Year : 2014 | Volume
: 11 | Issue : 1 | Page : 3--4
Serum electrolytes in children on chronic diuretic therapy for heart failure
Department of Paediatrics, University of Jos, Jos, Nigeria
Department of Paediatrics, University of Jos, Jos
|How to cite this article:|
Bode-Thomas F. Serum electrolytes in children on chronic diuretic therapy for heart failure.Nig J Cardiol 2014;11:3-4
|How to cite this URL:|
Bode-Thomas F. Serum electrolytes in children on chronic diuretic therapy for heart failure. Nig J Cardiol [serial online] 2014 [cited 2023 Mar 23 ];11:3-4
Available from: https://www.nigjcardiol.org/text.asp?2014/11/1/3/130039
Diuretic therapy plays a major role in heart failure management in children, as in adults. ,, Often this involves the combination of a loop diuretic such as furosemide or a thiazide, with a potassium sparing agent such as spironolactone. Loop diuretics, often called high ceiling diuretics because of the increasing diuretic responses they provide with increasing doses, are very effective and remain active even when renal impairment is present as may occur in severe cases of heart failure.  They are excreted by cells of the proximal convoluted tubule into the lumen of the nephron and exert their effect by inhibiting the Na/K/2Cl cotransporter that transports these ions across the lining cells of the proximal ascending limb of the loop of Henle. Therefore, they interfere with the reabsorption of sodium, potassium, and chloride ions and also calcium and magnesium ions and may deplete the blood levels of these electrolytes.  They may also result in acidosis as a result of the body's attempt to compensate for hypokalamia by exchanging hydrogen for potassium ions at the distal convoluted tubules. Nevertheless, they are often preferred to thiazides (which also cause sodium and chloride loss but act more distally) because they result in relatively less sodium loss compared with water loss.  Other reasons why loop diuretics may be preferred include the rapid relief of symptoms they are associated with, due both to the quicker onset of their diuretic effects and a direct and rapid onset venodilation that independently contributes to preload reduction.  Both the loop diuretics and the thiazides are often combined with potassium-sparing agents, such as spironolactone, which block the effect of aldosterone at the late distal convoluted tubule.  Thus, the different classes of diuretics cause 'sequential nephron blockade' because they all act at different sites of the nephron, combining either a loop diuretic or a thiazide (or both) with a potassium sparer may not only provide superior diuresis but also prevent hypokalamia, which is a major concern with the chronic use of loop and thiazide diuretics, especially when such a patient is also receiving digitalis.  This combination has been shown to hasten and enhance response to treatment in infants with congestive heart failure compared with the use of potassium supplements  and is more widely used in developing countries. Indeed, in adults the addition of spironolactone has been shown to significantly decrease both the death rate from congestive heart failure and the need for hospitalization. 
Diuretic therapy requires careful and regular monitoring of serum electrolytes and renal function. However, this is often not feasible in parts of the developing world, where the majority of children with chronic heart failure are those with structural heart diseases with limited access cardiac surgery. Many such children are maintained for years on these drug combinations, whereas awaiting definitive surgical treatment, whereas at the same time it is often not feasible to regularly check their serum urea and electrolyte levels. In such situations, the safety of this drug combination is often presumed, with the assumption that the potassium loss induced by the loop or thiazide diuretic is balanced out by the potassium retention caused by spironolactone. Similarly, effects of the other electrolyte losses often cannot be routinely monitored, and studies on the electrolyte profiles of children placed for protracted periods of time on these drug combinations are lacking.
The article by Sadoh et al.,  in this issue is an important contribution in this regard, as it attempts to address what must be a nagging question in the minds of many practitioners that are saddled with the chronic care of such children. After receiving these drug combinations (often for years), a few may be lucky enough to eventually receive the definitive treatment (surgery) but not many are so privileged. Too many succumb before ever receiving definitive treatment, usually from complications of the illness, but it is not known how many actually succumb to the complications of the chronic heart failure therapy they received, as opposed to those of the illness itself. The finding by Sadoh et al.,  that serum potassium values did not differ significantly between subjects on diuretics and their controls would seem to, barring contrary evidence, affirm the safety of the prolonged use of these drug combinations at least as far as serum potassium levels are concerned. Furthermore, the authors found no significant difference between subjects that had received these drug combinations for less than 6 weeks (compared with those who had received them for longer), with respect to their serum electrolytes, urea, and creatinine. However, 6 weeks would appear to be a relatively short time within which to adequately assess the effects of the chronic use of these drugs on the parameters assessed.
The authors rather highlight hyponatremia as potentially the most important concern in these cases. This is not surprising, as all three groups of diuretics (loop diuretics, thiazides, and potassium sparers) cause sodium loss but to varying degrees so that their combined chronic use would significantly deplete sodium levels. Although they found no significant differences in the mean serum sodium levels of subjects compared with controls, the authors admit that more subjects than controls had hyponatremia (without stating the actual numbers or percentages). They also state that none of the subjects had severe hyponatremia or its complications such as seizures. Nevertheless, given the wide range in the duration of diuretic therapy in the subjects, it might have been helpful if the authors had tried to directly correlate serum sodium levels with the duration of diuretic therapy. Arbitrarily selecting 6 weeks as a cutoff point for comparison probably also did not allow sufficient time for evaluation of the effect of chronic diuretic use on serum sodium and indeed the other electrolytes. They did find significantly lower chloride levels in subjects compared with controls, but the clinical implications of this were not discussed.
Nevertheless, the article rightly draws attention to the potential danger of hyponatremia in children on diuretic therapy for chronic heart failure. This point is perhaps even more important in older children, in whom many practitioners would emphatically advise a low salt diet. The findings of this study suggest that significant hyponatremia could become a potent threat if such patients are also placed on a strict low salt diet, especially where the serum electrolytes cannot be monitored as often as required.
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