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How the Cord Clamp Injures Your Baby?s Brain

By
George M. Morley, M.B., Ch. B., FACOG
This paper describes a major error in modern obstetrical practice, namely, routi
ne premature clamping of the umbilical cord. Some sections require medical knowl
edge for full comprehension and the language is very technical, but overall, med
ical jargon is avoided or explained in terms that most expectant parents can und
erstand. 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 on
ly repeatedly breathed but till all pulsation in the cord ceases. As otherwise t
he child is much weaker than it ought to be, a portion of the blood being left i
n 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 officia
l notification, medical academia and its peer review press have yet to acknowled
ge the possibility of any error. Public exposure and knowledge of the issue is i
ntended to accelerate correction of the error. The nature of the injury caused b
y this practice unhappily precludes a cure; for the unfortunate parents of an im
paired child, the knowledge may assuage any guilt they may have and give them re
assurance 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 clam
ped and cut at the earliest convenient time after birth. [1][2] At premature bir
ths and when the newborn is depressed or "at risk," immediate cord clamping is r
outinely performed in order to rush the child to a resuscitation table and to ob
tain 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 transfus
ion gives the baby too much blood, (hypervolemia) while neonatal intensive care
units (NICU) are filled with weak, fast - clamped newborns exhibiting signs of s
evere blood loss [5], pallor, hypovolemia (low blood volume) anemia, (low blood
count) hypotension (low blood pressure), hypothermia (cold), oliguria (poor urin
e output), metabolic acidosis, hypoxia (low oxygen supply), and respiratory dist
ress (shock lung) to the point that some need blood transfusions and many more r
eceive 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 c
ells, the term anemia is used; the blood is "dilute." Polycythemia means there a
re too many red cells "concentrated" blood. The "-volemia" terms refer to the to
tal volume of blood in the child?s heart and blood vessels; blood vessels are el
astic 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 "ball
oon." Too little blood volume (hypovolemia) lets the balloon and the heart colla
pse; 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 q
uantity of blood. An anemic baby may be hypervolemic -too much fluid, and a poly
cythemic child may be hypovolemic - dehydrated. A normal child that suffers acut
e 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 resto
re 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 r
outinely give a child too much, or too little, blood; mammals that routinely giv
e their offspring the wrong amount of blood for survival become extinct in one g
eneration.
Erasmus Darwin?s late clamping method is safe because the tie is placed on vesse
ls that the child has already closed physiologically (by natural constriction) a
fter 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 placenta
l life support system and starting the child?s life support systems without sign
ificant interruption of life support during the changeover process. Oxygen suppl
y 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 quick
ly from lack of oxygen; they do not regenerate, and asphyxiation (choking / lack
of oxygen) for about six minutes will cause permanent brain damage. [6]
Normal Cord and Placental Function after Birth (No Cord Clamp Used)
Before birth, the lungs are filled with fluid and very little blood flows throug
h 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 ch
ild is crying and pink, the cord vessels clamp themselves. During this interval
between birth and natural clamping, blood is transfused from the placenta to est
ablish blood flow through the lungs. Thus the natural process protects the brain
by providing a continuous oxygen supply from two sources until the second sourc
e 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 t
hrough 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 chang
ing the fetal circulation to the adult circulation - the one-sided heart (body b
lood flow only) changes to a two-sided heart (blood flows through the lungs, the
n through the body.) Ventilation of the lungs and placental transfusion effect t
his change. This is a very basic account of a very complex process. [8] It all h
appens 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 c
ord during the changeover process disrupts these life support systems and may ca
use serious injury.
The Effects and the Injuries of Immediate Cord Clamping (ICC)
The American College of Obstetricians and Gynecologists (ACOG) and the Society o
f Obstetricians and Gynecologists of Canada (SOGC) advocate immediate cord clamp
ing 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 functi
on. Blood, which normally would have been transfused to establish the child?s lu
ng 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 estab
lish 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 deli
vered, and the uterine contraction that delivers the child may also squeeze in s
ome placental transfusion before the fast clamp can be applied; however, cord cl
amping before the first breath [9] always causes some degree of asphyxia and los
s of blood volume:
1. It totally cuts off the infant brain?s oxygen supply from the placenta bef
ore lungs begin to function.
2. It stops placental transfusion -the transfer of a large volume of blood (u
p to 50% increase in total blood volume) that is used mainly to establish circul
ation through the child?s lungs to start them functioning.
