HCAP risk. Abbreviations: HCAP = healthcare-associated pneumonia; MRSA = methicillin-resistant Staphylococcus aureus. *Other combinations may also be used. Dosing may need adjustment for patients with renal insufficiency.  INPATIENT TREATMENT Inpatient treatment is provided in Tables 65-6 through 65-9. Inpatients not admitted to the ICU benefit from coverage for both atypical organ isms and cell-walled organisms. If trying monotherapy, use a respiratory fluoroquinolone, although this is discouraged (see above) to avoid resistance and Clostridium difficile outbreaks. Do not use monotherapy with macrolides or doxycycline; use aminopenicillins or cephalosporins and a macrolide or doxycycline. Patients ill enough for ICU care are optimally treated with combina tion agents, including an aminopenicillin or cephalosporin with either a respiratory fluoroquinolone or a macrolide. Penicillin-allergic patients can receive a respiratory fluoroquinolone with either aztreonam or clindamycin. For patients at risk for Pseudomonas infection, includ ing those with chronic structural lung disease, patients on high-dose steroids, and patients recently in an ICU, add coverage with at least two agents active against the organism. This may include an antipseu domonal β-lactam such as piperacillin-tazobactam or cefepime with a respiratory fluoroquinolone. Alternatively, a carbapenem, such as imi penem, along with either a fluoroquinolone or aminoglycoside, may be appropriate. Treat penicillin-allergic patients with a monobactam along Tintinalli_Sec08_p0425-0472.indd 445 8/1/19 2:10 PM

lactam such as piperacillin-tazobactam or cefepime with a respiratory fluoroquinolone. Alternatively, a carbapenem, such as imi penem, along with either a fluoroquinolone or aminoglycoside, may be appropriate. Treat penicillin-allergic patients with a monobactam along Tintinalli_Sec08_p0425-0472.indd 445 8/1/19 2:10 PM 446 SECTION 8: Pulmonary Disorders with a fluoroquinolone. If the combination does not include two drugs with antipseudomonal activity, then consider adding in an aminoglycoside. Patients admitted to the ICU with healthcare-associated pneumo nia require coverage for methicillin-resistant S. aureus with drugs such as vancomycin or linezolid.23,24 DISPOSITION AND FOLLOW-UP Most patients with CAP do not require hospitalization. 25 Many factors influence the prognosis and outcome of CAP . There are multiple clinical decision tools available to assist in the disposition process. The Pneumonia Severity Index is the best studied and recommended tool; many perceive it to be accurate but hard to use (although online tools exist) (Table 65-10). The CURB-65 rule looks at the presence of confusion, uremia >7 mmol/L, respiratory rate ≥30 breaths/min, diastolic blood pressure ≤60 mm Hg, and age ≥65 years old. 21 The CRB-65 uses the same variables but eliminates the uremia measurement. Patients with a CURB-65 or CRB-65 score of <2 have a low mortality rate, but neither the CURB-65 nor CRB-65 score is as well studied or validated as the Pneumonia Severity Index. Scoring systems provide a starting point for evaluation of the patient. Some patients may be eligible for admission based on other social or medical factors not assessed by these scores, but their best utility for scoring systems is as a tool to increase the number of appropriate patients treated on an outpatient basis and to limit unnecessary admissions. Admission decision patterns for CAP patients among emergency physicians are widely variable and often not linked to illness or patient factors. After admission, the next decision is to determine which patients require admission to the ICU. Admit patients with sepsis or those requiring mechanical ventilation to an ICU setting. Other criteria for ICU admission include a markedly elevated respiratory rate, a Pa o 2/ Fio2 ratio ≤250, multilobar infiltrates, confusion, uremia with a BUN >20 milligrams/dL, leukopenia, thrombocytopenia, hypothermia, hyponatremia, lactic acidosis, and asplenia (Tables 65-10, 65-11, and 65-12). Pneumonia Severity Index class V and CURB-65 patients with a score of ≥3 may need intensive care. 21 Most patients will achieve some measure of resolution within 3 to 5 days after the initiation of antibiotics. Many hospitalized patients can be switched to oral antibiotics at approximately 3 days and subsequently discharged to complete a course of therapy. However, about half of patients are still symptomatic at 30 days, with a significant minority of patients experiencing chest pain, malaise, or mild dyspnea even 2 to 3 months after treatment. Educate patients about smoking cessation and moderation of alcohol use, and provide information about rest, nutri tion, hydration, follow-up, and the importance of pneumococcal and influenza vaccination. TABLE 65-10 Pneumonia Severity Index Step 1: Assignment to risk class I •   Age >50 y old •   Comorbid conditions •   Neoplastic disease •   Cerebrovascular disease •   Congestive heart failure •   Renal disease •   Liver disease •   Physical examination abnormalities •   Altered mental status •   Pulse >125 beats/min •   Respiratory rate >30 breaths/min •   Systolic blood pressure <90 mm Hg •   Temperature <35°C (95°F) or >40°C (104°F) If any criteria positive, go to Step 2 which is collecting more laboratory and other data and assigning points (Table 65-11).

