## Objectives: To study the degree and timing of maternal hyperglycemia following betamethasone therapy in nondiabetic patients and establish a prophylactic dose of insulin. ## Methods: Forty-five patients receiving betamethasone 12 mg i.m. at 7 am on two consecutive days were randomized to no in
Randomized, controlled trial of insulin for acute poststroke hyperglycemia
โ Scribed by Michael McCormick; Donald Hadley; John R. McLean; Jennifer A. Macfarlane; Barrie Condon; Keith W. Muir
- Publisher
- John Wiley and Sons
- Year
- 2010
- Tongue
- English
- Weight
- 245 KB
- Volume
- 67
- Category
- Article
- ISSN
- 0364-5134
No coin nor oath required. For personal study only.
โฆ Synopsis
Abstract
Objective
Poststroke hyperglycemia is common and is associated with increased risk of death and dependence, but appropriate management remains uncertain. Glucose potassium insulin (GKI) infusion did not benefit patients with moderate poststroke hyperglycemia in a recent trial. Using magnetic resonance imaging (MRI), previous studies identified a relationship between recruitment of ischemic tissue to the final infarct and hyperglycemia, possibly mediated by brain lactic acidosis.
Methods
We undertook a randomized, placeboโcontrolled trial of GKI infusion in patients with blood glucose >126mg/dl (7mmol/l) within 24 hours of ischemic stroke. The primary endpoint was infarct growth on MRI between baseline and day 7. Brain lactate concentrations were measured with magnetic resonance spectroscopy.
Results
Forty patients were randomized, 15 to saline and 25 to GKI infusions of different durations. Capillary blood glucose concentrations were lowered significantly from 6 to 12 hours after GKI initiation. There was no significant difference on any measure of infarct growth between the GKI and saline groups. In a secondary analysis, GKI was associated with significantly greater infarct growth in patients with complete intracranial vessel occlusion compared with controls (p = 0.011 for groupโvessel status interaction). Brain lactate levels increased in control subjects, but were significantly lower with GKI infusion. Predominantly asymptomatic hypoglycemia occurred in 76% of GKIโtreated subjects.
Interpretation
GKI infusion within 24 hours of stroke lowered blood glucose and attenuated an increase in brain lactate, but did not affect cerebral infarct growth. Exploratory analysis found that GKI infusion was associated with greater infarct growth in patients with persistent arterial occlusion, and with a high incidence of asymptomatic hypoglycemia. ANN NEUROL 2010;67:570โ578
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