This is rarely associated with hypervolemia, where the association is typically iatrogenic, e.g., administration of hypertonic sodium bicarbonate. More commonly, hypernatremia is the result of a combined H2O and volume deficit, with losses of H2O in excess of Na+. Elderly individuals with reduced thirst and/or diminished access to fluids are at the highest risk of hypernatremia due to decreased free H2O intake. Common causes of renal H2O loss are osmotic diuresis secondary to hyperglycemia, postobstructive diuresis, or drugs (radiocontrast, mannitol, etc.); H2O diuresis occurs in central or nephrogenic diabetes insipidus (DI) (Chap. 168. Disorders of the Anterior Pituitary and Hypothalamus). In pts with hypernatremia due to renal loss of H2O, it is critical to quantify ongoing daily losses in addition to calculation of the baseline H2O deficit (Table 1-2).
Treatment: Hypernatremia The approach to correction of hypernatremia is outlined in Table 1-2. As with hyponatremia, it is advisable to correct the H2O deficit slowly to avoid neurologic compromise, decreasing the serum [Na+] over 48-72 h. Depending on the blood pressure or clinical volume status, it may be appropriate to initially treat with hypotonic saline solutions (1/4 or 1/2 normal saline); blood glucose should be monitored in pts treated with large volumes of D5W, should hyperglycemia ensue. Calculation of urinary electrolyte-free H2O clearance is helpful to estimate daily, ongoing loss of free H2O in pts with nephrogenic or central DI (Table 1-2). Other forms of therapy may be helpful in selected cases of hypernatremia. Pts with central DI may respond to the administration of intranasal DDAVP. Stable pts with nephrogenic DI may reduce their polyuria with hydrochlorothiazide (12.5-50 mg/d). This diuretic is thought to increase proximal H2O reabsorption and decrease distal solute delivery, thus reducing polyuria. Pts with lithium-associated nephrogenic DI may respond to amiloride (2.5-10 mg/d), which decreases the entry of lithium into principal cells in the distal nephron by inhibiting the amiloride-sensitive epithelial sodium channel (ENaC). Notably, however, most pts with lithium-induced nephrogenic DI can adequately accommodate by increasing their H2O intake. Occasionally, nonsteroidal anti-inflammatory drugs (NSAIDs) or COX-2 inhibitors have also been used to treat polyuria associated with nephrogenic DI, reducing the negative effect of local prostaglandins on urinary concentration; however, the nephrotoxic potential of NSAIDs typically makes them a less attractive therapeutic option. |
Section 1. Care of the Hospitalized Patient