Abstract 220: Cerebral Angioedema in a Patient with Refractory Hypertension and Intracerebral Hemorrhage

Introduction/Purpose There is emerging evidence to implicate bradykinin in the development of cerebral edema. In the periphery, its association to the development of angioedema is well known. However, the relationship of peripheral angioedema to the development of cerebral angioedema is not well established. Angioedema may occur in patients receiving antihypertensive medication, and alteplase for acute ischemic stroke (1), however, the concurrent involvement of cerebral vasculature is not well studied. Moreover, the connection with cerebral edema ‐ cytotoxic or vasogenic ‐ remains poorly understood. Here we present a patient with an intracerebral hemorrhage (ICH) in the setting of refractory hypertension, who developed angioedema, and ultimately fulminant cerebral edema. We aim to investigate whether angioedema may extend beyond a systemic response and into the cerebral vasculature, contributing to further neurological compromise. Materials/Methods A retrospective review was conducted for one patient. Data, including history, exam, imaging, and clinical interventions were analyzed. All identifiers were removed. Results A 51‐year‐old African American woman with a medically refractory hypertension on multiple home medications presented with aphasia, and a blood pressure of 220/110 mm Hg. An initial non contrast head CT revealed a 60‐cc left basal ganglia intracerebral hemorrhage. CTA of the head and neck were negative for an underlying structural abnormality. She required intubation soon after presentation due to obtundation. No interval re‐hemorrhage was noted on repeat head CT. A contrast enhanced MRI was also unrevealing. 48 hours later she was noted to have orolingual edema and an angiotensin converting enzyme inhibitor (ACEi) and diltiazem were discontinued. In the ensuing days, due to difficult to control hypertension despite being on multiple antihypertensives, an angiotensin II receptor blocker (ARB) was introduced. However, this was discontinued and reintroduced several days later only to be discontinued again due to orolingual edema. She also had a failed extubation attempt due to hypoxemia and stridor, and received FFP, decadron, and racemic epinephrine. 2 days later she developed bradycardia and had neurologic deterioration progressing from initial right hemiparesis to complete unresponsiveness on examination. A noncontrast head CT showed no interval re‐hemorrhage but did show new areas of hypodensity involving the bilateral occipital lobes, the brainstem, the left temporal lobe, and uncal herniation. Hypertonic saline was started, however the patient progressed to brain death. Conclusion This case highlights the potential link between systemic angioedema, and fulminant cerebral edema and rapid neurologic decline. Previous literature has described potentially parallel mechanisms behind peripheral angioedema and cerebral edema (2). Angioedema may also influence progression from vasogenic to cytotoxic cerebral edema. As vasogenic edema develops, the increased tissue pressure can lead to ischemia and exacerbate cytotoxic edema (3). The significance of posterior circulation involvement is noteworthy, as ischemic infarctions here can lead to neurological deficits and are associated with vasogenic edema due to blood‐brain barrier disruption, such as in posterior reversible encephalopathy syndrome (PRES). Further investigation is required to explore acute intracerebral effects of angioedema. Physicians should consider cerebral angioedema in patients with both peripheral angioedema and neurological deterioration.