• Jean-Louis Chiasson, Nahla Aris-Jilwan, Raphaël Bélanger, Sylvie Bertrand, Hugues Beauregard, Jean-Marie Ekoé, Hélène Fournier, and Jana Havrankova.
• Division of Endocrinology-Metabolism, Centre hospitalier de l'Université de Montréal, and the Department of Medicine, Université de Montréal, Montréal, QC. jean.louis.chiasson@umontreal.ca
• CMAJ. 2003 Apr 1; 168 (7): 859866859-66.

AbstractDiabetic ketoacidosis and the hyperglycemic hyperosmolar state are the most serious complications of diabetic decompensation and remain associated with excess mortality. Insulin deficiency is the main underlying abnormality. Associated with elevated levels of counterregulatory hormones, insulin deficiency can trigger hepatic glucose production and reduced glucose uptake, resulting in hyperglycemia, and can also stimulate lipolysis and ketogenesis, resulting in ketoacidosis. Both hyperglycemia and hyperketonemia will induce osmotic diuresis, which leads to dehydration. Clinical diagnosis is based on the finding of dehydration along with high capillary glucose levels with or without ketones in the urine or plasma. The diagnosis is confirmed by the blood pH, serum bicarbonate level and serum osmolality. Treatment consists of adequate correction of the dehydration, hyperglycemia, ketoacidosis and electrolyte deficits.

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