How the Cord Clamp Injures Your Baby’s Brain

By George Malcolm Morley, M.B., Ch.B., FACOG (morley@cordclamping.com)

This paper describes a major error in modern obstetrical practice, namely, routine premature clamping of the umbilical cord. Some sections require medical knowledge for full comprehension and the language is very technical, but overall, medical jargon is avoided or explained in terms that most expectant parents can understand. The error was defined very clearly over 200 years ago:

---

"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, (Charles Darwin’s grandfather) Zoonomia, 1801

---

Despite repeated publications illustrating the effects of the error, and official notification, medical academia and its peer review press have yet to acknowledge the possibility of any error. Public exposure and knowledge of the issue is intended to accelerate correction of the error. The nature of the injury caused by this practice unhappily precludes a cure; for the unfortunate parents of an impaired child, the knowledge may assuage any guilt they may have and give them reassurance regarding future births.

Modern obstetrics ignores the normal functions of the cord and placenta from the moment that the child is born, and in most hospitals the umbilical cord is clamped and cut at the earliest convenient time after birth. [1][2] At premature births and when the newborn is depressed or "at risk," immediate cord clamping is routinely performed in order to rush the child to a resuscitation table and to obtain cord blood samples for medico-legal purposes. [3][4] Placental blood, which ought to have been in the child, is either thrown away or used to provide stem cells or other commercial products.

Doctors are taught (and believe) that delayed cord clamping / placental transfusion gives the baby too much blood, (hypervolemia) while neonatal intensive care units (NICU) are filled with weak, fast - clamped newborns exhibiting signs of severe blood loss [5], pallor, hypovolemia (low blood volume) anemia, (low blood count) hypotension (low blood pressure), hypothermia (cold), oliguria (poor urine output), metabolic acidosis, hypoxia (low oxygen supply), and respiratory distress (shock lung) to the point that some need blood transfusions and many more receive blood volume expanders. [2] [5]

At this point, an explanation of the terms anemia, polycythemia, hypovolemia and hypervolemia is required. Blood is a mixture of red cells and plasma, a fluid. Blood is usually about half cells and half plasma. When blood contains too few cells, the term anemia is used; the blood is "dilute." Polycythemia means there are too many red cells "concentrated" blood. The "-volemia" terms refer to the total volume of blood in the child’s heart and blood vessels; blood vessels are elastic and are constantly filled by the heart pumping blood through them, like a long, circular balloon.

Too much blood volume (hypervolemia) overworks the heart and overfills the "balloon." Too little blood volume (hypovolemia) lets the balloon and the heart collapse; it makes no difference if the blood is diluted or concentrated. Anemia and polycythemia are about the quality of blood; hypo- and hyper-volemia are about quantity of blood. An anemic baby may be hypervolemic -too much fluid, and a polycythemic child may be hypovolemic - dehydrated. A normal child that suffers acute blood loss will have a normal blood count and low blood volume (hypovolemia.) During recovery from the hemorrhage, blood volume is restored with fluid (plasma), and the child becomes anemic (diluted blood) as it takes much longer to restore the lost red cells. Early infant anemia is a strong indication that the child has suffered significant previous blood loss.

Before birth, the cord and placenta "breathe" for the baby. Humans and all other mammals have evolved, over millions of years, a very safe mechanism for closing umbilical cords at birth without interrupting "breathing," and ensuring optimal survival of their offspring. An occasional natural accident such as a ruptured cord may rarely occur, but it is biologically impossible for that mechanism to routinely give a child too much, or too little, blood; mammals that routinely give their offspring the wrong amount of blood for survival become extinct in one generation.

