Anaphylaxis-Associated Cerebral Infarction: A Case Report

Anaphylaxis is a severe, potentially life-threatening allergic reaction that primarily affects the respiratory and cardiovascular systems. While neurological complications are rare, cerebral infarction may occur due to anaphylaxis-induced hypoperfusion, endothelial dysfunction, and a hypercoagulable state. The mechanisms underlying this association remain poorly understood, and reports of anaphylaxis-related stroke are scarce. A 75-year-old man with a history of diabetes mellitus and hypertension developed respiratory distress and loss of consciousness shortly after a bee sting. He was diagnosed with anaphylactic shock and treated with adrenaline, glucagon, and aggressive fluid therapy. Despite hemodynamic stabilization, he developed persistent left-dominant quadriplegia. Magnetic resonance imaging (MRI) revealed acute ischemic stroke confined to the cortical branches of the middle cerebral artery (MCA) bilaterally, with restricted diffusion on diffusion-weighted imaging (DWI) and decreased apparent diffusion coefficient (ADC) values. Magnetic resonance angiography demonstrated a signal void in the right MCA and stenosis of the left MCA. Perfusion-weighted imaging using time-to-maximum maps indicated prolonged transit time in the infarcted regions, which closely corresponded to the DWI lesions, suggesting that most of the hypoperfused tissue had already progressed to irreversible infarction. Given the extensive infarction and high risk of hemorrhagic transformation, single antiplatelet therapy was selected for secondary stroke prevention. While his neurological symptoms partially improved, he remained functionally dependent at discharge. Cerebral infarction is a rare but serious complication of anaphylaxis, especially in patients with underlying cerebrovascular risk factors. Early recognition of neurological deficits, prompt neuroimaging, and comprehensive hemodynamic stabilization are crucial in preventing irreversible brain ischemia. The underlying pathophysiology is thought to involve multiple mechanisms, including systemic hypotension, mast cell degranulation-induced endothelial dysfunction, transient or persistent cerebral vasoconstriction, and a hypercoagulable state triggered by inflammatory mediators. Considering the etiology of anaphylaxis-associated ischemic stroke is critical for guiding appropriate management strategies. This case highlights the importance of a multidisciplinary approach in managing anaphylaxis-related stroke. Further studies are warranted to clarify the pathophysiological mechanisms and develop tailored therapeutic strategies for this rare but severe condition.