Intracranial hypertension after resection of cerebral arteriovenous malformations. Predisposing factors and management strategy.

BACKGROUND AND
PURPOSE: Surgical excision of cerebral arteriovenous malformations (AVMs) may be complicated by postoperative breakthrough edema and hemorrhage and by intracranial hypertension. Embolization, staged resection, and meticulous surgical technique have decreased but not completely eliminated this complication. In this study we prospectively assess the prevalence of intracranial hypertension after excision of cerebral AVMs, examine factors predisposing to this complication, and document the outcome of aggressive monitoring and treatment of elevated intracranial pressure (ICP).
METHODS: During a 4-year period at a single institution, 32 consecutive patients with cerebral AVMs underwent surgical excision after staged embolization. All patients underwent postoperative monitoring of ICP and a uniform management protocol of intracranial hypertension.
RESULTS: Intractable intracranial hypertension was encountered after resection of 9 of 32 cerebral AVMs, including 3 of 20 (15%) AVMs 6 cm or less in maximum diameter and 6 of 12 (50%) AVMs greater than 6 cm in maximum diameter. This complication occurred in 5 of 10 (50%) lesions located in distal or border-zone locations, in 4 of 9 (44%) AVMs arising directly off proximal cerebral arteries, and in none of 13 AVMs in other locations. Preoperative single-photon emission-computed tomography perfusion scans were performed in 17 patients and demonstrated parenchymal hypoperfusion beyond the AVM nidus in 5 of 10 AVMs 6 cm or less in maximum diameter, none of which manifested postoperative intractable ICP. Hypoperfusion was observed on single-photon emission-computed tomography in 7 of 7 AVMs greater than 6 cm that were studied by this modality, and intractable ICP was observed postoperatively in 5 of these cases despite preoperative staged embolization in every case. Patients with symptomatic intractable ICP were treated with intravenous short-acting barbiturates under a strict critical care protocol. There was no instance of uncontrollable intracranial hypertension or break-through edema while on barbiturate therapy. There was no permanent morbidity related to this treatment and no mortality or new disability morbidity in this series.
CONCLUSIONS: We conclude that intractable intracranial hypertension remains a common complication after resection of a subgroup of cerebral AVMs despite preoperative embolization, modern neuroanesthesia and critical care management, and microsurgical technique. A proactive management protocol aimed at ICP control is safe and effective in the management of this complication.