Commentary:
A lawsuit can be difficult to defend when an allied healthcare professional and collaborating physician fail to communicate or coordinate care.
The Case:
Prior to becoming pregnant, a 29-YOF (5’1”, 155 lbs., G1 P0), was diagnosed with polycystic ovarian syndrome. The patient received all her prenatal care from a certified nurse midwife (CNM), and her pregnancy was noted as unremarkable. The patient took Prometrium® for the first trimester to avoid a miscarriage. An OB physician reviewed the patient’s initial ultrasound completed at 20 weeks and the results showed an appropriate gestational-age fetus and normal amniotic fluid and volume. A subsequent ultrasound, reviewed by the same supervising OB physician, revealed a size consistent with dates of a 34-week, six-day old fetus, and normal amniotic fluid index.
Seventeen days after the second ultrasound, the patient experienced spontaneous rupture of membranes at 5:00 a.m., and presented to the hospital at 6:54 a.m. On examination, she was noted to be 3 cm, 60 percent effaced, and -2 station. A limited ultrasound confirmed a vertex presentation. She was more than 37 weeks pregnant.
Upon admission, the patient was started on Pitocin® 2mU at 8:00 a.m. An hour later, an epidural was placed. At 9:44 a.m., the CNM was called and provided an update on the patient’s status. Fetal monitor strips reported the presence of short-term variability, average long-term variability, positive accelerations of moderate intensity, and what the nurse deemed a late deceleration. The patient was turned to her right side and the bed was placed in Fowler’s position.
By 10:00 a.m., the late decelerations had resolved and the patient was noted to have early decelerations. At 11:18 a.m., the Pitocin drip was at 8mU and she was 9.5 cm dilated, 100 percent effaced, and 0 station. Pitocin was decreased to 4mU at 11:43 a.m. By 11:45 a.m., she had an interior lip present that continued to be present between pushing efforts.
At 12:00 p.m., the CNM was at the patient’s bedside. There was no MD present during labor and delivery. The patient pushed for two hours and 22 minutes and delivered a 6 lb., 5 oz. male infant at 2:22 p.m. The umbilical cord was wrapped around the infant’s shoulders twice. Apgar scores were three, six, and seven. The infant was limp with minimal respiratory effort, requiring mask ventilation and intubation. Later that day, the infant was transferred to a children’s hospital.
In the NICU, the infant developed apneic episodes with associated tonic-clonic movements. A stat CT was negative and an MRI the next day was interpreted as showing acute subacute ischemic injury to the bilateral thalami, posterior limb of the internal capsules, and bilateral corona radiata. A placental pathology report revealed mature placenta of 367 grams—findings consistent with maternal malperfusion and marginal villous infarct, increased syncytial knots, and intervillous fibrin.
The child, now 4 years old, has severe developmental delay. He is wheelchair-bound with significant spasticity and dystonia, and has feeding difficulties, reflux, respiratory distress, and weak ocular muscles. In addition, the child has cerebral palsy with minimal head control and does not open his hands. He is microcephalic, nonverbal, and will require total care throughout his life. Previously, the child had a number of findings associated with genetic abnormalities. However, after being seen and tested by genetics specialists, no known clinically significant parameters were identified in the array analysis. The child has had multiple hospitalizations over the years.
Multiple defense expert witnesses included professionals in neuroradiology, pediatric neurology, maternal fetal medicine, and neonatology. The expert witnesses testified the injury was caused by prenatal intermittent chronic ischemia. Testimony also stated that a hypoxic ischemic brain injury occurred prior to delivery. The hypoxic ischemic insult to the brain was moderate, prolonged, and intermittent, and occurred over several hours and possibly several days. The experts stated the hypoxic ischemic injury was likely due to uteroplacental insufficiency, and most likely secondary to chronic intermittent umbilical cord compression, the prenatal cord wrapped around the shoulders twice, and prenatal placental nutritional deficiency.
Plaintiff’s expert witnesses testified the injuries were due to a number of factors including failure to recognize and promptly respond to abnormal fetal heart rate and uterine activity, failure to complete intrauterine resuscitation, failure to improve fetal oxygenation, and failure to safely manage Pitocin infusion in the face of tachysystole. Other factors included failure to provide an appropriate resuscitation team during delivery in the presence of Category 3 fetal tracing in the second stage. In addition, the MRI performed the day after birth indicated a near total or profound asphyxia injury.
Despite the efforts of defense counsel to argue the injuries were not caused by the care, the case was settled due to the lack of communication between the CNM and the supervising OB. Physicians using allied health professionals are responsible for making sure these professionals are adequately trained, know their limitations, and know when to contact the supervising physician when they encounter anything beyond a normal presentation.
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