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Debate Stirs Over Diagnosis, Low Apgar Scores


 

CABO SAN LUCAS, MEXICO — Some obstetricians see pediatricians and neonatologists as adversaries when it comes to reducing the risk of a lawsuit after delivering a baby with low Apgar scores.

The alledged problem: Most pediatricians, neonatologists, and pediatric neurologists don't follow a 2003 monograph produced by the American College of Obstetricians and Gynecologists (ACOG) and the American Academy of Pediatrics (AAP) that sets criteria for declaring that a newborn has hypoxic ischemic encephalopathy (HIE), which is an essential component of cerebral palsy, said O. Richard Depp, M.D., at a conference on obstetrics, gynecology, perinatal medicine, neonatology, and the law.

Until recently, pediatricians and neonatologists who saw a newborn who was not doing well and had depressed Apgar scores simply labeled the problem as HIE. “That is no longer appropriate,” said Dr. Depp, professor of ob.gyn. at Thomas Jefferson University and Drexel University, Philadelphia.

No one should presume a diagnosis of HIE until other causes have been excluded and criteria for HIE have been met, he said. (See sidebar.) Until then, the only appropriate label—and one less likely to spark litigation—is neonatal encephalopathy, which may be due to a number of causes, many of which occur before labor and delivery, according to the monograph.

“I think there is a real need for education among our colleagues in other specialties, because I don't think they've really read this,” Dr. Depp said during the conference, which was sponsored by Boston University and the Center for Human Genetics.

Not so, countered Avroy A. Fanaroff, M.B., in a commentary after Dr. Depp's talk. “Our pediatricians are trained to be very cautious about their use of terminology and to apply the ACOG criteria before they put down HIE,” he said. Dr. Fanaroff is professor and chairman of pediatrics and professor of reproductive biology at Case Western Reserve University, Cleveland.

“You practice in one of the pediatric capitals of the world,” responded Dr. Depp. He asked how many obstetricians in the audience of 150–200 people felt comfortably sure that the pediatricians in their hospitals were familiar with the monograph. Less than a handful raised their hands.

An obstetrician from Atlanta stepped up to the microphone and said, “We're fighting for our lives from the plaintiffs' attorneys, who say, 'Well, can you dispute the fact that this pediatric neurologist says this is HIE?' [The neurologist] wasn't there! He doesn't even know what he's saying!”

Dr. Depp suggested that it's time for chairs or division chiefs “to sit down and talk about how they will address this problem in a prospective manner.” At Jefferson University, he sat down with the chairpersons of pediatrics and anesthesia to negotiate an agreement on the proper use of terms such as HIE and neonatal encephalopathy.

Only recently have physicians attempted to distinguish between neonatal encephalopathy and hypoxic ischemic encephalopathy, he noted.

A 1999 international consensus statement, titled, “A template for defining a causal relation between acute intrapartum events and cerebral palsy” provided the first clear guidance and was endorsed by 16 medical organizations, including ACOG (BMJ 1999;319:1054–9).

ACOG and the AAP followed with the monograph, “Defining the pathogenesis and pathophysiology of neonatal encephalopathy and cerebral palsy” (Obstet. Gynecol. 2003;102:628–36).

Dr. Fanaroff agreed that differentiating hypoxic ischemic encephalopathy from neonatal encephalopathy is a complex task. “There are a whole lot of things that need to be sorted out. There are some that are acute events, others that are chronic, others that are acute and chronic, and others that are due to genetics or infection,” Dr. Fanaroff said.

“I think we're all treading on very thin ice, and walking on eggshells” when labeling problems in a newborn's chart.

HIE Criteria Essentials

Four prerequisites must be met in proposing that hypoxic ischemic encephalopathy caused moderate to severe neonatal encephalopathy, resulting in cerebral palsy:

1. Fetal umbilical cord arterial blood obtained at delivery with evidence of metabolic acidosis (pH less than 7 and base deficit of 12 mmol/L or more).

2. Early onset of moderate or severe neonatal encephalopathy in infants born at 34 weeks' gestation or later.

3. Spastic quadriplegic or dyskinetic cerebral palsy.

4. Exclusion of other identifiable causes such as coagulation disorders, infectious conditions, trauma, or genetic disorders.

The monograph also discusses other criteria that together suggest an intrapartum insult occurred.

Source: Defining the pathogenesis and pathophysiology of neonatal encephalopathy and cerebral palsy (Obstet. Gynecol. 2003;102:628–36).

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