Cocaine is associated with acute cardiopulmonary toxicity, including vasospasm-mediated ischemia. In patients with elevated D-dimer and renal impairment limiting CT pulmonary angiography (CTPA), pulmonary perfusion scintigraphy may be used to evaluate suspected pulmonary embolism (PE). We describe a case in which a high-probability perfusion scan following recent cocaine use mimicked PE, which was subsequently excluded by magnetic resonance angiography (MRA).

CASE INFORMATION:  A 59-year-old woman with chronic obstructive pulmonary disease, stage III chronic kidney disease, remote PE, and polysubstance use presented with several days of chest pain and dyspnea. She reported crack cocaine use two days prior. Laboratory evaluation demonstrated an elevated D-dimer (6.07 mg/L FEU), mildly elevated troponin, and acute-on-chronic renal dysfunction (creatinine 2.7 mg/dL; eGFR 19.7 mL/min/1.73 m²). Chest radiography was unremarkable. Because renal dysfunction limited CTPA, pulmonary perfusion scintigraphy was performed; ventilation imaging could not be completed. The study demonstrated multiple bilateral moderate-to-large peripheral wedge-shaped perfusion defects without corresponding radiographic abnormalities, interpreted as high probability for PE and new compared with a remote baseline study.

Anticoagulation was initially considered but ultimately discontinued after multidisciplinary evaluation given the discordant clinical picture and recent cocaine exposure. Bronchodilator therapy produced symptomatic improvement. Subsequent contrast-enhanced pulmonary MRA demonstrated no pulmonary arterial filling defect to suggest acute PE. The patient remained stable without anticoagulation and was discharged.

DISCUSSION:  Cocaine-associated pulmonary vasoconstriction has been reported to produce regional perfusion abnormalities that can mimic thromboembolic disease on lung scintigraphy. In this patient, recent crack cocaine exposure, multiple apparent perfusion defects, and absence of emboli on subsequent pulmonary MRA suggest transient pulmonary vasoconstriction as a potential explanation for the discordant imaging findings. Underlying COPD may further complicate interpretation through regional alterations in ventilation and perfusion. This case highlights the importance of correlating scintigraphic findings with clinical history and confirmatory imaging rather than interpreting a high-probability perfusion pattern in isolation.

CONCLUSION:  Recent cocaine exposure should be considered a potential confounder when pulmonary perfusion imaging suggests PE, particularly when confirmatory vascular imaging is discordant. Recognition of this uncommon imaging mimic may help prevent unnecessary anticoagulation and its associated risks.