An open letter to obstetricians about fetal asphyxia from a pathologist’s perspective.

I have been a perinatal pathologist for over 30 years and an expert witness in approximately 600 obstetrical malpractice cases. Because I try to be honest and unbiased, I am often a plaintiff’s witness because I cannot find evidence to substantiate many claims made about placental pathology. Yet, I think there is a strong case to be made that obstetricians are not guilty in the vast majority of “bad baby” cases based on our scientific understanding, and the incompleteness of our knowledge, of fetal asphyxia (suffocation).

First, consider the history of the association of cerebral palsy and birth complications. The first observations were by John Little who recorded his experiences with children on whom he performed percutaneous tenotomy to relieve spasticity. Even back then he proposed that suffocation was a probable etiology. Perhaps modern studies of fetal asphyxia began the experimental manipulation of guinea pigs by Dr. Windle, who demonstrated the wide variation in fetal neurological outcome with experimental conditions of directly applied intrauterine anoxia by cord or uterine arterial clamping. In the 1950’s Dawes and other physiologists developed a precise experimental model of asphyxia in monkeys. They covered the mouth and nose immediately at birth, preventing respiration, and then followed the physiologic and neurologic consequences. In the vicinity of 15 minutes of such asphyxia, the infants would begin to develop brain damage.

There was a serious problem with these studies: the brain injury was an isolated neuronal necrosis, not the wide sheaths of necrosis of white and gray matter seen in the brains of children with cerebral palsy. An explanation of this discrepancy was discovered on an island off of Puerto Rico in a studies led by Dr. Ron Myers in the 1960’s. The epiphany came, at least as published, from a single experimental animal. The mother had become agitated and acidotic from the anesthesia just prior to performing the usual experiment. The fetus developed not the expected neuronal necrosis but extensive white gray matter necrosis. Other experimental manipulations that produced a more prolonged mild fetal acidosis followed by cardiovascular collapse or acute total asphyxia, led to brain injury similar to that seen in cerebral palsy. Dr. Myers went on to refine these studies and describe 4 patterns of brain injury depending on the pattern of asphyxia. However, there are two key points: 1) The state of the infant prior to an acute asphyxial event determines the outcome and 2) The development of the extensive white gray brain lesion likely occurs very quickly during a collapse of cardiac perfusion. Dr. Myers once told me that the most difficult problem in his experiments was that the fetal monkeys often died during the procedures because death quickly followed the conditions of brain injury.

The practical conclusions are that the 15-minute window to prevent brain injury only occurs in a previously non-acidotic animal. Once cardiac decompensation occurs in a partially asphyxiated infant, there is very little time to rescue the infant. There is no way to predict by current technology the prior degree of brain acidosis and potential for brain swelling after rescue. Unless we a willing to preform Cesarean section on all infants with repetitive late decelerations or deep variable decelerations as soon as detected, there will be infants who cannot be successfully rescued in time to prevent brain injury. This makes delivery of infants at risk  of cerebral palsy a game of Russian roulette.

As an anatomical pathologist, I can’t help thinking that a better approach is to understand the exact anatomy causing intrauterine asphyxia. The delivery of one of my own daughters was a case in point. Her tracing was showing deep variables. I was fortunate to be working with some very smart and innovative fetal maternal medicine physicians. One of whom, using ultrasound found the equivalent of an occult cord prolapse that was being stretched and compressed with each contraction. He reasoned that this was not going to improve and my wife and I agreed to go ahead with a Caesarian section before the tracing showed more severe changes.  I believe this was the correct decision, and more importantly I think it is potentially a generalizable and logical strategy for managing non-reassuring fetal heart tracings. Some causes may be treatable my manipulation of the position of the cord, providing maternal oxygen, or developing novel ways to operatively change fetal or umbilical cord position. In others, Caesarian section may be indicated before fetal cardiac collapse and brain necrosis can occur.

I am a pathologist, so this suggestion is certainly presumptuous. I would like to know how often during an abnormal fetal heart tracing the obstetrician knows the anatomic conditions causing the tracing. I do understand that in some infants, particularly with intrauterine growth restriction, the fetus may not be able to compensate for contractions of labor and become acidotic. In many cases, I suspect anatomic compromise of umbilical cord blood flow is an important component of fetal asphyxia both in labor and in unexplained fetal death.

In an attempt to understand umbilical cord compromise, a medical student and I set up an arrangement for in vitro flow through umbilical cords. We did not have a specific agenda, but just borrowed a plastic baby doll, and started manipulating. Eventually we switched to PVC pipe pieces of fixed diameter. The conclusion of our study was that if the cord was wrapped around a pipe and then the remaining end twisted, the only important factor in stopping flow was the distance from the end of the wrapping to the end of the cord. In other words, the shorter the cord segment, the less torsion needed to stop flow. This is perhaps a self evident conclusion in that twisting a short versus a long segment increases the pitch, that is the twist per cm, and it is likely that the pitch determines when the vein will collapse. In vivo, our experimental length would correspond to the distance from the placenta to the first wrapping of the cord. This wrapping creates a short cord, as can be seen with tightening of a nuchal cord at delivery.

I don’t propose wrapping as the only mechanism of umbilical flow compromise or of fetal asphyxia. I did review the literature and I think there is room for increasing our understanding of the basic mechanisms that can occlude such flow. My only goal is to encourage investigation of the correlation of the fetal heart rate tracing with the real time cord anatomy in patients with abnormal heart tracings.

This same concern with the actual anatomy of asphyxia also applies to understanding stillbirth. Using abruption as a model of the findings in the infant of fetal asphyxia, the same visceral findings associated with asphyxia from placental separation occur in many unexplained stillbirths. This is not surprising given the limited number of things that can actually kill a fetus in utero. Yet, we have made little progress in understanding or preventing this asphyxia. I would plea that best time to investigate the anatomic details of “cord accidents is while the fetus is still in utero. In fetal death there is no Doppler image of umbilical cord blood flow, but recent reports demonstrate detailed visualization of the umbilical cord with an MRI. Adding an MRI study to an open ended clinical history and an expert autopsy could provide a better understanding of many stillbirths.

Fetal asphyxia is not something to fear as a potential for litigation. Quite the opposite, further research and understanding of the anatomic and physiologic causes in patients is the key to reducing infant morbidity and mortality, and reducing unjustified law suits.

 

 

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