A Refutation of ACOG’s Report on Cerebral Palsy

By George M. Morley, M.B., Ch. B., FACOG Cordclamping.com

A major error in modern obstetrical practice is routine premature clamping of the umbilical cord. Thousands of obstetricians have been taught that immediate cord clamping is an acceptable, standard obstetrical procedure, and millions of newborns have been subjected to it. Cerebral palsy (CP), along with other injuries, can result from premature cord clamping.

A task force of the American College of Obstetricians and Gynecologists (ACOG) issued a report on Neonatal Encephalopathy and Cerebral Palsy; the chairman states: "Scientific evidence shows that neonatal encephalopathy and cerebral palsy are largely not caused by labor and delivery events." The president of ACOG says the report is useful for educating doctors, parents and jurors and that "adverse outcome has nothing to do with medical negligence or error." The report offers doctors legal care; for patients, there is little hope, the causes of brain damage are "unpreventable."

In relation to the report, the January 2003 "Obstetrics & Gynecology" ("Green Journal") published a "knowledge survey" of OB’s [1] on the etiology and pathophysiology of neonatal encephalopathy and its relationship to CP. "Don’t know" was the most frequent response to the multiple-choice questions. The task force chairman also admits that the "true genesis ... of these injuries" has not yet been defined; he also states "most cases of CP are the result of multi-factorial and unpreventable causes that occur either during fetal development or in the newborn after delivery." In fact, the true genesis of these injuries is clearly illustrated in the correct answers to his questions:

"In cases of intrapartum asphyxia sufficient to result in cerebral palsy, injury to organ systems other than the brain ... results from redistribution of cardiac output in an effort to achieve brain sparing."

In other words, "In cerebral palsy cases that follow intrapartum asphyxia, the brain is the last organ to be damaged by deficient cardiac output." This is a classic description of the sequential organ injury to kidneys, liver, lungs, heart and then the brain, caused by hypovolemic shock. Intrapartum asphyxia is most frequently due to cord compression (e.g. tight cord around the neck) that impedes cord venous blood flow (the child’s oxygen supply) and shifts fetal blood volume to the placenta; the child is typically born limp and pallid blue--in shock. Asphyxia is coupled with hypovolemia. Such neonates seldom exhibit signs of brain damage immediately, they do not convulse at birth.

ACOG Practice Bulletin 138 (B138) states:

"Immediately after delivery of the neonate, a segment of umbilical cord should be doubly clamped, divided and placed on the delivery table pending assignment of the 5-minute Apgar score."

ACOG’s routine treatment (B138) of these depressed neonates is immediate cord clamping to obtain cord blood pH studies. The child’s only functioning source of oxygen--the placenta--is amputated together with 30 percent to 50 percent or more of its natural blood volume. Total asphyxia is imposed until the lungs function, and the depressed (asphyxiated, hypovolemic) child starts its extra-uterine life in hypovolemic shock.

Immediate ventilation may not reverse the asphyxia if there is not enough blood volume to perfuse the pulmonary blood vessels adequately; thus the immediately clamped neonate is very prone to hypoxia and ischemia--and to hypoxic ischemic encephalopathy (HIE). An Apgar score of less than seven at five minutes is an indicator of future neurological defect [2].

By relieving the cord compression, (unwinding the cord from around the neck, loosening the true knot) placental circulation reverses the asphyxia and placental transfusion rapidly reverses the hypovolemia. Pulmonary resuscitation with the placental circulation intact will usually result in a pink, crying newborn (with an intact brain) within five minutes. Transfusion of oxygenated placental blood that increases blood volume by less than 50 percent prevents hypoxic, ischemic injury.

The brain of the immediately clamped, depressed newborn is very probably uninjured at birth. Deterioration into encephalopathy is certainly multi-factorial. Deficient brain perfusion (ischemia) due to hypovolemia, low cardiac output and low blood pressure is the central factor. Hypoxia and acidemia due to poor lung perfusion are additional factors as is renal shut-down.

Hypoglycemia probably results from inadequate perfusion of the liver, causing deficient conversion of glycogen into glucose. The areas of the brain that are the most metabolically active suffer first--from hypoxia, acidosis and loss of nutrients, all compounded by inadequate tissue perfusion. Depending on degree, neuron necrosis may involve the whole cortex, or it may be very limited to one of the brain-stem nuclei or the germinal matrix. These lesions are, in essence, infarcts, necrosis resulting primarily from inadequate tissue perfusion.

The multiple factors involved are NOT, as ACOG claims, unpreventable; they can all be avoided completely by not clamping the umbilical cord.

"Another thing very injurious to the child, is the tying and cutting of the navel string too soon; which should always be left till the child has not only repeatedly breathed but till all pulsation in the cord ceases. As otherwise the child is much weaker than it ought to be, a portion of the blood being left in the placenta, which ought to have been in the child."

--Erasmus Darwin, Zoonomia, 1801 [3]

ACOG recommends and teaches immediate amputation of the placenta at birth to obtain cord blood studies for medico-legal documentation; the results have no bearing on child care. B138 was first published in 1993. Every cesarean section baby, every depressed child, every premie, and every child born with a neonatal team in the delivery room has its cord clamped immediately to facilitate the panicked rush to the resuscitation table. The current epidemic of immediate cord clamping coincides with an epidemic of autism.

