- Email: [email protected]
Hypertriglyceridemia in infants with bronchopulmonary dysplasia
506
The Journal of Pediatrics September 1989
Editorial correspondence
the ECMO-treated infants. The majority of lesions consisted of bilateral, multifocal neuronal necrosis and vascular thromboses. No left-sided predominance was observed. Drs. Schumacher and Donn state that the literature suggests a left-sided predominance of intracranial injury. We believe that it is not appropriate to compare the distribution of hemorrhage and stroke in a premature, very low birth weight population with that in term or near term infants with pulmonary hypertension treated with ECMO. A recent study by Klesh et al. 1 of infants with persistent pulmonary hypertension showed that cerebral infarction was present in eight infants. In these infants, only one right-sided lesion was found. The remainder of the lesions were diffuse or bilateral in distribution. Certainly, ECMO is not a risk-free therapy, but the survival rates and neurodevelopmental outcome of infants treated with ECMO at our institution are encouraging. We share the concern that Drs. Schumacher and Donn express about the acute and long-term effects of ligation of the vessels in the right side of the neck. However, we are also concerned that other variables, such as perinatal asphyxia, pre-ECMO ventilatory therapy, and changes in global cerebral hemodynamics during ECMO, may be ignored or overlooked as important factors in the pathogenesis of neurologic injury.
George A. Taylor, MD Associate Professor of Radiology and Pediatrics The Johns" Hopkins Medical Institutions Baltimore, MD 21205 Bitlie L. Short, MD Associate Professor of Pediatrics Children's National Medical Center Washington, D.C. 20010 REFERENCE
1. Klesh KW~ Murphy TF, Scher MS, Buchanan DE, Maxwell EP, Guthrie RD. Cerebral infarction in persistent pulmonary hypertension of the newborn. Am J Dis Child 1987;141:852-7.
Hypertriglyceridemia in infants with
bronchopulmonary dysplasia To the Editor: Wareham et at. (J PED~ATR1989;114:458-60) presented two patients with BPD and associated hypertriglyceridemia while they were receiving enteral feedings. The cause of the hypertrigtyceridemia was not determined, but besides some BPD-related factors, the authors stated that long-term treatment with theophylline, sympathomimetics, and thiazide diuretics may have altered lipid metabolism. Another drug that was given to both patients may be responsible
for the abnormal lipid metabolism; chloral hydrate is known to alter hepatic function, 1 and the human newborn infant appears to be more sensitive to chloral hydrate--induced hepatic dysfunction than the adult, z In addition, the use of chloral hydrate to sedate newborn infants has never been carefully studied. Because of the significant chloral hydrate-induced toxic effects,1,3 we suggest that chloral hydrate should not be used for long-term sedation until the risks and benefits of its use in the infant and neonate can be determined.
Jose L. Gonzalez, MD George H. Lambert, MD Jonathan Muraskas, MD Craig L. Anderson, MD Division of Neonatology Department of Pediatrics Stritch School of Medicine Loyola University Medical Center Maywood, IL 60513 REFERENCES
1. Harvey SC. Hypnotics and sedatives. In: Gilman AG, Goodman LS, Rail TW, Nurod F, eds. Goodman and Gilman's the pharmacologic basis of therapeutics. 7th ed. New York: Macmillan, 1985:339-71. 2. Lambert GH, et al. An association between chloral hydrate and direct hyperbilirubinemia in the newborn. Pediatrics (in press). 3. Laptook AR, Rosenfield CR. Chloral hydrate toxicity in a preterm infant. Pediatr Pharmacol 1984;4:161-5.
Reply To the Editor." The point by Dr. Gonzalez et at. is well taken. Neonatologists frequently use medications for which there is little or no information specific to newborn infants. Chloral hydrate is widely used for sedation of premature infants and certainly may have unexpected side effects. Concerning our two patients, it is difficult to sort out the potential effect of chloral hydrate on the hypertriglyceridemia because so many other factors changed during these patients' treatment period. More information on the effects of chloral hydrate in premature infants would be welcome, but discontinuing its use while the data are forthcoming may not be reasonable. Some form of sedation is frequently necessary, and chloral hydrate seems to be the safest choice in many cases. Substitution of a less well known and therefore potentially riskier medication may not be wise. We need more pharmacologic information on the medications that are commonly used in the treatment of preterm infants.
