EDITORIALS

more ominous and will require early bronchoscopy.

Putting the use of the 1970's instrument, the bronchofiberscope, into perspective in regard to hemoptysis is necessary. Most 1970's articles on hemoptysis dwell on the use of this fine instrument. In my opinion no bronchoscopy, especially for blood streaking and frank but nonmassive hemoptysis, is complete or adequate without the use of the bronchofiberscope. The diagnostic yield will be improved and the risks are acceptable if the examination is done as soon as possible after the beginning of the hemoptysis requiring bronchoscopy. None the less, this instruihent does not replace good clinical judgment and is probably overused for many reasons including monetary considerations. In cases of massive hemoptysis the use of a rigid bronchoscope for emergency examination seems more advantageous than using a bronchofiberscope. The selection of which scope to use for hemoptysis seems less important, however, than the close active communication and cooperation between the experienced pulmonary physician and the skilled thoracic surgeon. THOMAS A. NEFF, MD Chief, Pulmonary Service Denver General Hospital Associate Professor of Medicine University of Colorado Medical School, Denver REFERENCES 1. Lyons HA: Differential diagnosis of hemoptysis and its treatment. Basics of RD 5:26-30, Nov 1976 (Published by American Thoracic Society, New York City) 2. Stinghe RV, Mangiulea VG: Hemoptysis of bronchial origin occurring in patients with arrested tuberculosis. Am Rev Resp Dis 101:84-89, Jan 1970

We Have Come a Long Way THE HISTORICAL PIECE by Ilza Veith which appears elsewhere in this issue serves as a good reminder of how far medicine in the West, and indeed in the Western world, has come in the last 100 years. In one sense 100 years seems a long time, but compared with today's human life expectancy of more than 70 years, it really is not. It is safe to say that change in medicine has been at least as dramatic as change in the little town of Tiburon, California, since the 1870's, and it could even be that there has been relatively more ''progress" in medicine-a statement that today's real estate entrepreneurs in that part of California might conceivably wish to challenge. We have surely come a long way in a mere century and the mind boggles at what medicine will be able to do 100 years hence in the 2070's. Tiburon will seem to have hardly progressed at all by com-

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parison. And it is sobering to realize that some who are being born today will live to see and experience these changes which are inevitable but -MSMW yet to come.

Acute Renal Failure ACUTE RENAL FAILURE, discussed by Dr. Mendoza elsewhere in this issue, has changed over the last decade.12 The causes are more readily ascertained; the treatment has attained the status of conventional, and the prospects for those children who sustain irreversible damage are better. The decline in the prevalence of poststreptococcal glomerulonephritis has been very noticeable in the Northern and Western United States where scarlet fever and streptococcal pharyngitis were the common infections antecedent to the nephritis. In Hawaii and the southeastern part of the United States where the climate is warm and humid, the disease is prevalent and its antecedent infection is impetigo.3 The seasonal incidence and immunologic responses differ depending on whether pharyngitis or skin infection is the antecedent. In other respects the disease is the same. Better housing and nutrition, more effective use of antibiotics or the natural history of the disease may account for the decline in streptococcal pharyngitis and the associated decrease in nephritis induced in this way. The good prognosis customarily associated with nephritis affecting children appears to continue.4'5 The hemolytic-uremic syndrome, described in detail by Dr. Mendoza, is enigmatic. It appears to be a modern disease not present to any degree two or three decades ago. It is more prevalent in Argentina, South Africa and the Western United States. Its cause remains obscure. Our experience has been that the disease may leave the kidney severely injured more often than the experiences cited by Dr. Mendoza.6 The children who suffer permanent damage are among those who are severely oliguric or anuric on admission. However prolonged, oliguria, even to six weeks, is compatible with complete recovery. Acute tubular necrosis as noted often is preventable. The tendency, common a decade ago, to have children referred who had been given excessive quantities of 5 percent glucose and 0.2 percent saline solution (the ward all-purpose solution) to the point where they had hyponatremia, has fortunately reversed. Giving isotonic sodium chloride, Ringers lac-

