Abstract Introduction Primary spontaneous pneumothorax (PSP) typically affects tall, thin young men and has long been linked to cigarette smoking. Recent evidence, however, implicates both vaping and marijuana inhalation as additional risk factors. The exposure to heated aerosols and chemical vapors can injure alveolar structures, contributing to bleb development and predisposing the lung to collapse.¹1³ We describe a patient who developed recurrent, bilateral spontaneous pneumothoraces following heavy e-cigarette and marijuana use. Case Description A 30-year-old male with a daily habit of vaping and marijuana consumption presented with sudden-onset dyspnea and pleuritic chest pain. One month earlier, he had sustained a right-sided pneumothorax treated with chest tube drainage but resumed vaping after recovery. Imaging revealed a large right pneumothorax (approximately 70-80% collapse) and a smaller left-sided pneumothorax (20-30%). Bilateral chest tubes were placed for decompression. He later underwent right-sided video-assisted thoracoscopic surgery (VATS) with apical bleb resection and both mechanical and talc pleurodesis, with plans for a staged procedure on the opposite side. Laboratory studies, including alpha-1 antitrypsin level (189 mg/dL), were normal. Aside from a low BMI (17.8 kg/m²) and ongoing vaping, no additional risk factors were identified. Discussion Both vaping and marijuana smoking have been increasingly recognized as potential precipitants of PSP. Repeated exposure to heated hydrocarbons and fine particulates may provoke oxidative damage, inflammation, and alveolar disruption, ultimately fostering bleb or bullae formation.1-4 Deep inhalation techniques and breath-holding commonly associated with marijuana use may further increase intrathoracic pressure, promoting apical bullae formation and subsequent rupture.5-7 Definitive management of recurrent or bilateral PSP often requires surgical intervention—most effectively, VATS with blebectomy and pleurodesis—to prevent recurrence. This case highlights the growing concern that vaping and marijuana use can contribute to severe pulmonary complications in young adults. Comprehensive cessation counseling and close follow-up are essential to mitigate recurrence risk and improve clinical outcomes. References 1.Sharma A, et al. Cureus. 2019;11(12):e6304. 2.Bonilla A, et al. J Med Case Rep. 2019;13(1):283. 3.Skertich NJ, et al. J Pediatr Surg Case Rep. 2019;47:101209. 4.Brashier B, et al. J Clin Med. 2022;11(15):4352. 5.Bense L, et al. Respir Med. 2018;137:123-128. 6.Hedevang O, et al. Eur J Cardiothorac Surg. 2017;52(4):679-685. 7.Ribeiro LI, et al. Breathe (Sheff). 2016;12(3):222-230. This abstract is funded by: None
BACKGROUND:Polycystic liver disease (PLD) comprises a spectrum of inherited disorders characterised by progressive cyst development and highly variable clinical manifestations. A significant subset of patients develops debilitating symptoms and despite advances, a unified treatment algorithm is lacking. AIM:To review current evidence for medical, interventional and surgical management of PLD and identify gaps preventing an integrated, evidence-based care pathway. SUMMARY:Somatostatin analogues (SSAs) are the principal disease-modifying therapy, producing modest but reproducible liver-volume reductions of 3-7% and clinically meaningful symptom improvement in selected patients with diffuse small-to-medium cystic disease. Other pharmacologic strategies have shown limited or inconsistent benefit and currently have no established role outside research settings. Interventional radiologic and surgical options provide more substantial debulking but are phenotype-dependent. Partial hepatectomy offers the largest volume reduction but carries high morbidity and liver transplantation (LT) remains the only curative option for advanced disease, with excellent long-term outcomes but significant perioperative risk. Across all modalities, heterogeneous endpoints limit meaningful comparison and hinder integration of therapies into a unified treatment pathway. CONCLUSION:A phenotype-driven management framework and coordinated research strategy incorporating standardised volumetrics, symptom scoring and prospective multicentre cohorts are urgently needed to define optimal sequencing of medical, interventional and surgical therapies in PLD.
Abstract Introduction Small-cell lung carcinoma (SCLC) is the most aggressive and the most common neuroendocrine tumor of the lung. It usually presents as a centrally-located mass or mediastinal lesion with pleural metastasis and metastatic pleural effusion (MPE) being less common. Primary pleural involvement without lung lesion is extremely rare in SCLC. We report the case of a nonsmoker male with history of asbestos exposure, found to have pleural effusion and nodular pleural thickening on imaging without any lung mass or mediastinal lymphadenopathy. Cytology of pleural fluid confirmed SCLC. Case Description A 66-year-old nonsmoker male without any medical history presents with a 3-month history of progressively worsening shortness of breath, cough, pleuritic chest pain and a 20 lbs weight loss. Patient denied any associated hemoptysis, night sweats or loss of appetite. Patient worked as a plumber with a 25 year history of asbestos exposure. He was hemodynamically stable. Examination revealed decreased air entry on left with dullness to percussion and decreased tactile fremitus without cyanosis, clubbing, edema or lymphadenopathy. Laboratory data was unremarkable. Imaging studies showed a massive left-sided pleural effusion (Figure 1a) with nodular pleural thickening without any lymphadenopathy. Findings were concerning for mesothelioma. Thoracocentesis yielded exudative lymphocyte-predominant fluid with cytology consistent with SCLC (Figure 1b). Subsequent imaging failed to show any parenchymal abnormality or evidence of distant metastasis. Patient was started on ciplastin and etoposide. He had rapid re-accumulation of pleural effusion requiring chemical pleurodesis. Discussion Significant pleural effusion requiring thoracocentesis is present in less than 3% patients with SCLC. Pleural effusion in SCLC is mostly secondary to atelectasis of the lung caused by endobronchial lesion or due to external compression of the lymphatics caused by mass. Pleural metastasis and MPE are uncommon with isolated pleural SCLC being rare and with only a few cases reported. Recognition of SCLC cells in pleural fluid with staining positive for chromogranin, synaptophysin and TTF-1 has proven extremely helpful in establishing diagnosis. Treatment approach in patients with isolated pleural SCLC should be similar to those with limited disease SCLC involving chemoptherapy and thoracic radiation. Treatment should also focus on symptom control and preventing recurrence of effusion. Conclusion This case highlights the importance of considering SCLC in the differential for isolated unexplained exudative pleural effusion, even in the absence of associated parenchymal or mediastinal abnormalities. Establishing early diagnosis will have implications on prognostication and management as isolated pleural SCLC should be treated similar to limited-stage SCLC. This abstract is funded by: None
