ACOG has published literature setting birth trauma causation criteria to deny justice to children and to defend against lawsuits. Sims Weymuller and Liz McLafferty wrote about this topic. The article was published by WSAJ in Trial News.

Introduction

Brains need oxygen. When deprived of oxygen, brain cells die. One of the more devastating forms of birth injury occurs when there is not enough oxygen in a baby’s blood (hypoxia) and/or the blood flow is restricted (ischemia) causing an injury to the baby’s brain (encephalopathy) during the birth process (intrapartum). Occurring together, this injury mechanism is commonly called hypoxic-ischemic encephalopathy, or “HIE”, and can result in a range of neurologic outcomes from mild cognitive delays to severe conditions including cerebral palsy. Most HIE injuries are preventable through carefully managed obstetrical care.

Litigating these cases can be challenging due to a host of factors, not the least of which are the influential industry forces working to stack the deck against injured children seeking justice. The American College of Obstetricians and Gynecologists (ACOG) has gone out of its way to publish literature not to help further the obstetrical care, but to defend lawsuits. Their latest effort, Neonatal Encephalopathy and Neurologic Outcome (“NENO”), is purportedly a “consensus” document with a new approach. Rather than establish a crisp set of diagnostic criteria through a fair and disciplined meta-analysis, ACOG appears to have hand-selected certain “markers” and grouped them into a nebulous “constellation” of factors that is tailor-made for defense counsel [1].

Two Editions and a Lot of Smoke

In 2003, ACOG published its Neonatal Encephalopathy and Cerebral Palsy (1^st Ed.), which created stringent criteria for establishing intrapartum HIE. ACOG’s Task Force claimed that, in order for a baby to have suffered an acute intrapartum hypoxic event sufficient to cause Cerebral Palsy, four “Essential Criteria” must be met, and there are “five other criteria that collectively suggest intrapartum timing”. The four “essential” criteria had little to no epidemiological support in the literature. In 2014, ACOG published a second edition and re-titled it Neonatal Encephalopathy and Neurologic Outcome (“NENO”). The new version backed off its more stringent requirements in favor of supplying defense counsel with a universe of vagaries to obfuscate causation. The ACOG Task Force came to 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 which neonatal encephalopathy is attributable to an acute intrapartum event [2].” ACOG abandoned the phrase “essential criteria” (i.e. impossible criteria) in their 2^nd Ed., in favor of a “constellation of markers” (i.e. “nobody can say with certainty” criteria). The current ACOG standard purports to:

…compile a constellation of markers concerning neonatal status, contributing events, and developmental outcome to determine if they are consistent with acute hypoxiaischemia and may not be explained by other etiologies. Thus, when more of the elements from each of the item categories are met, it becomes increasingly more likely that peripartum or intrapartum hypoxia-ischemia played a role in the pathogenesis of neonatal encephalopathy [3].

The “constellation” framework does not recommend a minimal number of markers for making accurate diagnoses of HIE with acceptable level of specificity and thus is of little or no use to the obstetrical staff monitoring labor and delivery or to the clinicians who care for newborns. ACOG provided no guidance on the importance or priority of any given marker nor did it establish the minimum number of criteria required for an HIE diagnosis. Moreover, the methodology for arriving at the “constellation” appears to be merely a process of “consensus” rather than a true meta-analysis of the available literature. Were it the latter, ACOG would have had to consider significant contradictory literature. The resulting utility in practice and admissibility into evidence of NENO are questionable at best. If this “consensus” document of unknown methodology were to be admitted, however, its utility for the defense is clear. The authors appear to have kept in mind the goals of defense counsel: the more nebulous, the better. In the time since the ACOG published NENO, we have already seen defense experts gleefully wallow in the vagaries of the new standards as they attempt to exsanguinate our causation case. “Of course, some of the criteria are met here” they say, “but there just aren’t enough markers to state the cause with any certainty.”

ACOG’s Faulty Assumptions

ACOG couples the “constellation” framework with several faulty assumptions. ACOG assumes in NENO that developmental delays must be preceded by neonatal issues and encephalopathy in order to be considered an HIE injury. Yet studies have demonstrated that more mild forms of neonatal distress and hypoxia can impact cognition later on in development [4]. ACOG further assumes that prenatal factors are primarily to blame for neurologic injury, relying on a flawed and poorly designed study [5]. Meanwhile ACOG ignores a study with improved selection criteria and MRI-confirmed HIE injury in all subjects which found that the intrapartum period was the critical causal period and which reported on other studies that found the same [6].

Constellation Nebuli: ACOG’s Latest Criteria for (Not) Diagnosing HIE

The “constellation of markers” is comprised of two categories. The first category is: Neonatal Signs Consistent with an Acute Peripartum or Intrapartum Event, and it includes four subcategories. The second category is: Type and Timing of Contributing Factors That Are Consistent With an Acute Peripartum or Intrapartum Event. Rather than adopt this arbitrary subcategorization scheme, we discuss below the more specious categories.