mination abnormalities •   Altered mental status •   Pulse >125 beats/min •   Respiratory rate >30 breaths/min •   Systolic blood pressure <90 mm Hg •   Temperature <35°C (95°F) or >40°C (104°F) If any criteria positive, go to Step 2 which is collecting more laboratory and other data and assigning points (Table 65-11). If all negative, then assign to risk class I. TABLE 65-11 Pneumonia Severity Index Risk Classes II to V Criteria Points Demographics Male gender Age (y) Female gender Age (y) – 10 Nursing home resident 10 Coexistent illness Neoplastic disease 30 Congestive heart failure 20 Cerebrovascular accident 10 Renal disease 10 Liver disease 10 Physical examination Abnormal mental status 20 Pulse ≥125 beats/min 20 Respiratory rate >30 breaths/min 20 Blood pressure (<90 mm Hg) 15 Temperature <35°C (95°F) or >40°C (104°F) 10 Ancillary studies Arterial pH <7.35 30 BUN ≥30 milligrams/dL 20 Sodium >130 mEq/L 20 Glucose >250 milligrams/dL 10 Hematocrit <30% 10 Pao2 <60 mm Hg 10 Pleural effusion 10 Summary points risk assignment Sum of points <70 = risk class II Sum of points 71–90 = risk class III Sum of points 91–130 = risk class IV Sum of points >130 = risk class V TABLE 65-12 Prediction of Mortality From Pneumonia Class Points Mortality (%) Treatment Recommendation I No predictors 0.1 Outpatient II <70 0.6 Outpatient III 71–90 2.8 Individualized IV 91–130 8.2 Inpatient V >130 29.2 Inpatient  ASPIRATION PNEUMONIA INTRODUCTION AND EPIDEMIOLOGY Aspiration is the inhalation of oropharyngeal contents into the respiratory tract. 26-29 Aspiration pneumonia is the inhalation of infectious material from the oropharynx into the lower respiratory tract that causes infection of the lung parenchyma. 29 Aspiration alone does not cause pneumonia. Approximately half of healthy adults aspirate when sleeping. Aspira tion pneumonitis is an irritation and inflammatory response to aspirated material. Pneumonitis can develop when the aspirated material has a low pH (<2.5) or when other components of the aspirate cause an inflammatory response. Tintinalli_Sec08_p0425-0472.indd 446 8/1/19 2:10 PM

hy adults aspirate when sleeping. Aspira tion pneumonitis is an irritation and inflammatory response to aspirated material. Pneumonitis can develop when the aspirated material has a low pH (<2.5) or when other components of the aspirate cause an inflammatory response. Tintinalli_Sec08_p0425-0472.indd 446 8/1/19 2:10 PM CHAPTER 65:  Community-Acquired Pneumonia, Aspir ation Pneumonia, and Noninf ectious Pulmonar y Infiltra tes      447 TABLE 65-13 Risk Factors for Aspiration29,31 •   Advanced age •   Altered level of consciousness •   Anatomic abnormality of upper airway •   Dementia •   Esophageal disorders •   Gastroesophageal reflux •   Neuromuscular/neurologic disease •   Poor oral hygiene •   Prior history of aspiration •   Prolonged supine position •   Retained gastric material •   Tube feedings PATHOPHYSIOLOGY Aspiration pneumonia is a result of a complex interplay of the aspirated material, aspirated volume, pH, patient physiology, and pulmonary defense mechanisms. There is a large overlap in the etiology, symp toms, and bacterial flora of aspiration pneumonia and CAP , which often makes clinical differentiation difficult. In addition, over the years, microbiology patterns of aspiration pneumonia have changed. Risk factors for aspiration pneumonia include prior history of aspiration, altered level of consciousness, anatomic abnormality of the airway, neuromuscular disease, GI disease, retained gastric contents, percutaneous gastric or jejunal tube, nasogastric tube, prolonged supine position, poor oral hygiene, and advanced age 31 (Table 65-13). Oral hygiene risk factors for development of aspiration pneumonia include four or more decayed teeth, gingivitis, periodontitis, periodontal disease–causing organisms in saliva, and dental plaque. 32 Medications that decrease saliva production also predisposed to higher oral bacterial counts. Medications (diuretics, anticholinergics, anxiolytics, antipsy chotics, levodopa) can reduce salivary flow and lead to increased oral bacterial counts. Aspiration in younger patients tends to result from obtundation sec ondary to intoxication, seizures, or medication overdose. If a large vol ume of fluid is aspirated, it may lead to asphyxia. Y ounger patients with aspiration pneumonia may remember the aspiration incident several days earlier or have a history of substance abuse with frequent periods of amnesia or loss of consciousness. Aspiration in older patients results from preexisting risk factors such as enteral feeding, anatomic abnormalities (head, neck, and esopha gus), physiologic abnormalities of the mechanisms of deglutition and decreased immune response (cellular and humeral), decreased mucosal ciliary function, decreased mucus production, and decreased cough reflex. An increased stimulus is needed to provoke a cough reflex in older patients. Aspiration pneumonia is the second leading cause of infection in nursing homes, behind urinary tract infections. 