Erasmus Darwin’s late clamping method is safe because the tie is placed on vessels that the child has already closed physiologically (by natural constriction) after it has received the right amount of blood; the tie does no harm because it virtually does nothing. Safe cord closure at birth involves closing the placental life support system and starting the child’s life support systems without significant interruption of life support during the changeover process. Oxygen supply and blood to carry the oxygen are crucial to life support; blue blood contains little oxygen, red (pink) blood is saturated with oxygen. Brain cells die quickly from lack of oxygen; they do not regenerate, and asphyxiation (choking / lack of oxygen) for about six minutes will cause permanent brain damage. [6]

Before birth, the lungs are filled with fluid and very little blood flows through them; the child receives oxygen from the mother through the placenta and cord. This placental oxygen supply continues after the child is born until the lungs are working and supplying oxygen -that is, when they are filled with air and all the blood from the right side of the heart is flowing through them. When the child is crying and pink, the cord vessels clamp themselves. During this interval between birth and natural clamping, blood is transfused from the placenta to establish blood flow through the lungs. Thus the natural process protects the brain by providing a continuous oxygen supply from two sources until the second source is functioning well.

Placental blood transfusion occurs by gravity or by contraction of the mother’s uterus which forces blood into the child. [7] Transfer of blood into the child through the cord vein can occur after the arteries are closed (no cord pulsation). The transfusion is controlled by the child’s reflexes (cord vessel narrowing) and is terminated by them when the child has received enough blood (cord vessel closure). The switch from placental to pulmonary oxygenation also involves changing the fetal circulation to the adult circulation - the one-sided heart (body blood flow only) changes to a two-sided heart (blood flows through the lungs, then through the body.) Ventilation of the lungs and placental transfusion effect this change. This is a very basic account of a very complex process. [8] It all happens usually within a few minutes of birth, and when the cord pulsations have ceased and the child is crying and pink, the process is complete. Clamping the cord during the changeover process disrupts these life support systems and may cause serious injury. 

The American College of Obstetricians and Gynecologists (ACOG) and the Society of Obstetricians and Gynecologists of Canada (SOGC) advocate immediate cord clamping at birth [3] [4] before the child has breathed. This instantly cuts off the placental oxygen supply and the child remains asphyxiated until the lungs function. Blood, which normally would have been transfused to establish the child’s lung circulation, [9] remains clamped in the placenta, and the child diverts blood from all other organs to fill the lung blood vessels. [1]

After immediate clamping, the normal term baby usually has enough blood to establish lung function and prevent obvious brain damage, but it is often pale, weak, and slow to respond. Occasionally, a child will cry as soon as the head is delivered, and the uterine contraction that delivers the child may also squeeze in some placental transfusion before the fast clamp can be applied; however, cord clamping before the first breath [9] always causes some degree of asphyxia and loss of blood volume:

1. It totally cuts off the infant brain’s oxygen supply from the placenta before lungs begin to function.
2. It stops placental transfusion -the transfer of a large volume of blood (up to 50% increase in total blood volume) that is used mainly to establish circulation through the child’s lungs to start them functioning.

While ICC is a danger to all newborns, if a child is born asphyxiated and depressed following fetal distress from cord compression (e.g. a tight cord around the neck) [10] immediate cord clamping may very well be fatal. [9][1] A child deprived of oxygenated placental blood before birth is in dire need of oxygenated blood after birth. Immediate clamping in such circumstances [11] often produces a hypovolemic and asphyxiated child who cannot begin to breathe adequately to relieve the asphyxia; oxygen in the lungs will never reach the brain if the newborn does not have enough blood to flow from lungs to brain. [12]

The medical term for the condition that causes cerebral palsy (CP) is hypoxic, ischemic encephalopathy. (HIE) Hypoxic means lack of oxygen - the child has no placental oxygen supply; ischemic means lack of blood flow - half of the child’s blood is in the placenta; encephalopathy means brain damage. HIE is often treated with blood transfusion or blood volume expanders after a large part of the child’s own oxygenated blood has been discarded with the placenta. In addition, babies with HIE usually develop anemia.

