Fetal monitoring experts have long understood the mechanism of early decelerations as a simple reflex response to transient compression of the fetal head during labor. The fact that they are unrelated to any type of oxygenation issue for the fetus is evident in that early decelerations are the only deceleration that is allowed in a category 1 (normal) fetal heart rate tracing. But there is a theory regarding head compression gaining traction in birth injury cases. The concept is based on a hypothesis that extracranial pressure occurring during uterine contractions or maternal pushing can result in neurologic injury to the infant that does not necessarily present at birth but rather shows up later, well after the neonatal period. This theoretical mechanism of injury has even been given a very scientific sounding name, cranial compression ischemic encephalopathy (CCIE).1 While this theory may have an impressive name, it has no valid scientific basis. Unfortunately, the lack of scientific evidence to support CCIE has not prevented the theory from being successfully used by the plaintiffs' bar. Plaintiffs' allegations related to this theory of injury will often revolve around excessive uterine activity, prolonged labor, prolonged pushing or second stage, early decelerations, and use of uterine stimulants such as oxytocin. To effectively defend against these allegations, clinicians must understand the basis of the CCIE hypothesis and be able to articulate the lack of evidence for such allegations. This column discusses the basic tenets of the concept and provides clinicians with resources for debunking allegations of fetal head compression during labor as a cause of brain damage when there is no evidence of compromise at birth.

During labor and birth, extracranial pressure from both uterine contractions and maternal expulsive efforts is exerted on the fetus. The CCIE theory hypothesizes increased intracranial pressures from the normal extracranial pressures during labor result in hypoxic-ischemic brain injury even in a normally oxygenated fetus, and without evidence at delivery of the usual correlates to poor neonatal outcome such as low Apgar scores, metabolic acidemia in umbilical arterial cord blood, or a need for resuscitation at birth. The premise is that the pressure of uterine contractions and/or pushing efforts of the mother force the fetal head against the maternal pelvis hard enough to cause the fetus' intracranial pressure to surpass cerebral perfusion pressure and result in focal points of cerebral ischemia and injury, including cerebral palsy (CP).1-4

Recently, Heyborne published a systematic review using a 3-stage framework to address the evidence related to the CCIE theory.* The 3 questions forming the basis of the review are as follows4:

1. What is the effect of uterine contractions or maternal pushing efforts on extracranial pressure?

2. Is extracranial pressure transmitted across the cranium resulting in increased fetal intracranial pressure?

3. How would increased intracranial pressure (if it occurred) impact the fetal brain?

Following an exhaustive literature review in each of these 3 areas of inquiry, Heyborne concluded that while there can be extracranial pressures as high as 120-500+ mm Hg during the intrapartal period, such pressures are "not directly transmitted to the fetal intracranial space" and that the fetal brain is "well-protected from extracranial forces that occur during labor."4^(pe83)

The fact that the scientific evidence does not support this particular theory of causation for ischemic brain injury or CP is not preventing it from being used successfully in birth injury cases. A simple Web search of "head compression in labor causes brain damage" will result in several advertisements for plaintiffs' attorneys, some with graphic illustrations and seemingly scientific monographs on the subject. Clinicians and risk managers should proactively take steps to prepare for the defense of allegations tied to the CCIE theory. Recommendations for healthcare enterprises from a risk management perspective include the following:

1. Ensure that risk managers, nurses, midwives, and physicians are aware of the CCIE theory and educated regarding the lack of scientific validity.

2. All clinical staff, regardless of background, should be comfortable discussing the normal physiology of labor and should possess a good understanding as well as an ability to articulate the physiology of uterine activity during the different phases and stages of labor, as well as the relationship of uterine activity to fetal acid-base.

3. Multidisciplinary fetal monitoring education should include the specific mechanisms of various deceleration types, as well as their relationship to the fetal oxygen pathway; clinicians should be comfortable explaining the information in plain language.

4. Second-stage pushing and labor support should be well-documented, and the open-glottis style of pushing should be the primary method employed.

5. If litigation arises and the CCIE theory is offered related to causation, the defense should retain experts familiar with the theory and the evidence against its validity; clinicians should be adequately prepared for deposition questions on CCIE and related allegations such as excessive uterine activity or improper management of first- or second-stage labor.

In closing, while the burden of proving obstetric malpractice clearly falls on the plaintiff, junk science such as the CCIE theory can create serious problems for the defense of an unwarranted or frivolous claim. The best defense approach is a knowledgeable and well-prepared team of nurses, midwives, and doctors who understand the physiology and can comfortably, yet authoritatively, rebut the allegations during deposition and trial.

-Lisa A. Miller, CNM, JD

Founder

Perinatal Risk Management and Education Services

Portland, Oregon

References