Browse the corpus

CHAPTER 66:  Lung Empyema and Absc ess      449 involving the respiratory, cardiovascular, and immune systems or may be due to the infiltration of malignant cells. Some common noninfec tious causes of pulmonary infiltrates are congestive heart failure, aspiration pneumonitis, and pulmonary embolism. CLINICAL FEATURES The main symptom of noninfectious pulmonary infiltrates is dyspnea. Some disorders present with hemoptysis, cough, chest pain, or fatigue. Fever can also be a symptom of autoimmune disease exacerbation. It may be impossible to clinically differentiate a noninfectious source from an infectious source of fever in the ED. Table 65-15 lists the most common causes of acute noninfectious pulmonary infiltrates and their key clinical features, pathophysiology, and chest radiology findings. 41-48 Diffuse alveolar hemorrhage is the most common manifestation of pul monary vasculitis from asymptomatic chest radiograph abnormalities to severe respiratory failure. 45,48 TREATMENT Treatment is guided by the main differential diagnosis. Assess gas exchange with pulse oximetry in all patients, and use selective arterial blood gas analysis in patients who are ill, hypoxemic, or with underlying chronic lung disease; use noninvasive or mechanical ventilation as needed. Definitive treatment for noninfectious pulmonary disease depends on the underlying cause and will occur after ED stabilization. Many of the disorders listed in Table 65-15 are treated acutely with corticosteroids such as methylprednisolone (0.5 to 1 gram IV). 49 Additional immunosuppressive drugs may be initiated by the admitting physician. DISPOSITION AND FOLLOW-UP Patients suspected of having a noninfectious cause of pulmonary infil trates require testing beyond the capabilities of the ED. Hospitalization should be based on the severity of the medical illness, with attention to hypoxemia, hypercapnia, and work of breathing. Stable patients with mild symptoms may be referred to a pulmonologist, rheumatologist, or another specialist for further outpatient evaluation and treatment. REFERENCES The complete reference list is available online at www.TintinalliEM.com. Lung Empyema and Abscess Sharon E. Mace Eric Anderson  EMPYEMA INTRODUCTION AND EPIDEMIOLOGY Empyema is pus in the pleural space. A parapneumonic effusion is a pleural effusion associated with a lung infection, usually pneumonia but infrequently a lung abscess. Bacterial pneumonia with a parapneumonic effusion is the most common precursor, seen in about 60% of empyema patients. 1 Other causes of empyema are complications of chest surgery (22%), trauma (4%), esophageal perforation (4%), complications of chest tube/thoracentesis (4%), an extension from a subdiaphragmatic infection (3%), and assorted triggers (7%), including a hemothorax, chylothorax, or hydrothorax that becomes infected due to a systemic infection with hematogenous spread such as septicemia. 1,2 CHAPTER Of the approximately 1 million pneumonia patients hospitalized each year in the United States, 20% to 40% develop a parapneumonic effu sion; 5% to 10% of patients with a parapneumonic effusion develop an empyema. 3,4 Mortality in adults is about 20%. 5 With the advent of antibiotics, the incidence of empyema decreased in the first half of the 20th century, but since the 1990s, the incidence of empyema has increased in the United States and worldwide.

