Legally Speaking: The GBS defense that wasn't

Because of the potential jury verdict exposure, infant brain injury cases attract litigation even when the plaintiff's arguments are not scientifically or biologically plausible. It's often more expedient to settle such an action even when there is no negligence because juries can allocate extraordinary awards simply out of sympathy for the child's plight and the perceived cost of medical care and supervision.

THE FACTS

The patient was a G4P3 with a twin gestation and an estimated date of confinement of January 27 who had begun receiving prenatal care at a high-risk clinic the previous July. Her medical history was significant for a vaginal termination of pregnancy 2 years before at 13 weeks, a miscarriage 2 years before that at 8 weeks, a normal, spontaneous vaginal delivery 6 years previous, and delivery of twins 7 years before, at 36 weeks. During an office visit on August 17, at 16 weeks' gestation, her cervix was noted to be long, closed, and posterior; on August 31, it was fingertip. On September 19, the patient was group 1-cm dilated.

During the woman's visit on September 28, the obstetric resident who saw the patient performed an examination, which included an ultrasound, and ruled out placenta previa. Notes from a speculum exam indicated no dilatation (on interview, he indicated that if there was any, he would have documented that) and no pooling. Both fern and nitrazine tests were negative. The differential diagnosis for the white fluid included possible rupture of membranes (ROM), an infection, and physiologic discharge. The obstetric resident ruled out ROM and determined that the patient was not in labor because she was not having regular contractions.

The patient next presented to the hospital at 23½ weeks on October 6, at approximately 6 PM, complaining of contractions. Examination showed that she was fully dilated, and she was admitted and prepped for an emergent cesarean delivery (CD).

Twin "A" was delivered by CD at 6:58 PM from a breech presentation. His Apgar scores were 6 and 7 at 1 and 5 minutes, respectively, and he weighed 950 g. Despite intubation and resuscitation in the OR and maximum intervention with mechanical ventilation, high FiO₂s, beractant, antibiotics, packed cell transfusions, and vasopressors, he never stabilized and died just over 24 hours after delivery.

Twin "B," who was delivered at 6:59 PM from a transverse lie, weighed 895 g and had Apgars of 6 and 7 (the operative report for the CD notes Apgars of 8 and 8). He was also intubated in the OR and achieved a 10-minute Apgar of 8. By 7:15 PM, Twin B was in the neonatal intensive care unit and on mechanical ventilation with 100% oxygen. A chest x-ray showed bilateral granularity with air bronchograms consistent with respiratory distress syndrome. Lines were placed; he had a culture and was begun on antibiotics and prophylactic phototherapy and given beractant. One of the fetal placental sacs had mild acute chorioamnionitis. Blood cultures were negative. The placental-fetal culture grew moderate Haemophilus influenzae but the placental-maternal culture had no growth after 3 days.

During the course of his admission, Twin B had a relatively rocky respiratory course. He required several re-intubations and supplemental oxygen, plus selective intubation for collapse of a large part of his right lung, and suffered a left pneumothorax. Several cranial ultrasounds (U/S) were also done, the first of which was suspicious for bilateral early germinal matrix hemorrhage, with a choroid plexus hemorrhage unable to be ruled out. The second cranial U/S, done several days later, showed periventricular white matter changes consistent with periventricular leukomalacia (PVL). A third study demonstrated less prominent PVL changes. Another U/S, done approximately 2 weeks before discharge, demonstrated cystic changes consistent with evolving PVL. On December 30, the baby was discharged with provisions for home oxygen, pulse oximetry, and VNS follow-up.