The obvious correct way to resuscitate the depressed child is to keep the cord and placenta functioning while ventilating the lungs. [1][9][12] If a child is born depressed with a knot in the cord, should the knot be loosened or tightened? [11] A newborn depressed from lack of blood and lack of oxygen [10] is quickly restored to normal with a large transfusion of oxygenated placental blood and is unlikely to develop HIE. [12] Rapid restoration of oxygenation is crucial in preventing brain damage in the depressed child, and that child must have enough blood to transport oxygen to the brain. If hypoxic brain damage has occurred before birth, placental oxygenation and transfusion will not cure it after birth - nothing will - but progression of the damage will be prevented. Blood transfusion given after the child has developed HIE will not restore the dead brain cells. Blood transfusions given in the NICU are usually examples of "too little and much too late."

Fetal distress (intra-partum asphyxia [13]) from cord compression, such as occurs with a cord prolapsed during labor (a cord squeezed between the head and the cervix,) may be rapidly reversed by relieving the compression - elevating the presenting part (head) or changing the mother’s position. The fetal heart rate and monitor tracing soon return to normal, and at delivery by emergency c-section, the child may show no sign of asphyxiation. The same result can be obtained at birth in a child asphyxiated with a tight cord around the neck by reducing (unwinding) the cord and allowing the placental circulation to resuscitate the child. [1] The current standard obstetrical practice is to clamp the cord immediately to obtain a cord pH [3][4] - this maximizes the asphyxiation and hypovolemia, and accelerates HIE; the life-saving blood in the placenta is thrown away while parts of the child’s brain die.

The varying degrees of cerebral palsy and spastic paralysis are usually evident soon after birth in the movement and reflexes of the child, but lesser degrees of hypoxic, ischemic brain damage may remain hidden for years. [6] Iron deficiency anemia in infants is associated with learning disorders and behavioral problems to the point of mental retardation when these children reach grade school; [14] the degree of mental retardation increases with more severe degrees of infant anemia. [15]

At birth, no newborn is anemic; adequate iron is supplied from the mother regardless of her iron status. Any newborn that receives a full placental transfusion at birth has enough iron to prevent anemia during the first year of life. [13] It is, therefore, reasonable to conclude that full placental transfusion will prevent the mental retardation, behavioral disorders and learning disabilities that occur following infant anemia.

The immediately clamped newborn may be missing one third to one half of its normal blood volume and is very prone to develop infant anemia, [13] and as shown previously, it is also at risk for hypoxic, ischemic brain damage at birth. While some studies on treatment of the anemia in infancy have shown some behavioral improvement, most studies show no improvement or prevention of the brain dysfunction following correction of anemia, [16] making it difficult to establish a cause and effect relationship between anemia and brain dysfunction.

In HIE and CP (severe brain dysfunction) anemia develops AFTER the brain is damaged. Moderate hypovolemia and hypoxia at birth will produce infant anemia; it may also cause undiagnosed minor brain damage [6] that will later produce behavioral defects. Evidence strongly points to infant anemia and behavioral brain dysfunction having a common cause - immediate cord clamping; in other words, both anemia and brain dysfunction are effects, not a cause and an effect.

In a comprehensive review of cord clamping in 1982, Linderkamp concluded: "immediate clamping can result in hypovolemia and anemia. - A medium placental transfusion appears to be more appropriate in order to avoid the risk of hyperviscosity, whereas iron deficiency in later infancy is probably less dangerous." And in a similar review in 1981, Peltonen stated: "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." Within a few years, reports of these unharmed, "normal," anemic infants being mentally retarded in grade school began to appear in the literature.

While Linderkamp never proved that "hyperviscosity," (a hematocrit of >65%) was any risk at all to a newborn, Peltonen’s remarks were based on his observations of newborns’ chests viewed under a fluoroscope, and he described incomplete filling of the cardiac ventricles (decrease in heart size) following immediate clamping; his use of the word "fatal" indicates that, after immediate clamping, he witnessed a cardiac arrest that was not reversed. His blunt advice to avoid the procedure (he mentions no exceptions) emphasizes that the "normal" child may not be free from risk. He did not advise repeating his experiment; ACOG and SOGC [3] [4] do. Cardiac arrest, or inadequate cardiac output for a few minutes, will produce permanent brain damage.