Apgar Scores

An Apgar Score is a measure of the physical condition of a newborn infant obtained by adding points (2, 1, or 0) for heart rate, respiratory effort, muscle tone, response to stimulation, and skin coloration. The score is typically recorded at intervals of one, five and (sometimes) ten minutes after birth. A score of 10 represents the best possible condition.

ACOG states that an Apgar greater than or equal to seven at five minutes makes HIE an unlikely cause of neonatal encephalopathy. The data cited is largely specific to cerebral palsy, a severe injury that can result from HIE, and not to other forms of HIE. Recent studies contradict this claim, including one which found that 36% of children treated for HIE (in this case, with whole-body hypothermia) had Apgar scores greater than five at five minutes[7].

Fetal Umbilical Artery pH Less than 7.00

The pH of arterial blood flowing through the umbilical cord (from the baby) may provide evidence of the metabolic condition of the baby at birth. Providers often obtain “cord blood gas” readings, including the pH and the base excess, because lack of oxygen to the baby can cause acidosis in the blood which impacts the pH. In some but not all cases the pH will be lower, and the base excess higher, when acidosis occurs. ACOG maintains that a pH of less than 7.0 “increases the probability that neonatal encephalopathy had an intrapartum hypoxic component” and that if the pH is above 7.2, it is “unlikely that intrapartum hypoxia played a role in causing neonatal encephalopathy.” Of course, no studies suggest that a child with a pH greater than 7.2 cannot have suffered an HIE, just that it is unlikely, but this does not stop defense counsel and their experts from treating any blood gasses over 7.2 pH as virtually dispositive on causation. Meanwhile, the criteria as stated leave a gray area between 7.0 and 7.2. Supporting literature that ACOG cited suggests that this range does not rule out intrapartum HIE [8]. Drawing from a large number of studies, the authors analyzed the likelihood of impairment at various blood gas levels. The study found that infants with a pH under 7.0 are 12 times more likely to suffer serious long-term neurologic damage than those with normal blood gases and that infants with a pH in the 7.01 – 7.19 range are 2.2 to 2.4 times more likely to suffer long-term neurologic injury than babies with higher values. Moreover, other studies have found significant portions of infant cohorts diagnosed with neonatal encephalopathy had cord blood pH values greater than 7.0 and, in some cases had no suggestion of metabolic acidosis[9].

Neuroimaging Evidence of Acute Brain Injury

The timing of the brain birth injury can be an important component of a birth trauma case. If the child was injured before or after birth by some agent other than medical care, proving causation will be difficult. In some circumstances, brain imaging (ultrasound, CT or MRI) can help establish the timing of the injury. ACOG asserts that an MRI obtained between 24 hours and 96 hours of life will show the timing of a cerebral injury, and an MRI taken between 7 days and 21 days of life will show the full extent of the injury.

Like other tissue, brain tissue swells and takes a certain amount of time to reach its peak. If it shows swelling, the first MRI may demonstrate that a recent injury took place, likely in the intrapartum period. If the swelling has receded by the second MRI, timing is further confirmed. This imaging can also establish the degree and type of injury. In such cases an expert pediatric neuro-radiologist may be able to see injuries to the areas of the brain that are fed by the blood vessels that did not get enough well oxygenated blood during delivery. For example, an MRI of a typical parasagittal cerebral injury can demonstrate areas of cell death in a characteristic “watershed” pattern that tracks the vascular distribution that was impacted by the HIE.

While quite helpful if the MRI are timed just so, this is the “gold standard” in diagnostics and rarely occurs in the real world. The challenge to the lawyer representing an injured child is that this imaging either occurred or it did not. Some amount of imaging is typically conducted in the presence of concerning signs and symptoms (difficult delivery, low Apgars, seizures, low pH, etc.), but not always. It often requires proactive involvement by an experienced neonatologist or NICU staff. Many birth centers lack the required equipment or expertise for proper MRI imaging, and it can be risky to transport already injured neonates for imaging that likely entails sedation.

Multisystem Organ Failure

When the body is starved of oxygen, it may begin to prioritize delivery of what oxygen it has in reserve. The brain being a top priority, the body may shunt oxygenated blood away from other organs to the brain. Depending on the degree of this “brain-sparing” shunting in an oxygen deprived baby, it may result in multisystem organ failure at the time of birth. Examples of multisystem organ failure that ACOG includes are renal injury, hepatic injury, hematologic abnormalities, cardiac dysfunction, metabolic derangements, and gastrointestinal injury. ACOG includes multisystem organ failure in its “constellation” but admits that “the severity of brain injury seen on neuroimaging does not always correlate with the degree of injury to other organ systems.” This is consistent with studies that have shown significant percentages (25% [10], 30% [11] and 36% [12]) of neonates who suffered HIE that demonstrated no evidence of multisystem organ failure.

