Cerebral vasospasm treatment

The principal options for Cerebral vasospasm treatment and treating delayed cerebral ischaemia are haemodynamic augmentation and endovascular therapy.

Cerebral vasospasm treatmentAlternative therapies include intra-aortic counter pulsation (IABC), therapeutic hypothermia dedicated Cerebral vasospasm treatment and barbiturate coma.

The concept of haemodynamic augmentation – also referred to as hypertension, hypervolemia, hemodilution or triple-H therapy—in patients with aneurysmal subarachnoid haemorrhage evolved out of two important observations.

The first was the strong association between cardiovascular variables, cardiac output, and blood pressure in the days and weeks ensuing aneurysmal subarachnoid haemorrhage (aSAH), Cerebral vasospasm treatment and clinical outcomes, such as symptomatic vasospasm and long-term neurologic function.

The second observation was that cerebral vasospasm is characterized by a shift in cerebro-vascular resistance away from the penetrating arterioles to the major branches of the circle of Willis and their proximal branches; vessels that are incapable of effective autoregulation.

As a result, CBF becomes passively dependent on systemic blood pressure, increasing the risk of cerebral ischaemia. Using the Poiseuille relationship, it can be predicted that efforts to increase systemic blood pressure or to decrease blood viscosity will ameliorate cerebral perfusion and reverse ischaemia through Cerebral vasospasm treatment .

Since the 1970’s various investigators had observed significant improvement in neurologic function after initiating haemodynamic augmentation with colloid fluid expansion and through Cerebral vasospasm treatment .

The randomized controlled studies evaluating the efficacy of haemodynamic augmentation therapy in aneurysmal SAH and Cerebral vasospasm treatment are limited.

Rosenwasser et al noted that a strategy of blood pressure control with vasodilators in addition to volume expansion with packed red blood cell transfusion and albumin was associated with a significantly lower rate of symptomatic vasospasm and death when compared to the strategy of blood pressure control with diuretics in 30 patients who were being studied before they underwent aneurysm clipping.

In 82 patients who were randomly assigned to receive albumin fluid boluses titrated to normal or high filling pressures, Lennihan et al discovered that high filling pressures were not associated with any significant change on CBF or CBV as measured by xenon CT, nor were there any differences in the rate of symptomatic Cerebral vasospasm treatment , cerebral infarction, or 3-month Glasgow outcome scale.

In a study of 32 patients randomized to hypertensive/hypervolaemic vs normotensive/normovolaemic management protocols, Egge et al reported no difference in vasospasm rates, as measured by single proton emission computed tomography (SPECT), or 1-yr Glasgow outcome scale, whereas a higher rate of complications, viz., haemorrhage, coagulopathy, congestive heart failure were noted in the hypertensive/hypervolaemic group.

When the results of these three trials were pooled into a systematic review under Cerebral vasospasm treatment , no significant effect of prophylactic triple-H therapy on the rate of symptomatic vasospasm or death were noted.

A Cochrane meta-analysis also reached a similar conclusion, although Cerebral vasospasm treatment carried its own importance.

The inherent limitations of triple-H therapy are (1) The association of haemodynamic augmentation with severe complications such as congestive heart failure, non-cardiogenic pulmonary oedema, myocardial ischaemia, intracranial haemorrhage, global ischaemia and death; (ii) failure to reverse neurologic deterioration in certain patients; and (iii) Contraindications to its use such as the presence of significant pre-existing cardiopulmonary dysfunction.

To augment cardiac output, an inotropic agent (dobutamine) was administered in combination with hypervolaemic preload enhancement to 23 patients with vasospasm whose neuro logic examination failed to improve after pre load enhancement alone. It was noted that a 52% increase in cardiac index, and clinical reversal of ischaemic symptoms was evident in 18 out of 23 patients who underwent Cerebral vasospasm treatment .

In a recent study, xenon CT was used to evaluate CBF in 16 patients with symptomatic vasospasm who underwent volume expansion combined with either mean arterial pressure augmentation with phenylephrine or cardiac output augmentation with dobutamine. The increase in mean CBF was similar in both the groups.

It has been postulated that the Cerebral vasospasm treatment including wider pulse pressure and enhanced pulsatile flow associated with the administration of inotropic agents may ameliorate flow through the collateral vessels and through the microvasculature.

 

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