On March 12, 2012, plaintiff – who was approximately 37 weeks pregnant – was traveling through Virginia with her husband on their way back to North Carolina. She reported having back pains and went to the emergency room. Once there, she was transferred to another hospital for OB care and came under the care of the defendant.
Defendant took an initial pelvic exam that showed cervical dilatation of 1-2 cm, 70% effacement and -3 station with membranes intact. Defendant determined there were no signs of labor at that time and confirmed plaintiff had nonobstructing renal stones, which explained her back pain. Plaintiff was then admitted and treated for pain management. An initial evaluation done shortly after admission by defendant of the electronic fetal heart rate using external monitoring was “reactive.”
On March 14, 2012, a decision was made to induce labor as plaintiff had reached 38 weeks gestation. That evening, defendant placed a cervical ripening balloon to begin the inducement process. At approximately 8:14 a.m. on March 15, 2012, defendant assessed plaintiff’s progress to be 4/80/-2 and Pitocin was started at 2 mu/min. Pitocin then was incrementally increased per protocol. At approximately 1:11 p.m., defendant ruptured plaintiff’s membrane, which had clear fluid, and an IUPC was placed.
During the late afternoon and early evening, plaintiff’s contractions increased and had periods of tachysystole. At approximately 5:12 p.m., the nurses caring for plaintiff received orders to increase the Pitocin to 30 mu/min from 24 mu/min. An exam performed 10 minutes later showed plaintiff’s progress at 8/90/-1. Plaintiff continued to receive Pitocin until the end of the night.
On March 16, 2012, at approximately 12:15 a.m., the L&D nurse assessed plaintiff’s progress to be 10 cm dilated and at a 0 station. Plaintiff began pushing even though the head was at 0 station. After about an hour and a half of pushing with no progress, plaintiff requested a c-section, which the defendant refused, saying there was no indication for a c-section. Plaintiff was instructed to stop pushing at that point. She was instructed to start pushing again two hours later, this time from +2 station. Due to maternal exhaustion, a vacuum was applied by defendant for eight minutes and was removed once the baby crowned. Baby was finally delivered at 5:07 a.m. with APGAR scores of three at one minute, three at five minutes, four at 10 minutes and seven at 15 minutes. Diffuse scalp trauma was noted at delivery and positive pressure ventilation with oxygenation was given. On admission to the NICU, the baby was noted to have marked molding, bruising caput (left), cephalohematoma, abrasion to the left side of the head with very dark bruising and redness to forehead and neck. She also exhibited nasal flaring and facial drooping. Imaging, including a CT scan, ultrasound and MRI, showed evidence of trauma and hypoxic ischemic brain injury. The baby continued to be hyperirritable with a problem with oxygenation saturation which required intubation. Blood work showed abnormalities consistent with liver and kidney dysfunction.
At two days old, a neurologist diagnosed the baby with severe hypoxic ischemic encephalopathy. The baby required care from multiple specialties over her short life. She was assessed as having hypotonia, seizures, decreased movement, dysfunctional feeding/swallowing, dysfunctional breathing, difficulty feeding, hypothermia, blindness and acquired microcephaly. A G-tube was placed for feeding, she was globally delayed in all function, had no independent function and was wheelchair dependent. Over the three years of her life, she continued to decline, and at the end required Hospice care. She died on April 2, 2015. The cause of death listed on her death certificate was “anoxic encephalopathy”.
Plaintiff’s experts opined that one of the adverse effects of Pitocin is hyperstimulation of the uterus or tachysystole and its effect on fetal well-being. Among other things, tachysystole from Pitocin can increase the strength and/or duration and/or frequency of contractions. Any one of these can affect the ability of the fetus to tolerate the decreased delivery of blood flow via the umbilical cord or placenta.
During the contractions, either one of these structures are compressed which decreases the blood flow to the fetus. This causes intermittent hypoxia. With tachysystole, the compression of these structures can be prolonged or exaggerated. With increased frequency of contractions, the baby can have a shorter resting interval between contractions and less time to recover from the periods of hypoxia occurring during each contraction. Over time this can decrease the fetal reserve and the baby’s ability to tolerate labor and in turn can lead to ischemia of brain tissue. In addition, in certain labors where there is tachysystole the contractions cause repetitive/recurrent compression on the fetal head. This head compression can directly cause hypoperfusion in the brain and ischemia of the brain tissues. Head compression can be evident on fetal heart rate monitoring with early decelerations.
Plaintiff’s experts opined that the defendant was required under the standard of care to recognize there were periods of tachysystole with recurrent early decelerations and either marked variability or minimal variability of the fetal heart rate and to take the appropriate steps to try to resolve these issues, by either reducing or discontinuing the Pitocin and performing intrauterine resuscitation interventions such as oxygen, change of position and bolus of fluid. If these measures are not successful in resolving the non-reassuring status of the fetus, then a change in the plan of delivery should be considered, discussed with the patient and implemented. If remote from delivery, that change would be performing a cesarean section.
It was plaintiff’s experts’ opinion that if the defendant had complied with the standard of care and had reduced the Pitocin at 1730 on March 15, 2012, along with instituting uterine resuscitation, the contractions would have become normal and the fetal response would have improved within 15 minutes. However, it was also plaintiff’s experts’ opinion that if these measures failed to correct the issues, then a C-section should have been discussed with the plaintiff and performed by 6:30 p.m. on March 15, 2012. If these measures had been done, the injury to the baby’s brain and her death would have been avoided.[19-T-143]
Type of action: Medical malpractice/wrongful death
Injuries alleged: HIE, cerebral palsy
Verdict or settlement: Settlement
Attorneys for plaintiff: Charles J. Zauzig, Melissa G. Ray and David Haynes, Woodbridge