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Hypoglycemia Is Associated With Increased Postburn Morbidity and Mortality in Pediatric Patients*

Jeschke, Marc G. MD, PhD1,2,3; Pinto, Ruxandra PhD4; Herndon, David N. MD5,6; Finnerty, Celeste C. PhD5,6,7; Kraft, Robert MD5,6

doi: 10.1097/CCM.0000000000000138
Pediatric Critical Care

Objective: The objective of this study was to determine the prevalence of hypoglycemia after burn injury and whether hypoglycemia is associated with increased postburn morbidity and mortality.

Design: Cohort analysis.

Setting: Academic pediatric burn hospital.

Patients: This analysis included 760 pediatric burn patients, who were stratified according the number of hypoglycemic episodes (< 60 mg/dL glucose) they experienced while in the ICU. Clinical outcomes and metabolic and inflammatory biomarkers were analyzed during the first 60 days post admission. Patients with one or more hypoglycemic events were matched with patients not experiencing any event using propensity score matching, and outcomes and biomarker expression were compared between groups.

Measurements and Main Results: Eighty-four patients had one episode of hypoglycemia, 108 patients had two or more episodes of hypoglycemia, and 568 patients never experienced hypoglycemia. Patients with one or more hypoglycemic episodes had longer hospitalization, as well as more frequent infections, sepsis, multiple organ failure, and death (p < 0.05). The 166 propensity score–matched patients with one or more hypoglycemic events had greater inflammatory and metabolic responses, prevalence of sepsis, multiple organ failure, and mortality than burn patients without hypoglycemic (p < 0.05).

Conclusions: Hypoglycemic episodes correlate with injury severity and inhalation injury. When adjusted for injury severity, hypoglycemia is associated with significantly higher postburn morbidity and mortality.

1Ross Tilley Burn Centre, Sunnybrook Health Sciences Centre, University of Toronto, Toronto, ON, Canada.

2Division of Plastic Surgery, Department of Surgery, University of Toronto, Toronto, ON, Canada.

3Department of Immunology, University of Toronto, Toronto, ON, Canada.

4TECC Program Sunnybrook Health Sciences Centre, University of Toronto, Toronto, ON, Canada.

5Shriners Hospitals for Children and University of Texas Medical Branch, Galveston, TX.

6Department of Surgery, University of Texas Medical Branch, Galveston, TX.

7Sealy Center for Molecular Medicine and the Institute for Translational Sciences, University of Texas Medical Branch, Galveston, TX.

* See also p. 1315.

Dr. Jeschke had full access to all of the data in the study and takes responsibility for the integrity of the data and the accuracy of the data analysis.

Supplemental digital content is available for this article. Direct URL citations appear in the printed text and are provided in the HTML and PDF versions of this article on the journal’s website (http://journals.lww.com/ccmjournal).

Drs. Jeschke, Pinto, Herndon, and Finnerty received support for article research from Shriners Hospitals for Children (8490, 71008, 8640, 8760, 79135, 71001, and 84080), National Institutes of Health (NIH) (R01-GM56687, R01-GM087285-01, T32-GM008256, P50-GM60338, KL2RR029875, and UL1RR029876), National Institute of Disability and Rehabilitation Research (H133A020102, H133A70019, and H133A070026), CFI Leader’s Opportunity Fund (Project #25407), Canadian Institutes of Health Research (grant #123336), and Physicians’ Services Incorporated Foundation (Health Research Grant Program). Their institutions received grant support from NIH. The funding organizations played no role in the design and conduct of the study; in the collection, management, analysis, and interpretation of the data; or in the preparation, review, or approval of the manuscript.

For information regarding this article, E-mail: marc.jeschke@sunnybrook.ca

© 2014 by the Society of Critical Care Medicine and Lippincott Williams & Wilkins