By adopting Erasmus Darwin’s resuscitation method for all births and by obtaining birth blood studies from a heel stick, healthy babies with intact brains would be the routine and lawsuits would disappear. However, OB’s "don’t know;" ACOG and the "Green Journal" teach them not to know. For the trial lawyers, it is essential that the "true genesis" of cerebral palsy remains unknown, because that "true genesis" (B138) is a standard of medico-legal care; thus, no obstetrical fault exists; the medico-legal professions are at fault.

ACOG’s "cases of intrapartum asphyxia sufficient to result in cerebral palsy" do not, therefore, necessarily need to end in "unpreventable" tragedy. Fetal cord compression, such as occurs in cord prolapse, produces definite signs on the fetal heart rate (FHR) monitor; these are late FHR decelerations and prolonged FHR decelerations. If these are not corrected, and if they are neglected and progress, fetal brain damage will eventually occur, rapidly followed by fetal demise. Prompt diagnosis, prompt delivery and resuscitation with the placental circulation intact will result in a normal child (see Figure B).

This pathology and its correction by means of physiology can be demonstrated at any "normal" delivery as follows:

The scalp FHR lead should be left attached, the child delivered gently into a warm blanket, and the umbilical cord immediately closed between finger and thumb about 10 centimeters from the umbilicus.

The FHR will decelerate quickly to about 60 bpm and the cord vein between thumb and umbilicus will empty completely into the child. If the child does not breathe or cry, the heart rate will remain low, and the color will change from purple-pink (normal at birth) to pallid blue (vaso-constriction and asphyxia). Eventually, the normal child will gasp and start breathing due to high CO2 levels; the heart rate will increase, the color may improve, but the pallor will persist.

Few midwives or obstetricians will be able to observe, without interference, a deep, prolonged FHR deceleration on a non-breathing newborn for a period of 60 seconds. Common sense will soon release the finger and thumb. Watch the cord vein distend while the child receives the placental transfusion. When breathing starts, the pallid, purple child will turn a ruddy pink, the deep, prolonged FHR deceleration will rapidly recover, and in a minute or two the Apgar score will be 10 or higher. This ruddy-pink, squirming, bawling child with an intact cord has a normal blood volume.

On the other hand, some, following the ACOG and trial lawyers’ protocol B138, may immediately doubly clamp and cut the cord (distal to the compressing thumb) and send a sample to the lab for cord blood gases; this child will be pale, somewhat slow to respond and may have some retraction respiration--this "normal" child is missing a large portion of its normal blood volume.

In each scenario, a deep, long FHR deceleration "indicating asphyxia sufficient to cause brain damage" will be recorded on the monitor strip. In the first scenario, the effects are temporary, completely reversed and of no significance; in the second, one may have to wait until the child is in grade school to prove that the prolonged hypovolemia and subsequent anemia did not affect the integrity, growth and development of the child’s brain [4]. If the five-minute Apgar score is below seven, the neurological prognosis is poor [2]. Match the FHR tracing with that in Figure A.

Figure A [5] shows the effects of immediate cord clamping and imposed pulmonary asphyxia on a monkey. Figure B [5] shows the results of fetal asphyxia (generated by maternal anoxia) followed by resuscitation without cord clamping--with the placental circulation intact. Monkeys treated according to Figure A developed cerebral palsy after a long FHR deceleration. The monkey in Figure B was normal after a long FHR deceleration.

Immediate cord clamping (ICC) at birth was used routinely in these primate studies to produce asphyxia and brain damage; ICC is used routinely on human newborns to obtain cord blood specimens for medico-legal use.

In Figure A, very low blood pressure results in ischemic brain damage. In Figure B, blood pressure (blood volume) maintains brain perfusion despite hypoxia.

Professor Peltonen [6] studied (fluoroscopically) the effects of cord clamping before the first breath and noted virtual cardiac collapse due to decreased venous return until blood flow through the lungs occurred. He concluded:

"On the basis of these observations, it would seem that the closing of the umbilical circulation before aeration of the lungs has taken place is a highly unphysiological measure, which should thus be avoided. Although the normal infant survives without harm, under certain unfavorable conditions the consequences may be fatal."

It would appear that Peltonen immediately clamped the cord of an already compromised neonate that promptly had an irreversible cardiac arrest, and he decided never to do it again; ACOG Bulletin advises ICC on all compromised neonates. Most normal infants do survive ICC without apparent harm. Placental transfusion [7] is generated mainly by gravity or by uterine contraction. At normal delivery, the contraction that delivers the child may simultaneously squeeze into the child an adequate blood volume; some transfusion may occur in the second stage of labor when half the child is in the vagina while the placenta is being compressed.

If the child is delivered from the squatting position, downward, gravity will effect transfusion before a fast clamp can be applied. However, as long as pulsations are present, blood is flowing into the placenta, and return flow into the child is not guaranteed, especially if the vein is compressed. Natural cord closure does guarantee a blood volume optimal for survival [7].