Cerebral Palsy
While ICC is a danger to all newborns, if a child is born asphyxiated and depres
sed 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 depri
ved of oxygenated placental blood before birth is in dire need of oxygenated blo
od after birth. Immediate clamping in such circumstances [11] often produces a h
ypovolemic and asphyxiated child who cannot begin to breathe adequately to relie
ve the asphyxia; oxygen in the lungs will never reach the brain if the newborn d
oes not have enough blood to flow from lungs to brain. [12]
The medical term for the condition that causes cerebral palsy (CP) is hypoxic, i
schemic encephalopathy. (HIE) Hypoxic means lack of oxygen - the child has no pl
acental oxygen supply; ischemic means lack of blood flow - half of the child?s b
lood 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 chil
d?s own oxygenated blood has been discarded with the placenta. In addition, babi
es with HIE usually develop anemia.
The obvious correct way to resuscitate the depressed child is to keep the cord a
nd placenta functioning while ventilating the lungs. [1][9][12] If a child is bo
rn 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 r
estored to normal with a large transfusion of oxygenated placental blood and is
unlikely to develop HIE. [12] Rapid restoration of oxygenation is crucial in pre
venting brain damage in the depressed child, and that child must have enough blo
od to transport oxygen to the brain. If hypoxic brain damage has occurred before
birth, placental oxygenation and transfusion will not cure it after birth - not
hing will - but progression of the damage will be prevented. Blood transfusion g
iven after the child has developed HIE will not restore the dead brain cells. Bl
ood 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 occur
s with a cord prolapsed during labor (a cord squeezed between the head and the c
ervix,) may be rapidly reversed by relieving the compression - elevating the pre
senting 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, t
he child may show no sign of asphyxiation. The same result can be obtained at bi
rth in a child asphyxiated with a tight cord around the neck by reducing (unwind
ing) 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 part
s of the child?s brain die.
Learning Disorders and Mental Deficiency
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 o
f hypoxic, ischemic brain damage may remain hidden for years. [6] Iron deficienc
y anemia in infants is associated with learning disorders and behavioral problem
s 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 regard
less 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] I
t is, therefore, reasonable to conclude that full placental transfusion will pre
vent 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 norm
al blood volume and is very prone to develop infant anemia, [13] and as shown pr
eviously, 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 im
provement, most studies show no improvement or prevention of the brain dysfuncti
on 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 dama
ged. Moderate hypovolemia and hypoxia at birth will produce infant anemia; it ma
y also cause undiagnosed minor brain damage [6] that will later produce behavior
al defects. Evidence strongly points to infant anemia and behavioral brain dysfu
nction having a common cause - immediate cord clamping; in other words, both ane
mia and brain dysfunction are effects, not a cause and an effect.
In a comprehensive review of cord clamping in 1982, Linderkamp concluded: "immed
iate clamping can result in hypovolemia and anemia. - A medium placental transfu
sion 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 r
etarded 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 fill
ing of the cardiac ventricles (decrease in heart size) following immediate clamp
ing; his use of the word "fatal" indicates that, after immediate clamping, he wi
tnessed a cardiac arrest that was not reversed. His blunt advice to avoid the pr
ocedure (he mentions no exceptions) emphasizes that the "normal" child may not b
e 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 pro
duce 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 ret
ardation and behavioral disorders. Immediate cord clamping has become increasing
ly common in obstetrical practice over the past 20 years; today, rates of behavi
oral disorders (e.g., ADD/ADHD) and developmental disorders (e.g., autism, Asper
ger?s, etc) continue to climb and are not uncommon in grade school.
Respiratory Distress Syndrome
The premature baby is much more vulnerable to injury from immediate cord clampin
g than the robust term child. The brain is at an earlier stage of development an
d 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 (hy
povolemia) [13][9] resulting from immediate cord clamping and poor blood flow th
rough the lungs. Hyaline membrane disease (HMD) is diagnostic for RDS; under the
microscope, the HMD of "shock lung" - RDS - in adults and geriatric patients ap
pears the same as HMD in newborns.
* Immediate cord clamping in newborn foals can cause RDS and HMD, and simila
r 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 th
e 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 reflexi
ve effort to draw blood into the thorax; in adults with terminal hypovolemic sho
ck, it is seen as gasps of "air hunger." Newborns with optimal blood volumes fro
m placental transfusion do not exhibit retraction respiration. For years, there
has been abundant and overwhelming evidence that neonatal RDS is caused by inter
ruption of the placental transfusion by a cord clamp; however, to the medical pr
ofession, the cause of neonatal RDS remains a mystery. By allowing every newborn
to have a normal placental transfusion, iatrogenic RDS, and the hypoxia and bra
in damage that accompany it, should be completely preventable.
Lung Maturity, Surfactant and RDS
A 34 week preemie has no surfactant in its lungs which are, as defined by curren
t perinatal concepts, immature, yet it readily cries and turns a ruddy pink colo
r 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." Surfa
ctant lowers the surface tension of water and lessens the tendency of alveoli (a
ir sacs) to collapse. The newborn lung is erectile tissue, [19] which expands an
d "erects" the alveoli with the onset of pulmonary blood flow. [20][21] Ventilat
ion relaxes pulmonary arterioles and massive pulmonary blood flow distends the l
eft 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 e
rection (aeration) of the alveoli.
