Because glucose is an effective osmole, hyperglycemia leads to hyponatremia by causing an osmotically driven shift of water from cells into the extracellular compartment, resulting in dilution of serum sodium. This osmotic shift can be estimated by a correction factor that predicts a 1.6 mEq/L decrease in sodium for every 100 mg/dL rise in glucose. However, validation studies of this correction factor have suggested that the decrease in sodium may be even greater, from 2.4 to 4.0 mEq/L, depending on the plasma glucose level.4 Thus, in this patient, the corrected sodium would be 135 mEq/L or greater based on which correction factor is used. In patients with intact renal function, the osmotic shift in water to the extracellular compartment caused by glucose is somewhat balanced by an osmotic diuresis also driven by glucose. The result is usually a mild decrease in serum sodium. A patient on dialysis cannot respond with diuresis, and therefore hyponatremia tends to be more pronounced. In this case, the treatment is to remove the osmotic driving force, which will require immediate IV insulin. Subcutaneous insulin is not recommended for managing critical hyperglycemia. Free water intake will likely worsen underlying hyponatremia. Although the patient missed his hemodialysis session, hyponatremia is not a primary indication for urgent dialysis; correction of hyperglycemia is the first line of treatment. In addition, this patient has no other indications for activating immediate hemodialysis, such as critical hyperkalemia or volume overload.
- Initiate IV short-acting insulin therapy.
4. Hillier TA, Abbott RD, Barnett EJ. Hyponatremia: evaluating the correction factor for hyperglycemia. Am J Med 1999;106:399-403.
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