Incident Diabetes in Survivors of Critical Illness and Mechanisms Underlying Persistent Glucose Intolerance: A Prospective Cohort Study

Objectives: Stress hyperglycemia occurs in critically ill patients and may be a risk factor for subsequent diabetes. The aims of this study were to determine incident diabetes and prevalent prediabetes in survivors of critical illness experiencing stress hyperglycemia and to explore underlying mechanisms. Design: This was a prospective, single center, cohort study. At admission to ICU, hemoglobin A1c was measured in eligible patients. Participants returned at 3 and 12 months after ICU admission and underwent hemoglobin A1c testing and an oral glucose tolerance test. Blood was also collected for hormone concentrations, whereas gastric emptying was measured via an isotope breath test. β-cell function was modeled using standard techniques. Setting: Tertiary-referral, mixed medical-surgical ICU. Patients: Consecutively admitted patients who developed stress hyperglycemia and survived to hospital discharge were eligible. Measurements and Main Results: Consent was obtained from 40 patients (mean age, 58 yr [SD, 10], hemoglobin A1c 36.8 mmol/mol [4.9 mmol/mol]) with 35 attending the 3-month and 26 the 12-month visits. At 3 months, 13 (37%) had diabetes and 15 (43%) had prediabetes. At 12 months, seven (27%) participants had diabetes, whereas 11 (42%) had prediabetes. Mean hemoglobin A1c increased from baseline during the study: +0.7 mmol/mol (–1.2 to 2.5 mmol/mol) at 3 months and +3.3 mmol/mol (0.98–5.59 mmol/mol) at 12 months (p = 0.02). Gastric emptying was not significantly different across groups at either 3 or 12 months. Conclusions: Diabetes and prediabetes occur frequently in survivors of ICU experiencing stress hyperglycemia. Based on the occurrence rate observed in this cohort, structured screening and intervention programs appear warranted. 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 (https://ift.tt/29S62lw). Salary support was provided to Dr. Kar from a Royal Adelaide Hospital A.R. Clarkson Scholarship. Dr. Ali Abdelhamid received funding from Royal Adelaide Hospital Research Committee A.R. Clarkson Scholarship. Dr. Phillips disclosed that she was supported by an Royal Adelaide Hospital Early Career Fellowship and a Royal Adelaide Hospital A.R Clarkson Scholarship. Dr. Jones disclosed that her husband has participated in the advisory boards and/or symposia for Novo Nordisk, Sanofi, Novartis, Eli Lilly, Merck Sharp & Dohme, Boehringer Ingelheim, and AstraZeneca and has received honoraria for this activity; received funding from National Health and Medical Research Council (NHMRC) Career Development Fellowship. Dr. Deane’s institution received funding from GlaxoSmithKline, and he received funding from Baxter, Cardinal, Fresenius Kabi, and Takeda. This study was funded by a Royal Adelaide Hospital Research Committee NHMRC Near Miss Grant (to Dr. Deane); received funding from a NHMRC Early Career Fellowship. This work was performed at the Intensive Care Unit, The Royal Adelaide Hospital, North Terrace, Adelaide, SA, 5000, Australia. For information regarding this article, E-mail: Palash.kar@adelaide.edu.au; p_kar@hotmail.com Copyright © by 2018 by the Society of Critical Care Medicine and Wolters Kluwer Health, Inc. All Rights Reserved.

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