Electrolyte derangements and diuretic misuse in the elderly

Hypo- and hypernatremia occur frequently in elderly patients, representing severe complications leading to adverse events and, ultimately, to death. Hyponatremia develops either as a consequence of excessive water retention or solute depletion, or a combination of both. The normal kidney is capable of excreting any water excess, preventing the occurence of hypo-osmolar syndromes. Therefore, hyponatremia due to water retention requires an important defect in renal diluting ability. This commonly occurs because of central hypovolemia, nephron hypoperfusion, excessive fractional reabsorption in the proximal tubule and reduced fluid delivery to the distal nephron. Under these circumstances, while solute flee water formation is curbed by the reduced delivery of fluid, ADH-independent water abstraction can be unaltered, thus reclaiming a larger fraction of the inflow to the distal nephron. This leads to the excretion of a reduced volume of concentrated urine even in the absence of ADH, causing water retention and reduced diluting power. ADH secretion and high vasopressin levels in the plasma, caused by altered hypothalamic function, further contribute to the onset of hyponatremia. Drugs, heart failure, renal failure, cerebrovascular disease are frequent conditions capable of initiating this pathophysiological sequence. The most frequent cause of low plasma sodium in old age is represented by diuretic-induced Nadepletion. To the extent that sodium loss during diuretic treatment reduces the effective plasma volume and activates thirst, volume is defended by water intake, leading to dilution of residual solutes by a normal volume of solvent. In the aging subject, diuretic-induced K-depletion may represent a more common cause of hyponatremia than Na-loss. Hypernatremia is probably more common than hyponatremia in the elderly. It is caused almost exclusively by important water loss without equivalent solute losses. Dehydration can be caused by fever, coma, insufficient water supply during hospitalization or nursing home care, loss of thirst mechanism, diarrhea, vomiting, heat stroke, mental clouding, stroke, dementia and cerebrovascular disease. Careful clinical examination of the patients, and medical history identify the symptoms of the effective volume contraction due to solute depletion, as opposed to the prevalent signs of cerebral edema and hypertension characterizing water retention. The treatment of excess solvent retention requires techniques of excreting large volumes of hypotonic fluids with the aid of loop diuretics, while reinfusing part of the volume lost with hypertonic solutions that quantitatively replace the solutes excreted. The treatment of solute depletion requires the replenishment of either sodium, or potassium, or both, delivered with the minimal volume required. Water deficit and the attendant hypernatremia can be corrected by replenishing with either hypotonic solutions or with dextrose-containing f(uids the calculated losses. Simple mathematical formulas allow the correct calculations of the volumes and amounts of electrolytes necessary for replenishing the losses, effectively correcting hypo or hypernatremia.