D103-13 Butane Hash Oil-Induced Inhalational Lung Injury in a Young Adult: The Diagnostic Challenges

Abstract Introduction Butane hash oil (BHO) is a concentrated tetrahydrocannabinol (THC) extract increasingly used by young adults seeking potent cannabis effects. Inhalation introduces hydrocarbons, lipids, and thermal byproducts into the respiratory tract, causing cytotoxicity, inflammation, and exogenous lipid deposition. BHO-induced lung injury represents a novel form of e-cigarette or vaping product use-associated lung injury (EVALI) and may mimic infection or cardiogenic pulmonary edema, complicating diagnosis. Awareness is limited, but early recognition is critical to guide supportive care, avoid unnecessary interventions, and enable rapid recovery. Case Description A 26-year-old man with hypertension, obesity, and chronic marijuana use presented with three days of progressive exertional dyspnea, hemoptysis, and intermittent retrosternal chest pressure. He denied fever, chills, orthopnea, or sick contacts. On presentation, blood pressure was 167/117 mmHg, oxygen saturation 97% on room air, and exam revealed bibasilar crackles and trace lower extremity edema. Labs showed elevated troponin (139.8 → 134.1 ng/L), pro-BNP 607 pg/mL, and mildly elevated inflammatory markers; renal and hepatic function were normal. Chest radiography demonstrated cardiomegaly with bilateral patchy opacities. Chest CTA revealed multiple bilateral nodular opacities with central lucency and mediastinal lymphadenopathy (Figure 1a). Further history revealed BHO inhalation mixed with marijuana consumption one week prior. Echocardiography showed a dilated left ventricle with severe systolic dysfunction (EF 25%) and a small pericardial effusion; coronary angiography confirmed non-ischemic cardiomyopathy. Bronchoscopy was deferred due to cardiac instability. The patient received aggressive diuresis, guideline-directed heart failure therapy, and empiric antibiotics. Symptoms resolved, and repeat CT seven days later demonstrated near-complete resolution of pulmonary opacities and regression of lymphadenopathy, supporting hydrocarbon-induced lung injury over infection or embolic disease (Figure 1b). Upon discharge, he was counseled on strict avoidance of inhalational substances, and referred for outpatient pulmonary follow-up. Discussion BHO-induced inhalational injury is an emerging, hydrocarbon-driven cause of acute lung injury in young adults. Radiographic features including nodular opacities with central lucency, bilateral patchy infiltrates, and mediastinal lymphadenopathy can mimic necrotizing pneumonia or cardiogenic pulmonary edema, emphasizing the importance of a detailed exposure history and careful imaging interpretation. Unlike traditional EVALI, BHO injury typically resolves rapidly with supportive care and avoidance of exposure. Coexisting cardiomyopathy can obscure the clinical picture, but early recognition allows rapid clinical and radiographic recovery, avoids unnecessary invasive procedures, and mitigates long-term sequelae. Clinicians should maintain a high index of suspicion for BHO toxicity in young adults presenting with acute respiratory symptoms and inconclusive infectious or cardiac workups. This abstract is funded by: None