34 It is the leading cause for transfer from nursing home to the hospital and the leading cause of death in nursing home patients. 34 In nursing home patients, the aspiration incident may not be witnessed, and time of aspiration will be unknown. CLINICAL FEATURES AND TREATMENT Symptoms of aspiration pneumonitis tend to develop rapidly, with onset of shortness of breath, bronchospasm, hypoxia, and low-grade fever within a few hours of the aspiration. Symptoms typically resolve within 48 hours. Recent research by Driver et al 36 demonstrated that 8% of patients developed aspiration pneumonia after emergency endotracheal intubation. There were no intubation factors that were different in those patients who developed aspiration pneumonia and those who did not.

ration. Symptoms typically resolve within 48 hours. Recent research by Driver et al 36 demonstrated that 8% of patients developed aspiration pneumonia after emergency endotracheal intubation. There were no intubation factors that were different in those patients who developed aspiration pneumonia and those who did not. The National Emergency Airway Registry III investigators demonstrated witnessed aspiration in 5% of emergency endotracheal intubations, and occult aspiration occurs in 22% to 50% of prehospital emergency intubations. Aspiration syndromes include aspiration pneumonia, aspiration pneumonitis (Mendelson’s syndrome), acute airway obstruction, exogenous lipoid pneumonia, chronic interstitial fibrosis, Mycobacterium fortuitum pneumonia, and diffuse aspiration bronchiolitis 39 (Table 65-14). There is a broad spectrum of physical presentations for patients with aspiration pneumonia. The nursing home patient may appear in no distress and present with decreased appetite, weakness, altered sensorium, or fever; vital signs may be normal or show fever, tachycardia, tachypnea, and hypotension. Y ounger patients with acute aspiration of solid or liquid material may present in a more dramatic fashion with cough, shortness of breath, and possible hypoxia. Rales, rhonchi, and wheezes may exist. Unilateral (total occlusion) or sonorous (partial occlusion) breath sounds may be present in the case of occlusion of a mainstem bronchus. Aspiration of irritative substances such as oils, sterile gastric contents with pH of ≤2.5, activated charcoal, diatrizoic acid, or alendronate sodium all can cause an intense inflammatory reaction. Aspiration of pills such as potassium, iron, or metformin can cause local inflam mation and may lead to bronchial stenosis. Sucralfate and pomegranate supplements can expand when in contact with the bronchial mucosa and cause bronchial obstruction. A few patients may require chest CT to evaluate for lung abscess or foreign body, as aspiration is a risk factor for pulmonary abscess formation. After obtaining blood (and possibly adequate sputum) cultures, initiate antibiotic treatment, but do not delay antibiotics to obtain cultures. Clindamycin, a carbapenem, ampicillin-sulbactam, and moxifloxa cin are all reasonable treatments for suspected community-acquired aspiration pneumonia. 30 Bronchodilators aid aspiration-induced bronchospasm. DISPOSITION Healthy persons who aspirate small volumes of nontoxic material may be observed for a short time, approximately 1 to 2 hours, and if stable and reliable, discharged to return for worsening symptoms. Antibiotic treatment is not needed for witnessed aspiration of a small amount of nontoxic liquid provided the patient’s symptoms (cough, low-grade fever) resolve within 24 to 48 hours. Most patients with community-acquired aspiration pneumonia require admission. It is difficult to clinically distinguish aspiration pneumonia from non–aspiration-related pneumonia. 30 The history and clinical environment (older patient, nursing home, sedation, dysphagia, poor dentition, substance abusing) will lead to an impression of aspira tion pneumonia. The same admission guidelines apply to aspiration pneumonia as for other pneumonias.  NONINFECTIOUS PULMONARY INFIL TRATES INTRODUCTION AND EPIDEMIOLOGY A noninfectious pulmonary infiltrate is a radiologic abnormality that is not due to an infection. Suspect it when no other infectious findings exist or after antibiotics fail to improve symptoms.

