The plaintiff mother received prenatal care at defendant ob/gyn practice, predominately from Dr. A, between August 29, 2013 and April 15, 2014. There was no issue with that care.
At 4:16 am on April 14, 2014, the plaintiff was admitted to defendant hospital at 36 weeks, 6 days because of increasing contractions. An epidural was started at 8:06 am. Labor was managed by Dr. B from 8:00 am up to and including delivery of the infant at 5:06 pm. Dr. B was the daytime on-call attending for defendant ob/gyn practice and Dr. A (who was on vacation, but in the office) came to deliver the infant when Dr. B called to inform her that the patient was fully dilated. Dr. A arrived at about 4:50 pm or 16 minutes before delivery.
Labor was reported to be routine until 2:30 pm. At that time, the fetal heart rate monitor (FHR) showed fetal tachycardia to 165 bpm. The patient was 7 cm dilated, 90% effaced, and the infant was at +1 station. Oxytocin was started at 4 MUmin. At 3:25 pm, the patient was fully dilated and the oxytocin was stopped because of long variable decelerations, which had started at 3:10 pm, some of which had a late component. At that time, there was still good beat-to-beat variability. Tachysystole had begun at 3:15 pm.
The infant was at +4 station as of 4:20 pm, and the FHR continued to deteriorate from “bad” Category II strips to Category III strips, with decreasing beat-to-beat variability over that time until 4:36 pm, when variability was absent. At that time, maternal fever also was noted, from 99.7°F to 102.3°F. When Dr. A arrived at about 4:50 pm, she reviewed the FHR monitor and instructed the mother that her infant had to be delivered now. Because the head was so far down (at +5 station), Dr. A believed the infant could be delivered faster vaginally than with a cesarean section. At vaginal delivery at 5:06 pm, meconium and a tight nuchal cord x 1 were present. The mother’s temperature at delivery was 100.6°F.
The infant’s Apgars were 1, 3, and 4. Pediatrics was in the room at the time of delivery and suctioned the meconium but the infant’s heart rate was less than 60 beats per minute (bpm). Tactile stimulation and positive pressure ventilation (PPV) did not improve the heart rate. At 52 seconds, a neonatal airway specialist was called. At 2:27 minutes, the anesthesiologist arrived to assist. At 3:59 minutes, the pediatric resident made an unsuccessful attempt to intubate the infant. Another unsuccessful attempt at intubation was made at 4:17 minutes, by the pediatric attending. At 5 minutes, the neonatal airway specialist arrived and at 5:21 minutes, another unsuccessful attempt at intubation was made. Finally, at 6:10 minutes, Pediatrics successfully intubated the infant.
A cord venous blood gas indicated a pH of 6.905, CO2 of 94.9, PAO2 of 28.1, bicarbonate of 17.3, and a base excess of 16.7.
The infant’s initial neurological examination showed pupils pinpoint and equal bilaterally, no reaction to light, no tone, no spontaneous movement or eye opening, and no reflexes. He was diagnosed with “severe encephalopathy secondary to perinatal hypoxic – ischemia and DIC.” Although there were no detectable subclinical seizures on electroencephalogram, the physicians suspected seizure activity on physical examination and, as a result, the infant was treated with phenobarbital. He was placed on hypothermia protocol from birth until April 19, 2014. On April 21, 2014, magnetic resonance imaging was performed and the infant was noted to have an “acute” right thalamic infarct, measuring 1.1 x 1.3 cm. In addition, there was a finding of a posterior fossa subdural hematoma, as well as some arachnoid hemorrhage. Almost every note refers to the fact that the infant was suffering from “severe hypoxic ischemic encephalopathy (HIE).”