EDITORIALS

tate solution or chloride bicarbonate solutions to children whenever their perfusion is compromised is very important. Where acidosis coexists, as it often does, we use an ampule of 50 ml (50 mEq) of sodium bicarbonate added to 1 liter of 0.45 percent of sodium chloride (this solution has the following composition in mEq per liter: sodium, 121; chloride, 73; bicarbonate, 48) and infuse the solution at a rate of 20 ml per kg of body weight per hour until it is clear that perfusion is adequate. At that point, further expansion of extracellular fluid volume is contraindicated. Children with the nephrotic syndrome are prone to the development of acute tubular necrosis (ATN). When they have been in remission and suddenly have a relapse with massive proteinuria and contraction of plasma volume, shock and ATN may develop.7 They may need a prompt infusion of extracellular-like fluid to create enough edema to support circulation. If acute tubular necrosis does occur, it usually is not severe. We have found it useful to give mannitol to children with acute hemoglobinuria or myoglobinuria. We give 0.5 grams per kg of body weight as a 20 percent solution over a 15 to 30 minute period and then match further fluid input to urine output (or give slightly less fluid than urine output) using a 4 percent mannitol solution in 0.2 percent sodium chloride until the urine is seen to be free of pigment.8 Where there has been an acute release of myoglobin or hemoglobin the clearing usually takes less than 12 hours. This method avoids significant changes in extracellular fluid volume or osmolality. Acute renal failure in the neonatal period is a special case that has been the subject of a recent review.9 Therapy of acute renal failure has been well defined. The challenge of manipulating body composition that made treatment exciting to physicians and sometimes put a patient at risk has given way to straightforward strategies so clearly outlined in Dr. Mendoza's review. I would only emphasize one point and suggest another. Undertaking hemodialysis or pentoneal dialysis by an

experienced group at a relatively early stage on well defined criteria, uncluttered by attempts to avoid dialysis, has made an important difference. Hypertonic dialysate (4.5 percent dextrose solution) used as peritoneal dialysate is very helpful in removing extra fluid. Adequate dwell times (longer than 30 minutes) are needed to avoid inducing hypernatremia and to assure effective removal of extra fluid. While dialysis even in ex-

perienced hands carries some risk, the risk is minimal compared with leaving a patient with serious volume or compositional problems which dialysis could readily correct. The point I would draw attention to is the probable advantage of more aggressive nutritional therapy. There are data in adults that suggest the value to patients of giving intravenous nutrition that provides 50 to 100 percent of needed energy and amino acids.'0"11 In children with renal failure, net urea nitrogen production was progressively suppressed in response to increases in glucose administration given through a catheter placed in a central vein. Net urea nitrogen production was further reduced and nitrogen retained as body

protein when these children were also given essential amino acids.12 The risk of central vein catheters while appreciable probably is less than the risk of severe malnutrition. While no clear guidelines for instituting its use have emerged, experience with intravenous nutrition in surgical patients strongly supports the initiation of intravenous nutrition in patients with renal failure before cachexia has become obvious. Since children have a disadvantage in that the ratio of energy expenditure to energy stores is less,'3 it would seem logical to begin therapy soon after the onset of an illness in which intake is compromised. Undernutrition may be another factor, and a preventable one, that makes children with renal failure more susceptible to infection.'4 MALCOLM A. HOLLIDAY, MD Professor of Pediatrics Children's Renal Center University of California, San Francisco School of Medicine REFERENCES 1. Holliday MA: Acute renal failure. Pediatrics 35:478, 1965 2. Lieberman E: Management of acute renal failure in infants and children. Nephron 11:193-208, 1973 3. Wannamaker LW: Differences between streptococcal infections of the throat and of the skin. N Engl J Med 282:78, 1970 4. Dodge WF, Spargo BH, Travis LB, et al: Poststreptococcal glomerulonephritis: a prospective study in children. N EngI J Med 286:273-278, Feb 10, 1972 5. Lewy JE: Clinico-pathological correlations in acute poststreptococcal glomerulonephritis. Medicine 50:453, 1971 6. Tune BM, Leavett TJ, Grebble TJ: The hemolytic uremic syndrome in California: A review of 28 nonheparinized cases with long-term follow-up. J Pediatr 82:304-310, 1973 7. Egan TJ, Kenny FM, Jarrah A, et al: Shock as a complication of the nephrotic syndrome. Am J Dis Child 113:364-368, 1967 8. Orloff S, Potter DE, Holliday MA: Acute renal failure, In Smith CA (Ed): The Critically Ill Child. Philadelphia, W. B. Saunders, 1977, p. 127 9. Reimold EW, Don TD, Worthen HG: Renal failure during the first year of life. Pediatrics 59:987, 1977 10. Abel RM, Beck CH, Abbott WM, et al: Improved survival from acute renal failure after treatment with intravenous L-amino acids and glucose: Results of a prospective double-blind study. N Engl J Med 288:695, 1973 11. Asbach HW, Stoeckel H, Schiiler HW, et al: The treatment of hypercatabolic acute renal failure by adequate nutrition and haemodialysis. Acta Anaesthesiol Scand 18:255, 1974 12. Abitbol CL, Holliday MA: Total parenteral nutrition in anuric children. Clin Nephrol 5:153-158, 1976 13. Holliday MA: Intravenous nutrition in children with uremia. Am J Clin Nutr. (In press) 14. Law DK, Dudrich SJ, Abdow NI: The effects of protein calorie malntutrition on immune competence of the sturgical patient. Surg Gynecol Obstet 139:257, 1974

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Acute renal failure.

EDITORIALS more ominous and will require early bronchoscopy. Putting the use of the 1970's instrument, the bronchofiberscope, into perspective in re...
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