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Washington University Experience | VASCULAR | Hypoxia-Ischemia, fetal-neonatal | White Matter | 9A0 Case 9 History
Case 9 History
The patient was a 39 week EGA 3260 gram infant with history of diaphragmatic hernia diagnosed in-utero, admitted to the NICU on 8/23. At birth, the infant cried spontaneously, but had very little respiratory effort and, therefore, required intubation. Apgars were 3, 4, and 7. He had no obvious dysmorphic features. On initial neurological exam, he was described as having symmetric strength and hypotonia. He was treated with ventilatory and cardiovascular support, requiring inhaled nitric oxide, multiple fluid boluses, and blood transfusions. The patient was started on ECMO on 8/27. Multiple head ultrasounds were performed without evidence of intracranial hemorrhage. On 8/29 the patient was described as responsive to stimulation, with spontaneous eye opening, reactive pupils and bilateral cortical fisting. ECMO was continued for 19 days. On the morning of the 9/13 a head ultrasound demonstrated a 1.4 cm left parietal intraparenchymal hemorrhage. Because of the need for anticoagulation while on ECMO, the presence of intraparenchymal CNS hemorrhage was felt to be an indication for urgent discontinuation of ECMO. The medical care team and parents agreed that after discontinuation of ECMO, his care should be redirected at comfort measures. The patient was taken off ECMO support at 2250, and was then extubated without spontaneous respirations, heart rate, or spontaneous movement. At autopsy there was hemorrhage involving left parietal lobe and subarachnoid space, diffuse hypoxic/ischemic damage involving cortex, basal ganglia and thalamus and subcortical white matter. There is global subacute hypoxic/ischemic damage, ranging from pallor of the white matter, pyknotic nuclei, marked astrocytosis, activated microglia, and perivascular calcifications to frank infarction with neuronal nuclear pyknosis, macrophages, neuropil vacuolation, astrocytosis, axonal spheroids, calcifications, and vascular prominence. Immunohistochemical staining for glial fibrillary acidic protein (GFAP) was performed and highlights reactive astrocytes.
