Management of Hyperglycemic Crises: Diabetic Ketoacidosis and Hyperglycemic Hyperosmolar State

Abstract

Diabetic ketoacidosis (DKA) and hyperglycemic hyperosmolar state (HHS) are the most serious and life-threatening hyperglycemic emergencies in diabetes. DKA is more common in young people with type 1 diabetes and HHS in adult and elderly patients with type 2 diabetes. Features of the 2 disorders with ketoacidosis and hyperosmolality may coexist. Both are characterized by insulinopenia and severe hyperglycemia. Early diagnosis and management are paramount. Treatment is aggressive rehydration, insulin therapy, electrolyte replacement, and treatment of underlying precipitating events. This article reviews the epidemiology, pathogenesis, diagnosis, and management of hyperglycemic emergencies.

Keywords: Diabetes; Diabetic ketoacidosis; Hyperglycemic emergencies; Hyperglycemic hyperosmolar state; Management of hyperglycemic emergencies.

Figure 1

Pathogenesis of Hyperglycemic Emergencies Hyperglycemia and accumulation of ketones bodies result from a relative or absolute insulin deficiency and excess counter-regulatory hormones (glucagon, cortisol, catecholamines, and growth hormone). Increased Ketone Bodies and ketoacidosis. Decrease in insulin levels combined with increased in counter-regulatory hormones, particularly epinephrine causes the activation of hormone sensitive lipase in adipose tissue and breakdown of triglyceride into glycerol and free fatty acids (FFAs). In the liver, FFAs are oxidized to ketone bodies, a process predominantly stimulated by glucagon. The two major ketone bodies are β-hydroxybutyrate and acetoacetic acid. Accumulation of ketone bodies leads to a decrease in serum bicarbonate concentration and metabolic acidosis. Higher insulin levels present in HHS inhibit ketogenesis and limit metabolic acidosis. Increased Glucose Production in DKA and HHS. When insulin is deficient, hyperglycemia develops as a result of three processes: increased gluconeogenesis, accelerated glycogenolysis, and impaired glucose utilization by peripheral tissues. Hyperglycemia cause osmotic diuresis that lead to hypovolemia, decreased glomerular filtration rate and worsening hyperglycemia.

Figure 2

Management of Hyperglycemic Emergencies *Subcutaneous Insulin Protocol has not been validated for HHS Modified by permission of Diabetes Care from the American Diabetes Association Consensus Statement on Hyperglycemic Crises, 2009 .