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Washington University Experience | VASCULAR | Hypoxia-Ischemia, fetal-neonatal | White Matter | 5A0 Case 5 History
Case 5 History ---- The patient was a former 26 week EGA infant male (twin B) born on 04/14 via Cesarean-section to a 31-year-old G1, now P1 mother. The pregnancy was complicated by in utero death of twin A, delivered at 19 weeks gestation in a setting of preterm labor with premature rupture of membranes (PROM), treated with metronidazole, ampicillin, and azithromycin. Cervical cerclage was placed at 19 weeks to facilitate the viability of this patient (twin B). At 24 weeks, the mother experienced preterm labor and was treated with nifedipine, terbutaline, and steroids. The pregnancy was further complicated by maternal asthma, hypertension, possible chorioamnionitis, intra-uterine growth retardation, and breech presentation. This patient was delivered by a C-section secondary to fetal tachycardia and footling breech presentation. APGAR scores were 2 at 1 minute, 2 at 5 minutes, and 6 at 10 minutes; the infant failed to spontaneously cry, and demonstrated bradycardia. He required suctioning and bag mask ventilation for 3 minutes, chest compressions for 1 minute, and intubation, with subsequent recovery of heart rate. His birth weight was noted to be 790 grams (25% percentile). He was stabilized and transferred to the NICU for the duration of his life. He had a very complicated hospital course, most of which was attributable to prematurity. His main issues were severe cystic bronchopulmonary dysplasia, pulmonary hypertension, and pulmonary interstitial emphysema, which were treated with surfactant, caffeine, nitric oxide, several courses of dexamethasone, aminophylline, and sildenafil. He required prolonged ventilatory support and had a tracheostomy placed on 09/13. Sedation and paralytics were required to minimize agitation. He was given continuous tPA infusion to disrupt possible thromboemboli in his vasculature, but this intervention did not provide significant improvement in his pulmonary hypertension. Neurologically, the patient had a few minor issues noted soon after birth. A patent ductus arteriosus was noted on initial echocardiogram; therefore Indocin was administered on day of life 2. The infant's platelets remained stable, creatinine increased, therefore, Indocin was discontinued. Given the increased risk of IVH in the setting of Indocin, a head ultrasound was obtained on day of life 3 which revealed tiny bilateral subependymal hemorrhages, and no intraventricular hemorrhage. An ultrasound on day of life 10 showed resolution of the previously noted hemorrhages. However, a calcification lateral to the right frontal horn was concerning for possible TORCH infection. His urine CMV was negative. Neurology was consulted to evaluate his ventriculomegaly and abnormal development. MRI performed on 10/03 revealed a tiny focus of susceptibility adjacent to the frontal horn of the right lateral ventricle, consistent with blood product versus focal calcification. The ventricular system was reported to be of normal size and configuration. There was also diffuse white matter injury with a small brain. An additional ultrasound study of the head was performed on 10/21 in the setting of tPA administration for microemboli in the vasculature; this study revealed lateral and third ventricular size at the upper limit of normal, without intracranial hemorrhage. On 12/17, the patient had worsening respiratory and metabolic acidosis, likely secondary to sepsis/multiorgan failure and the family decided to withdraw support. ---- Autopsy revealed an immature brain with hypoxic/ischemic damage characterized by diffuse white matter loss, gliosis and focal cavitation, focal ulegyria and hydrocephalus ex vacuo.
