Endovascular therapy to treat symptomatic vasospasm
aft(prenominal) aneurysmal subarachnoid hemorrhage
(aSAH) has become a mainstay in many centers. Cerebral
vasospasm, defined as correctable vasoconstriction
of the intracranial vasculature, is found in approximately
30% to 70% of patients later aSAH, although
perhaps only one-third to one-half of these patients
will dampen symptoms and/or delayed ischemic
neurologic deficits (DINDs). DINDs remain the leading
cause of stroke, morbidity, and death rate after
aSAH (1). The Fisher grade (Table 1) (2), scoring the
amount of blood seen on the initial head computed
tomography (CT) scan, remains a dangerous predictor of
the severity of vasospasm to be anticipated and the
incidence of CT demonstrable infarction and associated
morbidity and mortality. Whether patients presenting
with aSAH are more apparent to develop
vasospasm, if treated by endovascular coiling versus
craniotomy and clipping, is a matter of young debate
with evidence supporting both claims (35) and no
prospective study as of yet performed.
Medical therapy, including the administration of
nimodipine for 21 days station bleed, regardless of the
presence of vasospasm, and triple-H (hypervolemia,
hypertension, and hemodilution) therapy once
vasospasm has been identified have improved outcomes
after aSAH and averted vasospasm-induced
DINDs in some patients. Some patients, however,
will suffer ravage cerebral ischemia despite
these efforts. Neurointerventional techniques, including
intra-arterial administration of vasodilators such
as papaverine and transluminal billow angioplasty
(TBA), have gained good results and have emerged as
a more aggressive approach for such patients (6).
These endovascular techniques (intra-arterial infusion
of medication and angioplasty) have their own associated
risks and benefits, and feud exists over
the best method (7). At what point to intervene with
endovascular interference has...If you want to get a full essay, order it on our website: Orderessay
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