sion; 5% to 10% of patients with a parapneumonic effusion develop an empyema. 3,4 Mortality in adults is about 20%. 5 With the advent of antibiotics, the incidence of empyema decreased in the first half of the 20th century, but since the 1990s, the incidence of empyema has increased in the United States and worldwide. 3,6 Predisposing factors for empyema include aspiration (and the conditions causing this event, notably altered swallowing), respiratory disease impairing ciliary function, immunocompromise, malignancy, IV drug abuse, alcoholism, diabetes, gastroesophageal reflux disease, and poor oral hygiene.1 CLINICAL FEATURES Suspect empyema if symptoms of pneumonia (fever, cough, dyspnea, pleuritic chest pain, and malaise) do not resolve with therapy. The onset of empyema may be insidious, with patients appearing chronically ill with weight loss, anemia, and night sweats. Physical examination findings include decreased breath sounds, dullness to percussion, decreased tactile fremitus, and occasionally a friction rub. 7 Pain from an underlying effusion or empyema may cause splinting with respiration. If there is an underlying pulmonary infection, rales or rhonchi may exist. DIAGNOSIS Diagnostic criteria for empyema are aspiration of grossly purulent material on thoracentesis and at least one of the following: thoracen tesis fluid with a positive Gram stain or culture, pleural fluid glucose <40 milligrams/dL, pH <7.2, or lactate dehydrogenase >1000 IU/L. For empyema from tuberculosis, absolute lymphocyte count on pleural fluid is useful, although other markers such as interferon release assays or adenosine deaminase show promise. 4 Pleural biopsy is diagnostic in 55% to 70% of patients, demonstrating a granuloma and/or being culture positive. A pleural-based opacity on a chest radiograph, including a lateral decubitus film, suggests a pleural effusion or empyema. POCUS accurately identifies pleural effusions and empyemas, differentiates a loculated effusion from a mass, and guides thoracentesis and chest tube placement. A chest CT scan with IV contrast can assess for a loculated effusion or empyema and identify any other abnormalities present. TREATMENT The definitive treatment of an empyema is drainage and antibiotics.3,8 In addition, treat any underlying disease, especially pneumonia. NSAIDs or opioids can decrease pleuritic pain. Thoracentesis and drainage aid in the diagnosis and provide symptomatic relief for dyspnea. The common organisms in empyema stratified by associated pathology are listed in Table 66-1. 2,9 In about 40% of cases, cultures are negative,10 and anaerobic species are particularly difficult to culture. Newer molecular analysis or nucleic acid amplification technology may lead to a higher detection rate for the underlying pathogen(s). The choice of antibiotics depends on the clinical presentation, local patterns, and results of diagnostic studies including cultures. Most antibiotics have adequate penetration into the pleural space with the exception of the aminoglycosides. 11 The detection of an aerobic organ ism does not preclude antibiotic coverage for anaerobes because there is a 23% incidence of mixed aerobic and anaerobic infections, according to one study. 12 Thus, empiric antibiotic coverage usually includes anaerobic coverage as well as coverage for other pathogens as indicated by the clinical situation, at least initially until culture results are known. Choices for empiric therapy for anaerobes include a β-lactam with β-lactamase activity, such as piperacillin-tazobactam or ampicillinsulbactam, a carbapenem, or clindamycin.

robic coverage as well as coverage for other pathogens as indicated by the clinical situation, at least initially until culture results are known. Choices for empiric therapy for anaerobes include a β-lactam with β-lactamase activity, such as piperacillin-tazobactam or ampicillinsulbactam, a carbapenem, or clindamycin. Options for gram-negative aerobic pathogens are a second- or third-generation cephalosporin plus metronidazole, a carbapenem, or a β-lactam aminopenicillin with β-lactamase activity (e.g., piperacillin-tazobactam or ampicillinsulbactam). There are many antibiotic options for gram-positive Tintinalli_Sec08_p0425-0472.indd 449 8/1/19 2:10 PM

tive aerobic pathogens are a second- or third-generation cephalosporin plus metronidazole, a carbapenem, or a β-lactam aminopenicillin with β-lactamase activity (e.g., piperacillin-tazobactam or ampicillinsulbactam). There are many antibiotic options for gram-positive Tintinalli_Sec08_p0425-0472.indd 449 8/1/19 2:10 PM 450 SECTION 8: Pulmonary Disorders TABLE 66-1 Common Organisms in Empyema and Associated Pathology 2,9 Pathology Organism Pneumonia Streptococcus pneumoniae Staphylococcus aureus Pneumonia (unimmunized with Haemophilus influenzae type B vaccine) H. influenzae Lung abscess Mixed oropharyngeal anaerobes Aspiration pneumonia S. aureus Recent thoracotomy Gram-negative bacilli Chest trauma S. aureus Gram-negative bacilli Contiguous abdominal infection Gram-negative bacilli Anaerobes Esophageal rupture Mixed oropharyngeal organisms Postprocedure Methicillin-resistant S. aureus Pseudomonas Hospital-acquired empyema Methicillin-resistant S. aureus Pseudomonas Pneumonia in the setting of human immunodeficiency virus Tuberculosis Fungal infections organisms including a β-lactam, with the exception of coverage for methicillin-resistant Staphylococcus aureus, which requires vancomycin or other antibiotics that cover methicillin-resistant S. aureus. In patients with postprocedure or hospital-acquired empyema, consider coverage for methicillin-resistant S. aureus and Pseudomonas aeruginosa . Initial therapy often consists of two antibiotics to cover both Staphylococcus and anaerobes; monotherapy with a penicillin derivative or metronidazole is inadequate coverage. After initial drainage of the empyema plus IV antibiotics, switch to oral agents until there is clinical and radiographic improvement. Modify empiric antibiotics once culture results return and the clinical course is apparent. Fibrinolytics (e.g., urokinase, alteplase, or streptokinase) can improve drainage of loculated parapneumonic effusions and empyemas. The Multicenter Intrapleural Streptokinase Trial (MIST) 1 used intrapleu ral streptokinase, and MIST 2 used alteplase and DNAase for pleural infection. 13,14 The results are mixed, making fibrinolytics an option that may lessen the frequency of later surgical intervention. 15-17 A blinded randomized trial comparing double placebo, alteplase and DNase, alteplase and placebo, or DNAase and placebo found that DNase alone or alteplase alone was ineffective, but the combination of alteplase and DNase improved fluid drainage, decreased the frequency of surgical referral, and decreased the length of hospital stay. About one third of patients treated with antibiotics and chest tube drainage need surgical drainage. 15 The MIST 1 found no difference in mortality or need for thoracic surgery between large (15F to 20F), medium (10F to 14F), or small (<10F) tubes, but did report that pain was much decreased with the smaller tube sizes. 14 Video-assisted tho racoscopic surgery allows debriding of empyemas that fail tube thora costomy drainage and antibiotic therapy. Video-assisted thoracoscopic surgery can be followed by or converted to a thoracotomy if pleural fluid drainage remains insufficient.  LUNG ABSCESS INTRODUCTION AND PATHOPHYSIOLOGY Lung abscess is characterized by localized necrosis of the lung paren chyma and is typically caused by suppurative microbial infection. Initial infection is usually caused by aspiration of oral contents. Type 3 Streptococcus pneumoniae and S. aureus are major causes of lung abscess, with an increasing frequency of Klebsiella pneumoniae infection. 17 In a Japanese study, Streptococcus spp. (59.8%), anaerobes (26.2%), and Gemella spp. (9.8%) all existed in community-acquired lung abscesses.18 Mycobacterium tuberculosis and Actinomycetes spp. were more common in lung abscesses that extended to the chest wall.

