YOUR LEGAL RIGHTS WHEN OXYGEN LOSS INJURES YOUR BABY AT BIRTH
June 12th, 2025By David A. Bowling and Lauren P. Jones
A Multipart Series from the Bowling Law Firm, APLC
I. Introduction
As a firm with a major concentration in the representation of families of children who have suffered hypoxic-ischemic encephalopathy (“HIE”) and/or cerebral palsy, The Bowling Law Firm is frequently faced with challenges from defendants arguing that the birthing process was not the cause of our clients’ babies’ neurologic injuries.
We must confront contentions that the brain injuries were due to processes prior to labor and delivery, events after labor and delivery, infection, genetic or metabolic derangements, or a myriad of alternate proposed causes.
The obstetrical community, led by the American College of Obstetrics and Gynecology (“ACOG”), has a substantial interest in defeating claims of birth injury and has issued multiple publications setting forth rather stringent criteria which obstetricians assert must be satisfied before an injury can be said to be causally related to intrapartum events.
It is fair to argue that the ACOG publications are biased towards protecting the interests of its member obstetricians rather than the families of injured children which we represent.
Moreover, in at least several respects, there is a scientific basis to assert that not all the ACOG criteria always apply.
Nevertheless, as attorneys handling birth injury cases, the published ACOG criteria cannot be breezily dismissed or taken lightly. They must be thoroughly understood by the practitioner handling HIE and cerebral palsy anoxic/hypoxic birth injury cases.
II. The ACOG Criteria
In 2003, the Task Force on Neonatal Encephalopathy and Cerebral Palsy issued its report which handed down criteria which the Task Force indicated should be satisfied before it could be said that a child’s cerebral palsy was caused by an intrapartum hypoxic event. (Hankins, G. Neonatal Encephalopathy and Cerebral Palsy. ACOG/AAP. 2003.)
In 2014, the Task Force renamed the work “Neonatal Encephalopathy and Neurologic Outcome” for the Second Edition and recognized 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.” (D’Alton, M. Neonatal Encephalopathy and Neurologic Outcome. Second Edition. ACOG/AAP. 2019; p. XXI-XXII.)
In other words, the Task Force criteria are now a bit less rigid than originally formulated. ACOG takes a more flexible approach in which a broad array of factors is included in the causation assessment.
The threshold factor (“I. Case Definition”) to be considered is whether there is a meeting of the definition of neonatal encephalopathy, which is a “clinically defined syndrome of disturbed neurologic function in the earliest days of life in an infant born at or beyond 35 weeks of gestation, manifested by a subnormal level of consciousness or seizures, and often accompanied by difficulty with initiating and maintaining respiration and depression of tones and reflexes.”
Assuming the case definition is met, a series of factors regarding the baby (“II. Neonatal Signs Consistent with an Intrapartum Event”) are to be assessed.
One of the factors to be considered—although no longer an essential criterion—is the Apgar score. The Apgar score is a measure of the newborn infant’s physical condition.
Points are scored for heart rate, respiratory effort, muscle tone, response to stimulation, and skin coloration.
It is measured serially at one minute after birth, and again at five minutes.
A score of 7 to 10 is considered normal and indicates good health without the need for anything more than routine postdelivery care. The Task Force states that “if the Apgar score at five minutes is greater than or equal to 7, it is unlikely that peripartum hypoxia-ischemia played a major role in causing neonatal encephalopathy.”
The cord arterial blood gas value is an additional neonatal factor to be considered.
Cord blood gas analysis in a newborn tests a baby’s acid-base status. Since low oxygenation (hypoxia, or its more severe form, anoxia) results in blood that is too acidic (acidemia), the blood gas results can give information regarding the oxygenation status of the fetus during the labor and delivery process.
The Task Force establishes that a base deficit* greater than or equal to 12 increases the probability that neonatal encephalopathy, if present, had an intrapartum hypoxic component.
Another important consideration to assess for an intrapartum event is the imaging evidence.
According to ACOG, “MRI is the neuroimaging modality that best defines the nature and extent of cerebral injury in neonatal encephalopathy.”
