A42-18 Cracked Clues: Unmasking Cocaine Induced Interstitial Lung Disease

Abstract Crack/Cocaine is one of the most widely consumed illegal narcotics globally. It is well known to cause cardiovascular and neurologic complications. In contrast, its pulmonary manifestation—known as crack lung or cocaine-induced lung injury—is less frequently reported despite its potentially fatal course. This condition usually arises within 48 hours of inhalation and may be exacerbated by concurrent tobacco use, which amplifies airway and parenchymal damage through synergistic effects. Radiologic findings often reveal bilateral ground-glass opacities, consolidations, and interlobular septal thickening, reflecting the diffuse nature of the injury. A 70-year-old male with history of active smoking (50 pack-years) and no occupational exposure was referred to Pulmonology clinics due to abnormal imaging showing chronic interstitial lung disease. He was asymptomatic and denied use of respiratory therapies or illicit drug use. Bronchoscopy was deferred by the patient. Nonetheless, infectious and rheumatologic workup were negative. Few months after initial evaluation, patient arrived to ED with progressive shortness of breath associated with dry cough that started four weeks after discontinuing cigarette smoking. No fever, chills, or hemoptysis. Upon evaluation, he was found tachypneic in marked respiratory distress with hypoxemia and elevated A-a gradient requiring high-flow nasal cannula (40 liters, FiO2: 90%). Laboratories were unremarkable. New imaging showed progression of disease with confluent ground-glass opacities bilaterally, with essentially complete opacification of the left lung by ground-glass densities. He was started on broad-spectrum antibiotics and Methylprednisolone 1 mg/kg daily. Extensive infectious workup resulted negative however toxicology was positive for cocaine. Bronchoscopy was not performed due to high risk of respiratory decompensation as patient had advanced directive of do not resuscitate/do not intubate; thus was escalated to non-invasive positive pressure ventilation (FiO2: 100%) with peripheral saturation of 88-90%. Patient continued to clinically deteriorate and remained dependent of oxygen supplementation with 100% FiO2. Supportive therapy with Morphine was given and the patient was referred to hospice care. This case underscores the importance of considering cocaine-induced lung injury in patients with diffuse pulmonary infiltrates, even when there is denial or absence of reported drug use; particularly when infectious and autoimmune workups are unrevealing. Incorporating toxicologic screening into the diagnostic workup is essential, as early recognition and timely discontinuation of the substance can prevent further lung damage and improve outcomes. This abstract is funded by: None