Modern diuretic treatment.

Abstract

Thiazide diuretics form the mainstay of treatment for numerous conditions characterised by oedema, most notably congestive heart failure when there is a reduced glomerular filtration rate, increased aldosterone production, and increased sodium reabsorption from the renal tubules. Longstanding heart failure no longer responsive to a thiazide often responds dramatically to a loop diuretic, and a loop diuretic also rapidly relieves acute pulmonary oedema secondary to left ventricular failure. Resistant oedema, on the other hand, may respond favourably when diuretics that act on different parts of the renal tubule are given together?for example, thiazide plus a loop diuretic with or without the addition of an aldosterone antagonist. A thiazide or loop diuretic is prescribed together with spiro nolactone in the nephrotic syndrome and in cirrhosis of the liver complicated by ascites, both conditions being almost invariably associated with secondary hyperaldosteronism. Thiazides and spironolactone are often prescribed, too, in some cases of recurrent, idiopathic cyclical oedema, particularly of the ankles, associated with water retention. In this disorder, which is most often seen in premenopausal women and especially at menstruation, diuretics may have an initial cosmetic effect, but long term benefit is hard to establish. Thiazides are also often inappropriately prescribed in managing chronic lymph oedema or chronic ankle oedema associated with varicose veins and poor venous return. Only in a few of these patients is the oedema easier to control as a result of using diuretics; adequate elastic support is more appropriate. The requirement for diuretic treatment in managing oedema needs to be regularly reassessed in order not to exceed the necessary minimum dose of the least powerful diuretic that will suffice. When clinical judgment does not suffice, a useful means of measuring the loss of sodium and water is to observe the rate and extent of weight loss. Provided that the serum sodium concentration remains normal, 1 kg of water loss corresponds to 140-150 mmol(mEq) of associated sodium loss. Another useful assessment is to measure the 24 hour urinary sodium excretion: if this is below 10-20 mmol the diuretic treatment is inadequate, but if it is quite high (above 100 mmol) and body weight is not decreasing sodium excretion is satisfactory but sodium intake needs to be reduced. On the other hand, some patients are at risk of developing saline depletion with loss of tissue turgor, postural hypotension, and a rising serum urea concentration because of loss of interstitial fluid and a fall in plasma volume with poor renal perfusion. The diuretic dose in such patients may best be adjusted to allow mild ankle oedema in the evening, which will clear during the night in bed. Excessive diuresis will othe wise produce undue shrinkage of the plasma volume with resu tant secondary hyperaldosteronism and hypokalaemia. Excessively rapid clearance of oedema also causes malaise.