Therapeutic hypothermia: treatment for hypoxic-ischemic encephalopathy in the NICU

Baby M was born limp, blue, and without respiratory effort at 38 weeks gestation to a 38-year-old, gravida 5, para 1, woman. Delivery was vaginal after a rapid progression of labor leaving no opportunity for a cesarean section. No other complications were noted during labor but a large surge at delivery, later diagnosed as uterine rupture, initially raised concerns about placental abruption. Apgar scores were 1, 2, and 4 at one, five, and ten minutes, respectively. She was resuscitated in the delivery room, intubated, and transferred in critical condition to the neonatal intensive care unit (NICU) at the birth hospital. Her initial cord pH was 6.7 and was slightly improved at 7.17 on arterial blood gas after resuscitation. Our NICU team was consulted because of her severe neurologic depression. The birth hospital was within walking distance of our tertiary care center and our neurologists went to evaluate her for the hypothermia protocol. Her neurologic exam was notable for dilated and unresponsive pupils, no spontaneous movements, and diminished reflexes and tone, consistent with moderate-to-severe encephalopathy. Seizure activity began at one hour of age and consisted of lip smacking, which was later confirmed by electroencephalogram (EEG). Enrollment criteria were met based on respiratory depression at birth requiring intubation and continued need for ventilation, concern for placental abruption, cord pH less than 7, and encephalopathy on exam and EEG. After stabilizing her airway and achieving central access to treat acidosis and seizures, the team prepared her for transfer to our NICU. At this point, the primary concern became her neurologic status.