Multimodality Treatment of Low-Grade Ruptured Brain Arteriovenous Malformations Presenting with Life-Threatening

Vasileios Panagiotopoulos1,2, Parmenion P Tsitsopoulos3, Petros Zampakis2

  • 1Department of Neurosurgery, University Hospital of Patras, Greece.

Maedica
|July 5, 2021
PubMed

Introduction:Acute management of low-grade but life-threatening ruptured arteriovenous malformations (AVM) with simultaneous hematoma evacuation remains controversial. The current report aimed to present a case series of multimodality management of low-grade (Spetzler-Martin I-II) but life-threatening ruptured arteriovenous malformations. Methods:A consecutive case series of six Spetzler-Martin (SM) grade I-II ruptured AVM patients with concurrent life-threatening hematoma initially treated with hematoma removal and, when possible, with simultaneous AVM extirpation is presented. Supplementary treatment was also applied when deemed necessary. Median clinical follow-up was 15.6 months. Neurological assessment was performed on admission (Glasgow coma scale score - GCS) and at final follow-up (modified Rankin scale score - mRS). Results:Intraparenchymal hematoma was evacuated in all six cases, with simultaneous AVM extirpation in three cases. Preoperative embolization was done in one patient, whereas postoperative embolization was performed in three additional patients. Supplementary radiosurgery was applied in one patient. Complete AVM occlusion was achieved in all patients. At the final follow-up (15.6 months), 33.3% of patients were asymptomatic, 50% had a non-significant or slight disability (mRS score 1-2), whereas one patient died. All patients with preoperative GCS score of 8 or higher had a favorable outcome. Conclusion:Acute surgical hemorrhagic clot evacuation as first step, followed by simultaneous AVM extirpation when feasible, may result in favorable clinical outcome in ruptured low-grade (SM I&II) brain AVMs with life-threatening hematoma. Embolization has a supplementary role in the acute phase of treatment either by either securing the bleeding source preoperatively or occluding the residual malformation especially in cases of technically demanding AVM removal.

Related Concept Videos

Hemorrhagic Stroke l: Introduction01:17

Hemorrhagic Stroke l: Introduction

A hemorrhagic stroke is an acute neurological event that occurs when a weakened cerebral blood vessel ruptures, allowing blood to accumulate within or around the brain. The sudden release of blood forms a focal hematoma that increases intracranial pressure, displaces neural tissue, and can obstruct cerebrospinal fluid pathways. These effects may be compounded by intraventricular extension of the hemorrhage, cerebral edema, or compression of adjacent structures, all of which contribute to...
Hemorrhagic Stroke ll: Pathophysiology01:29

Hemorrhagic Stroke ll: Pathophysiology

A hemorrhagic stroke develops when a cerebral blood vessel ruptures, allowing blood to escape into the surrounding brain tissue, as in intracerebral hemorrhage (ICH), or into the subarachnoid space, as in subarachnoid hemorrhage (SAH). Because the skull is a rigid compartment, the sudden presence of extravascular blood rapidly increases intracranial pressure and compresses adjacent neural structures, leading to immediate tissue injury and impaired cerebral perfusion.Mass Effect and Primary...
Cerebral Edema ll: Pathophysiology01:22

Cerebral Edema ll: Pathophysiology

Vasogenic edema is a major form of cerebral edema characterized by abnormal accumulation of fluid in the brain’s extracellular space due to disruption of the blood–brain barrier (BBB). The BBB is a specialized structure composed of endothelial cells connected by tight junctions, supported by astrocytic endfeet and a basement membrane. Under normal conditions, it tightly regulates the movement of ions, proteins, and solutes between the bloodstream and brain parenchyma. When this barrier loses...