Angela D. Ramos

Childhood sequelae of infant lung disease: Exercise and pulmonary function abnormalities after bronchopulmonary dysplasia

To determine the long-term pulmonary sequelae and effect on exercise tolerance of bronchopulmonary dysplasia (BPD), we studied 10 children at a mean age of 10.4 years, who had been born prematurely, survived respiratory distress syndrome, and subsequently developed BPD, and compared them with eight age-matched normal children born at term. Pulmonary function tests and graded exercise stress tests were performed. Residual volume, the ratio between residual volume and total lung capacity, vital capacity, forced expiratory volume in 1 second, forced expiratory flow between 25% and 75% of vital capacity, and maximal expiratory flows at 80%, 70%, and 60% of total lung capacity were all abnormal (P less than 0.02) in the children with BPD, compared with control values. Pre-exercise transcutaneous CO2 tension was higher (P less than 0.05) in the BPD group than in the control group. At maximal workload, tcPCO2 remained high in patients with BPD compared with control values (P less than 0.05). Arterial oxygen saturation at maximal workload fell below pre-exercise levels in the BPD group (P less than 0.05) but not in control children. There were no differences in maximal oxygen consumption between the BPD group and control children. Exercise-induced bronchospasm occurred in 50% of the BPD group, but not in the control group. We conclude that long-term survivors of BPD have evidence of airway obstruction, hyperinflation, and airway hyperreactivity, compared with a control group. Aerobic fitness was not significantly different in the BPD and control groups, but was achieved in the BPD group at the expense of a fall in SaO2 and a rise in tcPCO2.

Phenobarbital Does Not Prevent Total Parenteral Nutrition-Associated Cholestasis in Noninfected Neonates

Cholestasis associated with total parenteral nutrition (TPN) is a serious complication of this therapy for which there is no known treatment other than beginning enteral feeds. Phenobarbital is commonly used in other cholestatic disease states, but its benefit in this syndrome has not been demonstrated. We conducted a retrospective review of phenobarbital use in neonates receiving concurrent TPN. Thirty-one noninfected neonates were studied. They were without evidence of intrinsic liver disease at the institution of exclusive TPN therapy. For the purposes of this study, TPN-associated cholestasis was defined as a serum bilirubin in excess of 3 mg/dl at postnatal age of 3 weeks or more. Fourteen of the study infants received phenobarbital therapy for neurologic indications. Sixty percent of the phenobarbital-treated infants developed TPN-associated cholestasis, as compared to 33% of the untreated patients. Phenobarbital therapy was not effective in preventing TPN-associated cholestasis.

Management of children with hyperbilirubinemia and green teeth

Discoloration of the teeth is a well-known complication of tetracycline administration in the child with developing teethJ ,2 Reports of liquid iron preparations causing incorporation of a black iron stain into dental structures and pigment deposition in the teeth of patients with disorders of porphyrin metabolism have also been described? ,4 However, the presence of green pigmented teeth in a child is a rare finding? -7 Previously, green staining of the teeth occurred in a small minority of newborn infants who survived severe jaundice from erythroblastosis fetalis. Advances in the diagnosis and management of infants with extrahepatic biliary atresia and neonatal hepatitis have allowed a population of children with cholestatic liver disease to survive beyond infancy. These children are often plagued by long-standing cholestasis and lifelong jaundice. We report two cases of children with green pigmented primary teeth. The presumed cause of the tooth staining was deposition of bilirubin and heme breakdown products in the tooth structure. CASE REPORTS

NEURODEVELOPMENTAL OUTCOME AT 3.5 YEARS OF AGE IN ECMO TREATED CHILDREN: RELATIONSHIP TO PRIMARY DIAGNOSIS † 1224

NEURODEVELOPMENTAL OUTCOME AT 3.5 YEARS OF AGE IN ECMO TREATED CHILDREN: RELATIONSHIP TO PRIMARY DIAGNOSIS † 1224

NEURODEVELOPMENTAL OUTCOME AND POTENTIAL FOR ACADEMIC DIFFICULTIES IN ECMO SURVIVORS AT FIVE YEARS OF AGE † 1192

Introduction. Neurodevelopmental outcome studies of school age children who required extracorporeal membrane oxygenation (ECMO) as a newborn due to severe cardiorespiratory failure suggest that these children are at greater risk for learning disabilities and mental retardation than in the general population. In an attempt to further clarify the nature of potential learning disabilities of children who received ECMO, we assessed the neurodevelopmental status of our ECMO survivors at five years of age.

CRANIAL CT AND NEURODEVELOPMENTAL OUTCOME IN ECMO NEONATES EXPERIENCING AN ARREST. 1626

Little is known on the long term neurodevelopmental impact of a cardiopulmonary arrest on neonates with intractable cardiorespiratory failure who are being treated with ECMO. We previously reported on survival and neurodevelopmental outcome in a cohort of ECMO treated neonates matched by diagnosis for arrest (AG) and non-arrest (NAG) status. The current study was undertaken to correlate the cranial CT scans with the neurodevelopmental outcome in the survivors of this cohort. CT scans were performed on the AG at a median of 15 days of age, and on the NAG at a median of 12 days of age. In the AG, CT scans were done at a median of 13 days post arrest. The timing of arrests included 27 prior to ECMO (including 11 at cannulation, and 3 infants with multiple arrests) and 2 post ECMO. At follow up, age 12 to 42 months, the discharge CT scans of 29/30 AG (32±12 months, Mean±SD) and 31/35 NAG (33±11 months) children were reviewed by a neuroradiologist who was blinded to patient arrest and outcome status. Major findings on CT included:*p=0.049 In the AG with CT findings of low perfusion injury (i.e. vascular border zone necrosis), all arrests occurred at cannulation. The one NAG infant with a low perfusion injury had profound intrapartum asphyxia and fetal bradycardia. On neurodevelopmental follow up, 3 infants were abnormal and 1 was suspect. In infants with CT findings of an infarct (i.e. necrosis in a vascular distribution), neurodevelopmental outcome included 1 child whose exam was normal, 2 suspect, and 4 abnormal. In conclusion, neonates meeting the criteria for ECMO, but who have also had an arrest are not at an increased risk for low perfusion injury to the brain over their non-arrest cohorts. The increased incidence of intracranial infarcts in this group deserves continued neurodevelopmental study. All infants with major findings on CT following treatment with ECMO are at very high risk for significant neurodevelopmental problems and require close long term follow up.Table