A47-45 When Dust Clouds the Picture, Coal Worker’s Pneumoconiosis Disguised as Volume Overload

Abstract Coal Worker’s Pneumoconiosis (CWP), often asymptomatic, occurs due to the inhalation of coal dust and may lead to restrictive lung disease characterized by the formation of nodular opacities, progressive fibrosis, and necrosis. It is characterized by the deposition of black, carbon-based pigments (anthracosis) in lymph nodes and peri-lymphatic areas. Simple CWP presents with multiple small nodules, chronic cough, and dyspnea. However, rarely does it lead to pleural disease, specifically transudative effusions as opposed to other occupational lung diseases such as asbestosis. Unilateral pleural effusions are usually either infectious or malignant, whereas cardiogenic effusions are typically bilateral. Here, described is an elderly male with a unilateral pleural effusion with newly diagnosed reduced heart failure as well as CWP, highlighting the diagnostic challenge of discerning cardiogenic effusions from pleural disease related to CWP. A 67-year-old Polish male, with prior bladder cancer, and chronic tobacco use presented with resting dyspnea, chronic lower-extremity edema, and worsening scrotal pain and edema. On physical examination, he had 3+ pitting edema bilaterally and was hypoxic, requiring supplemental oxygen. Computed Tomography imaging depicted a large right pleural effusion, mediastinal lymphadenopathy, and scrotal ultrasound (US) also confirmed diffuse scrotal edema. Laboratory studies revealed a Pro-BNP of 13,833 pg/mL. Point-of-Care Ultrasound confirmed a loculated, right-sided effusion. Echocardiogram revealed an ejection fraction of 20-25%, grade 3 diastolic dysfunction, suggesting new-onset heart failure. He was started on diuresis using intravenous furosemide. Given his history of cancer, smoking, and the unilateral effusion, malignancy was considered. He underwent thoracentesis, demonstrating a transudative effusion by Light’s Criteria (pleural studies: protein 2.1 g/dL, Lactate Dehydrogenase 75 U/L, albumin 1.1 g/dL, pH 8.1, glucose 119 mg/dL; serum protein 6.9 g/dL, LDH 190 U/L). Ultimately, he required Video-Assisted Thoracoscopic Surgery with pleural and lymph-node biopsies and PleurX catheter placement. Pathology confirmed reactive lymphoid hyperplasia with anthracotic pigment—suggestive of coal worker’s pneumoconiosis (CWP). Repeat imaging showed improvement in the effusion, and he was weaned off supplemental oxygen and discharged on guideline-directed medical therapy. Although the transudative nature of the effusion supports heart failure, anthracosis and reactive lymphoid hyperplasia seen on biopsy is suggestive of CWP-related pleural involvement. The patient’s unilateral effusion, persisting despite diuresis, argues against sole cardiac involvement. Here, CWP may have caused chronic pleural dysfunction, and thus one cannot rule out a mixed mechanism. This underscores the diagnostic complexity of a unilateral pleural effusion in heart failure and highlights CWP as a potential contributor to pleural disease This abstract is funded by: None