LEGALLY SPEAKING
Risk management in obstetrics and gynecology

The allegation that an infant suffered "brain injury" during delivery is the most challenging and difficult to overcome, both for the defendant physician and counsel. In many cases a verdict that seems inconsistent with the evidence results when the jury's overwhelming sympathy for the infant and the difficulties posted by current laws on admissibility of family history and genetic evidence take precedence over reassuring tracings, thorough and appropriately timed progress notes, supportive Apgar scores and blood gas results, and lack of evidence of genetic or congenital anomaly.

CASE STUDY: "BRAIN-INJURED" INFANT

By Mark J. Aaronson, Esq., and Andrew I. Kaplan, Esq.

THE FACTS:

The plaintiff, an 18-year-old gravida 2 para 1 with an estimated date of confinement (EDC) of October 27th, presented to the defendant hospital on October 20th for external version of a fetus in breech presentation. Of significance, the mother had gained only 11 lb during the pregnancy and an October 14th ultrasound confirmed a breech presentation and a fetus "slightly small" for gestational age (SGA).

The admitting history recorded by the nurse-midwife on the date of the external version indicated the mother had no contractions and no bleeding, and that the attending physician had successfully performed the version to vertex under sonographic guidance. After the procedure, spontaneous labor was noted, and the plaintiff experienced contractions every 3 to 4 minutes. Vaginal examination revealed that she was 90% effaced, 1-cm dilated, and -3/-2 station. Artificial rupture of membranes revealed clear fluid. At 12:45 pm, the nurse-midwife noted contractions every 5 to 7 minutes that lasted for 40 seconds, with a fetal heart rate between 140 to 160 beats per minute (bpm) on internal fetal scalp electrode.

At 1:15 pm, the nurse's note indicated prolonged decelerations of 60 bpm for 3 minutes, the patient was turned on her left side, and 10 L of oxygen was administered. The note also documented a change in amniotic fluid from clear to meconium-stained. The nurse-midwife and attending were notified and at bedside and the nurse-midwife noted quick recovery in FHR with scalp stimulation. At 1:26 pm and 1:35 pm, the attending who performed vaginal examinations noted a fetus with compound presentation, and this was followed by a 1:50 pm note by the nurse, who documented prolonged decelerations to 70 bpm, which lasted 70 seconds. A sterile vaginal examination by the nurse-midwife detected a questionable occult cord prolapse and the attending was notified. Because of the nonreassuring FHR tracing, the patient was prepared for cesarean delivery. At 2:00 pm, the patient was transferred to the OR, anesthesia was begun at 2:15 pm, and the first incision was made at 2:19 pm. The infant, delivered at 2:23 pm, weighed 5 lb, 1 oz with Apgars of 1, 8, and 10, and was transferred to the neonatal intensive care unit at 2:40 pm.

The NICU notes indicated the infant was born floppy and had meconium-stained skin. He was intubated and meconium was suctioned from below the cords. His initial heart rate of 66 bpm improved to 100 bpm after resuscitation, and he received naloxone. The infant was erroneously listed as AGA (average for gestational age) when, in fact, he was actually SGA. Cord blood gases revealed acceptable pH and bicarbonate values (venous pH 7.32, HCO₃ 30) and the initial blood gas taken in the NICU at 3:32 pm had a pH of 7.38, CO₂ of 44, and an O₂ of 213 on 100% oxygen, with HCO₃ of 26. No tremors or seizure activity were noted, and the newborn's cultures were negative.

Genetic consults were obtained when it was noted that the infant had dysmorphic features of prominent forehead, prominent alveolar ridges, and high-arched palate. His chromosomal studies were normal and U/S of the brain revealed slight fullness of the left lateral ventricle that was deemed within normal limits. The infant was discharged home on October 25th and his failure to thrive and "small stature syndrome" were investigated by several institutions, but no determination of the etiology was ever made.

THE ALLEGATIONS:

The plaintiff alleged that the failure to perform an earlier cesarean delivery resulted in birth hypoxia sufficient to cause mental retardation.

DISCOVERY:

The discovery process revealed that the plaintiff mother had an older child who had no developmental disabilities, but that the mother's older sister had two children who were mentally retarded. The plaintiff's expert pediatric neurologist obtained that history from the mother and included it in his report about physical examination of the infant plaintiff. This information was also found in multiple records of the infant's treatment, and thus was included in the materials to be submitted into evidence at the time of trial.

Neither the physicians who treated the infant after birth nor those who evaluated him to determine whether his condition had a genetic etiology could determine the specific cause of his problems, but they noted that a genetic or congenital etiology could not be excluded. None were of the opinion that the infant's difficulties were related to the birthing process itself. At 3 years of age, the infant exhibited skills of a 9-month-old child.

