In what hyponatremic states can a patient be hyperosmolar or hypertonic?
The two most clinically relevant occurrences of hyperosmolar hyponatremia are azotemia and hyperglycemia. Buildup of nitrogenous waste, that is, urea, in the setting of impaired kidney function increases plasma osmolality. If present alone, kidney dysfunction does not lead to a change in serum sodium concentration. However, if a simultaneous disorder in water balance leading to hyponatremia is present, hyponatremia with normal or elevated serum osmolality may result. Such patients are truly hypotonic , because the decreased sodium, an effective osmole, leads to a decrease in tonicity while urea, an ineffective osmole, does not increase tonicity.
In hyperglycemia, increased serum glucose increases both the total and effective plasma osmolality, leading to a hypertonic state. The hypertonic plasma draws water from the cells into the extracellular compartment, lowering the serum sodium concentration. For every 100 mg/dL increase in glucose above normal, the serum sodium falls by approximately 1.6 mEq/L even as tonicity rises due to the hyperglycemia. In cases of more severe hyperglycemia (i.e., serum glucose >400 mg/dL), the ratio approximates a 2.4 mEq/L drop in serum sodium for every 100 mg/dL rise in serum glucose. A similar process occurs with administration of mannitol. Any such correction factor is an approximation, and osmolality should be measured directly when clinically relevant.
