NAVLE Endocrine

Canine Diabetic Ketoacidosis Study Guide

Diabetic ketoacidosis (DKA) is a life-threatening complication of diabetes mellitus characterized by the biochemical triad of hyperglycemia, ketonemia (or ketonuria), and metabolic acidosis.

Overview and Clinical Importance

Diabetic ketoacidosis (DKA) is a life-threatening complication of diabetes mellitus characterized by the biochemical triad of hyperglycemia, ketonemia (or ketonuria), and metabolic acidosis. It represents one of the most common endocrine emergencies in veterinary medicine and requires intensive hospitalization with aggressive fluid therapy and insulin administration. DKA occurs when absolute or relative insulin deficiency prevents glucose from entering cells, forcing the body to rely on fat metabolism for energy, which produces acidic ketone bodies.

Approximately 65-70% of dogs with DKA are newly diagnosed diabetics at the time of presentation. Concurrent diseases are present in over 70% of cases, with the most common being acute pancreatitis (40-41%), urinary tract infections (20%), and hyperadrenocorticism (15%). The presence of hyperadrenocorticism is associated with significantly worse outcomes.

Ketone Body Characteristics Detection
Beta-hydroxybutyrate (BHB) Most abundant in DKA; technically a hydroxy acid, not a true ketone Point-of-care ketone meters (most sensitive); NOT detected by urine dipstick
Acetoacetate Only true ketoacid chemically; converts to BHB in presence of NADH Detected by urine dipstick (nitroprusside reaction)
Acetone True ketone; volatile; causes fruity breath odor Clinical detection (breath); partially by urine dipstick

Pathophysiology

Insulin Deficiency and Counter-Regulatory Hormones

DKA develops from an absolute or relative insulin deficiency combined with elevated counter-regulatory hormones (glucagon, cortisol, catecholamines, and growth hormone). In dogs, Type 1 diabetes mellitus (absolute insulin deficiency due to beta-cell destruction) is the most common form. The pathogenesis involves genetic predisposition, autoimmune mechanisms, and environmental factors.

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