Low plasma colloid osmotic pressure (with high capillary hydrostatic pressure) m
ay lead to initial pulmonary edema, but rapid hemo-concentration (fluid loss int
o systemic tissues) following placental transfusion [22] quickly corrects this s
ituation, and the lungs "dry out" physiologically. Surfactant may help to preven
t atelectasis and may, by lowering surface tension, lessen the force needed to i
nflate the lungs at birth [21].
However, surfactant is of little value if the child has insufficient blood volum
e to erect the alveoli. Surfactant does not cure RDS, and its absence does not c
ause RDS. Normal function of premature lungs (lung "maturity") depends much more
on placental transfusion and plasma colloid osmotic pressure than on the presen
ce of surfactant. Normal lung function supplies adequate oxygenation to the pree
mie?s growing brain.
Steroid Treatment and RDS
The administration of steroids to the mother before premature birth greatly redu
ces the incidence and severity of pulmonary complications (RDS) in the newborn p
reemie, regardless of when its cord is clamped; however, long term use of steroi
ds results in growth retardation. [23][24] A rational explanation of these pheno
mena is that steroids constrict the placental blood vessels, not to the point of
impairing respiration, but enough to impair nutrition and cause growth retardat
ion over the long term. Over the short term, placental vaso-constriction will sq
ueeze 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 t
he improvement in respiratory status.
Of course, not using a cord clamp would be much more effective and much less exp
ensive. In addition, it would avoid long-term growth retardation.
Persistent Fetal Circulation
Before birth, the fetal circulation bypasses the lungs with oxygenated blood fro
m the placenta. RDS impairs newborn lung oxygenation, putting brain cells at ris
k. Persistent fetal circulation (PFC) is often a component of RDS ? poor blood f
low through the lungs results in low pressure in the left atrium which allows th
e foramen ovale flap valve to remain open; PFC has a high mortality rate. The pl
acental 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 ass
ociated with cesarean section newborns [25] who typically have immediate cord cl
amping 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 Disease (HMD)
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) du
e 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 d
eficient nutrients (aerobic respiration) and lung cells die from starvation. Pro
tein exudation into alveoli through dying cells forms the hyaline material. Blee
ding into alveoli also occurs in severe RDS - as it does in the adult in acute p
ulmonary infarction - the patient coughs up pink blood. HMD indicates severe lun
g dysfunction and consequent poor oxygenation of the child?s brain.
Intra - Ventricular Hemorrhage (IVH) (Brain Hemorrhage)
IVH is often associated with RDS in preemies. [26] It has all the characteristic
s 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 nec
rosis (death) such as that produced by the intense vasospasm of hypovolemic shoc
k. Following restoration of blood volume, hemorrhage into the dead tissue and in
to the ventricle occurs. Later, absorption of dead tissue enlarges the ventricle
. These preemies have permanent neurological defects. No studies allowing preemi
es to close their own umbilical cords and to achieve normal blood volumes have e
ver been done.
Necrotizing Entero-Colitis (NEC)
This is a common bowel lesion in preemies (and some term newborns) with an ische
mic component and has all the characteristics of a bowel infarct - blood in the
stool and bowel perforation. Intense vasospasm of hypovolemic shock due to immed
iate clamping is a plausible explanation for the lesion. The placental transfusi
on normally supplies the newborn gut with extra blood flow in preparation for fe
eding and digestion.
Discussion
The purpose of all medical care should be the maintenance or restoration of norm
al (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 ob
servation (care) to detect any developing abnormalities. Natural childbirth incl
udes 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 treatme
nt. 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 un
derstand 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 f
unction without a constant oxygen supply. Other tissues can live for a while wit
hout oxygen using "anaerobic respiration" - a person may be "brain dead" followi
ng drowning, but have normal muscles, kidneys and other organs. The primate brai
n is at most risk during birth when its primary oxygen supply (placenta) is at t
he end of an exposed and vulnerable supply line (umbilical cord.) For species su
rvival, primates must have a virtually perfect, innate mechanism that rapidly es
tablishes the oxygen supply from the lungs while the placenta is still functioni
ng. That mechanism must then close the cord vessels to prevent the newborn from
bleeding to death after the cord is severed. Complicated anatomical and physiolo
gical changes occur during transfer of oxygenation from the placenta to the lung
s.
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 imaginar
y 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 ex
cuse or justification for ACOG?s / SOGC?s immediate clamping to obtain medico-le
gal 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, polycy
themia, and hyperviscosity. They ignore the fact that polycythemia (hematocrit >
65% - "too many red cells") occurs in many normal, healthy babies. [22][27] Doc
tors have made a normal laboratory reading into a disease because red cells incr
ease blood viscosity (stickiness). They have never defined what normal viscosity
is, but they have defined the hyperviscosity syndrome (HVS) as extremely poor b
lood flow through tissues. HVS is supposedly caused by "sticky" blood such as oc
curs 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 primar
ily 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 immedi
ately to prevent blood loss.
