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Journal of Neurosurgery 1999-Apr

Delayed neurological deterioration following resection of arteriovenous malformations of the brain.

يمكن للمستخدمين المسجلين فقط ترجمة المقالات
الدخول التسجيل فى الموقع
يتم حفظ الارتباط في الحافظة
M K Morgan
L H Sekhon
S Finfer
V Grinnell

الكلمات الدالة

نبذة مختصرة

OBJECTIVE

The aim of this study was to analyze delayed neurological deficits following surgical resection of arteriovenous malformations (AVMs).

METHODS

The authors report on a consecutive series of 200 patients with angiographically proven AVMs of the brain that were surgically resected between January 1989 and June 1998. The 30-day mortality rate for patients in this series was 1%, with one death caused by AVM resection and one death attributed to basilar artery aneurysm repair following successful AVM resection. The Spetzler-Martin grading system correlated well with the difficulty of surgery. No permanent incidence of morbidity resulted from resection of Grade I or II AVMs; the percentage of patients with a significant neurological deficit due to resection was 7.8% for those with Grade III lesions and 33.3% for those with Grade IV or V AVMs. However, this grading system did not accurately predict the development of delayed neurological deficits. Ten patients (5%) developed delayed neurological deficits after recovering from anesthesia and surgery. The delayed deficit was due to hemorrhage in four of the 10 patients and all four had undergone resection of AVMs measuring at least 4 cm in diameter. An increase in blood pressure during the first 8 postoperative days precipitated hemorrhage in these patients. Edema arising as a consequence of propagated venous thrombosis (two patients) was associated with extensive venous drainage networks rather than large AVM niduses. Both hemorrhagic and edematous complications can be included under the umbrella term of "arterial-capillary-venous hypertensive syndrome" to describe the common underlying pathogenesis accurately. An additional four patients developed a delayed deficit as a result of vasospasm. Vasospasm occurred when resection had involved extensive dissection of proximal anterior and middle cerebral arteries; in such cases the incidence of vasospasm was 27%.

CONCLUSIONS

On the basis of their analysis of these complications, the authors recommend strict blood pressure control for patients with lesions measuring 4 cm or more in diameter (particularly those with a deep arterial supply). Thromboprophylaxis with aspirin and heparin is prescribed for patients with extensive venous drainage networks, and prophylactic nimodipine therapy and angiographic surveillance for vasospasm are suggested for patients in whom extensive dissection of proximal anterior or middle cerebral arteries has been necessary.

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