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Hypervolemia in cerebral vasospasm

Raabe, A and Romner, Bertil LU (2006) In Journal of Neurosurgery 104(6). p.994-995
Abstract
Object. Arterial vasospasm is the most common cause of delayed ischemic neurological deficits (DINDs) and one of the major causes of disability following subarachnoid hemorrhage (SAH). Current management of vasospasm involves intravascular volume expansion and hemodynamic augmentation with the goal of increasing cerebral blood flow (CBF). The purpose of this study was to examine the effects of volume expansion on regional (r)CBF in patients with DIND following SAH. Methods. The authors measured quantitative rCBF on positron emission tomography (PET) scans in six patients with aneurysmal SAH who had developed clinical signs of vasospasm. All patients were kept in a euvolemic state prior to the onset of vasospasm. At the onset of vasospasm,... (More)
Object. Arterial vasospasm is the most common cause of delayed ischemic neurological deficits (DINDs) and one of the major causes of disability following subarachnoid hemorrhage (SAH). Current management of vasospasm involves intravascular volume expansion and hemodynamic augmentation with the goal of increasing cerebral blood flow (CBF). The purpose of this study was to examine the effects of volume expansion on regional (r)CBF in patients with DIND following SAH. Methods. The authors measured quantitative rCBF on positron emission tomography (PET) scans in six patients with aneurysmal SAH who had developed clinical signs of vasospasm. All patients were kept in a euvolemic state prior to the onset of vasospasm. At the onset of vasospasm, global and rCBF were measured before and after the administration of a normal saline bolus of 15 ml/kg administered over 1 hour. Two patients then received saline infusions of 5 ml/kg x hr over the following 2 to 3 hours and underwent hourly serial CBF measurements. Global and rCBF data were calculated in each patient. The mean rCBF in areas with low flow at baseline (<= 25 ml/[100 g x min]) increased from 19.1 +/- 3.0 to 29.9 +/- 9.7 ml/(100 g x min) (p = 0.02) with volume expansion. This change was sustained over the following 2 to 3 hours. Pulmonary capillary wedge pressure, mean arterial blood pressure, cardiac output, and central venous pressure did not change significantly during this intervention. Conclusions. In euvolemic patients with vasospasm, intravascular volume expansion with a normal saline bolus raised CBF in regions of the brain most vulnerable to ischemia. (Less)
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author
and
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Journal of Neurosurgery
volume
104
issue
6
pages
994 - 995
publisher
American Association of Neurosurgeons
external identifiers
  • wos:000238129100031
  • pmid:16776352
  • scopus:33745965953
  • pmid:16776352
ISSN
0022-3085
DOI
10.3171/jns.2006.104.6.994
language
English
LU publication?
yes
id
fe154088-f6be-4844-af4a-4d1354094369 (old id 406780)
date added to LUP
2016-04-01 16:36:40
date last changed
2021-06-23 01:32:34
@article{fe154088-f6be-4844-af4a-4d1354094369,
  abstract     = {Object. Arterial vasospasm is the most common cause of delayed ischemic neurological deficits (DINDs) and one of the major causes of disability following subarachnoid hemorrhage (SAH). Current management of vasospasm involves intravascular volume expansion and hemodynamic augmentation with the goal of increasing cerebral blood flow (CBF). The purpose of this study was to examine the effects of volume expansion on regional (r)CBF in patients with DIND following SAH. Methods. The authors measured quantitative rCBF on positron emission tomography (PET) scans in six patients with aneurysmal SAH who had developed clinical signs of vasospasm. All patients were kept in a euvolemic state prior to the onset of vasospasm. At the onset of vasospasm, global and rCBF were measured before and after the administration of a normal saline bolus of 15 ml/kg administered over 1 hour. Two patients then received saline infusions of 5 ml/kg x hr over the following 2 to 3 hours and underwent hourly serial CBF measurements. Global and rCBF data were calculated in each patient. The mean rCBF in areas with low flow at baseline (&lt;= 25 ml/[100 g x min]) increased from 19.1 +/- 3.0 to 29.9 +/- 9.7 ml/(100 g x min) (p = 0.02) with volume expansion. This change was sustained over the following 2 to 3 hours. Pulmonary capillary wedge pressure, mean arterial blood pressure, cardiac output, and central venous pressure did not change significantly during this intervention. Conclusions. In euvolemic patients with vasospasm, intravascular volume expansion with a normal saline bolus raised CBF in regions of the brain most vulnerable to ischemia.},
  author       = {Raabe, A and Romner, Bertil},
  issn         = {0022-3085},
  language     = {eng},
  number       = {6},
  pages        = {994--995},
  publisher    = {American Association of Neurosurgeons},
  series       = {Journal of Neurosurgery},
  title        = {Hypervolemia in cerebral vasospasm},
  url          = {http://dx.doi.org/10.3171/jns.2006.104.6.994},
  doi          = {10.3171/jns.2006.104.6.994},
  volume       = {104},
  year         = {2006},
}