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The association of hyperglycemia with cerebral edema in stroke.
Author(s) -
Léo Berger,
A. M. Hakim
Publication year - 1986
Publication title -
stroke
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.397
H-Index - 319
eISSN - 1524-4628
pISSN - 0039-2499
DOI - 10.1161/01.str.17.5.865
Subject(s) - medicine , edema , cerebral edema , midline shift , stroke (engine) , autopsy , anesthesia , surgery , computed tomography , mechanical engineering , engineering
A retrospective review of stroke patients admitted to our hospital revealed 39 patients diagnosed as suffering an acute completed ischemic stroke who also had had fasting (AC) serum glucose determinations and sequential computer tomography (CT) studies. The patients were divided into three groups on the basis of mean AC serum glucose: Group 1 (n = 12) mean serum AC glucose greater than 150 mg/dl; Group 2 (n = 13) mean serum AC glucose 100-150 mg/dl; and Group 3 (n = 14) mean serum AC glucose less than 100 mg/dl. CT scans performed on each patient were studied for the presence of midline shift and/or ventricular compression, which were interpreted as evidence of cerebral edema. The three groups were comparable with respect to mean age, average mean arterial blood pressure and initial infarct size. Our results show that in Group 1, 42% of the patients died within the first week following their CVA with clinical evidence of transtentorial herniation confirmed by CT or autopsy. In contrast, none of the Group 3 patients died and only one showed radiological evidence for cerebral edema. Group 2 patients showed intermediate mortality and evidence of cerebral edema. These trends were statistically significant at p less than 0.005. In addition, the combined hyperglycemic group (1 and 2) had a significantly higher rate of development of hypodensity on CT (p less than 0.05) than the normoglycemic group. Our findings suggest that patients with hyperglycemia in association with their CVA develop more pronounced cerebral edema and have a worse clinical outcome. Possible pathophysiological mechanisms that may underlie this observation are discussed.

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