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
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.
PATHOPHYSIOLOGY OF CEREBRAL VASOSPASM
Oxy Hb
Sonobe M,Suzuki J :Vasospasmogenic substance produced following subarachnoid
hemorrhage and its fate . Acta Neurochir(Wien) 44:97-106,1978
1
Asano T,Tanishima T et als:Possible participation of Free Radical Reactions initiated by clot lysis in the
Pathogenesis of Vasospasm after Subarachnoid Hemorrhage. In Cerebral Arterial Spasm.Proceedings
of the Second International Workshop,pp190-201(WilkinsRH ed),Baltimore:Williams&Wilkins,1980.
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.
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.
3
Endothelial
Dysfunction
4
Cortical Spreading Depression
Cortical Spreading Ischemia
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”)
Membrane
failure
Na+/K+ pump
Ca++ pump
ATP dependent
DELAYED ISCHEMIC DEFICIT
SECONDARY TO CEREBRAL VASOSPASM
THE “REAL VASOSPASM”
Ischemia:
Ke,
Na i ,
Ca i
Pre-clipping
Microcirculation
Delayed Ischemic Deficit
During ischemia
Vasospasm
Narrowing due to ultrastructural alterations
> 50% stenosis
Post-clipping
Sundt Th M Jr,Davis DH:Reactions of cerebrovascular smooth muscle to blood and ischemia:Primary
versus Secondary Vasospasm.In: Cerebral Arterial Spasm.Wilkins RH (ed),Baltimore,Williams&Wilkins, pp
244-250,1980.
TREATMENT OF CEREBRAL VASOSPASM
Level Microcirculation
Delayed Ischemic Deficit
1-Haemodynamic Management- Induced Hypertension, Hypervolemia
2-Calcium Antagonists
Level Willis Circle
Angiographycal Symptomatic Vasospasm
1-Prophylaxis: Early Surgery with cisternal washing,
Fenestration of Lamina terminalis, drainage of basal
cisterns, evacuation of ICH (Modern concept of Integrated
Management of the Disease SAH)
2-Therapeutic Management: Endovascular Angioplasty
“HAEMODYNAMIC THERAPY”
Disautoregulation
during SAH
Takeuchi H,Handa Y et als:Impairment of cerebral autoregulation during the development of
chronic cerebral vasospasm after subarachnoid hemorrhage in primates.Neurosurgery 28:4148,1991.
CBF= CPP ( MAP - ICP) n x r 4
8x 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.
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 90:25922605,1994.
*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
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.
MECHANICAL &
PHARMACOLOGICAL
ANGIOPLASTY
THANK YOU VERY MUCH !!!
Prof. Dr. Leónidas Quintana
Chief of Neurosurgery Service – Van Buren Hospital
Cathedra of Neurosurgery
Valparaíso University School of Medicine, Chile