A 21-year-old female, G1 P0, had been being followed at a community hospital for an unremarkable prenatal course. At 39 weeks gestation, she spontaneously ruptured membranes at 7:45 a.m. and presented to the emergency department about an hour later. She was transferred to Labor and Delivery for evaluation and was seen by the nurse midwife on-call. The patient was deemed to not be in labor, and fetal well-being was thought to be assured. She was sent home at 9:45 a.m., having been advised to return when her contractions were closer together.
At about 11:30 a.m., the patient returned to Labor and Delivery with her husband, where she was re-evaluated by the same obstetrical provider. The patient’s cervix was 1 cm dilated, 90% effaced, and the fetal head at -1 station. The fetal heart was monitored via electronic fetal heart monitor (EFM) for 13 minutes; the nurse midwife deemed the fetal heart rate pattern as unremarkable, gave the patient Benadryl, and sent her home, instructing her to return if her contractions did not increase by 7:00 p.m.
The patient returned by wheelchair to L&D at 6:45 p.m., grunting and bearing down. Her cervix was 9 cm dilated, 100% effaced and fetal head at +1 station. EFM revealed a fetal heart tracing with marked variability in the baseline heart rate, fluctuating between 120-180, and notable for repeated decelerations to 90 bpm. The patient labored for about two more hours before delivery occurred, during which time there were persistent, recurrent deep variable decelerations to 80-90bpm. The nurse midwife delivered a baby boy at 9:01 p.m. with Apgars of 1 at one minute and 3 at five minutes.
The baby initially appeared floppy and had an umbilical artery cord blood gas pH of 6.74. Resuscitation by the on call pediatrician was successful after 20 minutes and the baby had his first spontaneous movement at 30 minutes of life. The baby was then transferred to a tertiary care facility where he experienced seizure activity. A brain MRI confirmed findings consistent with hypoxic-ischemic encephalopathy., The baby developed additional symptoms of profound, permanent neurological deficits, including blindness and a severe seizure disorder.