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Cerebral Vasospasm post Subarachnoid Hemorrhage Pathophysiological bases for its Treatment General considerations

Cerebral Vasospasm post Subarachnoid Hemorrhage Pathophysiological bases for its Treatment General considerations Pathophysiology Treatment. Prof. Dr. Leónidas Quintana Chief of Neurosurgery Service – Van Buren Hospital

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Cerebral Vasospasm post Subarachnoid Hemorrhage Pathophysiological bases for its Treatment General considerations

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  1. Cerebral Vasospasm post Subarachnoid Hemorrhage Pathophysiological bases for its Treatment General considerations Pathophysiology Treatment Prof. Dr. Leónidas Quintana Chief of Neurosurgery Service – Van Buren Hospital Cathedra of Neurosurgery Valparaíso University School of Medicine, Chile

  2. AT THE WILLIS CIRCLE THE CEREBRAL VASOSPASM IS REALLY A “SPASM”? Ecker A., Riemenschneider P.A. : Arteriographic demonstration of spasm of the intracranial arteries with special reference to saccular arterial aneurysms. J. Neurosurg. 1951, 8:660-667.

  3. PATHOPHYSIOLOGY OF CEREBRAL VASOSPASM OxyHb SonobeM,Suzuki J :Vasospasmogenicsubstanceproducedfollowingsubarachnoidhemorrhage and itsfate . Acta Neurochir(Wien) 44:97-106,1978

  4. 1 AsanoT,Tanishima T et als:Possibleparticipation of Free Radical Reactionsinitiatedbyclotlysis in thePathogenesis of VasospasmafterSubarachnoidHemorrhage. In Cerebral Arterial Spasm.Proceedings of theSecond International Workshop,pp190-201(WilkinsRHed),Baltimore:Williams&Wilkins,1980.

  5. Quintana L,Konda R,Ishibashi Y,Yoshimoto T, Suzuki J.:The Effect of Prostacyclin on Cerebral Vasospasm- An Experimenta Study. Acta Neurochirurgica 62,187-193, 1982.

  6. CAM 2 Inflammation Chaichana KL, Pradilla G, Huang J, Tamargo RJ: Role of inflammation (leukocyte-endothelial cell interactions) in vasospasm after subarachnoid hemorrhage. World Neurosurg 73:22-41, 2010.

  7. 3 Endothelial Dysfunction

  8. Cortical Spreading Depression Cortical Spreading Ischemia 4 Membrane failure Na+/K+ pump Ca++ pump ATP dependent Intracranial Hypertension due to global increase CBV during aneurysm rupture, and difusse decrease of CBF Regional or focal decrease of CBF at microcirculation level (real “spasm”)

  9. DELAYED ISCHEMIC DEFICIT SECONDARY TO CEREBRAL VASOSPASM THE “REAL VASOSPASM” Ischemia: K e , Na i , Ca i Pre-clipping Microcirculation DelayedIschemicDeficit During ischemia Vasospasm Narrowingduetoultrastructuralalterations > 50% stenosis Post-clipping Sundt Th M Jr,DavisDH:Reactions of cerebrovascularsmoothmuscletoblood and ischemia:Primary versus SecondaryVasospasm.In: Cerebral Arterial Spasm.Wilkins RH (ed),Baltimore,Williams&Wilkins, pp 244-250,1980.

  10. TREATMENT OF CEREBRAL VASOSPASM LevelMicrocirculation DelayedIschemicDeficit 1-Haemodynamic Management- InducedHypertension, Hypervolemia2-Calcium Antagonists LevelWillisCircle AngiographycalSymptomaticVasospasm 1-Prophylaxis: EarlySurgerywithcisternalwashing, Fenestration of Lamina terminalis, drainage of basal cisterns, evacuation of ICH (Modern concept of Integrated Management of theDisease SAH)2-Therapeutic Management: EndovascularAngioplasty

  11. “HAEMODYNAMIC THERAPY” Disautoregulation during SAH TakeuchiH,Handa Y et als:Impairment of cerebral autoregulationduringthedevelopment of chronic cerebral vasospasmaftersubarachnoidhemorrhage in primates.Neurosurgery 28:41-48,1991. CBF= CPP ( MAP - ICP) nxr 4 8 x v x L The “triple H therapy” is recommended for prevention and treatment of the ischemic complications due to cerebral vasospasm. It´s recommended to perform more clinical trials to establish it´s real efficacy. ( evidence level III-V, grade C ) Circulation 90:2592-2605,1994.

  12. CALCIO ANTAGONISTS Nimodipine is strongly recommended for diminishing the bad results at the outcome, due to DID secondary to vasospasm. (Evidence level I-II; strenght of recommendation A) Circulation 90:2592-2605,1994. *Nimodipine improved the evolution of SAH due to ruptured aneurysm (good vs other and good or moderate vs other) in a ratio 1,86:1 and 1,67:1 *Nimodipine decreased the probability of deficit and/or mortality due to vasospasm in a ratio of 0,46:1 *Nimodipine decreased the probability of ischemic complications at CT scan in a ratio of 0,58:1

  13. TOPICAL NIMODIPINE I.V. NIMODIPINE ACTION OF NIMODIPINE ON CEREBRAL CORTICAL ARTERIES ARTERIES OF 1mm: 40% VASODILATION ARTERIES OF 160-300 u : 100% VASODILATION ARTERIES OF < 100 u : 200% VASODILATION Quintana L.:Acción de la Nimodipina en el Déficit Isquémico Retardado de la HSA (Action of Nimodipine on Delayed Ischemic Deficit of SAH), Rev. Chil. Neurocirug, Vol. 2 (3), 239-250,1988.

  14. MECHANICAL & PHARMACOLOGICAL ANGIOPLASTY

  15. THANK YOU VERY MUCH !!! Prof. Dr. Leónidas Quintana Chief of Neurosurgery Service – Van Buren Hospital Cathedra of Neurosurgery Valparaíso University School of Medicine, Chile

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