Bleeding source identification and treatment in brain arteriovenous malformations

N Mjoli1, D Le Feuvre, A Taylor

  • 1Department Neurosurgery, University of Cape Town, Cape Town, South Africa.

Arteriovenous malformation (AVM) patients who initially present with intracerebral haemorrhage may have an identifiable source of bleeding on angiogram, which can be a treatment target. Previous work suggests that the re-bleed rate may be lowered if a weak area is eliminated.A retrospective cohort study was conducted on patients who presented over a six-year period with a bled AVM. Cases were reviewed looking for the source of the hemorrhage by correlating haematoma location on CT or MRI and any angio-architectural weakness seen on digital subtraction angiography (DSA). Neuroendovascular notes were reviewed to identify the treatment targets. One hundred patients presented with a brain AVM with a 1.7:1 male: female ratio, 41 patients had an initial presentation of hemorrhage. The source of hemorrhage was identified in 18 subjects with 11 intranidal false aneurysms, five flow-related aneurysms, two associated aneurysms and one venous pouch. The location of haemorrhage on the presenting scan significantly correlated with the identified bleeding source using Chi-square analysis (P-value 0.039). Partial targeted embolization was used successfully in 90% with a 9% related technical complication rate not resulting in long-term morbidity or mortality. The mean follow-up period was 34 months with an annual hemorrhage rate of 0.7%. In just under half the patients with AVM bleeding a source of haemorrhage can be identified on DSA and in most cases this will be an intranidal false aneurysm. Flow-related and associated aneurysms in patients with brain AVM can cause haemorrhage and these patients are more likely to have SAH than intracerebral haemorrhage.These weak points are a good target for partial endovascular treatment, are usually accessible and may reduce the higher haemorrhage rate expected over the next two years.

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...
Brain Abscess l: Introduction01:26

Brain Abscess l: Introduction

A brain abscess is a focal, intracerebral infection characterized by a localized collection of pus within the brain parenchyma, resulting from microbial invasion and the body’s inflammatory response. It progresses through stages: early and late cerebritis, followed by early and late capsule formation, reflecting tissue destruction, immune response, and eventual encapsulation.Etiology and PathogenesisCausative organisms vary with source and host factors, often involving polymicrobial infections,...