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DOI: 10.1055/s-0039-1679747
Subarachnoid Hemorrhage Secondary to a Dural Arteriovenous Fistula in a Patient with a Previous Vestibular Schwannoma Resection
Publication History
Publication Date:
06 February 2019 (online)
Introduction: Intracranial dural arteriovenous fistulas (DAVF) are rare lesions associated with dural sinus thrombosis, head trauma, tumors, infection, and previous surgical procedures. DAVF are not benign, with approximate annual subarachnoid hemorrhage (SAH) rates up to 8% and significant associated mortality. We present a patient with a history of a vestibular schwannoma (VS) resection who subsequently developed SAH secondary to an occult ipsilateral DAVF.
Methods: Case report and systematic literature review.
Results: A 50-year-old man with a history of left sided retrosigmoid craniotomy for vestibular schwannoma resection 19 years prior and previous tobacco presented with a severe headache that woke him from sleep. Although neurologically intact on arrival, while undergoing a head CT he became acutely unresponsive, requiring emergent intubation. Imaging findings included dramatic, diffuse SAH, with prominent projection throughout the basilar cisterns and left cerebellopontine angle, as well as associated intraventricular blood products and ventriculomegaly ([Fig. 1A]). Interval ventricular enlargement prompted placement of a right frontal external ventricular drain, after which his neurologic status improved to following commands in all extremities, with complete right abducens palsy. The patient was subsequently extubated and underwent a formal angiogram, which demonstrated a dysplastic and nonfunctional left posterior inferior cerebellar artery (PICA) that fed directly into a partially occluded transverse sinus ([Fig. 1B]). The dysplastic PICA was successfully occluded via endovascular embolization ([Fig. 1C]). On postoperative day 1, he developed new left-sided facial weakness, which resolved following a short course of steroids—as did the right abducens palsy. He subsequently completed an unremarkable convalescence, and was discharge to home on postoperative day 15, neurologically intact with mild headache.
Systematic literature review identified 5 prior patients who developed 6 DAVF after VS resection. Preceding cases were identified incidentally on routine follow-up imaging, or as a result of associated ischemic symptoms, all at ∼2 years after VS resection. One patient developed 2 sequential DAVF, the second of which presented shortly following treatment of the first. In all cases but 1, endovascular embolization techniques effectively treated the DAVF; the remaining lesion required surgical ligation. An excellent outcome, defined as complete obliteration without new deficit, was achieved in all cases.
Conclusion: We report the sixth case of DAVF developing after VS resection, and the first to have suffered SAH. Although rare, DAVF is a highly morbid potential sequela of VS resection. Correspondingly, follow-up imaging should be closely monitored for suspicious changes in the posterior circulation, with consideration for incorporating MRA into routine follow-up imaging at 2 years.

