Surgery · 2002
The effect of intraoperative duplex on the management of postoperative stroke.
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Sheehan Maureen K, Greisler Howard P, Littooy Fred N, Baker William H
Аннотация
BACKGROUND: Stroke after carotid endarterectomy (CEA) may be a result of intraoperative ischemia, embolism, or thrombosis at the operative site. Intraoperative duplex should eliminate the occurrence of a severe internal carotid artery (ICA) thrombosis and, thus, negate the benefit of reoperation. This article will detail the results of our evolving treatment algorithm for immediate versus delayed post-CEA neurologic deficit (ND).
METHODS: We studied patients who had an ND after CEA from 1988 to 2000. Results. Thirty-two patients (3.2%) had a post-CEA ND (26 related stroke or transient ischemic attack, 6 other); 31 had a satisfactory intraoperative duplex post-CEA, 1 was not tested. Fifteen patients awoke from operation with a related deficit, 5 of whom were re-explored and all had a patent ICA. One patient without lateralizing signs who was not re-explored had extensive thrombosis at postmortem. The remaining 9 all had a duplex-proven patent ICA. Ten patients had a lucid interval before their related ND. Six patients were re-explored and all had thrombosed ICAs; 5 of the 6 improved postthrombectomy. Four patients were not re-explored for various reasons; a carotid thrombosis was not later diagnosed in any of these patients.
CONCLUSIONS: Intraoperative and postoperative duplex has modified our treatment of post-CEA stroke. No longer are all patients re-explored. Patients with a normal intraoperative duplex who awaken with an immediate stroke do not usually have occlusive thrombus and routine re-exploration does not benefit these patients. Patients who have an ND develop after a lucid period may have a thrombosed ICA despite a normal intraoperative duplex, and unless there is a timely normal duplex, re-exploration is recommended and appears to benefit these patients.
METHODS: We studied patients who had an ND after CEA from 1988 to 2000. Results. Thirty-two patients (3.2%) had a post-CEA ND (26 related stroke or transient ischemic attack, 6 other); 31 had a satisfactory intraoperative duplex post-CEA, 1 was not tested. Fifteen patients awoke from operation with a related deficit, 5 of whom were re-explored and all had a patent ICA. One patient without lateralizing signs who was not re-explored had extensive thrombosis at postmortem. The remaining 9 all had a duplex-proven patent ICA. Ten patients had a lucid interval before their related ND. Six patients were re-explored and all had thrombosed ICAs; 5 of the 6 improved postthrombectomy. Four patients were not re-explored for various reasons; a carotid thrombosis was not later diagnosed in any of these patients.
CONCLUSIONS: Intraoperative and postoperative duplex has modified our treatment of post-CEA stroke. No longer are all patients re-explored. Patients with a normal intraoperative duplex who awaken with an immediate stroke do not usually have occlusive thrombus and routine re-exploration does not benefit these patients. Patients who have an ND develop after a lucid period may have a thrombosed ICA despite a normal intraoperative duplex, and unless there is a timely normal duplex, re-exploration is recommended and appears to benefit these patients.