A 19-year-old female with mild persistent asthma, borderline personality disorder, and substance abuse presented with three days of a non-productive cough and dyspnea. She endorsed generalized malaise and body aches, without fever or chills.
In the emergency department she was tachypneic and hypoxic to 87% on room air. A chest X-ray showed a streaky opacity in the left lingula and possible trace bilateral pleural effusions. Her labs were significant for a WBC count of 10.9, with a differential of 38% neutrophils, 19% lymphocytes, 32% eosinophils (absolute count of 3,500/cubic mm). She was started on ceftriaxone and azithromycin with concern for community acquired pneumonia. Her urine drug screen was positive for cocaine, amphetamines, benzodiazepines, and cannabinoids.
She endorsed starting to smoke crack cocaine three weeks prior to her presentation, with her last use two days prior. Prednisone was initiated. With continued hypoxia despite antibiotics and steroids she underwent a high resolution CT of the chest that showed low lung volumes and extensive multifocal band like opacities in the lower lobes consistent with atelectasis but could not rule out an infection.
Pulmonary was consulted and performed a bronchoscopy that revealed inflamed and hyperemic airways with bronchoalveolar lavage return that was cloudy and mucoid, but no evidence of hemorrhage. Laboratory studies from her lavage revealed 1076 WBCs/cubic mm, 55% of which were eosinophilis. Bacterial, viral, AFB, and fungal studies were unremarkable. Transbronchial biopsy of the left lower lobe was consistent with eosinophilic pneumonia. With continuation of prednisone at 40mg per day, her hypoxia and eosinophilia resolved. She was counseled to avoid cocaine and other illicit substances, and was discharged in good condition to finish a seven-day course of prednisone.
This patient’s presentation was consistent with acute eosinophilic pneumonia (AEP) related to crack cocaine inhalation. Cocaine in its native form can be injected intravenously or inhaled intranasally for its desired effects, but cannot be smoked for inhalation. In its free-base form also known as “crack” cocaine, it can be smoked. Cocaine abuse has been associated with numerous adverse manifestations, especially on the cardiopulmonary systems. It is associated with myocardial ischemia secondary to vasospasm, CHF, direct inhalant toxicity and diffuse alveolar damage with hemorrhage also known as “crack lung,” pulmonary arterial vasospasm mimicking a pulmonary embolus, pulmonary hypertension, AEP, and even respiratory failure with ARDS. In this case, a crack cocaine user presented with significant hypoxia, nonspecific chest X-ray abnormalities, with workup revealing AEP that responded well to steroids and avoidance of the offending agent.
AEP secondary to smoking crack cocaine is one of the less familiar, though clinically significant, adverse events observed with cocaine abuse. After taking a thorough social history regarding recreational drug use, clinicians should be suspicious for AEP when crack cocaine users present with hypoxia, nonspecific findings on imaging, and significant peripheral eosinophilia. Systemic steroids and abstinence from the drug are the mainstays of treatment.