Immediate cord clamping is clearly identified as a cause of newborn neurological (brain) injury ranging from neonatal death through cerebral palsy to mental retardation and behavioral disorders. Immediate cord clamping has become increasingly common in obstetrical practice over the past 20 years; today, rates of behavioral disorders (e.g., ADD/ADHD) and developmental disorders (e.g., autism, Asperger’s, etc) continue to climb and are not uncommon in grade school.

The premature baby is much more vulnerable to injury from immediate cord clamping than the robust term child. The brain is at an earlier stage of development and actively growing tissues are more easily damaged by lack of oxygen and lack of blood. The preemie’s most common problem and a leading cause of neonatal death is respiratory distress syndrome (RDS); it is caused by lack of blood volume (hypovolemia) [13][9] resulting from immediate cord clamping and poor blood flow through the lungs. Hyaline membrane disease (HMD) is diagnostic for RDS; under the microscope, the HMD of "shock lung" - RDS - in adults and geriatric patients appears the same as HMD in newborns.

• Immediate cord clamping in newborn foals can cause RDS and HMD, and similar lung lesions in newborn puppies and rabbits were produced by removal of blood volume after birth. [17]
• Landau completely prevented RDS/HMD in sectioned newborns by suspending the placenta and cord like an I.V. to give a full placental transfusion. [18]
• Kinmond virtually prevented RDS in preemies by giving a partial placental transfusion; none of these babies needed blood transfusion in the NICU. [2]

Retraction respiration, which is seen in the initial stages of RDS, is a reflexive effort to draw blood into the thorax; in adults with terminal hypovolemic shock, it is seen as gasps of "air hunger." Newborns with optimal blood volumes from placental transfusion do not exhibit retraction respiration. For years, there has been abundant and overwhelming evidence that neonatal RDS is caused by interruption of the placental transfusion by a cord clamp; however, to the medical profession, the cause of neonatal RDS remains a mystery. By allowing every newborn to have a normal placental transfusion, iatrogenic RDS, and the hypoxia and brain damage that accompany it, should be completely preventable.

A 34 week preemie has no surfactant in its lungs which are, as defined by current perinatal concepts, immature, yet it readily cries and turns a ruddy pink color when it has an optimal blood volume - no cord clamp used; the lungs behave in a most mature way that conflicts with the current idea of lung "maturity." Surfactant lowers the surface tension of water and lessens the tendency of alveoli (air sacs) to collapse. The newborn lung is erectile tissue, [19] which expands and "erects" the alveoli with the onset of pulmonary blood flow. [20][21] Ventilation relaxes pulmonary arterioles and massive pulmonary blood flow distends the left atrium and closes the foramen ovale (changes the heart from one-sided to two-sided) - the child turns pink. Placental transfusion maintains blood flow and erection (aeration) of the alveoli.

Low plasma colloid osmotic pressure (with high capillary hydrostatic pressure) may lead to initial pulmonary edema, but rapid hemo-concentration (fluid loss into systemic tissues) following placental transfusion [22] quickly corrects this situation, and the lungs "dry out" physiologically. Surfactant may help to prevent atelectasis and may, by lowering surface tension, lessen the force needed to inflate the lungs at birth [21].

However, surfactant is of little value if the child has insufficient blood volume to erect the alveoli. Surfactant does not cure RDS, and its absence does not cause RDS. Normal function of premature lungs (lung "maturity") depends much more on placental transfusion and plasma colloid osmotic pressure than on the presence of surfactant. Normal lung function supplies adequate oxygenation to the preemie’s growing brain.

The administration of steroids to the mother before premature birth greatly reduces the incidence and severity of pulmonary complications (RDS) in the newborn preemie, regardless of when its cord is clamped; however, long term use of steroids results in growth retardation. [23][24] A rational explanation of these phenomena is that steroids constrict the placental blood vessels, not to the point of impairing respiration, but enough to impair nutrition and cause growth retardation over the long term. Over the short term, placental vaso-constriction will squeeze blood into the child, giving it a placental transfusion before it is born. The extra blood volume, and possibly some hemo-concentration will account for the improvement in respiratory status.

