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Editorial: Normal short children.

failure, in diabetic ketoacidosis, in severe acidosis of any other origin, in extensive tissue damage, and, less frequently, in severe uncontrolled Addison's disease. Iatrogenic causes should not be forgotten, especially the administration of potassium supplements to patients with severe renal failure or to patients receiving spironolactone, in the absence of careful monitoring. When hypokalaemia is encountered one should first of all consider whether there is an inadequate dietary intake especially important in the elderly-whether the patient is taking diuretics, carbenoxolone, or corticosteroids, which could cause enhanced renal losses, or is taking purgatives which cause increased losses from the gut. If such causes are excluded one must consider intrinsic gastrointestinal disorders associated with malabsorption, fistulae, acute or chronic diarrhoea, and also renal abnormalities such as renal tubular acidosis. If the patient is hypertensive, and especially if there is an associated alkalosis, primary or secondary hyperaldosteronism should always be borne in mind. Since so small a percentage of the potassium is in the extracellular fluids the presence of hypokalaemia need not necessarily indicate an overall deficiency of potassium in the body and, conversely, there may be potassium depletion with the plasma potassium maintained in the normal range. It would be helpful if in clinical practice we could readily measure the intracellular potassium, but this is not so. For the moment at least measurement of erythrocyte, leucocyte, or muscle-cell potassium content is subject to too many difficulties and variables for general use. Undoubtedly the most accurate index to potassium depletion is the measurement of total body potassium in a whole-body monitor by counting the radioactivity from the natural isotope 40K which is present in the body, but the facilities are not universally available. Measurement of total exchangeable body potassium by the isotope dilution technique using 42K or 43K is a more readily available procedure, and it can give a useful indication of the potassium content of the body provided sufficient time is allowed for equilibration.2 Since precise measurement of body potassium is difficult the further investigation and management of most patients with hypokalaemia will be a matter for careful clinical appraisal. Causal factors should be corrected wherever possible, and the dietary potassium can be augmented with fruit and fruit juices. If digoxin is being given the dosage should be reduced or the drug omitted for a time in view of the increased sensitivity to its effect caused by alteration in the ratio of extracellular to intracellular potassium. If there is a need to continue diuretic therapy some prefer to change to a potassiumsparing diuretic such as amiloride or spironolactone, others will use a combined tablet containing the diuretic and potassium, and yet others will continue with thiazide or frusemide with separate oral potassium supplements. Ifpotassium supplements are used some patients prefer slow-release tablets of potassium chloride (Slow-K), each of which contains approximately 8 mEq of potassium, while others prefer effervescent tablets of potassium chloride (Sando-K), which provide 12 mEq of potassium. While no one disputes the need for potassium supplementation in patients with cardiac oedema, cirrhosis of the liver, and the nephrotic syndrome, it is uncertain whether all patients on diuretic therapy require potassium supplements. Doubt has been expressed previously by Healy et al.,3 while Down et al.4 have shown that supplements are not retained in patients on diuretic therapy if they are not potassium-depleted. This week (p. 316) Dr. H. J. Dargie and his colleagues show that total body potassium was not reduced in non-oedematous hypertensive patients receiving frusemide for one year, despite the presence in some of mild hypokalaemia. Provided a careful assessment is made of the individual circumstances in all cases, and provided that there is continuing supervision, oral potassium supplementation does not seem to be an essential part of diuretic therapy.