Obstetrics, Neonatology, Pediatric Neuroradiology
Ref. # 934101
A 34 year-old woman, gravida-8 para-3, had uneventful prenatal care. She presented to the ER six days overdue because her OB was unsure of the presentation of the fetus. An ultrasound showed the baby was in a vertex position. A non-stress test was reactive. Two days later she presented again complaining of contractions and leaking fluid. Upon exam there was no vaginal discharge and a non-stress test was reactive, so the patient was sent home. Six days later she presented for induction. At 0809 she was 2 cm dilated, 50% effaced and at minus two station. Fetal heart rate monitor tracings were reactive and she was in early labor. At 1640 a cytotec was inserted; a second insertion was placed at 0305 the next morning. At 0750 she was 3 cm dilated, 70% effaced and the baby was still at high station. Pitocin was started. At 0930 the OB left the hospital for personal reasons. A resident attended. Notes at 0955 reported positive long-term variability with occasional mild variables. Contractions were every one or two minutes. Her membranes were artifically ruptured. At 1206 there was a spontaneous deceleration of fetal heartbeats per minute after a contraction. The baseline dropped from the 140's to the 70's for one minute. At 1211 there was another deceleration to the 60's for 90 seconds. The woman was 6 cm dilated. Pitocin was turned off. Another three-minute deceleration began at 1213. The woman was 8 cm dilated. There were four more decelerations of 60-90 seconds until 1225, when the replacement OB assigned in the morning arrived and examined the woman for the first time. The woman was fully dilated. She was instructed to push. For the next 15 minutes the fetal heartbeat remained around 60 beats per minute. Pitocin was started again. At 1240 the resident unsuccessfully applied a vacuum to the baby's head while it was at plus two station. The OB attempted four more vacuum attempts and the baby was delivered at 1259. Apgars were 1 at one minute, 4 at five minutes, and 4 at ten minutes. The arterial cord pH was 6.61. According to the attending pediatrician the baby was placed under a warmer bed with no spontaneous movements, apneic, heart rate less than 40 beats per minute. The baby was intubated and transferred to the neonatal intensive care unit. The admission note mentioned a shoulder dystocia unrecorded in the OB notes. The baby developed seizure activity and was started on phenobarbitol. Dilatin was administered later. A CAT scan was consistent with global ischemia. A head ultrasound showed "small lateral ventricles likely secondary to edema." Cerebral spinal fluid tests showed 280 white blood cells and 0 red blood cells. The diagnosis was suspected meningitis. Six days later the non-responsive baby was transferred to a major medical center. An MRI was positive for severe hypoxic ischemia. The baby remained brain-damaged for six months until her death six months later. Two medQuest obstetricians independently opined the care rendered was negligent. The tracing was reassuring throughout until 1206. At 1211 the resident should have measured the scalp pH to assess the baby's well being. Delivery via C-section should have taken place by 1215. Upon arrival the second OB should have immediately performed the C-section at 1225 but instead negligently instructed the woman to push. The five attempts at vacuum extraction constituted negligence. A medQuest neonatologist reported that the diagnosis of "presumptive meningitis" was in error. No cultures were ever positive for either bacterial or viral pathogens. The infant's leukocytosis was not secondary to an infection as was thought, but to her severe seizure disorder. By the time of delivery the infant had suffered irreversible neurologic injury secondary to enduring 52 minutes with a profound bradycardia. The entirety of the infant's medical care was necessary to treat her resultant hypoxic-ischemic encephalopathy and its sequelae. A medQuest pediatric neuroradiologist reported the head ultrasound images two days post-delivery demonstrated hyperechogenicity of the white matter and effacement of the ventricles consistent with the appearance of diffuse brain swelling. The sequelae of the profound asphyxia were demonstrated on the CT brain scan four days later and a brain MRI at the major medical center. The brain swelling on the ultrasound was a result of the same profound asphyxia insult that resulted in the changes on the subsequent MRI.