ncreasing frequency of Klebsiella pneumoniae infection. 17 In a Japanese study, Streptococcus spp. (59.8%), anaerobes (26.2%), and Gemella spp. (9.8%) all existed in community-acquired lung abscesses.18 Mycobacterium tuberculosis and Actinomycetes spp. were more common in lung abscesses that extended to the chest wall. 18 Primary lung abscess can occur in individuals in good health or in those prone to aspiration. Approximately 80% of lung abscesses are primary, 19 and the overall reported mortality rate varies between 1% and 38.2%.18,20,21 Secondary lung abscess is associated with malignancy, immunosuppression, extrapulmonary infection, sepsis, or complications of surgery. The mortality rate in secondary lung abscess is often >50%. Lung abscesses present for <1 month are termed acute, and those pres ent for >1 month are chronic. Lung abscess may also develop as a result of hematogenous spread of infectious material to the lung parenchyma or complicating lung infarction. Think of hematogenous spread from another infectious focus, such as endocarditis, in those with multiple lung abscesses. Other less common causes of pulmonary abscess include penetrating chest trauma or fungal and parasitic infections. Primary and metastatic neoplasms and inflammatory conditions such as Wegner’s granulomatosis and sarcoidosis may also manifest as pulmonary cavitary lesions and become infected (Table 66-2). CLINICAL FEATURES Lung abscess typically has an indolent course, with patients presenting after 2 to 4 weeks of symptoms. Symptoms include cough, fever, pleuritic chest pain, hemoptysis, weight loss, and night sweats. The development of the infection is slow, so fever, tachycardia, and tachypnea are often absent. The cough may or may not be productive. DIAGNOSIS Chest radiograph may show an area of dense consolidation or an airfluid level inside of a cavitary lesion, indicating that the abscess cavity communicated with a bronchiole. Bronchiole communication occurs in most patients with lung abscess. Chest CT will diagnose cavitary lesions with and without bronchiolar communication. Conditions that may appear cavitary on a chest radiograph include infected bullae, pleural fluid collection with bronchopleural fistula, loop of bowel extending through a diaphragmatic hernia, hiatal hernia, and objects lying on or TABLE 66-2 Cavitary Lung Lesions Infectious Bacterial Anaerobic abscess Aerobic abscess Infected bullae Tuberculosis Actinomycosis Pleural empyema Fungal Coccidioidomycosis Histoplasmosis Blastomycosis Aspergillosis Cryptococcus Parasitic Echinococcosis, Entamoeba histolytica Amebiasis, Paragonimus westermani Neoplastic Bronchogenic carcinoma (squamous cell or adenocarcinoma) Metastatic cancer (colorectal or renal) Lymphoma or Hodgkin’s disease Inflammatory Sarcoidosis Wegener’s granulomatosis Other Foreign body aspiration Tintinalli_Sec08_p0425-0472.indd 450 8/1/19 2:10 PM