The diagnosis of IVH is confirmed and the severity gradedby ultrasound through the anterior fontanelle or computedtomography examination. Grade 1 IVH is confined to thegerminal matrix; grade 2 is an extension of grade 1, withblood noted in the ventricle without ventricular enlargement; grade 3 is an extension of grade 2 with ventricular dilation; and grade 4 has blood in dilated ventricles and in thecerebral cortex, either contiguous with or distant from theventricle. Grade 4 hemorrhage has a poor prognosis, as doesthe development of periventricular, small, echolucent cysticlesions, with or without porencephalic cysts and posthemorrhagic hydrocephalus. Periventricular cysts often are notedafter the resolution of echodense areas in the periventricularwhite matter. The cysts may correspond to the developmentof periventricular leukomalacia, which may be a precursorto cerebral palsy. Extensive intraparenchymal echodensitiesrepresent hemorrhagic necrosis. They are associated witha high mortality rate and have a poor neurodevelopmentalprognosis for survivors.
Treatment of an acute hemorrhage involves standard supportive care, including ventilation for apnea and blood transfusion for hemorrhagic shock. Posthemorrhagic hydrocephalus may be managed with serial daily lumbar punctures, an external ventriculostomy tube, or a permanent ventricular-peritoneal shunt. Implementation of the shunt often is delayed because of the high protein content of the hemorrhagic ventricular fluid.
Conditions known to reduce uteroplacental blood flow or to interfere with spontaneous respiration lead to perinatal hypoxia, lactic acidosis, and, if severe enough to reduce cardiac output or cause cardiac arrest, ischemia. The combination of the reduced availability of oxygen for the brain resulting from hypoxia and the diminished or absent blood flow to the brain resulting from ischemia leads to reduced glucose for metabolism and to an accumulation of lactate that produces local tissue acidosis. After reperfusion, hypoxic-ischemic injury also may be complicated by cell necrosis and vascular endothelial edema, reducing blood flow distal to the
Pupils Mydriasis Miosis Unequal, poor light reflex
Electroencephalography Normal Low voltage changing to seizure Burst suppression to isoelectric activity
Duration >24 h if progresses, otherwise may 24 h to 14 days Days to weeks remain normal
Modified from Sarnat HB, Sarnat MS: Neonatal encephalopathy following fetal distress, Arch Neurol 33:696, 1976.
involved vessel. Typically, hypoxic-ischemic encephalopathy in the term infant is characterized by cerebral edema, cortical necrosis, and involvement of the basal ganglia, whereas in the preterm infant it is characterized by periventricular leukomalacia. Both lesions may result in cortical atrophy, mental retardation, and spastic quadriplegia or diplegia.
The clinical manifestations and characteristic course of hypoxic-ischemic encephalopathy vary according to the severity of the injury (Table 64-2). Infants with severe stage 3 hypoxic-ischemic encephalopathy are usually hypotonic, although occasionally they initially appear hypertonic and hyperalert at birth. As cerebral edema develops, brain functions are affected in a descending order; cortical depression produces coma, and brainstem depression results in apnea. As cerebral edema progresses, refractory seizures begin 12 to 24 hours after birth. Concurrently the infant has no signs of spontaneous respirations, is hypotonic, and has diminished or absent deep tendon reflexes.