The Task Force 2014 article goes on to state that “distinct patterns of neuroimaging abnormalities are recognized in hypoxic-ischemic cerebral injury in the infant born at or beyond 35 weeks of gestation and have prognostic value for predicting the later neurodevelopmental impairments.
If the results of the MRI or magnetic resonance spectroscopy obtained after the first 24 hours of life are interpreted by a trained neuroradiologist and no area of injury are noted, then it is unlikely that significant peripartum or intrapartum hypoxic-ischemic brain injury was a significant factor in neonatal encephalopathy.”
Testimony from neuroradiologists is almost invariably required in cerebral palsy/HIE cases to establish that the injury was caused by hypoxia and/or anoxia in the birthing process.
Although not a requirement for establishing the connection between labor and delivery and brain injury, ACOG also indicates that involvement of other organ systems can be a sign of intrapartum hypoxia. Quite often, this can be established by lab results showing kidney or liver injury.
After an assessment of these neonatal signs, the Task Force’s model moves to an assessment of “Type and Timing of Contributing Factors That are Consistent with an Acute Peripartum or Intrapartum Event.” A “sentinel event” such as a uterine rupture, severe abruptio placentae, umbilical cord prolapse, or maternal cardiovascular collapse would be deemed consistent with an intrapartum event.
But there are other ways that hypoxic or anoxic birth injuries can be caused, and in this respect, the Task Force article focuses on fetal heart rate monitoring which is the focal point of birth injury cases.
“Fetal heart rate monitor patterns consistent with an acute peripartum or intrapartum event” must be considered. The Task Force states a fetus which shows an abnormal heart rate pattern on initial monitoring likely has a pre-existing injury and that the outcome may not be improved by urgent delivery.
However, “the patient who presents with a category I (normal) fetal heart rate pattern that converts to category III (abnormal)… is suggestive of intrapartum timing of a hypoxic – ischemic event.” (D’Alton, M. Neonatal Encephalopathy and Neurologic Outcome. Second Edition. ACOG/AAP. 2019; p. 210.)
The Task Force suggests that in addition to determining whether the imaging shows damage, the imaging should be assessed to determine if the “Timing and Type of Brain Injury Patterns Based on Imaging Studies [is] Consistent with an Etiology of an Acute Peripartum or Intrapartum Event.”
This recognizes that brain damage evolves over time, with certain signs appearing at certain times after the insult occurs. Thus, the imaging evidence, although inadequate to precisely define the time of the insult, can often narrow the timeframe into a window of time which can include or exclude the labor and delivery period.
Again, The Bowling Law Firm frequently calls upon experts in the field of neuroradiology to assist with our birth injury cases.
There should also be an assessment of whether there is “no evidence of other proximal or distal factors that could be contributing factors.”
As stated from the outset, other potential explanations for brain injury will be offered by the defense, and the lawyer representing the patient’s family must be prepared to address questions of whether alternative causes could have accounted for the injury: infection, metabolic derangement, pre-existing injury, genetic abnormality, etc.
Finally, the Task Force suggests that consideration should be given to whether the “Developmental Outcome is Spastic Quadriplegia or Dyskinetic Cerebral Palsy.”
In this respect, even if the baby has cognitive deficits which meet other criteria for establishing an intrapartum cause, a child without motor deficits in the extremities will be met with expert testimony from the defense that the child could not have been injured in the birthing process.
There is, of course, a counter argument to this, but that is a matter for another installment of this series.
III. Conclusion
The framework for assessing causation set forth by the ACOG Task Force will likely be considered by the court and the jury in assessing a case alleging brain injury, hypoxic ischemic encephalopathy, and/or cerebral palsy from the birthing process.
This does not mean that the ACOG criteria must be perfectly met for a case to be successful.
To use but one example, although most babies injured due to hypoxia/anoxia during birth will have abnormal Apgars, some children who suffer neurologic devastation due to malpractice during labor and delivery will have normal Apgar scores.
And this topic will be the subject of the next installment of this series, Proving Causation In Hypoxic Ischemic Encephalopathy/Cerebral Palsy Birth Injury Cases.
