For lawyers who represent birth malpractice victims, few phrases conjure up as much ire and frustration as “the ACOG report,” the shorthand for a 2003 document put out by the American College of Obstetricians and Gynecologists (“ACOG”) called “Neonatal Encephalopathy and Cerebral Palsy: Defining the Pathogenesis.” Despite its title, the report made no effort to explain how a doctor could determine the cause of a particular child’s cerebral palsy, and it made no effort to explain how the incident of neonatal encephalopathy (i.e., newborn brain damage) could be reduced. (Bob Schuster has a little more on its origins, and MedScape has a summary of it.)
Rather, the sole purpose of the report was to prevent children with cerebral palsy caused by labor and delivery malpractice from obtaining compensation, which it accomplished by giving a cover to insurance company’s efforts to confuse judges and juries into believing that babies could survive hours without adequate oxygen and suffer no consequences. The report established core four “essential” criteria, and five “suggestive” criteria that, ACOG claimed, had to be met before a child’s cerebral palsy could be linked to hypoxia at birth.
Sure, in the “Task Force on Neonatal Encephalopathy and Cerebral Palsy,” ACOG dressed up their preordained conclusions in scientific and medical jargon and gave passing nods to basic principles of honest medical research, but the report was worthless from a medical standpoint. It wasn’t a real compilation of medical information, like a Cochrane Review or UpToDate, and it didn’t give any recommendations on how to diagnose or treat patients.
Instead, the report was used constantly in birth injury litigation by paid experts testifying on behalf of obstetricians and hospitals sued for ignoring the signs and symptoms of fetal distress and failing to treat fetal hypoxia. If you brought a hypoxia birth injury claim anywhere in the United States after 2003, you could be assured that the ACOG report would be front and center in the defense, with the veneer of “scientific” and “medical” proof.
ACOG wasn’t responsible for coming up with most of the “essential” and “suggestive” criteria, but instead cut-and-pasted them from the International Cerebral Palsy Task Force’s 1999 “template for defining a causal relation between acute intrapartum events and cerebral palsy,” available here. You can see a comparison of the ACOG and International guidelines on table 3 of this article.
The International Task Force’s criteria was suspiciously strict to begin with, like with their criteria for blood pH and Apgar scores.
The typical pH of blood is 7.35 or higher. When a baby is deprived of oxygen, their blood starts to become increasingly acidic, and the pH goes down. Before 1999, a variety of studies, like this 1987 study, showed that a pH as high as 7.20 was correlated with subsequent cerebral palsy. The International Task Force, however, said that oxygen deprivation in labor and delivery could only be tied to cerebral palsy if the pH of the blood in the baby’s umbilical arterial cord was 7.00 or lower. (As a 2010 article in the British Medical Journal in 2010 recounted, the 7.00 number wasn’t exactly evidence-based medicine: it was “derived through consensus, not through evaluation of collated summaries of evidence.”)
Apgar, in turn, is an inherently subjective measure by which a newborn is evaluated for their “Appearance, Pulse, Grimace, Activity, Respiration.” (Although “APGAR” seems like an acronym, the scoring system was devised by Dr. Virginia Apgar, and the acronym was made up later to fit the name.) The International Task Force said that, if a newborn didn’t have “Apgar scores of 0-6 for longer than 5 minutes,” then it was less likely the child’s cerebral palsy was caused by hypoxia. This was a rather dubious “criteria” to begin with, given a long line of research indicating that Apgar isn’t really that useful to predict long-term outcomes — it’s real use is just in deciding whether a newborn needs intervention or not.
ACOG, however, didn’t think that went far enough to help obstetricians, so made two changes to the International Task Force’s criteria, both of which were presumably calculated to thwart children with cerebral palsy from obtaining compensation.
First, ACOG adjusted the Apgar scores even further downward, from “scores of 0-6 for longer than 5 minutes” (the International criteria) to “Apgar score of 0-3 beyond 5 min,” despite the the International Task Force’s own conclusion that “duration of low Apgar scores is more likely to indicate the effectiveness of resuscitation than to predict outcome.” ACOG knew this was garbage; their own journal reported in 2001 that newborns with 5-minute Apgar scores below 7 were 31 times more likely to be diagnosed with cerebral palsy. A newborn with an Apgar of “0-3 beyond 5 minutes” — which means that, five minutes after birth, they are limp, gray, and unresponsive to stimuli, with nothing more than their breathing and a heartbeat — is not just more likely to have cerebral palsy, they run a serious risk of death.
Then, ACOG added the most dubious “factor” of all: “Exclusion of other identifiable etiologies, such as trauma, coagulation disorders, infectious conditions, or genetic disorders.” In other words, even if all the signs point towards brain damage being caused by oxygen deprivation during birth, then the paid experts for negligent doctors can still make up whatever they wanted whenever. This was terrible medicine — in clinical practical, doctors use the differential diagnosis, they don’t contort their analysis to avoid a particular outcome they don’t like — but it had ACOG’s stamp on it. Most of the defense expert witnesses I’ve dealt with settled on “undiagnosed intrapartum stroke” as their go-to bogus defense. Any time my client was obviously injured by oxygen deprivation, the defense witness said that the child actually suffered a stroke long before the birth, but nobody noticed it and there was no way to prove or disprove it.
All of which is why malpractice lawyers cringe at any mention of “the ACOG report.”
Not long ago, ACOG released its second edition, now renamed “Neonatal Encephalopathy and Neurologic Outcome.” Jane Brody at the New York Times has some exceedingly friendly coverage of it, which we’ll come back to in a moment.
