Dennis A. Velez, MD Cerebrovascular/Endovascular Neurosurgery Dept. of Neurological Surgery Vanderbilt University
Objectives To recognize cerebral vasospasm (CVS) as a treatable complication of aSAH To safely and effectively institute optimal medical management of CVS To recognize the different modalities used to diagnose CVS To learn to identify which patients may benefit from endovascular therapy for CVS
Definition CVS has been defined in various ways: Clinical vasospasm (delayed cerebral ischemia, DCI) Angiographic vasospasm TCD vasospasm Which one is more clinically relevant?
Pathophysiology Prolonged arterial contraction: oxyhemoglobin Structural changes in the arterial wall: arterial hyperplasia, platelet aggregation and edema-luminal narrowing, increased resistance, decreased blood flow Breakdown of blood products: oxyhemoglobin, serotonin, prostaglandins, catecholamines, histamine, angiotensin Inflammatory response: neurogenic and classic inflammation
Histological changes
Role of Hgb oxidation products
Intracellular signaling
Inflammatory Response
CVS Prediction: Patient-specific factors Clinical grade Blood volume and frequency of SAH Size and location of aneurysm(s) Cocaine use Sex Age Smoking Hypertension
Glasgow Coma Scale
Hunt and Hess Grading Scale
WFNS Grading Scale
Fisher Scale
Pathological Markers Endothelin 1 Leukocytosis Soluble adhesion molecules Lipid peroxides Cellular proliferation and Growth Factors Hypomagnesemia Genetic markers
Diagnostic Neurological Imaging DSA/Conventional angiography CT angiography/CT perfusion TCD SPECT DWI/PWI
TCD
CVS Treatment Options Triple “H” therapy Albumin 5%/Normal Saline Pressors Hemodilution Nimodipine Statins Lumbar drainage/ Head shaking Endovascular treatment: IA/TBA Intra-aortic balloon counterpulsation (IABC)
Lumbar Drainage
Head Shaking for CVS
Intra-aortic balloon counterpulsation