Different mechanisms can cause hyponatremia (Fig. 35-1).Pseudohyponatremia is a laboratory artifact that is present when the plasma contains high concentrations of protein or lipid. It does not occur when a direct ion-selective electrode determines the sodium concentration, a technique that is increasingly used in clinical laboratories. In true hyponatremia, the measured osmolality is low, whereas it is normal in pseudohyponatremia. Hyperosmolality, resulting from mannitol infusion or hyperglycemia, causes a low serum sodium concentration because water moves down its osmotic gradient from the intracellular space into the extracellular space, diluting the sodium concentration. For every 100 mg/dL increment of the serum glucose, the serum sodium decreases by 1.6 mEq/L. Because the manifestations of hyponatremia are due to the low plasma osmolality, patients with hyponatremia caused by hyperosmolality do not have symptoms of hyponatremia and do not require correction of hyponatremia.
Classification of true hyponatremia is based on the patient’svolume status (see Fig. 35-1). In hypovolemic hyponatremia, the child has lost sodium from the body. Water balancemay be positive or negative, but there has been a higher netsodium loss than water loss; this is often due to oral or intravenous (IV) water intake, with water retention by the kidneys to compensate for the intravascular volume depletion. Ifthe sodium loss is due to a nonrenal disease (e.g., diarrhea),the urine sodium concentration is very low, as the kidneysattempt to preserve the intravascular volume by conservingsodium. In renal diseases, the urine sodium is inappropriately elevated.
Patients with hyponatremia and no evidence of volumeoverload or volume depletion have euvolemic hyponatremia. These patients typically have an excess of total bodywater and a slight decrease in total body sodium. Some ofthese patients have an increase in weight, implying that theyare volume overloaded. Nevertheless, they usually appearnormal or have only subtle signs of fluid overload. In syndrome of inappropriate ADH (SIADH), there is secretion of ADH that is not inhibited by either low serum osmolality or expanded intravascular volume. Retention of watercauses hyponatremia, and the expansion of the intravascular volume results in an increase in renal sodium excretion. Hyponatremia in hospitalized patients is often due to SIADHsecondary to stress in the presence of hypotonic fluids.
SIADH      (emesis, diarrhea)  Glucocorticoid deficiency Nephrotic syndrome      Skin (sweating or burns)      Capillary leak
Urine Na+ variable Thiazide or loop diuretics      Acute or chronic renal failure Osmotic diuresis      Postobstructive diuresis      Polyuric phase of ATN      Renal tubular damage (e.g., obstructive uropathy)
Figure 35-1 Differential diagnosis of hyponatremia. Assessment of hyponatremia is a three-step process: (1) Determine if the osmolality is low; if yes, the patient has true hyponatremia. (2) Evaluate the patient’s volume status. (3) Determine the urine sodium concentration to help narrow the differential diagnosis. ATN, Acute tubular necrosis; SIADH, syndrome of inappropriate secretion of antidiuretic hormone.
SIADH is also associated with pneumonia, mechanical ventilation, meningitis, and other central nervous system disorders (trauma). Ectopic (tumor) production of ADH is rarein children. Infants can develop euvolemic hyponatremia asa result of excessive water consumption or inappropriatelydiluted formula.