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Symptoms: Pleuritic Chest Pain, Dry Cough, Blood-Tinged Sputum

Wiler, Jennifer L. MD, MBA

doi: 10.1097/01.EEM.0000357581.86072.df
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Dr. Wiler is the assistant chief of clinical operations in the department of emergency medicine and the medical director of the ED Observation Unit at Washington University and Barnes-Jewish Hospital in St. Louis.

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A 55-year-old man who recently emigrated from Kenya presented to the ED with right-sided pleuritic chest pain for two months. Over this same time, he also had a dry cough occasionally productive of blood-tinged sputum.

He denied a history of medication problems, but stated that he experienced fatigue, myalgias, subjective fevers, and night sweats over the past few weeks. Shown is the patient's initial chest radiograph.

What diagnosis are you concerned about, and what management would you initiate in the ED?

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Diagnosis:/ Pulmonary Tuberculosis

Tuberculosis is a communicable disease transmitted by respiratory droplets and caused by the bacteria Mycobacterium tuberculosis. This virulent organism is one of the most common causes of infectious disease-related deaths worldwide. M. tuberculosis can infect nearly every organ system in the body, including the musculoskeletal system (Pott's disease), urogynecological system, lymphatic system, gastrointestinal tract, periorbital/orbit system (most commonly choroidal tubercles or tuberculomas), cardiac system (pericarditis), and central nervous system. It also can cause extensive hematogenous dissemination (military TB).

TB progresses through three stages: primary infection in a previously naive host, a latent (noncontagious) stage, and reactivation (also known as chronic, endogenous, postprimary, recrudescent TB). The World Health Organization estimates that more than two billion people are infected with TB worldwide, and fewer than 13,000 new cases were reported last year in the United States, with most occurring in foreign-born persons and ethnic and racial minorities, according to the Centers for Disease Control and Prevention. HIV-associated TB accounts for approximately 10 percent of total U.S. TB cases.

Reactivation TB is the most common form of pulmonary TB, occurring in 90 percent of non-HIV-infected patients, usually from previously seeded lung tissue. Seeding preferentially occurs by the aerophilic Mycobacterium in the posterior apices of the lung (80–90%). Factors that precipitate reactivation of previously latent infection are unclear except for immunosuppression.

Primary infections can present with myriad symptoms, most commonly fever (approximately 70%) lasting two to three weeks. Pulmonary involvement occurs in about a third of patients, and can include pleuritic chest pain, pleural effusion (which can develop within weeks and last as long as a year), infiltrates (approximately 60%), and bronchial lymphadenopathy (hilar in more than 60%).

Reactivation TB can be difficult to diagnose clinically. Initially, more than half of patients report nonspecific symptoms of cough (with or without sputum production), weight loss, and fatigue; the other half report fever and night sweats. Hemoptysis may be present in 25 percent; nearly 30 percent report chest pain or dyspnea. No physical diagnostic finding is pathoneumonic for pulmonary TB. Patients with latent TB are asymptomatic, and do not present for primary evaluation of TB symptoms in the ED, but chest radiographic findings consistent with latent infection may be found incidentally.

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Radiographic findings of pulmonary TB depend on the severity and stage of infection. Findings can range from cavitations with air-fluid levels (up to 20% in reactivation cases), military pattern, hilar scarring, apical calcified granuloma (Simon focus), intrathorasic lymphadenopathy (primarily hilar and mediastinal), solitary nodule, infiltrates, bronchiectasis, and pleural effusion to atelectasis or no radiologic findings and a normal chest radiograph (up to 5% of cases during active infection). Computerized tomography is more sensitive in identifying small or apical lesions, and may be of value in equivocal cases but typically not in the ED.

Patients with suspected pulmonary TB should be placed in an airborne infection isolation room (negative pressure respiratory), and strict droplet precautions should be followed. Mantoux skin testing has little value in the ED, and is used to identify patients with latent TB.

The confirmatory diagnosis of TB is made by isolating the M. tuberculosis bacteria. For suspected pulmonary TB, expectorated sputum or bronchoscopic sampling should be done; the yield of positive sampling is as low as 20 percent. Body fluid smears positive for acid-fast bacilli (AFB) are the quickest way to diagnose TB, but have a sensitivity of 45 percent to 80 percent because bacteria other than M. tuberculosis are acid-fast. Culture identification is the gold standard to diagnose M. tuberculosis and required for drug sensitivity and genotype testing, but can take four to eight weeks to result. Results from newer nucleic acid amplification tests (NAAT) are available within two to 48 hours, and have a much higher sensitivity than AFB smears, but results stay positive for months despite clinical improvement and response to antibacterial treatment. Current CDC recommendations state that NAAT should “be performed on at least one respiratory specimen from each patient with signs and symptoms of pulmonary TB for whom a diagnosis of TB is being considered but has not yet been established, and for whom the test result would alter case management or TB control activities.” (MMWR 2009;58[1]:7.)

If the NAAT and AFB smear are positive, presume the patient has TB and begin treatment while awaiting culture results. If the NAAT is positive and AFB negative, use clinical judgment to ascertain if pharmacologic treatment is warranted while awaiting culture results and consider a NAAT retest. If NAAT is negative and AFB positive, test for inhibitors and retest NAAT. If NAAT is negative and AFB negative, use clinical judgment to determine if TB therapy is warranted while awaiting results of culture and additional diagnostic tests.

Pulmonary TB can result in numerous thoracic complications include pneumothorax, hemoptysis, brochiectasis, tuberculoma, and pulmonary necrosis. Prior to pharmacological treatment, massive hemoptysis from a pulmonary artery aneurysm rupture resulted in approximately five percent of TB deaths.

The eradication of TB is challenging because it requires multidrug therapy with consistent compliance for six to 12 months. There are currently 10 FDA-approved drugs for TB, but first-line treatment is isoniazid (INH), rifampin, ethambutol, and pyrazinamide. Joint guidelines from the CDC, the American Thoracic Society, and the Infectious Diseases Society of America published in 2003 recommend treatment protocols for patients with and without HIV. (MMWR 2003;52[RR-11]:1.) Multidrug-resistant (MDR) TB (resistant to INH and rifampin) and extensively drug-resistant (XDR) TB (resistant to INH, rifampin, fluoroquinolones, and either amikacin, kanamycin, or capreomycin) have emerged as infectious disease threats. With appropriate treatment regiments, patients with TB have a cure rate of 95 to 97 percent while the cure rate for MDR TB is only 50 to 60 percent. (Am J Respir Crit Care Med 2003; 167[4]:603.) Forty-nine cases of XDR TB were identified between 1993 and 2006, and noted to have a higher mortality rate than MDR TB. (MMWR 2007;56[11]:250.)

In the ED, exposure to patients with active pulmonary TB is a risk of our occupation. Many hospitals require periodic TB staff surveillance with PPDs to identify exposure and seroconversion. Early respiratory isolation of patients with presumed pulmonary TB is critical to decrease ED patient and staff exposure risks. Often patients with suspected active TB require inpatient evaluation and infectious disease specialist input.

This patient was placed in respiratory isolation, admitted to the hospital, and started on empiric anti-TB medications. A right thoracostomy tube was placed and effusion drained (see photo); fluid cultures were eventually positive for M. tuberculosis.

© 2009 Lippincott Williams & Wilkins, Inc.