Birth-Brain Injury Caused by Umbilical Cord Clamping:
From Imbecility and Cerebral Palsy to Minimal Mental Retardation
George Malcolm Morley, MB ChB FACOG
Figure 1 is a recording of total asphyxiation of a newborn primate delivered by C-section with electronic monitoring of Fetal Heart Rate, BP and Respiration. The cord was clamped and the head placed in a saline-filled bag at birth. Post mortem examination showed massive necrosis of basal ganglia and the cerebral cortex. Hypoxia did not injure this neonate’s brain.
During birth, the VIABILITY of the Central Nervous System and the myocardium are dependent on perfusion with nutrient blood that removes the waste products of aerobic and / or anaerobic metabolism. Deficient perfusion will result in tissue death – infarction – regardless of blood oxygen content.
The FUNCTIONS of the Central Nervous System and the myocardium (nerve impulses and muscle contraction) are dependent on aerobic metabolism – OXYGEN. Deficient oxygen supply results in loss of function. Deficient myocardial function (from ANY cause) will result in loss of perfusion and tissue infarction.
Cardiac arrest (no blood pressure for 15 minutes) infarcted the brain of the above monkey. Human neonates, born by C-section, are routinely oxygenated within minutes of birth and never have hypoxic heart failure causing zero blood pressure. However, the clinical course of the human newborn that progresses to brain ischemia and brain injury is often mimicked in the above tracing.
Cerebral Palsy (CP) is only the tip of an enormous iceberg of birth-brain injury.
The brain damage of CP begins after the baby is born. The main clinical signs are pallor, apathy, altered tone and difficulty feeding.
Ischemic Encephalopathy is diagnosed on MRI, the ischemia is generalized; blood flow through ALL the brain is deficient, regardless of oxygenation.
Ischemia is the pathogen.
At birth, the basal ganglia and the cortex are growing and metabolizing actively. In CP, they undergo ischemic necrosis – infarction.
The cause of the ischemia is heart failure – failure to generate an adequate blood pressure – resulting in deficient tissue blood flow.
1. Two types of heart failure are demonstrated in this experiment:
Gasping is retraction respiration, a reflex response to heart failure – a response to critically low BP and very low Central Venous Pressure.
Negative intra-thoracic pressure pulls venous blood into the lungs and heart, filling the ventricles.
Note the spikes of increased pulse rate as ventricles pump out blood, but with negligible effect on BP.
Now look at the spikes of diastolic blood pressure down to ZERO and below ZERO.
Blood is pulled backwards out of low-pressure peripheral arteries into the thoracic aorta.
Blood flows up and down the carotid arteries, pumped in, sucked out; very little blood flows through the brain.
Ischemic neuron necrosis probably begins at this point; then the myocardium fails progressively from anoxia. Ten minutes of cardiac arrest (and brain damage) follow.
At 25 minutes of asphyxia, resuscitation ventilates the lungs and oxygenates the blood; blood pressure and pulse rate are well restored.
Then blood pressure falls and at 50 mms Hg. GASPING begins again. The heart is oxygenated and perfect; why is it failing?
Look at the first action – the cord was clamped. Pulse rate and Cardiac Output fell 50%: WHY? 50% of venous return to the heart was clamped off.
50% of this monkey’s blood volume was clamped in its placenta.
Ventilation then opened the pulmonary circulation that filled with blood from all other organs – creating systemic blood loss and the falling BP.
The monkey stabilized with a low blood pressure maintained by gasping – hypovolemic heart failure. Remember this scenario.
This degree of anoxia never occurs at human birth, but the sequence of delivery, immediate cord clamping (ICC), and immediate resuscitation followed by collapse into pallor, hypotension, and gasping is not uncommon at human cesarean section. CP is rare, but large placental blood loss is quite routine.
Term CP babies have a somewhat different case history; all have an episode of asphyxia during birth.
The cause of asphyxia is cord compression – a tight nuchal cord, a true knot in the cord, a prolapsed cord and/or other cord accident situations.
The cord vein carries red, oxygenated blood. Compression impedes oxygen flow to the fetus – hypoxia. As oxygen is dissolved in blood, compression also impedes blood return to the fetus. Hypoxia entails Hypovolemia.
Net blood flow in cord compression is out of the baby into the placenta.
The end result is an engorged placenta and a hypoxic, exsanguinated baby.
These “hypoxic” babies are not born blue; they are ashen white and dishrag limp; no tone, no reflexes – dead – but with a pulsating cord.
Rational treatment is to remove the cord compression (loosen the knot, unwind and release the nuchal cord) and allow oxygenated placental blood transfusion to restore a normal blood volume and normal oxygenation.
Routine current treatment is immediate cord clamping and removal to a resuscitation table for immediate ventilation. Think about the resuscitated monkey – it had some blood volume to fill its lungs.
Little systemic blood is available to fill the lungs of the cord-compressed newborn.
After ICC, severe hypovolemic shock ensues with retraction respiration. Ischemic encephalopathy and CP follow.
The most metabolically active part of the preemie’s brain (and the most vulnerable to ischemia) is the germinal matrix. (GM) It functions from 23 weeks to 36 weeks gestation. It is extremely vascular with a copious blood flow; it “boils” out neuroblasts and spongioblasts that migrate out to grow and form the cerebral cortex.
Immediate cord clamping (ICC) amputates the large placenta and all its blood; retraction respiration is common; brain ischemia and infarction of high metabolism areas follow.
Because of extreme vascularity, hemorrhagic infarction of the G.M. occurs. Bleeding invades neighboring white matter and the ventricles – IVH – with massive brain damage. Most cerebral palsy babies are preemies.
Figure 4. The most metabolically active parts of the term neonate’s brain are in the nuclei of the inferior colliculi!