apply to aspiration pneumonia as for other pneumonias.  NONINFECTIOUS PULMONARY INFIL TRATES INTRODUCTION AND EPIDEMIOLOGY A noninfectious pulmonary infiltrate is a radiologic abnormality that is not due to an infection. Suspect it when no other infectious findings exist or after antibiotics fail to improve symptoms. Noninfectious infil trates occur in response to a wide variety of pathophysiologic processes TABLE 65-14 Aspiration Syndromes29,39 •   Acute airway obstruction •   Aspiration pneumonias •   Aspiration pneumonitis •   Chronic interstitial fibrosis •   Diffuse aspiration bronchiolitis •   Exogenous lipoid pneumonia •   Mycobacterium fortuitum pneumonia Tintinalli_Sec08_p0425-0472.indd 447 8/1/19 2:10 PM

rocesses TABLE 65-14 Aspiration Syndromes29,39 •   Acute airway obstruction •   Aspiration pneumonias •   Aspiration pneumonitis •   Chronic interstitial fibrosis •   Diffuse aspiration bronchiolitis •   Exogenous lipoid pneumonia •   Mycobacterium fortuitum pneumonia Tintinalli_Sec08_p0425-0472.indd 447 8/1/19 2:10 PM 448 SECTION 8: Pulmonary Disorders TABLE 65-15 Noninfectious Causes of Pulmonary Infiltrates Disease Pathophysiology Chest Radiography Findings Symptoms Allergic bronchopulmonary Aspergillosis Hypersensitivity reaction to Aspergillus fumigatus. Most common in patients with asthma or cystic fibrosis. Eosinophils fill small airways and alveolar spaces due to inflammation. Bronchiectasis. Branching tubular opacities may be seen, usually predominantly or exclusively involving upper lobes. Dyspnea, wheezing, productive cough; may have hemoptysis and occasionally fever. Acute eosinophilic lung disease Cause unknown. Association with new or binge smoking. Eosinophils accumulate in distal airways and alveolar and interstitial spaces. Nonspecific bilateral consolidations and reticular opacities. Dyspnea, fever, nonproductive cough, and wheezing. In acute forms, hypoxia and potential for rapid progression to respiratory failure. Steroid responsive. Hypersensitivity pneumonitis (extrinsic allergic alveolitis) Inflammation of the alveoli secondary to hypersensitivity in response to inhaled organic dust. Diffuse micronodular interstitial infiltrates. May see ground-glass densities in the lower or mid-lung fields. Bases spared. Fever, chills, malaise, cough, chest tightness, dyspnea, and headache. Organizing pneumonia (bronchiolitis obliterans organizing pneumonia [BOOP]) Inflammation of the bronchioles and surrounding tissues, leading to loss of the integrity of the bronchioles and organizing pneumonia without infection. Cryptogenic organizing pneumonia if immunocompromised or connective tissue diseases (e.g., SLE, rheumatoid arthritis, dermatomyositis). Patchy multifocal alveolar infiltrates without effusion. Cough, dyspnea, fever. Antinuclear cytoplasmic antibody (ANCA)–associated vasculitides: granulomatosis with polyangiitis (Wegener’s granulomatosis), Churg- Strauss syndrome Both systemic vasculitides of small and medium-sized vessels of unknown origin. Wegener’s characterized by necrotizing granulomatous vasculitis with involvement of upper respiratory tract, lung parenchyma, and kidneys. Churg-Strauss disease is an allergic eosinophilic condition. Most are asthmatic. Bilateral peripheral, patchy, alveolar infiltrates and nodules. Cough, dyspnea, allergic rhinitis/sinusitis. May have skin, coronary, or intestinal involvement. Acute interstitial pneumonia Idiopathic or secondary (chemical agents). Three stages: interstitial edema spreads to alveoli with hemorrhage and hyaline membrane formation (exudative), organization of fibrinous exudate (proliferative), scarring and cyst formation and honey comb fibrosis (fibrotic). Normal for first 12–24 h. Bilateral opacities with sparing of costophrenic angles. Minimal or no pleural effusion. “White lung” due to extensive consolidation. Rapid progression to respiratory failure. Mortality rate higher in those with comorbidities. Sarcoidosis Systemic granulomatous disease of unknown etiology. Noncaseating pulmonary granulomas. 4 stages: bilateral hilar adenopathy; bilateral hilar adenopathy with reticulonodular pulmonary opacities; pulmonary opacities only; pulmonary fibrosis. Dyspnea, cough, weight loss; skin lesions may also be found. May be asymptomatic. Anti–glomerular basement membrane antibody disease (Goodpasture’s syndrome) Autoimmune disease affecting the lungs and kidney due to autoantibodies to type IV collagen. Causes hemorrhagic interstitial pneumonitis.