John A. Wareham, MD Department of Neonatology Children's Hospital Greenville, SC 29605
The Journal of Pediatrics September 1989
Editorial correspondence
the ECMO-treated infants. The majority of lesions consisted of bilateral, multifocal neuronal necrosis and vascular thromboses. No left-sided predominance was observed. Drs. Schumacher and Donn state that the literature suggests a left-sided predominance of intracranial injury. We believe that it is not appropriate to compare the distribution of hemorrhage and stroke in a premature, very low birth weight population with that in term or near term infants with pulmonary hypertension treated with ECMO. A recent study by Klesh et al. 1 of infants with persistent pulmonary hypertension showed that cerebral infarction was present in eight infants. In these infants, only one right-sided lesion was found. The remainder of the lesions were diffuse or bilateral in distribution. Certainly, ECMO is not a risk-free therapy, but the survival rates and neurodevelopmental outcome of infants treated with ECMO at our institution are encouraging. We share the concern that Drs. Schumacher and Donn express about the acute and long-term effects of ligation of the vessels in the right side of the neck. However, we are also concerned that other variables, such as perinatal asphyxia, pre-ECMO ventilatory therapy, and changes in global cerebral hemodynamics during ECMO, may be ignored or overlooked as important factors in the pathogenesis of neurologic injury.
George A. Taylor, MD Associate Professor of Radiology and Pediatrics The Johns" Hopkins Medical Institutions Baltimore, MD 21205 Bitlie L. Short, MD Associate Professor of Pediatrics Children's National Medical Center Washington, D.C. 20010 REFERENCE
1. Klesh KW~ Murphy TF, Scher MS, Buchanan DE, Maxwell EP, Guthrie RD. Cerebral infarction in persistent pulmonary hypertension of the newborn. Am J Dis Child 1987;141:852-7.
Hypertriglyceridemia in infants with
bronchopulmonary dysplasia To the Editor: Wareham et at. (J PED~ATR1989;114:458-60) presented two patients with BPD and associated hypertriglyceridemia while they were receiving enteral feedings. The cause of the hypertrigtyceridemia was not determined, but besides some BPD-related factors, the authors stated that long-term treatment with theophylline, sympathomimetics, and thiazide diuretics may have altered lipid metabolism. Another drug that was given to both patients may be responsible
for the abnormal lipid metabolism; chloral hydrate is known to alter hepatic function, 1 and the human newborn infant appears to be more sensitive to chloral hydrate--induced hepatic dysfunction than the adult, z In addition, the use of chloral hydrate to sedate newborn infants has never been carefully studied. Because of the significant chloral hydrate-induced toxic effects,1,3 we suggest that chloral hydrate should not be used for long-term sedation until the risks and benefits of its use in the infant and neonate can be determined.
Jose L. Gonzalez, MD George H. Lambert, MD Jonathan Muraskas, MD Craig L. Anderson, MD Division of Neonatology Department of Pediatrics Stritch School of Medicine Loyola University Medical Center Maywood, IL 60513 REFERENCES
1. Harvey SC. Hypnotics and sedatives. In: Gilman AG, Goodman LS, Rail TW, Nurod F, eds. Goodman and Gilman's the pharmacologic basis of therapeutics. 7th ed. New York: Macmillan, 1985:339-71. 2. Lambert GH, et al. An association between chloral hydrate and direct hyperbilirubinemia in the newborn. Pediatrics (in press). 3. Laptook AR, Rosenfield CR. Chloral hydrate toxicity in a preterm infant. Pediatr Pharmacol 1984;4:161-5.
Reply To the Editor." The point by Dr. Gonzalez et at. is well taken. Neonatologists frequently use medications for which there is little or no information specific to newborn infants. Chloral hydrate is widely used for sedation of premature infants and certainly may have unexpected side effects. Concerning our two patients, it is difficult to sort out the potential effect of chloral hydrate on the hypertriglyceridemia because so many other factors changed during these patients' treatment period. More information on the effects of chloral hydrate in premature infants would be welcome, but discontinuing its use while the data are forthcoming may not be reasonable. Some form of sedation is frequently necessary, and chloral hydrate seems to be the safest choice in many cases. Substitution of a less well known and therefore potentially riskier medication may not be wise. We need more pharmacologic information on the medications that are commonly used in the treatment of preterm infants.
John A. Wareham, MD Department of Neonatology Children's Hospital Greenville, SC 29605