Diabetic ketoacidosis (DKA) is a serious complication of diabetes characterized by hyperglycemia, metabolic acidosis, and ketonemia. Elevated levels of ammonia in the blood, or hyperammonemia, can sometimes occur alongside DKA. This is significant because increased ammonia levels can contribute to neurological dysfunction.
The development of elevated blood ammonia in DKA is multifactorial. Insulin deficiency, a hallmark of DKA, promotes protein catabolism to provide substrates for gluconeogenesis. This breakdown of protein releases amino acids, which are then deaminated in the liver. Deamination produces ammonia, which is normally converted to urea for excretion. However, in DKA, the capacity of the urea cycle to process the increased ammonia load may be overwhelmed, resulting in hyperammonemia. Additionally, dehydration and impaired renal function, common in DKA, can further reduce the clearance of ammonia.