Of course, not using a cord clamp would be much more effective and much less expensive. In addition, it would avoid long-term growth retardation.

Before birth, the fetal circulation bypasses the lungs with oxygenated blood from the placenta. RDS impairs newborn lung oxygenation, putting brain cells at risk. Persistent fetal circulation (PFC) is often a component of RDS – poor blood flow through the lungs results in low pressure in the left atrium which allows the foramen ovale flap valve to remain open; PFC has a high mortality rate. The placental transfusion is an essential factor in effecting the shift from the fetal circulation to the adult circulation at birth, [8] and PFC is also commonly associated with cesarean section newborns [25] who typically have immediate cord clamping and who receive little or no placental transfusion. [1] After birth with the placenta removed, PFC bypasses the lungs and circulates de-oxygenated blood to the brain.

Hyaline membrane formation is diagnostic for RDS and indicates gradual death of lung tissue. If the newborn survives, lung scarring indicates permanent damage. HMD is, in essence, slow pulmonary infarction (death from lack of blood flow) due to poor perfusion and lack of blood borne nutrients. Lung tissue does not die from lack of oxygen - there is oxygen in the alveoli that rapidly exhausts the deficient nutrients (aerobic respiration) and lung cells die from starvation. Protein exudation into alveoli through dying cells forms the hyaline material. Bleeding into alveoli also occurs in severe RDS - as it does in the adult in acute pulmonary infarction - the patient coughs up pink blood. HMD indicates severe lung dysfunction and consequent poor oxygenation of the child’s brain.

IVH is often associated with RDS in preemies. [26] It has all the characteristics of a hemorrhagic infarct of the germinal matrix. (GM) The GM is a very active metabolic area of the preemie’s brain and is very prone to hypoxic, ischemic necrosis (death) such as that produced by the intense vasospasm of hypovolemic shock. Following restoration of blood volume, hemorrhage into the dead tissue and into the ventricle occurs. Later, absorption of dead tissue enlarges the ventricle. These preemies have permanent neurological defects. No studies allowing preemies to close their own umbilical cords and to achieve normal blood volumes have ever been done.

This is a common bowel lesion in preemies (and some term newborns) with an ischemic component and has all the characteristics of a bowel infarct - blood in the stool and bowel perforation. Intense vasospasm of hypovolemic shock due to immediate clamping is a plausible explanation for the lesion. The placental transfusion normally supplies the newborn gut with extra blood flow in preparation for feeding and digestion.

Discussion

The purpose of all medical care should be the maintenance or restoration of normal (healthy) form and function. Therefore, definition and recognition of normal form and function are essential before any treatment can begin. Normal healthy (physiological) childbirth does not require medical treatment; it does require observation (care) to detect any developing abnormalities. Natural childbirth includes the normal and the abnormal. A true knot in the umbilical cord occurs quite naturally, but it is not the routine, normal form of the cord; if it is a loose knot, it does not affect cord function, and it does not require medical treatment. If the knot is tight, it impedes the child’s oxygen supply and that requires treatment (restoration of the normal). The midwife or physician who does not understand the normal form and function of the umbilical cord is not qualified to treat or take care of the umbilical cord.

All primates (monkeys, apes and humans) have large brains that cannot live and function without a constant oxygen supply. Other tissues can live for a while without oxygen using "anaerobic respiration" - a person may be "brain dead" following drowning, but have normal muscles, kidneys and other organs. The primate brain is at most risk during birth when its primary oxygen supply (placenta) is at the end of an exposed and vulnerable supply line (umbilical cord.) For species survival, primates must have a virtually perfect, innate mechanism that rapidly establishes the oxygen supply from the lungs while the placenta is still functioning. That mechanism must then close the cord vessels to prevent the newborn from bleeding to death after the cord is severed. Complicated anatomical and physiological changes occur during transfer of oxygenation from the placenta to the lungs.

