The typical intensive care unit (ICU) patient with DKA is a known diabetic with insulin deficiency who has an event that causes an increase in growth hormone, glucagon, cortisol, or catecholamines, or an omission or deficiency of insulin. Occasionally, it may also be the presenting diagnosis for a new-onset diabetic patient. An underlying cause should always be excluded in the patient with DKA. The most common underlying etiologies include infection, myocardial infarction, stroke, and pancreatitis.

The physiology of DKA is fairly straightforward. The hyperglycemia in DKA results from gluconeogenesis and glycogenolysis in the liver and a reduced utilization of glucose by peripheral tissues. This, in turn, releases the inhibitory effect on glucagon, which when combined with low insulin levels results in more hepatic gluconeogenesis and glycogenolysis. Glucose levels can routinely run as high as 800 mg/dL. This level of hyperglycemia leads to dehydration and other electrolyte abnormalities because of the ensuing osmotic diuresis. Total-body stores of sodium, potassium, chloride, phosphorus, and magnesium are reduced by the polyuria that accompanies the diuresis. The serum potassium may be artificially elevated secondary to the profound acidosis. In addition, a factitious hyponatremia may occur in the setting of hyperglycemia. Therefore, the serum sodium must be corrected by increasing the sodium level by 1.6 mEq for each 100-mg/dL increase in serum glucose.