ACOG’s Three-Tiered System for Monitoring the Fetal Heart Rate

Electronic fetal monitoring (EFM) is an electronic method to record the fetus’s heartbeat and the mother’s contractions. The fetal heart rate (FHR) is the way a baby in utero tells the world how it is doing before it can speak. There are normal stresses of labor, to which most babies have a normal, regular reaction pattern – with brief accelerations of heart rate, while maintaining a regular, variable heartbeat over time, with small ups and downs. Then there are concerning patterns, where the baby’s heart rate decelerates during or after a contraction, or loses variability, or rises dramatically in an attempt to circulate more oxygenated blood to its organs. EFM can aid the practitioner in making delivery decisions because “the fetus will always experience decelerations that warn of the presence of hypoxia [13].” Since EFM shows earlier detection of the fetus in distress, it allows practitioners to better time obstetric interventions and delivery and avoid injury.

Entire volumes are dedicated to the reading and interpretation of FHR monitoring and that subject is beyond the scope of this article, but it is important to note the controversy of ACOG’s approach. In 2008, an ACOG-sponsored workshop proposed a three-tier system for classifying FHR tracings in which Category I tracings are considered “normal”, Category III tracings are considered “abnormal” and Category II tracings are “indeterminate [14].” Here is a summary of the categories:

Though EFM is meant to be a diagnostic tool to avoid injury to the mother and child, ACOG adopted these criteria and recommended that delivery need not occur during Category II tracings [15]. Yet, in NENO, under the constellation of factors for classifying HIE, ACOG agrees that if the fetal heart rate pattern converts to Category III, this “is suggestive of a hypoxic-ischemic event.” That is, accordingy to ACOG, delivery need only be expedited once a hypoxic event is already underway. EFM is meant to prevent hypoxia, not confirm damage to the brain once it has occurred. As one study declared: “[k]nowledge of fetal physiology would clearly require expeditious nursing actions before a Category III pattern develops. Waiting until there is absent baseline FHR variability with recurrent late decelerations or recurrent variable decelerations or bradycardia is, frankly ‘too little, too late [16].’”

CCIE: When Excessive Uterine Activity Causes a Hypoxic Injury to the Baby

Not included in ACOG’s recent publications is a mechanism of injury that helps explain those cases that don’t entirely fit the constellation criteria: comprehensive cerebral ischemic encephalopathy (CCIE). Typically, uterine contractions do not cause permanent injury to the baby. Fetuses can survive labor without apparent injury when resting intervals between contractions permit adequate re-oxygenation between contractions. However, prolonged and excessive uterine activity can result in CCIE [17]. The most prevalent measure of excessive uterine activity is short resting intervals: less than 60 seconds between contractions [18].

CCIE is a specific type of HIE. We see CCIE injuries when too much Pitocin is administered. Pitocin is a synthetic version of Oxytocin, the hormone that the body produces naturally to induce contractions. If too much Pitocin is administered, the uterus may contract too frequently, the contractions may last too long, or the uterus may not relax enough between contractions. Any of these occurrences, and often a combination of them, can prevent the fetus from reoxygenating, resulting in an HIE.

While defense counsel asserts in their Daubert challenges that CCIE is a new, made-up category of birth injury, research shows that knowledge of CCIE has been around for decades. As early as the 1960s, studies show that “a repetition of successive episodes of cerebral ischemia and also the deformation of the brain may lead to permanent damage of the central nervous system of the fetus [19].” In the 1980s and 1990s studies further showed that when a baby’s head is compressed, it can lead to “increased intracranial pressure and decreased cerebral profusion pressure” and “ischemic insult [20].” Indeed, Pitocin package inserts warn that strong or prolonged contractions could result in deceleration of the fetal heart rate and fetal hypoxia. The resulting head compression can result in localized ischemic injury (a lack of perfusion to the brain) that, unlike systemic acidosis, does not result in significantly increased blood gasses.

Conclusion

While ACOG’s constellation of criteria and suspect methodology present challenges to a successful birth trauma case, a careful examination can help clear the cloud of NENO dust. This article merely scratches the surface of the abundant countervailing literature ignored by ACOG and available to challenge thE admissibility of NENO. Marshalling those resources will shed light onto Constellation Nebula and reveal it for the defense litigation smoke-screen it truly is.

[1] Everything old is new again; as Joel Cunningham succinctly put it, “[i]n the area of birth-injury cases, the purpose of most of the litigation literature is to try to convince judges and juries of two things: (1) Depriving babies of oxygen during the birth process almost never causes brain injury; and (2) nothing an OB does or does not do can cause or prevent a baby from suffering a brain injury.” Cunningham, Joel. “The Litigation Literature.” Trial News, Volume 39-2. October 2003.

