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Washington University Experience | VASCULAR | Hypoxia-Ischemia, fetal-neonatal | Pontosubicular necrosis | 1A0 Case 1 History
Case 1 History --- The patient was a 34-week EGA age infant male born 4/5 via C-section to 28 year-old G4, P3 mother. Pregnancy was complicated by antenatal diagnosis of congenital heart disease and maternal urine drug screen positive for opiates and marijuana. The patient’s mother presented to OSH with vaginal bleeding, and, due to concern over placental abruption, C-section was performed. APGARs were 5 at 1 minute, 8 at 5 minutes. The infant was intubated after delivery and transferred to SLCH NICU where he remained for the duration of his life. He was placed on a continuous prostaglandin infusion secondary to his apparent cyanotic congenital heart disease (poor oxygen saturations). Echocardiogram on day of life (DOL)#1 revealed double outlet right ventricle with transposed great vessels, pulmonary atresia, a large patent ductus arteriosus, a large subaortic ventricular septal defect, and a small patent foramen ovale (left to right flow). Head sonogram on DOL#1 was normal; however, on DOL2, he also was noted to have minimal spontaneous movement. On DOL#3, the infant had episodes of increased pulmonary resistance and hypotension. Neurologically, he had minimal spontaneous movement and did not respond to stimulation. In the morning seizure activity was noted on the amplitude-integrated EEG for which he was given phenobarbital. Standard EEG was severely abnormal due to severe voltage suppression as well as burst suppression. The lack of state change and no response to stimulation were consistent with severe cerebral dysfunction. Head sonogram revealed a grade I subependymal hemorrhage on right side without intraventricular or intraparenchymal hemorrhage. The family decided to withdraw care and the patient expired on 4/9. Gross autopsy on 4/10 confirmed transposition of great vessels, patent ductus arteriosus, ventricular septal defect, and patent foramen ovale. ---- Neuroautopsy showed an immature brain (230 grams) with global ischemic injury consisting of bilateral neocortical ACA/MCA watershed infarcts (an unusual pattern in premature brains), pontosubicular necrosis, white matter necrosis in a periventricular distribution and focal germinal matrix hemorrhage.
