- Email: [email protected]
Feeding of premature infants—use of a simple formula
WILSON ET AL
23. Steindl P, Ferenci P, Dienes HP, Grimm G, Pabinger I, Madl C, et al. Wilson’s disease in patients presenting with liver disease: a diagnostic challenge. Gastroenterology 1997;113: 212-8. 24. Martins da Costa C, Baldwin D, Portmann B, Lolin Y, Mowat AP,
THE JOURNAL OF PEDIATRICS NOVEMBER 2000 Mieli-Vergani G. Value of urinary copper excretion after penicillamine challenge in the diagnosis of Wilson’s disease. Hepatology 1992;15: 609-15. 25. Tanner MS, Portmann B. Indian childhood cirrhosis. Arch Dis Child 1981;56:4-6.
26. Sternlieb I. Mitochondrial and fatty changes in hepatocytes of patients with Wilson’s disease. Gastroenterology 1968;55:354-67. 27. Sternlieb I. Fraternal concordance of types of abnormal hepatocellular mitochondria in Wilson’s disease. Hepatology 1992;16:728-32.
50 Years Ago in The Journal of Pediatrics FEEDING OF PREMATURE INFANTS—USE OF A SIMPLE FORMULA Abelson S. J Pediatr 1950;37:711-7.
Fifty years ago, the 2-year experience of a US Naval Hospital in feeding 311 premature infants a “simplified formula,” which consisted of half evaporated milk and half water, was reported in The Journal of Pediatrics. This mixture supplied 52% of calories from fat, 28% from carbohydrate, and 20% from protein. The feeding protocol included 36 to 72 hours of “drying out” (water and formula were withheld to relieve edema), after which gavage feedings were initiated at a volume of ~40 cc/kg/d. Glucose water and half-strength formula were used to transition to full-strength formula. By the second week of life, feeds were gradually advanced to provide 150 to 200 cc/kg/d (110-140 kcal/kg/d). Subcutaneous clyses of 5% dextrose were occasionally given for “apathy and signs of dehydration.” Intravenous fluids were reserved for those infants who required abdominal surgery. Nutritional supplements included multivitamins, crude liver extract, and iron. The author noted that transfusions were believed to be unnecessary, because the infants were “thriving and comfortable” in spite of anemia. The birth weight of the majority of infants (199/311) reported in this case series was between 2001 and 2500 g. Overall mortality was 17%; for infants weighing <1000 g, mortality was 100%. On average, infants regained birth weight at 2 weeks; thereafter, infants weighing 1001 to 1500 g gained 18.7 gm/kg/d and those weighing 1501 to 2000 g gained 12.7 gm/kg/d. Acidosis responsive to treatment with sodium bicarbonate was reported in 8 infants. None of the infants in this series developed retrolental fibroplasia, prompting the author to speculate that the high fat content of the formula might have prevented this disease. Clearly, the most striking change in the past 50 years has been in survival of the premature infant. Mortality in infants weighing <1500 g at birth is now <17% (~86% survival in infants weighing 750-1000 g, 94% in those weighing 1001-1250 g, and 97% in those weighing 1251-1500 g). The importance of early nutrition (including water) has been increasingly recognized, and the means by which we can provide both enteral and parenteral nutrition have improved. Although the quality and quantity of protein and other macronutrients and micronutrients supplied by premature infant formulas and human milk fortifiers have been significantly modified and improved, the current approach to the advancement of enteral feeds is remarkably similar despite a paucity of supportive data. Unfortunately, few trials have adequately addressed the critical question of how alterations in nutrient provision affect long-term growth, neurodevelopment, and morbidity in premature infants. Brenda B. Poindexter, MD Section of Neonatal-Perinatal Medicine Riley Hospital for Children Indianapolis, IN 46202
722
23. Steindl P, Ferenci P, Dienes HP, Grimm G, Pabinger I, Madl C, et al. Wilson’s disease in patients presenting with liver disease: a diagnostic challenge. Gastroenterology 1997;113: 212-8. 24. Martins da Costa C, Baldwin D, Portmann B, Lolin Y, Mowat AP,
THE JOURNAL OF PEDIATRICS NOVEMBER 2000 Mieli-Vergani G. Value of urinary copper excretion after penicillamine challenge in the diagnosis of Wilson’s disease. Hepatology 1992;15: 609-15. 25. Tanner MS, Portmann B. Indian childhood cirrhosis. Arch Dis Child 1981;56:4-6.
26. Sternlieb I. Mitochondrial and fatty changes in hepatocytes of patients with Wilson’s disease. Gastroenterology 1968;55:354-67. 27. Sternlieb I. Fraternal concordance of types of abnormal hepatocellular mitochondria in Wilson’s disease. Hepatology 1992;16:728-32.
50 Years Ago in The Journal of Pediatrics FEEDING OF PREMATURE INFANTS—USE OF A SIMPLE FORMULA Abelson S. J Pediatr 1950;37:711-7.
Fifty years ago, the 2-year experience of a US Naval Hospital in feeding 311 premature infants a “simplified formula,” which consisted of half evaporated milk and half water, was reported in The Journal of Pediatrics. This mixture supplied 52% of calories from fat, 28% from carbohydrate, and 20% from protein. The feeding protocol included 36 to 72 hours of “drying out” (water and formula were withheld to relieve edema), after which gavage feedings were initiated at a volume of ~40 cc/kg/d. Glucose water and half-strength formula were used to transition to full-strength formula. By the second week of life, feeds were gradually advanced to provide 150 to 200 cc/kg/d (110-140 kcal/kg/d). Subcutaneous clyses of 5% dextrose were occasionally given for “apathy and signs of dehydration.” Intravenous fluids were reserved for those infants who required abdominal surgery. Nutritional supplements included multivitamins, crude liver extract, and iron. The author noted that transfusions were believed to be unnecessary, because the infants were “thriving and comfortable” in spite of anemia. The birth weight of the majority of infants (199/311) reported in this case series was between 2001 and 2500 g. Overall mortality was 17%; for infants weighing <1000 g, mortality was 100%. On average, infants regained birth weight at 2 weeks; thereafter, infants weighing 1001 to 1500 g gained 18.7 gm/kg/d and those weighing 1501 to 2000 g gained 12.7 gm/kg/d. Acidosis responsive to treatment with sodium bicarbonate was reported in 8 infants. None of the infants in this series developed retrolental fibroplasia, prompting the author to speculate that the high fat content of the formula might have prevented this disease. Clearly, the most striking change in the past 50 years has been in survival of the premature infant. Mortality in infants weighing <1500 g at birth is now <17% (~86% survival in infants weighing 750-1000 g, 94% in those weighing 1001-1250 g, and 97% in those weighing 1251-1500 g). The importance of early nutrition (including water) has been increasingly recognized, and the means by which we can provide both enteral and parenteral nutrition have improved. Although the quality and quantity of protein and other macronutrients and micronutrients supplied by premature infant formulas and human milk fortifiers have been significantly modified and improved, the current approach to the advancement of enteral feeds is remarkably similar despite a paucity of supportive data. Unfortunately, few trials have adequately addressed the critical question of how alterations in nutrient provision affect long-term growth, neurodevelopment, and morbidity in premature infants. Brenda B. Poindexter, MD Section of Neonatal-Perinatal Medicine Riley Hospital for Children Indianapolis, IN 46202
722