Most obstetricians, pediatricians and especially their academic peers have never seen a child close its own cord; they are totally ignorant of the physiology of the process. Institutional dogma and misinformation have obliterated scientific thought and method, and have changed a healthy, normal process into an imaginary disease. They then advise curing the imaginary disease with an injurious cord clamp. Amputating a functioning placenta destroys the organ that is keeping the child alive and is preparing the child for life outside the womb. There is no excuse or justification for ACOG’s / SOGC’s immediate clamping to obtain medico-legal blood samples; [3][4] if indicated, a fine needle inserted into a pulsating cord artery will supply the same information without destroying the child’s life support system.

Doctors believe that placental transfusion causes hypervolemia, plethora, polycythemia, and hyperviscosity. They ignore the fact that polycythemia (hematocrit > 65% - "too many red cells") occurs in many normal, healthy babies. [22][27] Doctors have made a normal laboratory reading into a disease because red cells increase blood viscosity (stickiness). They have never defined what normal viscosity is, but they have defined the hyperviscosity syndrome (HVS) as extremely poor blood flow through tissues. HVS is supposedly caused by "sticky" blood such as occurs after the child has received "too much" blood.

However, HVS has never been described in a late clamped child; it usually occurs in immediately clamped newborns. HVS is a vaso-constriction syndrome due primarily to low blood volume and has very little to do with blood viscosity. [1] If, on very rare occasions, a child ever receives too much blood after natural cord closure, the condition should be properly diagnosed and the excess blood removed, just as if a cord ruptures spontaneously at birth, it should be clamped immediately to prevent blood loss.

The cord clamp is very useful for stopping bleeding from a ruptured cord; so doctors use it at every delivery to prevent bleeding. This usually stops placental transfusion, and hundreds of studies have been done to determine whether clamping before the transfusion is more beneficial than clamping after the transfusion, and hundreds more on clamping during the transfusion to get the "right amount" of blood into the baby. Linderkamp’s review [13] alone has over 200 references. Gunther’s study demonstrates that during placental transfusion, blood may flow into and out of the child until the right amount of blood is attained after the child is breathing. [7]

If the cord clamp were applied at the height of a uterine contraction that is forcing blood into the child at high pressure, [7] it could well trap too much blood in the child, blood that would have run back into the placenta if the clamp had not been used. Clamping between uterine contractions may leave too little blood in the child, making it impossible to decide when to clamp the cord.

It is generally understood (misunderstood) that too much blood causes jaundice and damages the brain. Hundreds more studies have been done on immediate clamping to resuscitate preemies and to measure cord pH values at birth for the benefit of risk managers. All of these studies on cord clamping are scientifically flawed; they have no physiological norm - not one of these studies included a physiological control set of babies delivered without the use of a cord clamp - normal babies that do not have too much or too little blood clamped in them.

Without an established norm, the cord clamp and its injuries are accepted as part of "normal" childbirth. Nearly all premature babies develop anemia that is "normal," and later, in school, are found to be mentally retarded. [15] [28] All received standard care as prescribed by medical academia; the anemia and mental retardation are the result of normal cord clamp birth injury.

The absurdity of the cord clamping / "too much blood" controversy is best illustrated by satirical analogy:

• Endo-tracheal intubation (a tube in the windpipe) is very useful for ventilating a newborn that is too depressed to breathe. Therefore, at every birth, a tube is placed in every child’s trachea to help it breathe. This prevents most newborns from crying, though some cry before the tube can be inserted and it then prevents further crying. Many studies are then done to find out if intubation before crying is more beneficial than intubation after crying. It is generally understood that too much crying may give the child too much oxygen and damage the eyes. Many more studies are done on immediate intubation (to document the carbon-dioxide content of the first breath for risk managers) and are compared to thousands of babies intubated after three minutes and after five minutes to find out what is normal.

