Neonatology, Pediatric Hematology/Oncology
Ref. # 842201
A large gestational age baby suffered a traumatic forceps delivery that was followed by an initial period of apnea requiring intubation and assisted respiration. The baby appeared mottled and cyanotic. Apgars were 4, 6 and 7-8 at 1, 5 and 10 minutes, respectively. A blood sample from the umbilical cord after birth had a pH of 7.21. Bruising was noted and a clavicular fracture was confirmed on X-ray. The next day the baby was lethargic. Electrolytes and blood glucose levels were normal. WBC was 25,000. A pH was not repeated. The next day the baby was jaundiced with a bilirubin level of 12.1 in the morning and 17.3 in the evening. Hemoglobin/hematocrit were 16.7/51%. Phototherapy was begun but by the next afternoon the bilirubin was 22.9. The baby was transferred to another hospital, where he underwent a double volume exchange transfusion. Diagnosis was renal vein thrombosis and a CT scan showed a subarachnoid hemorrhage. The baby's liver enzymes were elevated and platelets decreased, necessitating a second exchange transfusion. Three days later, during which cardiac problems had developed, the baby was transfused with platelets and fresh frozen plasma secondary to thrombocytopenia. Three more days later his total bilirubin was 34.5 total, 25.1 direct. Blood cultures were obtained and the baby was transferred to a major medical center. The blood culture was positive for E. coli. During the next 17 days treatment included a third exchange transfusion, antibiotics for sepsis, and Phenobarbital for seizures. Further evaluation indicated the presence of Hepatitis B antigen and mild bilateral hydrocephalus, possibly related to a Grade II intraventricular hemorrhage. The baby was subsequently diagnosed with cerebral palsy. A medQuest neonatologist opined the child's abnormal findings were the result of hypoxia and fetal distress. A traumatic delivery was further evidenced by numerous findings including: obvious bruising and fractured clavicle; hyperbilirubinemia related to the bruising; intraventricular bleeding (unusual in a full-term infant without asphyxia); early development of seizures; and microcephaly, a common sequela of birth asphyxia. There was a negligent failure to perform appropriate acid-base monitoring in the immediate postnatal period. This failure, combined with the injuries suffered during labor and delivery, caused the child's neurological and intellectual deficits. A medQuest pediatric hematologist/oncologist reported the child's hyperbilirubinemia was not treated in a timely fashion. The standard for exchange transfusion in a term baby is a bilirubin value of 20; for a high-risk infant such as the one concerned, the value is 18. The combination of thrombocytopenia and direct hyperbilirubinemia in a stressed newborn should have prompted a suspicion of sepsis, necessitating the drawing of blood cultures and the initiation of antibiotics. The baby was probably not born with neonatal hepatitis since there was no sufficient evidence within the first few weeks of life. The normal lag time in the hepatitis surface antigen becoming positive is 2-4 weeks, indicating it was transmitted during any one of the three exchange transfusions. The failure to follow standard pediatric care led to the child's debilitating central nervous system damage.