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Published on: October 27, 2020
Hyperglycemia and insulin resistance in cardiac arrest patients treated with moderate hypothermia
Matthew D Ettleson1, Vanessa Arguello, Amisha Wallia
1Division of Endocrinology, Metabolism, and Molecular Medicine (M.D.E., A.W., L.A., M.E.M.), Department of Medicine, and Department of Neurology (R.A.B.), Northwestern University Feinberg School of Medicine, Chicago, Illinois 60611; and Department of Internal Medicine (V.A.), University of Illinois at Chicago/Advocate Christ Medical Center, Chicago, Illinois 60453.
Insights
Hyperglycemia after cardiac arrest, not therapeutic hypothermia (TH), is linked to mortality. Post-arrest blood glucose levels predict survival, suggesting stress from the arrest itself causes elevated glucose.
Area of Science:
- Critical care medicine
- Cardiology
- Endocrinology
Background:
- Hyperglycemia following cardiac arrest and during therapeutic hypothermia (TH) is common, but its cause and impact on outcomes remain unclear.
- It is unknown whether hyperglycemia is a direct result of cardiac arrest or TH, or if it influences patient survival.
Purpose of the Study:
- To investigate the effect of TH on blood glucose (BG) levels in patients post-cardiac arrest.
- To determine the association between hyperglycemia and mortality in these patients.
Main Methods:
- A retrospective chart review of 62 patients undergoing TH after cardiac arrest.
- Analysis of BG levels from 72 hours pre-arrest to 48 hours post-TH, including insulin infusion rates.
- Correlation of BG levels and insulin resistance with survival to hospital discharge.
Main Results:
- Therapeutic hypothermia (TH) did not independently affect blood glucose (BG) levels.
- Nonsurvivors exhibited significantly higher mean BG levels (253 ± 112 mg/dL) compared to survivors (192 ± 69 mg/dL) between cardiac arrest and TH initiation (P = .016).
- No significant differences in BG, insulin infusion rates, or insulin resistance were observed between groups during or after TH.
Conclusions:
- Therapeutic hypothermia (TH) does not independently alter blood glucose (BG) levels in post-cardiac arrest patients.
- Elevated BG levels after cardiac arrest, prior to TH or insulin treatment, are associated with increased mortality.
- The severity of the cardiac arrest event is likely the primary driver of hyperglycemia in these patients.
Context:
It is unknown whether the hyperglycemia that follows cardiac arrest and during therapeutic hypothermia (TH) is due to the arrest or the TH, whether it is associated with adverse outcomes, or whether its treatment affects outcomes.
Objective:
The objective of the study was to determine the effects of TH on the blood glucose (BG) levels in postcardiac arrest patients and the effects of hyperglycemia on mortality.
Design:
This was a chart review of 62 patients undergoing TH after cardiac arrest between September 2005 and April 2008. BG levels from 72 hours before the arrest to 48 hours after TH and iv insulin infusion rates were analyzed and correlated with survival to discharge from hospital.
Setting:
The study was conducted at a tertiary, university referral center.
Patients:
PATIENTS undergoing TH after cardiac arrest participated in the study.
Interventions:
TH consisted of cooling as rapidly as possible to 33°C, holding that temperature for 24 hours, and then controlled rewarming to 37°C over 8 or 16 hours. Hyperglycemia was managed with iv insulin drip protocols.
Main Outcome Measure:
The relationship of cardiac arrest and hypothermia to hyperglycemia, with a key secondary outcome being the relationship of hyperglycemia to survival to discharge, was measured.
Results:
Analysis of glucose patterns showed no independent effect of TH on BG levels. Mean BG levels between cardiac arrest and the initiation of hypothermia were higher in nonsurvivors (253 ± 112 mg/dL, n = 48) than in survivors (192 ± 69 mg/dL, n = 24, P = .016). BG, insulin infusion rates, and insulin resistance during hypothermia, during rewarming, and 24-48 hours after hypothermia were not significantly different between the 2 groups.
Conclusions:
In patients treated with TH, the TH had no independent effect on BG levels. Mortality was associated with increased BG levels after cardiac arrest but before initiation of TH or an insulin drip. Likely, it is the severity of stress from the cardiac arrest that causes the hyperglycemia in these patients.
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