The cord clamp, like the endotracheal tube, is not a part of human anatomy. It is a dangerous surgical instrument with very limited indications for use. A clamp placed on the pulsating cord of a newborn that cannot breathe has the same effect as a clamp placed on the throat of a child that is crying - complete asphyxiation.

Natural cord closure and placental transfusion are just as normal and as healthy as is crying at birth. [1] The normal Apgar score at five minutes is 10 - a pink, active, crying baby - and many immediately clamped newborns do not achieve that score; low five minute Apgar scores correlate with neurological injury. [29] Windle states: "A child with a slight brain defect often appears no different from a normal child. His intelligence quotient may lie in the range considered normal, but one never knows how much higher it would have been if his brain had escaped damage in the uterus or during birth. [6]

The neurological disorders, memory and behavioral defects, and the corresponding brain lesions that Windle demonstrated in monkeys, were produced by interrupting placental oxygenation and circulation at birth and by delaying the onset of pulmonary oxygenation. They did not occur in newborn monkeys that delivered without interference with the cord and placenta. Strikingly similar neurological disorders and behavioral defects occur in human infants following a period of asphyxiation occurring between the cessation of placental oxygenation and the establishment of pulmonary oxygenation. The primary cause of these defects in human babies is premature clamping of the umbilical cord that stops placental oxygenation and placental transfusion. Windle’s experiment on monkeys is repeated every day on human newborns.

"Learning disabilities are increasing dramatically. One child in six is afflicted by autism, aggression, dyslexia, or attention deficit disorder. In New York, cases of learning disability rose 55 percent between 1983 and 1996, from 132,000 to 204,000. In California there were 11,995 reported cases of autism in 1998, up 210 percent from 1987." [30] The injuries alluded to by Erasmus Darwin over 200 years ago have been convincingly demonstrated in number, variety, and severity by the practice of immediate cord clamping.[3][4] This practice has increased greatly over the past twenty years. Discontinuing the use of the cord clamp until after physiological closure of the umbilical vessels will eliminate most of these injuries. However, the purpose of this paper is not only to avoid newborn injury, but also to ensure optimal survival. The child has the biological equipment and wherewithal to become the brightest and the best; non-use of the cord clamp helps to ensure that potential.

©Copyright George M. Morley February 21, 2002

References:

