May Case Summaries

Birth asphyxia assumed cause of neonatal encephalopathy

In 2004, a 17-year-old California girl was admitted to the hospital with near-term preeclampsia. The patient tested positive for strep on admission, which was appropriately treated during labor. Five days later, her labor was induced and she developed a fever, which was also treated, and she was ultimately delivered by cesarean section. She developed a severe infection with a fever as high as 104.^o F and required hospitalization for 2 weeks postpartum. The infant's Apgars were 2/3/3 and umbilical cord pH

was 7.18, base excess minus 5. The infant had serious brain damage, was transferred to a children's hospital, and was subsequently diagnosed with cerebral palsy.

The defense claimed that the patient was appropriately managed and the brain damage and CP were due to an infection or inflammatory process in utero just before delivery. The placental pathology showed "chorionitis and diciduitis." A settlement was reached during trial for $2.4 million. This provided $250,000 to the mother and $2.15 million to purchase an annuity for the child.

Legal perspective

In this case the decision was made to put forth a causation defense against the claim that the infant had a hypoxic-ischemic episode proximate to birth. Noting the positive strep culture, fever during labor, the maternal postpartum infection, and the placental findings, as well as no FHR evidence of ongoing damaging acidemia in labor, it was suspected the infant's injuries were from infection and not asphyxia at birth as the plaintiff's experts claimed. In the ACOG/AAP document on Neonatal Encephalopathy and Cerebral Palsy, one of the items necessary for assigning blame to asphyxia proximate to birth as a cause is that other causes or sources for the injury are ruled out, including infection, genetic disorders, and thromboembolic events. Thus, during discovery the placenta and cord were examined by an expert placental pathologist and evidence of infection in the placenta and in the fetal vessels was found. Also the fact that the pH was above 7.0 and the base deficit of 6 did not meet the threshold of 12, as described in the ACOG/AAP document, points to an inflammatory process as a possible cause for this child's CP diagnosis.

What happened in this lawsuit was unfortunate for the defense and ultimately forced them to settle the case. While the delivering hospital that obtained the cord gases made the correct determination of "respiratory acidosis" from the values, when the infant was transferred to the children's hospital, the diagnosis was written as "metabolic acidosis at birth." The error may have come from using string cites for gas results and assuming the two institutions used the same string order and not seeing the actual page of results. Nevertheless, once that was written those words and others like "birth asphyxiation," "asphyxia," "birth injury," and "severe hypoxia at birth" were written by subsequent treating consultants in literally hundreds of places in the child's records. Of course, metabolic acidosis is a better term than "asphyxic birth" or "perinatal asphyxia," but the better term as a diagnosis is neonatal encephalopathy, since that is a result and can have several causes.

While some of this could have been brought out in testimony and cross examination, jurors in general give credence to subsequent treating physicians as experts since they appear neutral as nondefendants and have actually taken care of the child. Unfortunately, determining that a "hypoxic-ischemic" event was the cause of the encephalopathy so early in the records, and all the consultants dutifully repeating it, probably prevented anyone from exploring independently the cause of the encephalopathy even though some knew of the severe maternal and placental infection. The result in the case was that the treating expert physicians all testified as to the "cause" as they had written in the chart, which led the defense to offer a settlement.