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Cerebral Vasospasm

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

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Cerebral Vasospasm

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

  2. 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 17-40% of those patients experiencing neurologic complication

  3. 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)

  4. Pathophysiology • The exact pathophysiology is unknown • Blood breakdown products in the subachanoidspace 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

  5. Histological changes

  6. Role of Hgb oxidation products

  7. Inflammatory Response

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

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

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

  11. TCD

  12. 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

  13. 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

  14. 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

  15. Triple-H therapy • Hypervolemia • Hemodilution • Hypertension

  16. Triple-H therapy—Hypervolemia/Hemodilution • Crystalloid + colloid solution(5% albumin ; Hexastarch/HAES ) • Volume expansion while monitoring • CVP level :keep 8-10 cm H2O • PCWP level: 16-18 mmHg • Ideal Hct: 30-40%

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

  18. Triple-H therapy--Hypertension When vasospasm • Hypertension was induced with phenylephrine or dopamine infusion • SBP: 160-200 mmHg

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

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

  21. 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 160-200 mmHg • Complication: pulmonary edema and rebleeding

  22. 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

  23. Thank you for your attention

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