Abstract Introduction Angioedema is defined as nonpitting, nonpruritic swelling of the deep subcutaneous or submucosal tissues, most commonly mediated by histamine or bradykinin. Etiologies include hereditary and acquired, idiopathic, and drug-induced (notably angiotensin-converting enzyme inhibitors (ACEi) or illicit drug use). Bradykinin-mediated angioedema associated with drug use typically presents without urticaria. We present a rare case of cocaine-induced angioedema. Case Presentation A 68 year old male with hypertension, polysubstance use disorder, and anxiety presented with abdominal pain and pronounced neck, oropharynx and tongue swelling without urticaria after cocaine intake that eventually required intubation. The patient had a history of recurrent airway compromise following cocaine use, and chronic lisinopril therapy for hypertension, both recognized risk factors for angioedema. On initial evaluation, Ludwig’s angina was originally considered due to bilateral edema being more pronounced on the right side, but there were no signs of bacterial infection or fluid collections on imaging or physical exam. Other differential diagnoses included opioid and cannabis exposure with a positive drug screen, but the clinical pattern and temporal association with cocaine use made that less likely, so he was treated with hydrocortisone and H1 and H2 blockers. With resultant decreased laryngeal edema, he was successfully extubated and discharged. Discussion The novelty of this case lies in the repeated episodes of airway compromise within 24 hours of cocaine ingestion, supporting a diagnosis of cocaine-induced angioedema, which is thought to be mediated by sympathomimetic effects leading to vasodilation, increased vascular permeability, and histamine release. While ACE inhibitor use is a more common cause, hereditary, infectious etiologies, and other drug exposures respond differently; this underscores the importance of a thorough differential diagnosis in acute upper airway swelling management. In this patient’s work up, laboratory evaluation supported a drug-induced etiology rather than hereditary angioedema, with elevated C1 esterase inhibitor and normal C3, C4 levels. The lack of family history or underlying lymphoproliferative disorders also suggests this. Importantly, the patient’s angioedema improved despite resumption of lisinopril. The patient’s ingestion of other drugs were more remote, and the rest of his medication regimen was not associated with angioedema. This case highlights the need for a high index of suspicion for cocaine-induced angioedema in patients with polysubstance use despite ACE inhibitor exposure. Management requires urgent airway assessment, exclusion of infectious causes, and a multidisciplinary approach, including substance use counseling and close monitoring for recurrence and comorbidities that may complicate the overall picture. This abstract is funded by: None
Phillip et al. (Fri,) studied this question.