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Stroke from carotid endarterectomy: when and how to reduce perioperative stroke rate?
G J de Borst1, F L Moll, H D van de Pavoordt
1Department of Vascular Surgery, St. Antonius Hospital, Nieuwegein, The Netherlands.
Insights
Most strokes after carotid endarterectomy (CEA) occur postoperatively due to thromboembolism. Continuous transcranial Doppler (TCD) monitoring during the immediate postoperative phase may help prevent these strokes.
Area of Science:
- Neurology
- Vascular Surgery
- Neurocritical Care
Background:
- Carotid endarterectomy (CEA) is a procedure to remove plaque from carotid arteries.
- Perioperative stroke is a significant complication of CEA.
- Understanding stroke mechanisms is crucial for prevention.
Purpose of the Study:
- To analyze mechanisms of perioperative stroke after CEA.
- To evaluate the role of intraoperative monitoring in stroke prevention.
Main Methods:
- Analysis of 599 CEAs performed between 1996-1999.
- Continuous intraoperative monitoring using electroencephalography (EEG) and transcranial Doppler (TCD).
- Classification of strokes by onset, outcome, and side; etiology assessed via imaging and re-exploration.
Main Results:
- 20 (3.3%) patients experienced perioperative stroke or death.
- Most strokes (16/20) occurred after a symptom-free interval (mean 18 hours).
- Common mechanisms included internal carotid artery occlusion (ipsilateral) and embolization.
Conclusions:
- Postoperative thromboembolism is the primary cause of stroke after CEA.
- Suggests implementing additional TCD monitoring in the immediate postoperative period.
- Enhanced monitoring may reduce stroke incidence following CEA.
Objectives:
To analyse four years of CEA with respect to the underlying mechanisms of perioperative stroke and the role of intraoperative monitoring in the prevention of stroke.
Patients And Methods:
From January 1996 through December 1999, 599 CEAs were performed in 404 men and 195 women (mean age: 65 years, range: 39-88). All operations were performed under general anaesthesia using computerised electroencephalography (EEG) and transcranial Doppler (TCD). Any new or any extension of an existing focal cerebral deficit, as well as stroke-related death were registered. Perioperative strokes were classified by time of onset (intraoperative or postoperative), outcome (minor or major stroke), and side (ipsilateral or contralateral). Stroke aetiology was assessed intraoperatively by means of EEG, TCD, completion arteriography or immediate re-exploration, and postoperatively by duplex sonography, computerised tomography (CT) or magnetic resonance imaging (MRI) of the head.
Results:
Perioperative stroke or death occurred in 20 (3.3%) patients. In four operations stroke was apparent immediately after surgery. Mechanisms of these strokes were ipsilateral carotid artery occlusion (1) and embolisation (3). In 16 patients stroke developed after a symptom-free interval (2-72 h, mean 18 h) due to occlusion of the internal carotid artery on the side of surgery (9). Other mechanisms were: contralateral occlusion of the internal carotid artery (1), postoperative hyperperfusion syndrome (1), intracerebral haemorrhage (1), and contralateral ischaemia due to prolonged clamping (1). In three procedures the cause was unknown.
Conclusions:
In our experience most strokes from CEA developed after a symptom-free interval and mainly due to thromboembolism of the operated artery. We suggest the introduction of additional TCD monitoring during the immediate postoperative phase.