Vasospasm is the prolonged intense constriction of the larger conduction arteries in the subarachnoid space,which initially surrounded by subarachnoid clot it is likely that spasmogens are released from the breakdown of red blood cell trapped by fibrin mesh in in the the abnormal environment of subarachnoid space.The etiology remain uncertain but appears to be related to the amount and distribution of blood in the subarachnoid space.
This may also be due to local mechanic pressure effects from the high pressure arterial bleeding of the aneurysm or from the clot itself.
Pathogenesis :(1,3)
The vasospastic artery has a structural and pathologic changes within the vessel wall, such as swelling and necrosis of the smooth muscle cells. Although the exact mechanism and cause of spasm have not been completely elucidated,a reasonable hypothesis is that one or more vasoactive substances contained in the blood in the basal cisterns induce changes in the cerebral arteries to cause severe constriction.
Several mediators have been postulated including serotonin
histamine,cathecolamine,prostaglandins,angiotensin,lipid
peroxidase,endothelin and oxyhemoglobin.
The component in the blood implicated in the pathogenesis of vasospasm is currently thouht to be oxyhemoglobin.
The cerebrovascular tone is regulated by a balanced between vasodilatating and vasoconstricting factors.
The suppressived interaction of oxyhemoglobin with endothelium derived relaxing factor nitric oxide (patent vasodilator) coupled with stimulated production of endo
thelin(potent vasoconstrictor) is the postulated cause
of vasocerebral spasm. In experimental vasospasm the increase in the perivascular concentration of oxyhemoglobin and deoxyhemoglobin parallels the time course of vasospasm. In support of this hypothesis,early intracra-
nial operation (within 48 hours) to remove extravasated subarachnoid blood has been shown to be effective in reducing the occurence of vasospasm and associated neurologic deterioration.
INCIDENCE:(1,3)
In study vasospasm accounted for 13,5% the overall morta
lity and major morbidity.
Not all patients with subarachnoid hemorrhage(SAH) will develop vasospasm and its severity,time course and prognosis are largely inpredictable.
The incidence and severity of delayed cerebral vasospasm have been shown to correlate with the amount and location of blood in the basal cisterns.
The frequency of occurence as determined by angiography is estimated to be 40% to 60%.
However,clinically significant and symptomatic vasospasm occurs at a lower frequency (20% to 30%).
This difference may be explained by the varying degree of vasospasm. As established lower limit of cerebral blood flow(CBF) compatible with normal brain function is appro
ximately 15 to 20 ml/100 g/min.
Thus considerable reduction in CBF can occur from vaso
spasm without clinical symptoms.
When symptomatic vasospasm develops, approximately 50% of the patients will die or be left with serious residual neurologic deficits.
Typically angiographically detectable vasospasm is not seen until 72 hrs after SAH, the incidence peaks 7 days after SAH and it is seldom seen after 2 weeks.The onset of vasospasm is generally 3-5 days after SAH, and duration of 2-4 weeks.
CLINICAL MANIFESTATION: (1,2)
Clinical manifestation most commonly gradually but may also occur abruptly include a decrease in the level of conciousness new onset of focal sign and mutism.
Hijdra et al found that the patients with delayed cerebral ischemia from vasospasm had a decreased in the level of conciousness that may be accompanied by but was never preceded by focal signs.
Progressive impairment in level of conciousness or increase in focal neurologic deficit occuring more than four days after SAH should raise the suspicion of cerebral vasospasm.
DIAGNOSIS: (2,3)
Cerebral angiography remains the gold standard for diagno
sing vasospasm which is seen as smooth vasoconstriction in cerebral vessel.
Vasospasm may be limited the area surrounding the rup
tured aneurysm or it may be widespread when it is asso
ciated with poor prognosis.
Although an angiogram remains the definitive diagnostic tool for vasospasm,and although transcranial Doppler ultrasonography (TCD) is unreliable as a measure of CBF in patients with SAH because vasospasm associated changes in vessel diameter, it has become valuable for diagnosing vaso
spasm non invasively prior the onset of clinical symptoms.
As the vessel diameter is reduced for a given blood flow,red blood cell velocity (FV) increases.
Hence, cerebralvasospasm is considered present when FV > 12o cm/sec or the ratio between the FV in the middle cerebral aretery(MCA) and the FV in the internal carotid artery(ICA) exceeds 3, should decrease with effective treatment.
TCD is increasingly being used to diagnose vasospasm especially in sedated and ventilated patients, as it has advantage of being a noninvasive bedside test and TCD results did not have any adverse influence on management or outcome.
Cerebral angiography should be performed in any patient with clinically suspected vasospasm despite negative TCD findings.
Other methods which can be used to diagnose vasospasm include photonemision tomography and positron emission tomography(PET).
PET has been performed in patients not responding to triple Htheraphy,the aim is to diagnose any hypoperfused area which are not infracted.
Which will benefit from an improvement in blood flow.
CBF values <20 ml/100g/min have been found in the affected hemisphere of patients with symptomatic vasospasm and values <12ml/100g/min have been asso
ciated with irreversible changes.
to be confinued
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