The biochemistry in diabetic ketoacidosis and hyperosmolar non-ketotic coma is often complex and difficult to interpret.

Sodium concentrations can be normal, low, or, high. The sodium concentration in patients with hyperosmolar non-ketotic coma is usually high, and reflects severe intracellular dehydration and total body water loss. The serum sodium depends on the following:

a. the diluting effect of movement of intracellular water to the extracellular space, particularly in the early stages of the illness;

b. loss through osmotic diuresis;

c. underlying renal function;

d. vomiting of oral fluid intake and diarrhea.

Hyperglycemia interferes with the measurement of sodium as the increased osmolarity in the extracellular compartment draws water from the intracellular compartment and dilutes the sodium:

Free fatty acid and triglyceride levels are high and will interfere with sodium measurement, making it falsely low.

Hyperkalemia is common initially, despite a total body deficit of potassium as a result of the diuresis. Hyperkalemia is mainly due to release of intracellular potassium because of the increased tissue catabolism driven by the insulin deficiency. Acidemia causing cellular potassium-hydrogen exchange plays a minor role.

A high-anion-gap metabolic acidosis is present in diabetic ketoacidosis with varying degrees of respiratory compensation. If patients with hyperosmolar non-ketotic coma have a metabolic acidosis, it is usually secondary to high lactate levels as a result of hypovolemia or due to precipitating factors such as septicemia or acute myocardial infarction. Urea and creatinine are often elevated secondary to dehydration. Creatinine and amylase may be falsely raised secondary to interference with the assay by ketone bodies.

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