[2] Neonatal Encephalopathy and Neuro – logic Outcome (2nd Ed.), ACOG, March 2014, p. xxi-xxii.

[3] 2nd Ed., Executive Summary, p. xxii.

[4] Odd, D.E. et al., (2009). “Resuscitation at birth and cognition at 8 years of age: a cohort study.” Lancet, 2009 May 9, 373 (9675):1615-1622; R. & Cooper, D., et al, (2012). “Perinatal cyanosis; long term cognitive sequelae and behavioral consequences.” Applied Neuropsychology Child. 1(1)48-52.

[5] Badawi, N., et al. (1998). “Intrapartum risk factors for newborn encephalopathy: the Western Australian case control study.” BMJ, 317(7172), 1554-1558.

[6] Martinez-Biarge, M., et al, (2013). “Antepartum and intrapartum factors preceding neonatal hypoxic-ischemic encephalopathy.”

[7] Wayock, C.P. (2014). “Perinatal risk factors for severe injury neonates treated with whole-body hypothermia for encephalopathy. Amer. J. Obstet. Gynecol.; Jul;211(1):41.e1-8. doi: 10.1016/j.ajog. 2014.03.033.

[8] Malin GL, Morris RK, Khan KS. Strength of association between umbilical cord pH and perinatal and long term outcomes: systemic review and meta-analysis. BMJ 2010;340:c1471.

[9] Korst, L.M. et al.¸(1999). “Acute fetal asphyxia and permanent brain injury: a retrospective analysis of current indicators.” Journal of Maternal and Fetal Medicine, 8 (3), 101-106 (finding 60% of neonates did not reveal metabolic academia); Jonsson, M., et al., (214). “Suboptimal care and metabolic academia is associated with neonatal encephalopathy but not with neonatal seizures alone: a population based clinical audit” (finding a rate of 40% without metabolic academia).

[10] Mohammed, L. et al. Multi-Organ Dysfunction in Neonates with HypoxicIschemic Encephalopathy, Med. J. Cairo Univ., Vol. 78, No. 1, December 461-467, 2010

[11] Phalan, J.P., et al., (1998). “Intrapartum fetal asphyxia brain injury with absent multiorgan system dysfunction” Journal of Maternal Fetal Medicine. 7, 19-22.

[12] Korst, L.M. et al.¸(1999). “Acute fetal asphyxia and permanent brain injury: a retrospective analysis of current indicators.” Journal of Maternal and Fetal Medicine, 8 (3), 101-106.

[13] Garite, Thomas J. Electronic Fetal Heart Rate Monitoring – Risks, Benefits, Future and Strategies to Avoid Pitfalls. Maternal Fetal Medicine, Touch Briefings, 2008, p. 60-62.

[14] Macones et al. The 2008 national Institute of Child Health and Human Development workshop report on electronic fetal monitoring: update on definitions, interpretations, and research guidelines. J Obstet Gynecol Neonatal nurs. 2008 Sept-Oct; 37(5); 510-5.

[15] Intrapartum Fetal Heart Rate Monitoring: Nomenclature, Interpretation, and General Management Principles. ACOG Practice Bulletin No. 106, American College of Obstetricians and Gynecologists. Obstet Gynecol. 2009 Jul; 114(10;192-202).

[16] Murray, et al. On NIG Workshop Report. J. Obstet. Gynecol. Neonatal Nurs. 2009; 38(1):4-5.

[17] Ater, Stewart & Jill Hunter. Compre – hensive Cerebral Ischemic Encepha – lopathy Associated with Excessive Uterine Activity (2014).

[18] MK Kunz et al., Incidence of uterine tachysystole in women induced with oxytocin, 42(1) J. Obstetric Gynecologic & Neonatal Nursing 12-18 (Jan 2013).

[19] Schwarcz RL, Strada-Saenz G, Althabe O, Fernandez-Funes J, Caldeyro-Barcia R. Pressure Exerted by Uterine Contractions on the Head of the Human Fetus During Labor (1969) In: Perinatal factors affecting human development. Pan Am Health Organ Sci Publi, pp 115-126.

[20] A.P. Harris, et al, Cerebral and Peripheral Circulatory Responses to Intracranial Hypertension in Fetal Sheep, 64 Circulation Research 991-1000 (1989); A.P. Harris et al., Efficacy of the Cushing Response in Maintaining Cerebral Blood Flow in Premature and Near-Term Fetal Sheep, 43 Pediatric Research 50-56 (1998); O’Brien, et al, Effect of Cephalic Pressure on Fetal Cerebral Blood Flow, 1 Am. J. Perinatology 223-226 (1984).