Hypervolemia in cerebral vasospasm
(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)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/406780
- author
- Raabe, A and Romner, Bertil LU
- organization
- publishing date
- 2006
- 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
- 2022-01-28 20:55:50
@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 (<= 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}},
}