Cerebral Vasospasm Saeed Fareghbal M.D QUMS Rajaei hospital Neurosurgery ward

Cerebral Vasospasm The main cause of morbidity and mortality with aneurysmal SAH was rebleeding Cerebral vasospasm is recognised as the main cause of substantial disability and death The incidence as high as 70% and another % of those patients experiencing neurologic complication

Cerebral Vasospasm Transient arterial narrowing The peak incidence is 3-10 days after SAH, and it can persist for weeks It can lead to delayed ischemic neurological deficit (stroke)

Pathophysiology The exact pathophysiology is unknown Blood breakdown products in the subachanoid space leading to narrowing of the arterial lumen RBC hemolysis and subsequent release of oxygen, Hb, and other active oxygen species Prolonged smooth muscle contraction Secondary effects -Vessel wall changes Hypertrophy, hyperplasia, and fibrosis

Histological changes

Role of Hgb oxidation products

Inflammatory Response

Risk Factors * Clinical grade Blood volume and frequency of SAH Size and location of aneurysm(s) Cocaine use Sex Age Smoking Hypertension

Clinical Presentation It characterised by confusion or decreased consciousness with focal neurological deficit dysphasia hemiparesis

Diagnosis CT scan TCD (transcranial Doppler) The gold standard: angiography SPECT

TCD

Cerebral Blood Flow Regional cerebral blood flow in health people :50-70 mL/min per 100 mg Symptoms of cerebral ischemia: < 20 mL/min per 100 mg Structure damage and neuronal death: flow < 15mL/min per 100 mg

Management Prevention of arterial narrowing Subarachnoid blood removal Prevention of dehydration and hypotension Calcium channel blocker :Nimodipine Reversal of arterial narrowing Transluminal balloon angioplasty Chemical angioplasty with intra-arterial papaverine Prevention and reversal of ischemic neurologic deficit Triple-H therapy

Nimodipine (Nimotop) Acts on cerebral arterials as a smooth muscle relaxant by blocking L-type(slow) calcium channels Increase in the volume of circulation plasma, induced hypertension, and hemodilution Used only in the prevention 60mg q4h po for 21 days IV 1mg/hour initially, increased after 2hrs to 2mg/hr, for 5-14 days

Triple-H therapy Hypervolemia Hemodilution Hypertension

Triple-H therapy — Hypervolemia/Hemodiluti on Crystalloid + colloid solution(5% albumin ; Hexastarch/HAES ) Volume expansion while monitoring CVP level :keep 8-10 cm H2O PCWP level: mmHg Ideal Hct: 30-40%

Triple-H therapy-- Hypertension Before vasospasm The target BP is controversial No HTN: SBP <110mmHg HTN: SBP is maintained at 20 % below baseline

Triple-H therapy-- Hypertension When vasospasm Hypertension was induced with phenylephrine or dopamine infusion SBP: mmHg

Complication of Triple-H Therapy Intracranial Exacerbation of cerebral edema Increase intracranial pressure hemorrhagic infarction in areas of previous ischemia

Complication of Triple-H Therapy Extra-cranial Pulmonary edema:17%, Dilutional hyponatramia:3%, delayed ischemic neurological deficit Myocardial infarction: 2%

Take Home Massage Vasospasm: 3-10 days after SAH S/S: deterioration in the mental status or focal neurological deficit Risk factor: the amount of blood clot Gold standard: angiography Nimodipine 60mg q4h po for 21 days No HTN:<110mmHg; HTN: 80% baseline Triple-H therapy: CVP 8-10 cm H2O; Hct 30-40%; BP mmHg Complication: pulmonary edema and rebleeding

Reference Tri-H therapy in the management of aneurysmal subarachnoid hemorrhage; Jon Sen, Antonio Belli;The Lancet Neurology Vol 2 October 2003 Sabiston Management of cerebral vasospasm in patients with aneurysmal subarachnoid hemorrhage; M. Al-Yamany, M.C. Wallace; Intensive care Med(1999)25: Basilar vasospasm following spotaneous and traumatic subarachnoid hemorrhage: clinical implications; J. F. Soustiel, V. Shik; Acta Neurochir (Wien) 2002,144: Therapeutic approaches to vasospasm in subarachnoid hemorrhage; Nicholas W. C.; Current Opinion Critical Care 2002,8: Cerebral vasospasm after subarachnoid hemorrhage; Nazli J., Stephan A.; Current Opinion Critical Care 2003,9:

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