Diagnosis and treatment of diabetic ketoacidosis and the hyperglycemic hyperosmolar state

Abstract

Diabetic 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.

Fig. 1: Schematic of the pathogenesis of diabetic ketoacidosis (DKA) and the hyperglycemic hyperosmolar state (HHS). Relative or absolute insulin deficiency stimulates hepatic glucose production, which results in hyperglycemia, osmotic diuresis and dehydration. In severe insulin deficiency, the liver will augment ketone body production, culminating in hyperketonemia and, eventually, acidosis. βOHB = β-hydroxybutyric acid; AcAc = acetoacetic acid. Photo: Chesley Sheppard

Fig. 2: Management of adult patients with DKA and HHS. Copyright ©2003 American Diabetes Association. From Diabetes Care 2003;26(1 Suppl): S109-17. Reprinted and adapted with permission from The American Diabetes Association.