Abstract

Diabetic ketoacidosis (DKA) is the leading cause of morbidity and mortality in children with type 1 diabetes mellitus (TIDM). Mortality is predominantly related to the occurrence of cerebral edema; only a minority of deaths in DKA are attributed to other causes. Cerebral edema occurs in ∼0.3% to 1% of all episodes of DKA, and its etiology, pathophysiology, and ideal method of treatment are poorly understood. There is debate as to whether physicians treating DKA can prevent or predict the occurrence of cerebral edema and the appropriate site(s) for children with DKA to be managed. There is agreement that prevention of DKA and reduction of its incidence should be a goal in managing children with diabetes. To explore these issues, the Lawson Wilkins Pediatric Endocrine Society (LWPES) and the European Society for Pediatric Endocrinology (ESPE) convened a panel‖ of expert physicians for a consensus conference. The meeting was chaired by Mark A. Sperling, MD, representing LWPES, and David B. Dunger, MD, representing ESPE. The Consensus statement was developed with close partnership between the ESPE and LWPES and the International Society for Pediatric and Adolescent Diabetes, all 3 organizations being represented by members who participated in the writing process. The statement also was endorsed by related organizations; the Juvenile Diabetes Research Foundation International, the World Federation of Pediatric Intensive and Critical Care Societies, the European Society for Pediatric Critical Care, the European Society of Pediatric and Neonatal Intensive Care, and the Australian Pediatric Endocrine Group were represented by invited participants. Each of the major topics had a presenter and recorder, responsible for review of the literature and providing evidence-based recommendations according to criteria used by the American Diabetes Association (see Appendix; levels of evidence are indicated in capital letters, in parentheses).1 Type 2 diabetes was not considered. All participants contributed … Address correspondence to David B. Dunger, Department of Paediatrics, University of Cambridge, Addenbrooke’s Hospital, Level 8, Box 116, Cambridge CB2 2QQ, United Kingdom. E-mail: dbd25{at}cam.ac.uk; or Mark A. Sperling, Department of Pediatrics/Endocrinology, Children’s Hospital of Pittsburgh, 3705 Fifth Ave, Pittsburgh, PA 15213. E-mail: masp{at}pitt.edu

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