With adequate water intake in the setting of severe hyperglycemia with osmotic diuresis, the BUN/creatinine ratio can be normal or low despite severe water and electrolyte losses and intracellular dehydration.
Hyperglycemia causes osmotic expansion of the extravascular compartment and dilutional hyponatremia. Plasma sodium is corrected to the following formula: Na (corrected) = Na (measured) + 0.016 × (glucose – 100), which gives a sodium level of 147 mmol/L in the absence of osmotic expansion.
Although patients can present with hyperkalemia, mainly resulting from mild acidosis and decreased activity of the sodium–potassium-ATPase pump leading to intracellular → extracellular shifts, patients with hyperosmolar hyperglycemia are truly potassium depleted as the result of osmotic diuresis and renal losses. Careful replenishment of potassium guided by plasma levels is critical to avoid arrhythmias, cardiac arrest, and respiratory muscle weakness.
Typically, diabetic ketoacidosis (DKA) is accompanied by severe metabolic acidosis characterized by pH less than 7.30 and bicarbonate less than 15 mmol/L.
Plasma osmolality can be calculated by the following formula: 2 × Na + glucose/18 + BUN/2.8, giving a result of 329 mOsm/kg in this patient (reference range, 285 to 295). Effective osmolality does not include BUN as urea freely crosses cell membranes. This patient’s effective osmolality is 323 mOsm/kg, consistent with a hyperglycemic hyperosmolar state (>320 mOsm/kg according to American Diabetic Association guidelines).
