254 such as frusemide, ethacrynic acid, and bumetanide can control severe fluid retention whatever the cause; but occasionally the response to conventional dosage is poor, and such cases give rise to the notion of diuretic resistance.
Patients with renal failure on regular hsemodialysis have their excess sodium and water removed by ultrafiltration, and this principle has been applied to overhydrated-non-uraemic patients thought to be resistant to diuretics. 1Dialysers with a high ultrafiltration capacity are modified by closure of one port of the dialysate compartment and collection of the ultrafiltrate through the other. A mean filtration rate of 30 ml/min enables 4-8 litres to be removed in 2-4 hours. Surprisingly, in view of such a rapid removal of fluid, the procedure is well tolerated and in the hands of routine dialysis staff the technique is simple, safe, and effective; but is it necessary? Asaba and his colleagues,2who advocate long-term evaluation of this method, treated nine patients who had shown "resistance to intensive diuretic therapy in hospital". Unfortunately they do not give details of their diuretic regimen. Five of their patients had renal failure and were severely nephrotic. Inability to control oedema in such patients is unusual. Apart from a low-salt diet, frusemide in very large doses of 1-3 g/day may be necessary together with an aldosterone antagonist and occasionally the infusion of hyperoncotic salt-poor albumin. The effect of diuretics in renal disease is limited by the low glomerular filtration-rate and by the pathophysiological changes in water and electrolyte handling. As the glomerular filtration-rate falls the fractional excretion of sodium and water rises, but even a high fractional excretion can be increased by a large dose of frusemide. Indeed frusemide remains effective until the glomerular filtration-rate has fallen below 3 ml/min. In these circumstances the drug is not well absorbed from the gastrointestinal tract and should be given intravenously.4 In patients with severe cardiac failure, continuous infusion of frusemide in low doses secures a controlled gentle diuresis with plasma concentrations well below those likely to cause deafness. 5 One of the patients in Asaba’s group had ascites due to cirrhosis-a condition in which resistance to diuretics is occasionally encountered, particularly in the absence of peripheral oedema. Vigorous attempts to remove ascitic fluid with diuretics or ultrafiltration are likely to cause hypovolxmia and acute ischxmic renal failure. The time-honoured principles of bed rest, rigid sodium restriction, and cautious diuretic therapy still apply. In the patient with gross ascites reinfusion of concentrated ascitic fluid, by the Rhodiascit procedure, will occasionally shorten the stay in hospital.6 Oedema resistant to diuretics is rare and suggests that - the underlying illness is terminal. Ultrafiltration may have a small role in special situations where speed is vital, such as urgent cardiac surgery. 1. Silverstein, M. E., Ford, C. A.,
Lysaght, M. J., Henderson, L. W. New Engl. J Med. 1974, 291, 747. 2 Asaba, H., Bergeström, J., Fürst, P., Shaldon, S , Wiklund, S. Acta med. scand 1978, 204, 145 3 Allison, M.E. M., Kennedy, A. C Clin Sci 1971, 41, 171. 4 Tilstone, W. J., Fine, A. Clin. Pharmac. Ther. 1978, 23, 644. 5 Lawson, D. H., Gray, J. M B, Henry, D. A., Tilstone, W. J. Br. med. J. 1978, ii, 476. 6. Moult, P
J A., Parbhoo, S P., Sherlock, S. Postgrad med. J. 1975, 51, 574.
YES, YOUR ADENOTONSILLECTOMY IS REALLY NECESSARY PAEDIATRICIANS and E.N.T. surgeons may differ about place of adenotonsillectomy in the management of recurrent sore throats, otitis media, and mouth breathing, but both agree that the operation should be done when adenotonsillar obstruction presents a threat to life. In the past 15 years several workers’-4 have described young children, usually under 4 years, with large tonsils, stridor when lying supine,s sleep apnceaand somnolence.7 These symptoms may be absent in the upright anxious child attending a clinic, and mothers’ stories should not be dismissed lightly. A chest X-ray may show cardiomegaly and pulmonary oedemagand the electrocardiogram reveals right heart strain, axis deviation, and hypertrophy.9 The differential diagnosis includes
cardiomyopathy, myocarditis, primary pulmonary hypertension, and nephrosis10 but a careful history, overnight observation, and blood-gas analysis may spare the child from a potentially dangerous cardiac catheterisation.11 If doubt remains the effect of nasopharyngeal intubation may be tried.12 Heart-failure should be treated with digoxin and diuretics and then the tonsils and adenoids-and not one without the other11—should be removed without delay. Oxygen therapy has dangers since these children may depend on hypoxic drive for respiration; sedation should be given cautiously if at all.s The pathophysiology of this condition is that chronic nasopharyngeal obstruction causes pulmonary hypoventilation, arterial hypoxæmia, and acidosis leading to pulmonary vasoconstriction and hypertension. This may happen in children whose tonsil and adenoid sizes are unexceptional, and other factors such as abnormalities of the epiglottis may be important. Why this condition has only lately been described is far from clear. One explanation is the reduction in number of adenotonsillectomies, but this operation is usually done at school age and most children with this syndrome are younger. A more likely explanation is that the common condition of adenotonsillar hypertrophy produces dramatic consequences only in the small minority of children (though perhaps more than are recognised) with some other predisposition to cardiopulmonary disease. Support for this notion comes from the observation that some 20% of people have a pronounced increase in pulmonary vascular resistance in response to hypoxia.13 The occurrence of this syndrome in homozygous twins" suggests a
genetic cause. Postoperatively the X-rays, cardiograms, findings return to normal-and the
and cardiac catheter symptoms disappear.
1. Harrington, R. Med. J. Aust. 1978, ii, 175. 2. Levy, A. M., Tabakin, B. S., Hanson, J. S., Narkewicz, R. M. New Engl. J. Med. 1967, 277, 506. 3. Noonan, J. A. Circulation, 1965, 32, suppl. 2, p. 164. 4. Luke, M. J., Mehnzi, A., Folger, G. M., Rowe, R. D. Pediatrics, 1966, 37, 762. 5. Macartney, F. J., Panday, J., Scott, O. Archs Dis. Childh. 1969, 44, 585. 6. Moffat, D. A. J. Pediat., 1976, 89, 510. 7. Mangat, D., Orr, W. C., Smith, R. O. Archs Otorhinolar. 1977, 103, 383. 8. Talbot, A. R., Robertson, L. W. ibid. 1973, 98, 277. 9. Ainger, L. E. Br Heart J., 1968, 30, 356. 10. Thanopoulos, B., Ikkos, D. D., Milingos, M., Foutakis, D. Acta pœdiat. scand. 1975, 64, 659. 11. Massumi, R. A., Savin, R. K., Pooya, M., Reichelderfer, T. R., Fraga, J. R., Rios, J. C., Ayesterian, E. Dis. Chest, 1969, 55, 110. 12. Kravath, R. E., Pollak, C P., Borowiecki, B. Pediatrics, 1977, 59, 865 13. Grover, R. F., Vogel, J. H. K., Averill, K H., Blount, S. G., Jr. Am. Heart
J. 1963, 66, 1.