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Arteriovenous malformation
From WikEM
Contents
Background
- Focal abnormal conglomerations of dilated arteries and veins in the brain parenchyma
- Arterial blood flows directly into draining veins without capillary beds creating high pressure channels
- May rupture, causing intracerebral hemorrhage +/- intraventricular hemorrhage. Mechanism of rupture incompletely understood.
- Prevalence 0.14%
- Congenital lesions
- Majority are sporadic, not familial
- Associated with Osler- Weber-Rendu disease and Sturge-Weber syndrome
- Lifelong risk of bleeding
- 2-4% per year, cumulative
Clinical Features
- Hemorrhage (most common)
- 42-72% of clinically apparent AVMs
- Usually by age 20-49
- Seizures
- Ischemia (by vascular steal – rare)
- Headaches
Differential Diagnosis
- Venous angioma
- Cavernous malformation
- Capillary telangiectasia
Evaluation
Work-up
- CT/CTA
- CT delineates acute hemorrhage, CTA to show abnormal vasculature
- MRI/MRA
- Vessels appear as abnormal flow voids
- Both better than CT for visualizing structures in relation to AVM
- Angiography
- Gold standard to evaluate the architecture including arterial feeding, venous drainage, and AVM-associated aneurysms
Evaluation
Management
- Surgical Resection
- Traditionally treatment of choice
- Radiosurgery (Gamma Knife or CyberKnife)
- Embolization (usually an adjunct treatment)
- Combination of above three in some cases
- Decision is based on AVM size, location, and patient factors
Disposition
- In cases of acute hemorrhage or neurological decline, obvious need for immediate neurosurgical consultation
- If patient presents with headache or seizure and lesion is then found, may simply warrant outpatient neurosurgical evaluation
