Abstract Introduction Angioedema is a potentially life-threatening condition characterized by localized, non-pitting swelling of subcutaneous or submucosal tissue. While commonly associated with allergic reactions or ACE inhibitor (ACEi) therapy, less recognized mechanisms include neurogenic bradykinin release following central nervous system injury. We present a case of severe oropharyngeal angioedema in a patient with long-term ACEi use that occurred after an intracranial hemorrhage, highlighting the interplay between neurogenic and pharmacologic triggers. Case Presentation An 83-year-old man with diabetes, hypertension, hyperlipidemia, and long-standing lisinopril use presented after an unwitnessed fall. Head computed tomography revealed acute bilateral frontal subdural hematomas and a small subarachnoid hemorrhage. Neurosurgery recommended conservative management with close neurochecks. On admission, the patient developed throat swelling and dysphagia without urticaria or respiratory distress. He received diphenhydramine, famotidine, and methylprednisolone with minimal improvement. Naso-laryngoscopy showed significant edema of the nasopharynx and epiglottis but patent vocal cords. Because of progressive airway compromise, the patient was intubated in the intensive care unit for airway protection. In the absence of an allergic trigger and given chronic ACEi exposure, bradykinin-mediated angioedema possibly worsened by neurogenic release following intracranial hemorrhage was diagnosed. Lisinopril was discontinued, and supportive care led to gradual resolution of edema. The patient was extubated after several days with resolution of airway swelling. His course was complicated by delirium and altered mentation attributed to the hemorrhage. He required no surgical intervention and was discharged on hospice care following goals-of-care discussions with family. Discussion Bradykinin-mediated angioedema can occur through impaired degradation, as with ACEi therapy, or through increased production from neurogenic release after central nervous system injury. Neurogenic inflammation from intracerebral hemorrhage may activate kallikrein-kinin pathways, increasing bradykinin production and vascular permeability. Diagnosis is clinical, supported by the absence of urticaria, normal complement levels, and lack of response to antihistamines or corticosteroids. Recognizing these features distinguishes it from histamine-mediated causes and guides management. Treatment focuses on early airway protection and discontinuation of ACEi. Targeted therapies such as icatibant or C1 esterase inhibitors may be considered in refractory cases. Conclusion This case highlights a rare interaction between neurologic injury and bradykinin-mediated angioedema in the setting of ACEi use. Clinicians should maintain a high index of suspicion for neurogenic or mixed-mechanism angioedema in patients with acute central nervous system pathology who develop airway edema. Prompt airway management and recognition of non-histaminergic mechanisms are essential to improve outcomes and prevent airway loss. This abstract is funded by: None
Wood et al. (Fri,) studied this question.
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