Contralateral stroke during carotid endarterectomy due to abnormalities in the circle of Willis

Andrea Moritz1, Gerda Koci, Barbara Steinlechner

  • 1Department of Anesthesia, General Intensive Care and Pain Control, Division of Cardiothoracic and Vascular Anesthesia and Intensive Care, University Hospital Vienna, Austria.

Insights

Approximately 10-20% of patients experience neurological deficits during carotid endarterectomy. Preoperative assessment of the circle of Willis can identify patients at risk for intraoperative cerebral ischemia, especially diabetics.

Area of Science:

  • Neurology
  • Vascular Surgery
  • Radiology

Background:

  • Carotid endarterectomy (CEA) involves cross-clamping the common carotid artery, which can lead to neurological deficits in 10-20% of patients.
  • Neurological deficits during CEA are primarily caused by embolization or cerebral hypoperfusion due to insufficient collateral blood flow via the circle of Willis.

Observation:

  • Some patients with specific anatomical variations benefit from detailed preoperative imaging to assess risks for intraoperative hypoperfusion.
  • Regional anesthesia allows for early detection of neurological symptoms, proving advantageous in high-risk patients.
  • A case study highlighted the early detection of bi-hemispheric brain ischemia in a diabetic patient with unknown circle of Willis abnormalities under regional anesthesia.

Findings:

  • Lack of adequate collateralization in the circle of Willis was confirmed post-surgery via perfusion-magnetic resonance imaging.
  • Symptomatic diabetic patients with low-grade internal carotid artery stenosis may have an increased risk of intraoperative cerebral ischemia.

Implications:

  • Preoperative assessment of circle of Willis function is crucial for identifying patients at risk during CEA.
  • Tailored intraoperative management, including shunt insertion and neurologic monitoring, can be planned based on preoperative risk assessment.
  • This approach can improve patient outcomes and reduce the incidence of neurological deficits following CEA.