(1179) Diffuse Alveolar Hemorrhage Triggered by Cocaine Use

Introduction: Over 42 million Americans have used cocaine in their lifetime. Cocaine affects multiple organ systems and is commonly known for its cardiovascular complications. One less reported but detrimental complication is diffuse alveolar hemorrhage (DAH), defined as widespread bleeding into the pulmonary alveolar spaces. Studies on cocaine-induced DAH are limited.

Description: 35-year-old male with a history of chronic opioid and tobacco use was found minimally responsive in a park. He reported no health issues before this incident. He was brought to the emergency room and was noted to be hypoxemic with oxygen saturation of 40% on room air, hypertensive (151/83), and tachycardic. He had shallow respirations, pinpoint pupils and coarse bilateral breath sounds. He was given narcan twice and required bag-mask ventilation, which improved his mental status. Chest X-ray showed diffuse pulmonary edema. Initial labs revealed urine toxicology positive for cocaine and fentanyl, and a blood alcohol level of 17. Urinalysis did not report blood or dysmorphic RBCs. He was started on BiPAP but could not tolerate it, soon developing bloody frothy hemoptysis. For worsening hypoxemia, he was intubated followed by bronchoscopy with bronchoalveolar lavage (BAL). BAL was consistent with DAH and cell count from BAL did not show any eosinophils. Vasculitis panel and bronchial lavage cultures were negative. 2D echo reported normal LVEF and normal wall motion. His hypoxemia improved, and he was extubated after 2 days and discharged home.

Discussion: Inhaled cocaine is absorbed well across the alveolar membrane and can lead to crack lung and pulmonary complications including reported cases of DAH. DAH can present with hemoptysis, fever, cough, chest pain and dyspnea. Clinically, these patients have acute hypoxic respiratory failure with diffuse pulmonary involvement on imaging that improves with mostly supportive care and occasionally requires corticosteroids if there is an associated acute eosinophilic pneumonia. The underlying mechanism is thought to be hypoxic alveolar epithelial capillary damage due to vasoconstriction or direct cytotoxicity, and barotrauma. Mortality is high, and patients are at risk of catastrophic results if not diagnosed and provided supportive care.