Dennis A. Velez, MDCerebrovascular/Endovascular Neurosurgery

Dept. of Neurological SurgeryVanderbilt University

ObjectivesTo recognize cerebral vasospasm (CVS) as a

treatable complication of aSAHTo safely and effectively institute optimal

medical management of CVSTo recognize the different modalities used to

diagnose CVSTo learn to identify which patients may

benefit from endovascular therapy for CVS

DefinitionCVS has been defined in various ways: Clinical vasospasm (delayed cerebral

ischemia, DCI)Angiographic vasospasmTCD vasospasmWhich one is more clinically relevant?

PathophysiologyProlonged arterial contraction: oxyhemoglobinStructural 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 gradeBlood volume and frequency of SAHSize and location of aneurysm(s)Cocaine useSexAgeSmokingHypertension

Glasgow Coma Scale

Hunt and Hess Grading Scale

WFNS Grading Scale

Fisher Scale

Pathological MarkersEndothelin 1LeukocytosisSoluble adhesion moleculesLipid peroxidesCellular proliferation and Growth FactorsHypomagnesemiaGenetic markers

Diagnostic Neurological ImagingDSA/Conventional angiographyCT angiography/CT perfusionTCDSPECTDWI/PWI

TCD

CVS Treatment OptionsTriple “H” therapyAlbumin 5%/Normal SalinePressorsHemodilutionNimodipineStatinsLumbar drainage/ Head shakingEndovascular treatment: IA/TBAIntra-aortic balloon counterpulsation (IABC)

Lumbar Drainage

Head Shaking for CVS

Intra-aortic balloon counterpulsation