Abstract Intro Pleural tuberculosis (TB) accounts for around 5% of TB cases in the United States. It typically presents with a unilateral, lymphocyte-predominant exudative effusion with elevated adenosine deaminase (ADA) levels. Classic fluid characteristics include a straw-colored appearance and loculations. The diagnosis is confirmed by Mycobacterium tuberculosis (MTB) growth in pleural fluid cultures or by pleural biopsy exhibiting caseating granulomas. This case highlights an unusual presentation of pleural TB with neutrophil-predominant effusion, mimicking bacterial empyema. Description A 36-year-old incarcerated male with a history of diabetes and schizophrenia was found to have patchy right upper lobe opacities and a right pleural effusion on chest x-ray during routine jail intake. He reported two weeks of dyspnea and night sweats. A TB workup was initiated - three sputum AFB smears and two MTB PCR tests resulted negative. Given his high-risk setting, empiric TB therapy with rifampin, isoniazid, pyrazinamide, and ethambutol (RIPE) was started. The patient was admitted to the hospital for scheduled pleuroscopy as ultrasound revealed loculated pleural fluid. Pleuroscopy revealed thick, yellow-green fibrinopurulent adhesions and loculations with cloudy amber fluid (Image 1), and two chest tubes were placed for drainage. Pleural fluid analysis was exudative with 99% neutrophils, lactate dehydrogenase 2462 U/L, and glucose 6 mg/dL, suggestive of bacterial empyema. RIPE therapy was stopped, and he was treated with antibiotics and intrapleural fibrinolytics with subsequent clinical improvement. After discharge, the patient’s ADA returned elevated at 112 U/L, and pathology showed granulomatous inflammation and necrosis. Three weeks later, pleural AFB cultures grew MTB. The patient was restarted on RIPE therapy for confirmed pleural TB. Discussion Pleural TB fluid analysis presents with lymphocyte-predominant fluid in 60-90% of cases. Neutrophil predominance is generally in the first few days of effusion, then lymphocytes become dominant after. In our patient, pleural fluid was sampled more than two weeks after initial effusion detection, a timeframe in which lymphocyte predominance would be expected. Cases of neutrophil-predominant pleural TB have been reported, often accompanied by additional features suggestive of TB. It is thought that chronic pleural infection causes an influx of neutrophils, leading to purulence and loculation. One study suggests that a non-lymphocytic effusion, when associated with elevated ADA levels 40 U/L and nodular pulmonary lesions, should raise suspicion for tuberculous etiology. In this case, the presence of extensive adhesions, loculations, and fibrinopurulent fluid on pleuroscopy, together with significantly elevated ADA, supports the explanation for neutrophil-predominant pleural fluid in confirmed tuberculosis empyema. This abstract is funded by: None
Montes et al. (Fri,) studied this question.
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