THE TRIAL:

At the trial, the plaintiff's expert ob/gyn testified that the attending physician departed from good and accepted practice in failing to perform a "crash" cesarean delivery. He did not criticize the attending's care between 12:00 pm and 1:55 pm on October 20th, but testified that the attending departed thereafter by not delivering the infant within 3 to 4 minutes after the second severe deceleration. On cross-examination, however, this expert conceded that if the normal cord pH was valid, it absolutely spoke against hypoxia during delivery. In fact, he conceded that the presence of a normal cord pH militated against hypoxia in the hour prior to delivery.

The plaintiff's pediatric neurology expert admitted that the cord blood gas results were "inexplicable" and seemed to rule out the theory of hypoxia during birth. He further conceded that the infant's NICU course was normal and spoke against a significant hypoxic insult. This expert's theory was that the infant had "secondary microcephaly," which supported his opinion that during delivery, the infant suffered hypoxia significant enough to cause mental retardation. That theory, however, contradicted the opinion of all of the physicians who had treated the infant after the birth that the child was born microcephalic. To support his opinion, the pediatric neurologist mixed and matched results from the Ballard scale and an intrauterine head growth circumference graph to arrive at the conclusion that the record of the infant as "AGA" and not "SGA" was accurate. At one point, this expert testified that if the infant was born 3 or 4 minutes earlier, he would have been "okay," but at another time, he used 15 minutes as the critical period.

Before the trial began, the court ruled that the family history of mental retardation could not be put before the jury. The plaintiff's pediatric neurologist admitted, however, that he had obtained that history from the mother and included it in his report on the physical examination. As such, defense counsel was allowed to sum up before the jury on the issue over plaintiff counsel's objection. However, the jury was specifically instructed to disregard any testimony on genetics or family history when they subsequently were charged on what evidence they could consider while deliberating.

The defendant's obstetrical expert testified that the attending handled the labor and delivery appropriately and that at no time did any of the FHR tracings show a late deceleration, much less a pattern of late decelerations. The low 1-minute Apgar was consistent with meconium, and after vigorous suctioning, the Apgars were very good. The defendant's neonatology expert testified that the 5- and 10-minute Apgars reflected good neonatal resuscitation, and the cord blood gases confirmed that there was no indication the newborn had sustained any perinatal asphyxia. She believed that if the infant had "head sparing," rather than microcephaly, this might be reflective of placental insufficiency, but because the baby was relatively microcephalic, there was no evidence of asphyxia. Finally, she testified that the infant did not show a consistent pattern of hypoxic ischemic encephalopathy.

The defendant's expert pediatric neurologist concurred, and based upon her own examination of the infant, testified that the child's problems were related to factors other than those that occurred at birth. She opined that the infant's symmetrical rather than asymmetrical IUGR suggested that the problems likely occurred at the time of conception, or during the first, second, or early third trimester, rather than on the date of delivery. To support that opinion, she pointed to the umbilical cord pH.

Finally, the defendant's expert pediatric neuroradiologist testified that none of the MRIs subsequently performed upon the infant showed any evidence of hypoxia. Of significance, the court would not allow the defense to call the first-year resident who had erroneously indicated "AGA" rather than "SGA" in the infant's chart, a note that was then carried through the entire neonatal record.

After lengthy deliberation, the jury returned a significant verdict for the plaintiffs. As of this writing, the verdict has been reduced by two thirds on posttrial motion, and an appeal to set aside the verdict as against the weight of the evidence is pending.

ANALYSIS:

The result of this case underscores the unpredictability of the trial process. Often, the trial court, in its discretion, will exclude testimony or evidence that is seemingly helpful to one side or the other. In this case, the jurors were all serving for the first time and no doubt were influenced by the court's refusal to allow them to weigh testimony on familial history, or to hear a witness explain the entry indicating that the infant was "AGA."

This case further underscores the significance of the presenting infant's condition, which can never be overlooked, no matter how defensible the medicine appears. Most jurors are loathe to send a profoundly damaged infant home empty-handed, absent an airtight defense on behalf of the delivering physicians. In this case, what would appear to be an insignificant error in charting made by a first-year resident allowed a seasoned plaintiff's expert to create an explanation for his opinions that injury occurred during the birthing process. Despite his concessions that the infant's blood work and diagnostic studies argued against his theories, the expert gave the jury enough of a basis, in their minds, to justify a verdict for the plaintiffs.

Mark J. Aaronson is a Founding Partner at Aaronson, Rappaport, Feinstein & Deutsch, LLP, New York, N.Y. Since graduating from Brooklyn Law School in 1969, he has spent virtually all of his legal career concentrating on defense litigation, specifically high-exposure medical malpractice cases as well as defense of product liability and construction claims.

Andrew I. Kaplan is a Partner at Aaronson, Rappaport, Feinstein & Deutsch, LLP. Mr. Kaplan graduated from Brooklyn law School in 1993 and has specialized in medical malpractice defense and health-care litigation since entering private practice.

 

Mark Aaronson. Legally Speaking: Case Study: "Brain-injured" infant. Contemporary Ob/Gyn Jun. 2, 2003;48:22-26.