The cord clamp is very useful for stopping bleeding from a ruptured cord; so doc
tors use it at every delivery to prevent bleeding. This usually stops placental
transfusion, and hundreds of studies have been done to determine whether clampin
g 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 i
nto and out of the child until the right amount of blood is attained after the c
hild is breathing. [7]
If the cord clamp were applied at the height of a uterine contraction that is fo
rcing blood into the child at high pressure, [7] it could well trap too much blo
od in the child, blood that would have run back into the placenta if the clamp h
ad not been used. Clamping between uterine contractions may leave too little blo
od in the child, making it impossible to decide when to clamp the cord.
It is generally understood (misunderstood) that too much blood causes jaundice a
nd 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 flawe
d; they have no physiological norm - not one of these studies included a physiol
ogical 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 par
t of "normal" childbirth. Nearly all premature babies develop anemia that is "no
rmal," and later, in school, are found to be mentally retarded. [15] [28] All re
ceived standard care as prescribed by medical academia; the anemia and mental re
tardation are the result of normal cord clamp birth injury.
The absurdity of the cord clamping / "too much blood" controversy is best illust
rated by satirical analogy:
* Endo-tracheal intubation (a tube in the windpipe) is very useful for venti
lating 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 n
ewborns 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 b
efore crying is more beneficial than intubation after crying. It is generally un
derstood 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 thou
sands of babies intubated after three minutes and after five minutes to find out
what is normal.
* All premature babies are intubated immediately as this gives them a normal
respiration Apgar score of 2 at one minute even when they do not have a heartbe
at. All ventilation is monitored so that no baby gets "too much oxygen." Torn vo
cal cords and pneumo-thoraces are an accepted part of this "normal" childbirth.
Doctors are surprised when told that babies born at home never have torn vocal c
ords, but they are all terrified of not using intubation on even a few newborns,
or even asking the mother?s consent about it, because immediate intubation is t
he Standard of Care set by the gods of Academia for use by trial lawyers.
The cord clamp, like the endotracheal tube, is not a part of human anatomy. It i
s 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 effe
ct as a clamp placed on the throat of a child that is crying - complete asphyxia
tion.
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 pin
k, active, crying baby - and many immediately clamped newborns do not achieve th
at score; low five minute Apgar scores correlate with neurological injury. [29]
Windle states: "A child with a slight brain defect often appears no different fr
om a normal child. His intelligence quotient may lie in the range considered nor
mal, but one never knows how much higher it would have been if his brain had esc
aped 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 interruptin
g placental oxygenation and circulation at birth and by delaying the onset of pu
lmonary oxygenation. They did not occur in newborn monkeys that delivered withou
t interference with the cord and placenta. Strikingly similar neurological disor
ders and behavioral defects occur in human infants following a period of asphyxi
ation occurring between the cessation of placental oxygenation and the establish
ment of pulmonary oxygenation. The primary cause of these defects in human babie
s is premature clamping of the umbilical cord that stops placental oxygenation a
nd placental transfusion. Windle?s experiment on monkeys is repeated every day o
n human newborns.
"Learning disabilities are increasing dramatically. One child in six is afflicte
d by autism, aggression, dyslexia, or attention deficit disorder. In New York, c
ases 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 gr
eatly over the past twenty years. Discontinuing the use of the cord clamp until
after physiological closure of the umbilical vessels will eliminate most of thes
e injuries. However, the purpose of this paper is not only to avoid newborn inju
ry, 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:
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Footnote:
In the February 2000, I formally requested that ACOG?s ethics and practice commi
ttees revoke ACOG Educational Bulletin 216 which was published in 1995. In the F
ebruary 2002 edition of OBSTETRICS & GYNECOLOGY, ACOG quietly announced, in very
small print on a back page (361), that Bulletin 216 has been withdrawn from cir
culation. I have yet to receive a formal reply from ACOG.
For the past seven years, thousands of obstetricians have been taught that immed
iate cord clamping is an acceptable, standard obstetrical procedure, and million
s of newborns have been subjected to it. Without any attempt at warning the prof
ession, ACOG has quietly relieved its officials from further responsibility for
an injurious procedure that is widely and naively performed by many practicing o
bstetricians. 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 standar
d care.
2. That the person who clamps the cord before the lungs are oxygenating the c
hild should have sound, documented, clinical justification for doing so and
3. That the person who clamps the cord immediately or prematurely is individu
ally responsible and liable for the resulting injuries.
George Malcolm Morley, M.B., Ch.B., FACOG
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 America
n 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.
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