Abstract

Introduction Arteriovenous malformations(AVMs) are high‐flow vascular abnormalities characterized by direct communications between arteries and veins of various complexities. Cerebral AVMs may manifest with new‐onset seizures or intraparenchymal (IPH) or subarachnoid hemorrhages (SAH). Life‐threatening bleeds may occur from the AVM nidus or associated aneurysms. We report a patient with hemorrhage from a complex AVM that included a prominent nidus and large inflow aneurysms requiring several endovascular techniques for treatment. Methods N/A Results A 35 year old male patient newly arrived from the Philippines with a history of hypertension presented to the hospital after being found unresponsive at home with frothing from the mouth and incontinence. The patient regained consciousness in the ER, complaining of a posterior headache which he had been experiencing for a week. NIHSS of 0 was noted with no neurological deficits. CT‐head revealed extensive SAH in interhemispheric falx anterior to and outlining the entire corpus callosum with intraventricular extension. CT‐ angiogram demonstrated a prominent AVM with a well‐developed nidus situated to the left of midline about the posterior corpus callosum. Two large inflow aneurysms, felt to be the rupture site, projecting from the proximal left pericallosal artery were also demonstrated. An incidental ACA aneurysm was also noted. Cerebral angiography redemonstrated these findings as well as the drainage of the AVM primarily through the straight sinus. Graded as Spetzler Martin 4. Common femoral approach was used. An access catheter was passed into the left ICA. The pericallosal artery was accessed with a detachable tip microcatheter which was further advanced past the inflow aneurysms into the main pedicle feeding the AVM nidus. The inflow aneurysms were accessed and embolized with coils using a second microcatheter prior to AVM embolization. This sealed off access to the aneurysms and parent vessel against liquid agent backflow. Onyx‐18 was then injected into the main AVM pedicle under a blank roadmap. Extensive but partial filling of the AVM was noted anteriorly but full embolization of the posterior aspect of the nidus was not achieved. Finally coiling of the ACA aneurysm was performed after accessing the right ICA. An MRI with and without contrast was performed and an expected acute infarction in the left ACA territory was observed. A repeat angiogram was performed a week later revealing posterior cerebral artery and posterior choroidal branches feeding the posterior 1/3 of the AVM. Embolization of three posterior feeding pedicles was subsequently performed utilizing dilute NBCA. Because of coil impaction the proximal pericallosal inflow aneurysm required re‐treatment with further coil placement 8 months after initial treatment. The patient has regular angiograms to monitor the AVM, which appears stable without significant residual shunting. Conclusion Ruptured AVMs are fatal events requiring careful treatment to prevent further bleeding while preserving viable brain tissue. AVMs are fragile formations of vessels which can receive collaterals from multiple targets and often have associated high risk features like inflow aneurysms. Accordingly endovascular treatment may require a mixture of techniques to ensure adequate and safe embolization. Regular monitoring of these structures and adjacent vessels is required to prevent any poor outcomes.

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