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 1740% 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 l RBC hemolysis and subsequent release of oxygen, Hb, and other active oxygen species Prolonged smooth muscle contraction Secondary effects -Vessel wall changes l 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 l hemiparesis l
Diagnosis CT scan TCD (transcranial Doppler) The gold standard: angiography SPECT
TCD
Cerebral Blood Flow Regional cerebral blood flow in health people : 50 -70 m. L/min per 100 mg Symptoms of cerebral ischemia: < 20 m. L/min per 100 mg Structure damage and neuronal death: flow < 15 m. L/min per 100 mg
Management Prevention of arterial narrowing l l l Subarachnoid blood removal Prevention of dehydration and hypotension Calcium channel blocker : Nimodipine Reversal of arterial narrowing l l Transluminal balloon angioplasty Chemical angioplasty with intra-arterial papaverine Prevention and reversal of ischemic neurologic deficit l 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 60 mg q 4 h po for 21 days IV 1 mg/hour initially, increased after 2 hrs to 2 mg/hr, for 5 -14 days
Triple-H therapy Hypervolemia Hemodilution Hypertension
Triple-H therapy — Hypervolemia/Hemodilution Crystalloid + colloid solution(5% albumin ; Hexastarch/HAES ) Volume expansion while monitoring CVP level : keep 8 -10 cm H 2 O l PCWP level: 16 -18 mm. Hg l Ideal Hct: 30 -40%
Triple-H therapy--Hypertension Before vasospasm The target BP is controversial No HTN: SBP <110 mm. Hg HTN: SBP is maintained at 20 % below baseline
Triple-H therapy--Hypertension When vasospasm Hypertension was induced with phenylephrine or dopamine infusion SBP: 160 -200 mm. Hg
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 60 mg q 4 h po for 21 days No HTN: <110 mm. Hg; HTN: 80% baseline Triple-H therapy: CVP 8 -10 cm H 2 O; Hct 30 -40%; BP 160 -200 mm. Hg 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: 1463 -1466 Basilar vasospasm following spotaneous and traumatic subarachnoid hemorrhage: clinical implications; J. F. Soustiel, V. Shik; Acta Neurochir (Wien) 2002, 144: 137 -144 Therapeutic approaches to vasospasm in subarachnoid hemorrhage; Nicholas W. C. ; Current Opinion Critical Care 2002, 8: 128 -133 Cerebral vasospasm after subarachnoid hemorrhage; Nazli J. , Stephan A. ; Current Opinion Critical Care 2003, 9: 113 -119
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