Diabetic ketoacidosis sometimes refered to as DKA develops when an absolute insulin deficiency and combined with excess contra-insulin hormones increase hepatic glucose production, thereby decreasing peripheral glucose utilization, and stimulating release of fatty acids from fat cells and production of ketones by the liver. These changes cause hyperglycemia, osmotic diuresis and acidosis.

This is much more common among persons with insulin-dependent diabetes mellitus or IDDM than among those with non-insulin-dependent diabetes mellitus (NIDDM).

DKA may be the initial manifestation of previously unrecognized insulin dependant diabetes mellitus. Usually however DKA develops in persons known to have diabetes. Patients with IDDM and expeience flulike illnessor pneumonia and who fail to take insulin or who do not receive extra insulin during the illness may develop DKA. Patients with NIDDM who are under severe stress may secrete more contra-insulin hormones; this in turn compromises limited insulin secretion, which may lead to DKA.

In the past before insulin was available, patients with diabetes often died of DKA; now with the care and treatment that is available, the mortality rate associated with Diabetic Ketoacidosis is less than 5%. Individuals who develop DKA experience pain and suffering, lose time from school or work, have increased hospitalization rates, and have high medical costs.

Ultimately, DKA results from a lack of insulin. Early recognition of metabolic disarray, by monitoring glucose and ketones and by properly using insulin and fluids, can prevent further decompensation. DKA should be considered preventable, said different way, when DKA occurs, a breakdown in patient care has occurred that should have been prevented.