Sarah Rehou1, Stephanie Mason, Marjorie Burnett, Marc G Jeschke. 1. 1Ross Tilley Burn Centre, Sunnybrook Health Sciences Centre, Toronto, ON, Canada. 2Division of General Surgery, Department of Surgery, Faculty of Medicine, University of Toronto, Toronto, ON, Canada. 3Division of Plastic and Reconstructive Surgery, Department of Surgery, Faculty of Medicine, University of Toronto, Toronto, ON, Canada. 4Department of Immunology, Faculty of Medicine, University of Toronto, Toronto, ON, Canada.
Abstract
OBJECTIVES: Metabolic alterations after burn injury have been well described in children; however, in adult patients, glucose metabolism and insulin sensitivity are essentially unknown. We sought to characterize metabolic alterations and insulin resistance after burn injury and determine their magnitude and persistence at discharge. DESIGN: Prospective, cohort study. SETTING: Tertiary burn centre. PATIENTS: Nondiabetic adults with an acute burn involving greater than or equal to 20% total body surface area. INTERVENTIONS: An oral glucose tolerance test was administered at discharge. MEASUREMENTS AND MAIN RESULTS: Glucose, insulin, and C-peptide levels were measured to derive surrogate measures of insulin resistance and β-cell function, including quantitative insulin sensitivity check index, homeostasis model assessment of β-cell function, homeostasis model assessment of insulin sensitivity, homeostasis model assessment of insulin resistance, and the composite whole-body insulin sensitivity index. Patients were grouped according to the degree of glucose tolerance: normal glucose tolerance, impaired fasting glucose/impaired glucose tolerance, or diabetes. Forty-five adults, 44 ± 15 years old and with 38% ± 14% total body surface area burned, underwent an oral glucose tolerance test at discharge. Median quantitative insulin sensitivity check index (0.348 [0.332-0.375]) and median homeostasis model assessment of insulin resistance (1.13 [0.69-1.45]) were abnormal, indicating insulin resistance and impaired insulin production at discharge. Two-thirds of patients (n = 28) met criteria for impaired fasting glucose/impaired glucose tolerance or diabetes. CONCLUSIONS: We have demonstrated that burn-injured adults remain hyperglycemic, are insulin resistant, and express defects in insulin secretion at discharge. Patients with lower burn severity (total body surface area, 20-30%) express similar metabolic alterations as patients with larger burns (total body surface area, ≥ 30%). Glucose tolerance testing at discharge offers an opportunity for early identification of burn patients who may be at high risk of prediabetes and diabetes. Our findings demonstrated that two-thirds of burn patients had some degree of glucose intolerance. With this in mind, surveillance of glucose intolerance post discharge should be considered. As hyperglycemia and insulin resistance are associated with poor outcomes, studies should focus on how long these profound alterations persist.
OBJECTIVES: Metabolic alterations after burn injury have been well described in children; however, in adult patients, glucose metabolism and insulin sensitivity are essentially unknown. We sought to characterize metabolic alterations and insulin resistance after burn injury and determine their magnitude and persistence at discharge. DESIGN: Prospective, cohort study. SETTING: Tertiary burn centre. PATIENTS: Nondiabetic adults with an acute burn involving greater than or equal to 20% total body surface area. INTERVENTIONS: An oral glucose tolerance test was administered at discharge. MEASUREMENTS AND MAIN RESULTS:Glucose, insulin, and C-peptide levels were measured to derive surrogate measures of insulin resistance and β-cell function, including quantitative insulin sensitivity check index, homeostasis model assessment of β-cell function, homeostasis model assessment of insulin sensitivity, homeostasis model assessment of insulin resistance, and the composite whole-body insulin sensitivity index. Patients were grouped according to the degree of glucose tolerance: normal glucose tolerance, impaired fasting glucose/impaired glucose tolerance, or diabetes. Forty-five adults, 44 ± 15 years old and with 38% ± 14% total body surface area burned, underwent an oral glucose tolerance test at discharge. Median quantitative insulin sensitivity check index (0.348 [0.332-0.375]) and median homeostasis model assessment of insulin resistance (1.13 [0.69-1.45]) were abnormal, indicating insulin resistance and impaired insulin production at discharge. Two-thirds of patients (n = 28) met criteria for impaired fasting glucose/impaired glucose tolerance or diabetes. CONCLUSIONS: We have demonstrated that burn-injured adults remain hyperglycemic, are insulin resistant, and express defects in insulin secretion at discharge. Patients with lower burn severity (total body surface area, 20-30%) express similar metabolic alterations as patients with larger burns (total body surface area, ≥ 30%). Glucose tolerance testing at discharge offers an opportunity for early identification of burn patients who may be at high risk of prediabetes and diabetes. Our findings demonstrated that two-thirds of burn patients had some degree of glucose intolerance. With this in mind, surveillance of glucose intolerance post discharge should be considered. As hyperglycemia and insulin resistance are associated with poor outcomes, studies should focus on how long these profound alterations persist.
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