Abstract Introduction Empyema is a pleural space infection that carries high morbidity, particularly among immunocompromised patients. Those with rheumatoid arthritis (RA) on tumor necrosis factor-α (TNF-α) inhibitors are predisposed to pyogenic and opportunistic infections. Differentiating rheumatoid pleural effusion (RPE) from infectious empyema remains a diagnostic challenge, as both may demonstrate exudative, neutrophilic fluid with low glucose, high lactate dehydrogenase (LDH), and low pH. Early recognition and drainage are critical to prevent deterioration. Case Presentation A 55-year-old woman with long-standing seropositive RA on adalimumab, sulfasalazine, and hydroxychloroquine presented with dyspnea and right-sided chest pain. Chest imaging revealed a moderate-to-large right pleural effusion without consolidation. Diagnostic thoracentesis yielded turbid exudative fluid with neutrophil predominance, glucose 2 mg/dL, LDH 2500 U/L, and pH 7.052, but Gram stain and cultures were negative. The findings were initially attributed to RPE related to high rheumatoid factor (RF) activity, and no drainage catheter was placed. Over the following week, her dyspnea worsened, and repeat imaging demonstrated enlarging loculated effusion with air-fluid levels. A second thoracentesis produced frank pus. Pleural fluid cultures subsequently grew Streptococcus intermedius, part of the Streptococcus anginosus group. A right-sided pigtail catheter was inserted, and intravenous vancomycin, cefepime, and metronidazole were initiated, later narrowed to ampicillin-sulbactam. Two doses of intrapleural tissue plasminogen activator (tPA) were administered with marked clinical improvement. Follow-up CT showed near-complete resolution, and she was transitioned to four weeks of oral amoxicillin-clavulanate. Immunosuppressive therapy was withheld during recovery. Discussion This case underscores the diagnostic overlap between RPE and empyema, particularly in RA patients on biologic therapy. RPE often presents as a sterile, low-glucose, low-pH exudate, yet identical biochemical findings may occur in infection.i Persistent or enlarging effusions, systemic toxicity, or worsening respiratory symptoms should prompt reevaluation and repeat drainage. S. intermedius, a microaerophilic organism associated with abscess formation, highlights the importance of considering anaerobic sources in immunosuppressed hosts.ii Intrapleural fibrinolytic therapy provided effective non-surgical management, aligning with MIST-2 trial principles. TNF-α inhibitors heighten infection risk, and temporary discontinuation during sepsis remains prudent.iii Empyema can masquerade as autoimmune pleuritis in RA. Clinicians must maintain vigilance for infection when low-glucose, low-pH effusions persist despite conservative care. Timely drainage, culture-directed antibiotics, and judicious management of immunosuppression are essential for optimal outcomes. References i Balbir-Gurman et al., “Rheumatoid Pleural Effusion.” ii Dyrhovden et al., “Pleural Empyema Caused by Streptococcus Intermedius and Fusobacterium Nucleatum.” iii Ali et al., “Clinical Use of Anti-TNF Therapy and Increased Risk of Infections.” This abstract is funded by: None
Gul et al. (Fri,) studied this question.