The report is a step in the right direction:
[F]or the current edition, the Task Force on Neonatal Encephalopathy determined that a broader perspective may be more fruitful. This conclusion reflects the sober recognition that knowledge gaps still preclude a definitive test or set of markers that accurately identifies, with high sensitivity and specificity, an infant in whom neonatal encephalopathy is attributable to an acute intrapartum event. The information necessary for assessment of likelihood can be derived from a comprehensive evaluation of all potential contributing factors in cases of neonatal encephalopathy. This is the broader perspective championed in the current report.
If ACOG is now admitting that their factors aren’t quite as clear-cut and inviolate as claimed back in 2003, and that the real diagnosis requires a more genuine review of the patient’s history, then I applaud them. If they’re just coming up with more excuses to cram in bogus theories about how the child must have been injured by something other than oxygen deprivation, then we’ll just fight it out in the courts.
ACOG backed off of the “pH of 7.00 or lower,” I presume in part because of the report in the British Medical Journal in 2010, “Strength of association between umbilical cord pH and perinatal and long term outcomes,” which noted the 7.00 number was “derived through consensus, not through evaluation of collated summaries of evidence,” and that the evidence supported an association between birth injuries and a pH up to 7.20. The Second Edition now says:
1. Fetal umbilical artery pH less than 7.0, or base deficit greater than or equal to 12 mmol/L, or both, increases the probability that neonatal encephalopathy, if present, had an intrapartum hypoxic component; lesser degrees of acidemia decrease that likelihood.
2. If the cord arterial gas pH levels are above 7.20, it is unlikely that intrapartum hypoxia played a role in causing neonatal encephalopathy
This is still artfully worded for litigation purposes — they could just as well admit a pH of 7.20 or lower “increases the probability that neonatal encephalopathy, if present, had an intrapartum hypoxic,” rather writing the two paragraphs separately — but it’s a start, and 7.00 is no longer a bright-line cut-off.
ACOG’s Apgar numbers are still absurd and self-contradictory:
A. Apgar Score of Less Than 5 at 5 Minutes and 10 Minutes
1. Low Apgar scores at 5 minutes and 10 minutes clearly confer an increased relative risk of cerebral palsy. The degree of Apgar abnormality at 5 minutes and 10 minutes correlates with the risk of cerebral palsy. However, most infants with low Apgar scores will not develop cerebral palsy.
2. There are many potential causes for low Apgar scores. If the Apgar score at 5 minutes is greater than or equal to 7, it is unlikely that peripartum hypoxia–ischemia played a major role in causing neonatal encephalopathy.
What does this even mean? If the issue is “Apgar score at 5 minutes is greater than or equal to 7,” why does the title say “Apgar Score of Less Than 5 at 5 Minutes and 10 Minutes?” Truth is, ACOG should scrap this altogether as an indicator of long-term birth injuries. As the National Institutes of Health say, “The Apgar score is not designed to predict the future health of the child.” Apgar is useful for clinicians trying to figure out if a newborn needs care, but it’s value in predicting future harm is limited (not least because of its subject nature), and it certainly shouldn’t be used as threshold for post hoc diagnoses.
That said, I do give ACOG credit for eliminating the “catch-all” they used to have, in which doctors were supposed to give more credence to wild speculations about potential causes than they were to the evidence in front of them. The “Exclusion of other identifiable etiologies, such as trauma, coagulation disorders, infectious conditions, or genetic disorder,” has been replaced with:
D. No Evidence of Other Proximal or Distal Factors That Could Be Contributing
Factors In the presence of other significant risk factors—such as abnormal fetal growth, maternal infection, fetomaternal hemorrhage, neonatal sepsis, and chronic placental lesions—an acute intrapartum event as the sole underlying pathogenesis of neonatal encephalopathy becomes much less likely.
There are problems with this analysis — “neonatal sepsis” can arise from the harm caused by hypoxia — and it’s more than a little daft to require no evidence of other potential factors (what happened to the “broader view” espoused earlier?), but at least it’s not a free-for-all of potential causes.
ACOG hasn’t given up its old ways but it is getting a little closer to the science and the medicine, and thus getting a little more honest. They couldn’t help themselves from recommending “changing the culture of health care delivery from one that names and blames to one that is dedicated to reducing medical errors through a constructive, nonthreatening and professional process,” as if obstetricians were children who needed gentle guidance rather than licensed professionals, but it was banal enough to be largely harmless.
Seeing the above, Jane Brody at the New York Times initially goes the right way:
In other words, doctors must be more forthcoming in reporting problems encountered during the care of pregnant women, especially at the time of labor and delivery. Such honesty can identify preventable causes of brain injuries in newborns and enable corrective action.
And then falls off the deep end:
But it would be helpful, too, for families to reconsider a leap to legal action whenever babies are born with a brain injury. Such suits put doctors on the defensive and make them unwilling to report problems that might have been prevented.
Brody was happy to call up the head of the ACOG Task Force and ask them all about the report, but it seems it wasn’t worth her time to talk to a family with a child that suffered a birth injury. My clients never “leap to legal action,” they come to it slowly and painfully as it dawns on them that they have a seriously disabled child who will need extensive care throughout the rest of their lives. They come to me with questions — they’ve noticed that even friendly, well-meaning doctors won’t give them a straight answer about what happened — and I don’t “leap” either. I review everything and then have it reviewed by an obstetrician. “Legal action” only happens when it’s clear a child was permanently disabled because some doctor or hospital couldn’t do their job right.
If some obstetricians are so morally bankrupt that the mere possibility of a lawsuit (one in which they’re unlikely to pay a dime out of pocket, even if the lawsuit is successful) is enough to make them go on giving newborns brain damage rather than reporting problems to improve their skills and their profession, then they have no business in medicine. The more ACOG works to prevent hypoxia instead of defending it, the less their doctors will have to worry about legal action.