Diabetic Ketoacidosis (DKA) is a severe, life-threatening complication of diabetes resulting from a profound deficiency of insulin. This condition creates a chaotic metabolic state characterized by dangerously high blood sugar, the production of acidic ketone bodies, and significant dehydration. Despite this severe dehydration, blood tests often show a low sodium level, a condition known as hyponatremia. This paradox is explained by two physiological mechanisms that alter the concentration and total amount of sodium in the body.
The Metabolic Foundation of DKA
The underlying cause of DKA is a lack of effective insulin, the hormone responsible for allowing glucose to enter the body’s cells for energy. Without insulin, cells starve, and the body releases stress hormones like glucagon and cortisol. This hormonal shift signals the liver to produce massive amounts of glucose through processes like gluconeogenesis, resulting in extreme hyperglycemia.
Insulin deficiency also triggers the breakdown of fat stores (lipolysis), releasing free fatty acids into the bloodstream. The liver converts these fatty acids into ketone bodies, such as acetoacetate and beta-hydroxybutyrate. These ketones are strong acids, and their accumulation overwhelms the body’s buffering capacity, leading to metabolic acidosis—the “K” and “A” components of DKA.
How High Glucose Dilutes Measured Sodium
The first reason for low measured sodium relates to fluid physics, not true sodium loss. Glucose is an osmotically active particle, meaning its concentration strongly influences water movement across cell membranes. When blood glucose levels become extremely high, the concentration of solutes in the plasma increases significantly.
This high concentration of glucose in the extracellular space creates an osmotic force that pulls water out of the body’s cells and into the blood vessels. The resulting influx of water increases the total volume of fluid in the plasma relative to the sodium present. When laboratory equipment measures the sodium concentration in this diluted blood sample, the result appears falsely low, even if the total amount of sodium in the body is near normal. This effect is referred to as dilutional hyponatremia.
The Role of Osmotic Diuresis in Sodium Loss
The second mechanism contributing to low sodium involves the kidneys and represents a true total body loss of the electrolyte. Normally, the kidneys filter glucose from the blood and reabsorb almost all of it back into circulation. In DKA, however, the blood glucose level far exceeds the kidney’s capacity to reabsorb it, typically around 180 to 200 milligrams per deciliter.
The excess, unreabsorbed glucose spills into the urine, a process called glycosuria. This high concentration of glucose in the renal tubules acts as a powerful osmotic agent, drawing large amounts of water into the urine. This excessive urination, known as osmotic diuresis, also carries along electrolytes, including sodium, chloride, and potassium, leading to their depletion. This mechanism results in the severe dehydration characteristic of DKA and ensures the patient has an absolute deficit of sodium. Frequent vomiting associated with DKA further depletes fluid and electrolytes from the gastrointestinal tract, exacerbating this loss.
Calculating and Restoring Sodium Balance
Because of the dilutional effect of glucose, the initial measured sodium value is unreliable for guiding treatment decisions. Clinicians must calculate a “corrected sodium” value to estimate the true sodium concentration if the blood glucose were normalized. This is done by adding 1.6 milliequivalents per liter (mEq/L) to the measured sodium for every 100 milligrams per deciliter (mg/dL) that the blood glucose is above 100 mg/dL.
The corrected sodium provides a more accurate picture of the patient’s water deficit and helps determine the appropriate type of intravenous fluids for resuscitation. If the corrected sodium is low or normal, initial treatment involves isotonic saline (0.9% sodium chloride) to rapidly restore blood volume and replace lost sodium and water. If the corrected sodium is high, a more hypotonic solution, such as 0.45% sodium chloride, may be used after initial volume restoration to address the relative excess of water loss. Careful, gradual replacement of both fluid and sodium is necessary to stabilize the patient.