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. 2024 Aug;67(8):1455-1479.
doi: 10.1007/s00125-024-06183-8. Epub 2024 Jun 22.

Hyperglycaemic crises in adults with diabetes: a consensus report

Guillermo E Umpierrez  1 , Georgia M Davis  2 , Nuha A ElSayed  3   4 , Gian Paolo Fadini  5   6 , Rodolfo J Galindo  7 , Irl B Hirsch  8 , David C Klonoff  9 , Rozalina G McCoy  10   11 , Shivani Misra  12   13 , Robert A Gabbay  3   4 , Raveendhara R Bannuru  3 , Ketan K Dhatariya  14   15
Affiliations

Hyperglycaemic crises in adults with diabetes: a consensus report

Guillermo E Umpierrez et al. Diabetologia. 2024 Aug.

Abstract

The American Diabetes Association (ADA), European Association for the Study of Diabetes (EASD), Joint British Diabetes Societies for Inpatient Care (JBDS), American Association of Clinical Endocrinology (AACE) and Diabetes Technology Society (DTS) convened a panel of internists and diabetologists to update the ADA consensus statement on hyperglycaemic crises in adults with diabetes, published in 2001 and last updated in 2009. The objective of this consensus report is to provide up-to-date knowledge about the epidemiology, pathophysiology, clinical presentation, and recommendations for the diagnosis, treatment and prevention of diabetic ketoacidosis (DKA) and hyperglycaemic hyperosmolar state (HHS) in adults. A systematic examination of publications since 2009 informed new recommendations. The target audience is the full spectrum of diabetes healthcare professionals and individuals with diabetes.

Keywords: Aceto-acetate; Acidosis; Anion gap; B-hydroxybutyrate; Diabetic ketoacidosis; Hyperglycaemia; Hyperglycaemic crises; Hypoglycaemia; Ketones; Ketonuria.

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Conflict of interest statement

GEU is supported by research grants from the National Institutes of Health (NIH) (NATS UL 3UL1TR002378-05S2) from the Clinical and Translational Science Award programme and from the NIH and National Center for Research Resources (NIH/National Institute of Diabetes and Digestive and Kidney Diseases [NIDDK] 2P30DK111024-06) and has served as a member of advisory boards for Dexcom and GlyCare. GMD is supported by a research grant from NIH/NIDDK Career Development Award K23DK122199, has received research support from Insulet and has consulted for Medscape. GPF has received honoraria and consultancy and lecture fees from Abbott, AstraZeneca, Boehringer Ingelheim, Lilly, MSD, Novo Nordisk, Mundipharma, Sanofi, Takeda and Servier. RJG is supported by the NIDDK of the NIH under award numbers P30DK111024-08, 1K23DK123384 and 1R03DK138255. RJG has also received research support (to Emory University, Atlanta, GA, USA) for studies from Novo Nordisk, Dexcom and Eli Lilly and consulting/advisory or honoraria/lecture fees from Abbott Diabetes, Dexcom, Eli Lilly, Novo Nordisk, AstraZeneca, Boehringer Ingelheim, Medtronic, and Bayer outside of this work. IBH has received research support from the NIH, Dexcom and MannKind and serves as consultant for Abbott Diabetes Care, Embecta and Hagar. DCK is a consultant for Afon, Atropos Health, GlucoTrack, Lifecare, Nevro, Novo Nordisk, Samsung and Thirdwayv. RGM is supported by the NIDDK of the NIH (R03DK127010 and R01DK135515), the National Institute on Aging of the NIH (R01AG079113), the Patient-Centered Outcomes Research Institute (DB-2020C2-20306), and the American Diabetes Association. RGM also serves as a consultant to EmmiEducation (Wolters Kluwer) on developing patient education materials related to diabetes and to Yale New Haven Health System’s Center for Outcomes Research and Evaluation on developing quality measures related to diabetes. SM holds a personal award from the Wellcome Trust Clinical Career Development Scheme (223024/Z/21/Z) and is supported by the National Institute for Health Research Imperial Biomedical Research Centre. SM also reports an investigator-initiated grant from Dexcom and has received speaker fees (donated to the institution) from Sanofi and Lilly. RAG has served as a consultant to Lark, Vida and Sweetch. RRB and NAE declare that there are no relationships or activities that might bias, or be perceived to bias, their work. KKD has received honoraria for travel, advisory boards and speaker fees from Abbott Diabetes, AstraZeneca, Boehringer Ingelheim, Novo Nordisk, Eli Lily, Menarini and Sanofi Diabetes. No other potential conflicts of interest relevant to this article were reported.

Figures

Fig. 1
Fig. 1
Pathogenesis of DKA and HHS. This figure is available as part of a downloadable slideset
Fig. 2
Fig. 2
The diagnosis criteria of (a) DKA and (b) HHS. This figure is available as part of a downloadable slideset
Fig. 3
Fig. 3
Clinical presentation in patients with DKA and HHS. This figure is available as part of a downloadable slideset
Fig. 4
Fig. 4
Treatment pathways for DKA and HHS. BOHB, β-hydroxybutyrate. This figure is available as part of a downloadable slideset
Fig. 5
Fig. 5
Transition to maintenance insulin administration in DKA. Calculation of the transition subcutaneous dose should account for hypoglycaemia risk factors and anticipated nutritional intake. Estimates can be made using a weight-based calculation or in those already on insulin, the preadmission insulin dose. Basal-bolus insulin is the preferred regimen and should be started 1–2 h before cessation of intravenous insulin. At discharge, dosing of basal-bolus insulin may change again considering hypoglycaemia risk. Follow-up plans should be in place to provide necessary support and training at discharge. NPO, nil per os (not by oral admnistration); T1D, type 1 diabetes; T2D, type 2 diabetes. This figure is available as part of a downloadable slideset
See this image and copyright information in PMC

References

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