Monitoring plasma sodium concentration for the first few days of diuretic therapy is prudent. This is especially true in elderly women, patients who ingest large volumes of water, or patients on nonsteroidal anti-inflammatory drugs. If hyponatremia develops, the treatment consists of stopping the diuretic, water restriction, and replacement of any sodium deficit by administering isosmotic saline (see Chapter VC1). This does not apply to edematous states (e.g., heart failure, cirrhosis with ascites, nephrotic syndrome, etc.) where massive edema is conjoined with a persistently shrunken effective arterial blood volume
FIGURE 5. Mechanisms of diuretic induced hyponatremia. (A) Thiazide diuretics. Since thiazides act on the distal tubule, they have no effect on the increased medullary hypertonicity. The action of ADH in the collecting tubules will allow water reabsorption into the hypertonic medullary interstitium. The decreased the free water excretion will increase the tendency to hyponatremia. (B) Loop diuretics. Since loop diuretics act on the TAL, they impair the generation of a medullary hypertonic interstitium. Upon ADH action, free water reabsorption will be limited by a lack of medullary hypertonicity and the tendency to hyponatremia is limited. (Modified and adapted from The Kidney: Physiology and Pathophysiology. Second edition. Seldin DW and Giebisch G. Chapter 28, with permission).
(EABV). In consequence, salt administration increases edema, but does not significantly augment EABV. Therapy is therefore primarily directed at reducing free water intake. If the hyponatremia is severe or symptomatic, administration of hypertonic saline may be necessary; a loop diuretic is generally added to prevent volume overload. Patients with moderate to severe hyponatremia have to be monitored closely as the rapid correction of volume contraction with isotonic saline will make the patient euvolemic. Once euvolemic, the patient will have an appropriately suppressed ADH secretion and the result will be the production of a dilute urine. The resultant rapid excretion of excess water will produce rapid correction of hyponatremia and will increase the risk for osmotic demyelination.
Paradoxically, loop diuretics are sometimes used in conjunction with hypertonic saline infusion in the treatment of hyponatremia. By limiting medullary hypertonicity, they decrease urinary concentration and net electrolyte-free water excretion. The combination reduces the risk of volume overload. .
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