1. Morley GM. Cord Closure: Can Hasty Clamping Injure the Newborn? OBG MANAGEMENT July 1998; 29-36.
2. Kinmond S et al. Umbilical Cord Clamping and Preterm Infants: a Randomized Trial. BMJ 1993; 306: 172-175
3. American College of Obstetricians and Gynecologists. Umbilical Artery Blood Acid-Base Analysis. Washington, D.C.: ACOG; 1995. Educational Bulletin 216.
4. Society of Obstetricians and Gynecologists of Canada. Policy statement No. 89. May 2000.
5. Faxelius, G. Raye, J. et al. Red cell volume measurements and acute blood loss in high-risk infants. Pediatrics 1977; 90(2): 273-281.
6. Windle W. Brain Damage by Asphyxia at Birth. Scientific American. 1969 Oct;221(4):76-84.
7. Gunther M. The transfier of blood between the baby and the placenta in the minutes after birth. Lancet 1957;I:1277-1280.
8. Morley GM. LETTERS OBSTETRICS & GYNECOLOGY, Vol 97, No.6,June 2001, 1024-1026
9. Peltonen T. Placental Transfusion, Advantage - Disadvantage. Eur J Pediatr. 1981;137:141-146
10. Cashmore J. Usher RH. Hypovolemia resulting from a tight nuchal cord at birth. Pediatr. Res 1973;7:339.
11. Morley, GM. LETTERS, OBG MANAGEMENT. February 1998, p. 14-16.
12. Morley GM. LETTERS, OBG MANAGEMENT. May 1999, p. 102-109
13. Linderkamp O. Placental transfusion: determinants and effects. Clinics in Perinatology 1982;9:559-592
14. Lozoff B. Jimenez E. Wolf AW. Long Term Development Outcome in Infants with Iron Deficiency. N Eng J Med 1991; 325: 687-94.
15. Hurtado EK et al. Early childhood anemia and mild to moderate mental retardation. Am J Clin Nut. 1999; 69(1): 115-9.
16. Lozoff B, Brittenham GM, Wolf AW et al. Iron deficiency anemia and Iron therapy effects on infant development test performance. Pediatrics 1987;79:981-995.
17. Mahaffey Leo W. Rossdale, PD. CONVULSIVE SYNDROME IN NEWBORN FOALS RESEMBLING PULMONARY SYNDROME IN THE NEWBORN INFANT; The Lancet 1959 1223-1225.
18. Landau DB. Hyaline membrane formation in the newborn: hematogenic shock as a possible etiological factor. Missouri Med1953; 50: 183.
19. Jaykka S. Capillary Erection and Lung Expansion. Acta Paediatr. 1965 [nppl] 109.
20. Jaykka S. An experimental study of the effect of liquid pressure applied to the capillary network of excised fetal lungs, Acta Paediatr. 1957; Supp 112:2-91.
21. Avery ME et al. The inflationary pulmonary force produced by pulmonary vascular distension in excised lungs. The possible relation of this force to that needed to inflate the lungs at birth. J. Clin. Invest. 1959; 38: 456-460.
22. Aziz S.F.A. Early Cord Clamping and its Effect on some Hematological Determinants of Blood Viscosity in Neonates. OBGYN.net Publications, January 2002
23. Bloom SL et al. Antenatal Dexamethazone and Decreased Birth Weight. OBSTETRICS & GYNECOLOGY 2001; 97: No. 4. 485-490
24. Vermillion ST. et al. Is Betamethasone Effective Longer than Seven Days after Treatment? OBSTETRICS & GYNECOLOGY 2001; 97 : No. 4. 491-493
25. Levine EM et al. Mode of Delivery and Risk of Respiratory Diseases in Newborns. OBSTETRICS & GYNECOLOGY 2001; 97: 439-42
26. Suarez RD et al. Indomethacin Tocolysis and Intraventricular Hemorrhage. OBSTETRICS & GYNECOLOGY Vol. 97 No. 6 June 2001 921-925.
27. Nelle M, et al. The Effect of Leboyer Delivery on blood Viscosity and other hemorrheologic parameters in full-term neonates. Am. J Obstet Gynecol 1993; 169(1) : 189-193
28. Hack M, et al., Outcomes in Young Adulthood for Very Low Birth-weight Infants. New Engl J Med, Vol. 346, No.3, Jan, 2002:149-157
29. Thorngren-Jerneck K. et al. A Population Based Register Study of One Million Term Births. Obstetrics & Gynecology 2001 Vol. 98 No. 1: 1024-1026
30. A.J. Chien, ZNet Commentary, February 06, 2002

Footnote:

In the February 2000, I formally requested that ACOG’s ethics and practice committees revoke ACOG Educational Bulletin 216 which was published in 1995. In the February 2002 edition of OBSTETRICS & GYNECOLOGY, ACOG quietly announced, in very small print on a back page (361), that Bulletin 216 has been withdrawn from circulation. I have yet to receive a formal reply from ACOG.

For the past seven years, 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. Without any attempt at warning the profession, ACOG has quietly relieved its officials from further responsibility for an injurious procedure that is widely and naively performed by many practicing obstetricians. It would be ethically and morally appropriate for ACOG TO ANNOUNCE TO EVERY OBSTETRICIAN IN VERY LARGE PRINT:

1. That immediate cord clamping is no longer officially sanctioned as standard care.
2. That the person who clamps the cord before the lungs are oxygenating the child should have sound, documented, clinical justification for doing so and
3. That the person who clamps the cord immediately or prematurely is individually responsible and liable for the resulting injuries.

George Malcolm Morley, M.B., Ch.B., FACOG (morley@cordclamping.com)

C.V.

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

Criticism, comment and refutation on this article is encouraged and may be sent to morley@cordclamping.com they will receive responses from the author.