Preemies, cesarean deliveries and especially the cord-compressed neonates are very likely to develop pathological hypovolemia following ICC. Natural cord closure will not heal brain damage incurred before delivery such as is seen in long decelerations caused by abruptio placenta; however, placental transfusion in such cases may halt progression of the injury.

Regarding cutting a cord that is around the neck:

"Let the loop be loosened to enable it to be cast off over the head ... [or] by slipping it down over the shoulders. ... If this seems impossible, it should be left alone; and in the great majority of cases, it will not prevent the birth from taking place, after which the cord may be cast off. ... Should the child be detained by the tightness of the cord, as does rarely happen, ... the funis may be cut. ...

" Under such a necessity as this, a due respect for one’s own reputation should induce him to explain, to the bystanders, the reasons which rendered so considerable a departure from the ordinary practice so indispensable. I have known an accoucheur’s capability called harshly into question upon this very point of practice. I have never felt it necessary to do it but once. ... The cord should not be cut until the pulsations have ceased."

--Charles D Meigs, M.D., 1842 [8]

One hundred and fifty years ago, ICC was regarded as malpractice. No publication since has contradicted Professor Meigs or Erasmus Darwin.

During 2002, ACOG published two articles [9,10] on HIE. Of the 284 neonates studied, all had confirmed HIE, all except six had cords clamped immediately as cord blood pH values were recorded on each child, and the six without cord pH values almost certainly had ICC to rush them to resuscitation. Therefore:

• All 284 neonates in the studies had ICC.
• Every neonate was hypoxic until the lungs functioned.
• Every neonate was deprived of up to 50 percent of its natural blood volume.
• Every neonate was deficient in oxygen transport capacity.
• Every neonate was subjected to hypoxia and ischemia (hypovolemia) after birth.
• All 284 neonates developed HIE after birth.
  

One of the studies reported synchronous damage to the heart, liver and kidneys that is typical of injury occurring in hypovolemic shock. Thus ACOG has published virtual proof that ICC causes brain damage; absolute proof will be provided by a study on similarly depressed neonates that are resuscitated with the placental circulation intact and none develop HIE (see Figure B).

The birth brain injury litigation bonanza for trial lawyers began with fetal monitoring in the 1960s; it also spawned the neonatology and perinatology professions. Expert detection and handling of fetal distress and fetal resuscitation by specialists were expected to prevent brain damage and subdue the litigation crisis. After more than 30 years of intensive study, investigation, publication, education, litigation and billions of dollars down the drain, the "Green Journal" now publishes a "knowledge survey" revealing that most practicing obstetricians "don’t know" much about neonatal brain damage.

As mentioned above, the author of the report admits that the "true genesis" of these injuries is not defined, and ACOG reports that most brain damage is "unpreventable." The members of the study may be indoctrinated with the ACOG dogma that the cord clamp is harmless and that placental transfusion is pathological. ICC is the true genesis of HIE and the subsequent cerebral palsy; ICC is preventable, as is CP.

Parents, patients and practicing obstetricians suffer lifelong misery from this failed multi-factorial and multi-professional enterprise that was supposed to save newborn brains. The medico-legal professions, perinatal specialists and obstetrical academia continue to benefit. The lay public has no problem comprehending that immediate amputation of a functioning placenta is harmful to the newborn child.

Not one publication over the past 200 years, peer reviewed or otherwise, endorses the practice of immediate cord clamping; all relevant articles and opinions condemn it, yet ACOG and trial lawyers promote it to practicing obstetricians for medico-legal protection. ICC has become standard practice, and obstetricians who want to treat the child correctly are placed in the dilemma of choosing legal self-protection and chancing newborn injury, or losing legal protection by violating the standard of care.

To end this dilemma and the medico-legal terror and suffering, patients should demand, and practicing obstetricians should provide, an informed consent document stating that the newborn’s cord will not be clamped until all pulsations have ceased and until the child is breathing and pink and that resuscitation, if needed, will be done with the placental circulation intact.

A scalp or heel blood sample at birth to confirm oxygenation status is just as valid as a cord blood sample. The practicing obstetricians may thus be able to restore some semblance of dignity and respect to their profession by discarding and ignoring the advice of their tort counselors, academic peers, publishers and sub-specialists. The scarcity of injured newborns and empty NICU’s may have a very negative impact on various parties; the abundance of healthy babies will be welcome news to everyone else.

My letters published in the "Green Journal," June 2001, asking ACOG to provide an informed consent document for B138 remain unanswered, as do formal complaints regarding B138 to ACOG and the AMA. These parties have remained silent, and they have the right to remain silent; their silence speaks louder than words. ACOG’s report on cerebral palsy is either a colossal error or a grotesque attempt to cover up B138.

George M. Morley graduated from Edinburgh University Medical School in 1957, completed a residency in OB/GYN in 1962, and practiced obstetrics and gynecology until his retirement in 1999. He is board certified in OB/GYN, and a Fellow of the American College of Obstetrics and Gynecology.

© Copyright G. M. Morley, M.B., Ch.B., FACOG, April 2002