Ref. # 414301
A 29-year-old G2P1 mother gave birth via C-section because of severe fetal bradycardia that did not respond to position changes. Previous fetal heart tracings had been reactive. The male infant's Apgar scores were 1, 2, 6 and 7 at 1, 5, 10 and 15 minutes, respectively. In the delivery room he was intubated, ventilated, treated with epinephrine, and placed with an umbilical venous catheter. He was hypotonic and unresponsive to pain stimuli, with fixed pupils and some gag activity. Later his pupils were reactive and he was grimacing on suctioning. By Day 3 he was weaned from the respirator. A CT scan showed a saggital sinus thrombosis. At Day 18, on discharge, the infant was alert and active and had good tone. Pathological study of the placenta showed an infarction involving 25% of the placental surface. Over the next three years it became evident the boy suffered from Choreoathetotic, a form of cerebral palsy. Symptoms include low muscle tone, weakness, wild and unrestrained movements, and the inability to stand unsupported. Mobility depends on the use of a walking frame or wheelchair. The motor disabilities extend to the speech apparatus: the boy cannot produce spoken language. He has good receptive language ability--showing relatively intact cognitive functioning--which has been harnessed for computer-assisted communication. He cannot control the passage of fluids and solids through the mouth and throat and has frequent vomiting. He is prone to respiratory tract infections and was recommended for the placement of a gastric tube and gastric fundoplication. A medQuest pediatric neurologist reported the pattern of impairment is characteristic of damage to deep structures in the forebrain, including the basal ganglia and thalamus. Such damage is most often seen after a severe but relatively brief asphyxic insult, usually in a term baby. In a study of 11 infants with similar damage to the basal ganglia, the children were subjected to asphyxia which began with an irreversible bradycardia, and who were delivered by emergency C-section. Given the evidence of infarction in the placenta and a saggital sinus in the infant, it would appear that a hyper-coagulable state in the maternal-fetal circulation produced an acute infarction of the placenta, resulting in an asphyxial insult to the fetus. In the future the child will require aids for mobility, including equipment that interfaces with his communicative devices. His health can be expected to be precarious. He will require skilled nursing care as well as medical interventions. Although at risk for an early death due to respiratory complications, he can be reasonably expected to live into his thirties or beyond.