C59-02 Distinguishing Crack Lung From Pneumonia Like Shadows : A Case Report and Literature Review

Abstract Introduction Crack lung is an acute pulmonary syndrome that develops within hours to days after inhalation of freebase cocaine, presenting with respiratory distress, hypoxemia, hemoptysis, fever, and diffuse pulmonary infiltrates due to acute alveolar injury and inflammation. Its presence is frequently overlooked because often mimics community-acquired pneumonia or COPD exacerbation. The recurrent injury, chronicity, and long-term radiologic outcomes are seldomly reported. Case Presentation A 55-year-old African American woman with bipolar disorder, hypertension, and chronic cocaine use presented with acute dyspnea after smoking crack cocaine. Urine drug screen showed cocaine, BNP 379 pg/ml. Chest CT-angiography revealed bilateral lower-lobe ground-glass and consolidative opacities without pulmonary embolism suggestive of possible differentials: diffuse alveolar damage, hemorrhagic alveolitis, and pneumonitis. Infectious workup was negative, including viral, streptococcus pneumonia, and legionella. She clinically improved with short course prednisone, bronchodilators, and diuretics weaning off high-flow oxygen to nasal cannula. Although follow-up imaging showed persistent opacities. Three months later, after recurrent cocaine use, she returned with similar clinical and radiological findings, confirming cocaine-induced lung injury rather than a new infection. Discussion Cocaine inhalation can cause lung toxicity through a combination of direct epithelial toxicity, intense inflammation, and microvascular disruption, leading to diffuse alveolar damage, hemorrhagic alveolitis, or pneumonitis as seen in our patient. Imaging often reveals bilateral ground-glass opacities that closely mimic infection or pulmonary edema 1. Although many acute cases typically resolve with supportive therapy, pneumonia from cocaine inhalation requiring ICU admission may progress to respiratory failure, with reported mortality rates up to 30%. Cocaine-induced acute eosinophilic pneumonia has better prognosis with rapid recovery. Habitual inhalational use of “crack” cocaine has been linked to recurrent alveolar hemorrhage and microvascular injury with elevated endothelin-1 levels 2. HRCT studies demonstrate premature emphysematous changes even in asymptomatic users 3. Repeated toxic inhalational exposures precipitate cumulative lung injury, increasing risk of fixed airflow limitation and potentially irreversible structural damage 4. Interstitial fibrosis caused by chronic cocaine use can lead to respiratory insufficiency and increased mortality. Our patient experienced recurrent cocaine-induced pneumonitis with persistent radiologic abnormalities, despite initial clinical improvement. This pattern represents an underrecognized form of relapsing pulmonary injury rather than transient inflammation alone. Unlike most published cases that resolve after abstinence, this case demonstrates the cumulative lung damage and radiologic pattern with recurrent abuse. The need for increased awareness, addiction intervention and social worker’s support is critical for prevention of crack lung. References: PMIDs: 1. 32995177 2. 11948058 3. 18545829 4. 11224724 This abstract is funded by: NA