C48-14 Smoke and Mirrors: Unmasking Cocaine- Induced Acute Alveolar Damage

Abstract Introduction Acute pulmonary toxicity associated with smoking crack cocaine (“Crack lung”) is characterized by respiratory distress from diffuse alveolar damage and hemorrhagic alveolitis. Without a social history, clinicians may mistake the condition for infectious pneumonia, acute respiratory distress syndrome (ARDS) from a number of etiologies, interstitial lung disease, and many others. Treatment is primarily supportive, but defined treatment regimens have yet to be established. Uncommonly, in the most severe cases, patients will require invasive mechanical ventilation. Case presentation A 32-year-old female was brought into the emergency department via emergency services with dyspnea and small-volume hemoptysis. She had received intramuscular epinephrine, nebulized ipratropium-albuterol, intravenous magnesium, and intravenous methylprednisolone enroute to the hospital. She was noted to be hypoxemic and encephalopathic. She was initially supported with supplemental oxygen via nonrebreather mask but required intubation for hypoxemic respiratory failure and airway protection. She was started on broad spectrum antibiotics for possible infectious pneumonia. A urine drug screen was positive for cocaine. She was subsequently intubated and proceeded to imaging. CT of the chest revealed diffuse, patchy consolidations. (Figure 1. ) Bronchoscopy was performed and serial aliquots from a bronchoalveolar lavage were collected. These samples were blood-tinged, but not progressively hemorrhagic. The following day, the patient was maintaining appropriate oxygenation and mental status was improving. She was extubated to a high-flow nasal cannula and oxygen requirements decreased over the following days. Her infectious workup, including respiratory cultures, was unremarkable and antibiotics were discontinued. She was weaned off of supplemental oxygen and discharged with a diagnosis of pulmonary cocaine toxicity. Discussion This case of acute pulmonary toxicity secondary to cocaine inhalation underscores the importance of maintaining a broad differential when encountering a patient with respiratory distress, hemoptysis, and diffuse alveolar opacities on imaging. Management is typically supportive with supplemental oxygen. When cases are severe, invasive mechanical ventilation may be necessary. Literature suggests succinylcholine should be avoided when there is concern for cocaine intoxication due to an increased risk of hyperkalemia and cardiac arrhythmias. Previous case reports have described clinical and radiographic improvement with administration of glucocorticoids; however definitive data is lacking. Acute eosinophilic pneumonia may also be a confounding factor for improvement with steroids. Continued cocaine use can cause chronic fibrosis and persistent diffusion defects with recurrent hypoxic respiratory failure requiring mechanical ventilation. Early recognition of cocaine-associated acute lung injury is crucial to initiate appropriate supportive care and reduce the risk of recurrent respiratory failure. This abstract is funded by: none