A diagnostic approach to hyponatremia is outlined in list. The of hyponatremia show that it can be associated with normal, high, or low total body sodium content.
In some hyponatremic disorders, the serum osmolality is elevated; thus, the intracellular wa ter content is not increased, and no risk of brain edema exists. Hyperglycemia and the use of hypertonic mannitol may result in hyponatremia because of water shift from the intracellular to extracellular space. Hyponatremia associated with normal serum osmolality may be seen in patients with extreme hyperlipidemia and h proteinemia, resulting from methodologic errors in techniques to measure serum electrolyte concentration.
The increasing use of ion-selective electrodes for these measurements is making these causes of “pseudohyponatremia” uncommon. Hyponatremia may also be seen in patients who undergo transurethral resection of the prostate or hysteroscopy because of the absorption of large amounts of hypo-osmolar glycine or sorbitol irrigating solutions. Most hyponatremic disorders are associated with hypo-osmolality . In principle, hypo-osmolality can result from an increase in water intake and/or a decrease in renal water excretion. Under normal circumstances, the kidneys can excrete 16 to 20 L of water per day. Water excretion may be impaired secondary to a reduced GFR rate, impaired sodium chloride reabsorption in the renal segments of the distal or to suppress secretion in response to hypertonicity (syndrome of inappropriate ADH). Thus, for a patient to develop hyponatremia solely as a result of excess water intake is unusual. In primary polydispsia,the hyponatremia is caused by large water intake in the presence of impaired water or a excretion. Hyponatremia may also occur with modestly increased water intake in the presence of impaired GFK or decreased solute intake. In patients with decreased GFR, renal water excretion is impaired because of decreased delivery of filtrate to the distal nephron.
Patients with chronic starvation or beer potomania have deficient oral intake of solutes. Because renal water e cretion depends on osmolar intake, these patients may develop hyponatremia at a modestly increased level of water intake. More commonly, hyponatremia occurs as a result of the inability to dilute urine maximally because of reduction in the rate of salt absorption by the diluting segment, sustained nonosmotic release of ADH, or a combination of these two factors. In the disorders associated with decreased ECV, nonosmotic ADH release occurs and promotes water retention by the kidney. In addition, these patients have enhanced proximal sodium chloride reabsorption with diminished distal delivery These disorders may be associated with signs of either volume expansion or volume depletion SIADH is the prototype of the primary release of ADH or ADH-like substances.
It occurs most often in tera association with pathologic processes of the central nervous system or pulmonary system. Many medications one Coun can enhance the release of ADH or can potentiate its(dashed effect. The circulating ADH allows excessive water absorption in the collecting duct with a modest expansion of the extracellular fluid volume.