The effect of head of bed elevation on cerebrovascular dynamics in mild or moderate cerebral vasospasm following aneurysmal subarachnoid hemorrhage
Stroke is the leading cause of disability and the third leading cause of death. One type of stroke, aneurysmal subarachnoid hemorrhage accounts for approximately 7% of all strokes. One of the complications associated with aneurysmal subarachnoid hemorrhage is cerebral vasospasm. The sustained constriction of one or more intracranial blood vessels may result in additional cerebral ischemia or infarction. Vasospasm may begin from 3 to 5 days after the subarachnoid hemorrhage and continue up to 21 to 28 days after the bleed.In the patient with aneurysmal subarachnoid hemorrhage, a delicate balance exists between preventive measures to decrease the consequences of immobility and the need to support optimal cerebral perfusion to prevent secondary brain injury. Based on tradition and consensus in individual institutions, the degree of head elevation during vasospasm has been limited by some clinicians in an attempt to minimize vasospasm and/or its sequelae. As a result, some individuals have remained on bedrest for weeks. However, prior to this study, no scientific investigation has been conducted to demonstrate the effect of head of bed elevation on cerebrovascular dynamics in vasospasm following aneurysmal subarachnoid hemorrhage.This study is descriptive and quasi-experimental. Twenty subjects, between days 3 and 14 post aneurysmal subarachnoid hemorrhage in mild or moderate vasospasm, underwent head of bed elevations in a 0--20--45--0 degree sequence. Middle cerebral artery flow velocities and middle cerebral artery to internal carotid artery ratios, the determinants of cerebral vasospasm, were recorded in each position using transcranial Doppler technology. Descriptive and inferential statistics were computed. No patterns or trends were found that indicate head of bed elevation increases vasospasm. As a group, there were no statistically significant differences within subjects at the different head positions (p ≤ 0.05). In addition, no individuals increased to severe vasospasm with the head of bed elevations at 20 and 45 degrees. In general, increasing the head of the bed did not cause harmful changes in cerebral blood flow. The fact that one individual did experience an increase from mild to moderate vasospasm indicates the value of being able to monitor vasospasm during head of bed elevation. Additional studies with a larger sample size, longer duration of head of bed elevations, and/or increased head of bed elevations are warranted.
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