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Washington University Experience | VASCULAR | Infarct, watershed | 12A0 Case 12 History
Case 12 History ---- This patient was a former 34-week estimated gestational 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 which included transposition of the great vessels, ventricular septal defect, and pulmonary atresia. The infant was delivered via C-section secondary to concern over placental abruption. APGARs were 5 at 1 minute and 8 at 5 minutes. He was placed on a continuous prostaglandin infusion secondary to his apparent cyanotic congenital heart disease (poor oxygen saturations). He remained intubated and was given replacement surfactant. Echocardiogram on day of life 1 revealed double outlet right ventricle with transposed great vessels, pulmonary atresia, and a small patent foramen ovale (left to right flow). A large patent ductus arteriosus and a large subaortic ventricular septal defect both with left to right flow were also noted. Head sonogram on day of life 1 was normal. On day of life 2, he developed respiratory acidosis requiring additional ventilatory support. He also was noted to have minimal spontaneous movement and did not move in response to stimulation. He required phototherapy for hyperbilirubinemia. On day of life 3, infant had episodes of increased pulmonary resistance with desaturations which responded to increased respiratory support. He also had episodes of hypotension which responded to fluid boluses. From a neurologic standpoint, the infant continued to have an abnormal exam with decreased spontaneous activity and lack of response to stimulation. Continuous amplitude integrated EEG revealed decreased baseline activity but no specific seizure activity. On day of life 5, infant became increasingly hypotensive requiring milrinone infusion with decreasing urine output with continued minimal spontaneous movement and hypotonia. Additionally, in the morning seizure activity was noted on the amplitude-integrated EEG for which he was given phenobarbital. 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 the right side without intraventricular or intraparenchymal hemorrhage. Given the infant’s difficult to manage hypotension and extremely poor neurodevelopmental prognosis, his family decided to withdraw care. He expired on 4/9. ---- Gross autopsy was notable for transposition of great vessels, patent ductus arteriosus, ventricular septal defect, and patent foramen ovale. Brain weight was 230 grams. Histological sections of the frontal lobes show evidence of focally severe hypoxic/ischemic injury, manifested by marked neuronal nuclear pyknosis, mild neuronal loss, astrocytic and microglial proliferation, neuropil vacuolation and parenchymal dyscohesion. The most caudal occipital section lesion was apparently older.