nly; pulmonary fibrosis. Dyspnea, cough, weight loss; skin lesions may also be found. May be asymptomatic. Anti–glomerular basement membrane antibody disease (Goodpasture’s syndrome) Autoimmune disease affecting the lungs and kidney due to autoantibodies to type IV collagen. Causes hemorrhagic interstitial pneumonitis. Diffuse, bilateral, predominantly alveolar densities with sparing of the apices and costophrenic angles. Fatigue, dyspnea, cough with hemoptysis; may have simultaneous hematuria. Drug-induced pneumonitis Causes include chemotherapeutic, immunosuppressive, antimicrobial, and herbal agents. Typically, bilateral interstitial infiltrates. Cough, mild fever, dyspnea. Potentially hypoxia. Chemical pneumonitis Inflammatory reaction to the presence of foreign sub stance, such as barium, petroleum distillates, pesticide, or irritating gases. Diffuse alveolar and interstitial infiltrates. History of exposure or aspiration of sub stance; acute dyspnea, cough, and possibly wheezing. Radiation pneumonitis Interstitial pulmonary inflammation seen in 5%–15% of patients with thoracic radiation treatment. Subtle hazy ground-glass densities to marked patchy infiltrates or homogenous consolidation. Air bronchograms are commonly present. Symptoms occur 1–6 months after treatment: low-grade fever, cough, fullness in the chest. Alveolar cell carcinoma, often called bronchiolar or bronchioloalveolar carcinoma Adenocarcinoma originating in a terminal bronchiole and spreading across the alveolar walls. Peripheral alveolar infiltrates. May see peripheral nodule or mass. Often severe coughing dyspnea and copious sputum production. May mimic pneumonia, but no fever, leukocytosis, or response to antibiotics. Leukemic infiltrates Most common in myeloid leukemia when peripheral blast cell counts exceed 100,000/mL. Primitive myeloid leukemic cells invade through the endothelium of the lung capillary beds, yielding hemorrhage. Interstitial or alveolar infiltrates. Diffuse infiltrates associated with hypoxia and need for intubation; focal infiltrates associated with coexistent pneumonia. Respiratory distress, hypoxemia, and may progress to respiratory failure. Fat emboli ED presentations are typically after trauma, associated with long bone fracture. Interstitial prominence, suggesting interstitial edema. Radiographic findings may be delayed by hours after trauma Dyspnea, cough, hemoptysis, and pleural pain. May be associated with confusion, stupor, delirium, and a petechial skin rash, most commonly on the chest. Alveolar hemorrhage In the setting of chemotherapy induction for leukemia and thrombocytopenia (<20,000/mL), hemorrhage filling alveoli is common from endobronchial and interstitial sources. Also seen with SLE. Focal or diffuse alveolar infiltrates. Dyspnea, hemoptysis; symptoms are frequently less severe than radiographic appearance would predict. Acute respiratory distress syndrome Reaction of the lung to a number of precipitating causes, including sepsis, trauma, surgeries, transfusions, and therapeutically induced immunosuppression. Classically, patchy peripheral infiltrates that extend to the lateral lung margins suggest the diagnosis. Hypoxia, tachypnea, rales. Abbreviation: SLE = systemic lupus erythematosus. Tintinalli_Sec08_p0425-0472.indd 448 8/1/19 2:10 PM