Transient Cerebral Ischemia from Perfusion Injury: A Case Report of Autoregulatory Disruption in the Brain

Background Cerebral autoregulation allows for the metabolic demands of the brain to be regulated by maintaining cerebral perfusion dependent on systemic blood pressure. Certain conditions, like surgery and stroke, can impair cerebral autoregulation, leading to cerebral hyperperfusion, hypoperfusion, and resultant cell death. This case highlights the importance of recognizing autoregulatory disruption in perfusion-related ischemic stroke in the setting of vascular surgery. Case Presentation A 29-year-old man presented with left critical limb ischemia, with etiology as a left brachial artery thrombus in the setting of left subclavian artery dissection. He underwent a left common carotid artery to left brachial artery bypass with thrombectomy. On examination post-surgery, he developed global aphasia and right hemibody weakness and hemisensory deficit, not present before surgery. CT head showed sulcal effacement in the left middle cerebral artery (MCA) distribution with preserved gray-white differentiation and rightward 1–2 mm midline shift. CT angiography of head/neck revealed no large vessel occlusion. CT perfusion revealed decreased cerebral blood flow, decreased blood volume, and increased time to drain within the left MCA distribution. He was not a thrombolytic or thrombectomy candidate, given recent surgery and lack of large vessel occlusion (LVO). For cerebral edema treatment, he was given mannitol 1g/kg, followed by hypertonic saline 3%. MRI head obtained the following day, showing diffusion restriction in the left frontoparietal cortex, sparing subcortical regions. As his exam improved, hypertonic saline was weaned. Repeat MRI head showed progression of cytotoxic edema, with etiology suspected hypoperfusion related ischemic injury. Neurologic exams continued to improve, and was discharged to inpatient rehabilitation. Conclusion Based on the imaging findings, we believe there was transient hyperperfusion during surgery, causing acute cerebral edema, followed by transient hypoperfusion as seen on CT perfusion. We postulate this is failure of cerebral autoregulation post-carotid clamping, followed by hypoperfusion-related ischemic injury.