FIGURE 4: Autoradiogram showing greatest perfusion after 60 seconds in nuclei of the brainstem auditory pathway. From Kety (1962).
FIGURE 5: Diagram of the auditory pathway
6. These necrotic Inf. Coll. are from a child that died of suffocation.
7. This monkey with necrotic Inf. Coll. was “mildly” asphyxiated 5 years before its brain was examined.
Monkey: normal colliculi.
Monkey: Five years after “minor” asphyxiation.
The monkey was neurologically normal, however, its mental responses were not normal.
When food was placed in one of two containers, and the monkey released after one minute, it chose correctly 50% of the time. Non-asphyxiated normal monkeys chose correctly 90+% of the time.
The monkey had very defective recent memory; it could not pay attention to the food for one minute – it had attention deficit disorder, ADD.
Many 5-year-old children have ADD, and ADHD, and learning and behavioral disorders, and autism, ASD and Asperger’s syndrome. They fill special education classes across the continent. They have a common denominator – mental deficiency – a low IQ.
If the mid-brain nuclei are as susceptible to ischemic infarction as are the basal nuclei and the cortex, high-resolution radiography should demonstrate this in cerebral palsy children, and possibly in autistic children. MRI studies of the inferior colliculi have never been done on “special education” (SE) children.
As it is, there is plausible proof that many SE children had severe hypovolemia and brain ischemia during birth – immediate CC and intra-placental blood loss.
Dozens of studies correlate infant iron deficiency anemia (during the first year of life) with low IQ in grade school and learning disabilities.
In 1999, a large study from Dade Co. FL compared infant hemoglobin levels with a standard IQ test result in grade school:
“The effect of hemoglobin was significant after all covariates were entered into the equation [odds ratio (OR): 1.28; 95% CI: 1.05, 1.60]. Therefore, for each decrement in hemoglobin, risk of mild or moderate mental retardation increased by 1.28, even after we controlled for all other variables in the equation.” (Hurtado)
Normal placental transfusion (no cord clamping) provides enough hemoglobin and iron to prevent anemia during the first year of life.
Immediate cord clamping causes hypovolemia, hypotension, ischemia and subsequent infant anemia.
Therefore, for each decrement in hemoglobin, a corresponding amount of hemoglobin was clamped in the placenta at birth, – with equivalent increased risk of mental retardation in grade school.
How many newborns are at risk for serious blood loss during birth, for anemia after birth, and for mental deficiency?
“Sick neonates are one of the most [anemic] heavily transfused groups
of patients in modern medicine.” N A
What “group” of patients is prone to blood loss? Mothers have placenta previa and abruption placenta with massive blood loss, and they also have post partum hemorrhages that cover the delivery room floor. Four times more newborns receive blood transfusions than mothers!
ACOG advocated immediate cord clamping for many years to obtain cord arterial blood pH for medico-legal documentation. All studies on babies with cerebral palsy have routine cord pH studies – routine ICC. For many years, every CP baby has had ICC.
ICC was epidemic in the 1980’s and 1990’s; it still is. ACOG has withdrawn the Practice Bulletins that advocate ICC, but has not issued any warning of the known injurious effects of ICC.
C-sections usually have ICC. C-section babies are 4 times more likely to be autistic than vaginal deliveries.
Babies from complicated deliveries are more likely to be autistic than spontaneous deliveries. They routinely have ICC with immediate transfer to resuscitation.
A recent follow up study on home births reported zero autism cases in grade school. In Amish communities with many midwife deliveries (cord clamping is delayed until the placenta has delivered), there is no autism epidemic.
But autism is widely regarded as a genetic inherited trait – many more boys than girls are autistic – it is surely sex linked. However, when newborn rats are asphyxiated, then resuscitated, some have no brain damage; most are female. Most of the neurologically impaired ones are MALE! Newborn male rats have a higher metabolic rate than female rats – their brains are more susceptible to ischemic damage.
The pulse rate of the average human term male fetus is higher than the female. Male brains are at higher risk of ischemic damage than female brains.
Admission of women to college and university is increasing. For every 100 women receiving bachelor’s degrees, just 73 men get one. Is this (lower male IQ) the result of universal ICC over the past 25 years?
1968 William Windle, who did most of the primate work on brain damage, said this:
9. “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.”
William Windle, 1968
Figure 10. This monkey was delivered while its mother was asphyxiated in pure nitrogen. Its cord was not clamped.
The pulse rate and BP fell with hypoxia, and recovered with resuscitation.
Placental transfusion (PT) filled the lung blood vessels after ventilation and before cord clamping. PT also filled the gut, the liver, the kidneys, the skin and the brain with blood.
The PT was clamped in the baby, not in the placenta. PT generated very adequate blood pressure and copious tissue perfusion. Placental transfusion prevents birth brain damage.
Figure 11. The human equivalent of this monkey is the red baby on the handout.
Birth Brain Injury and Cord Clamping
Normal newborn blood volume Blood volume? Cord pH normal
1882 "Infants which have had the benefit of late ligation of the cord are red, vigorous, and active, whereas those in which the cord is tied early are apt to be pale and apathetic." Lusk WT (1882) The Science and Art of Midwifery
1801 “Tying and cutting of the navel string too soon is very injurious to the child; 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; 1801
1992,1993 Clamping delayed for five minutes produced routine Apgar scores of 10. Linderkamp ‘1992,1993
1982 “… immediate cord clamping can cause hypovolemia, hypotension and anemia …” Linderkamp ‘1982
1981 “Thus [clamping before the first breath] is unphysiological and should be avoided; under certain unfavourable circumstances the consequences may be FATAL.” Peltonin 1981
1994-2002 “To obtain a cord pH, doubly clamp a segment of cord immediately.” ACOG BULLETIN 138
2003 Cowan F …Neonatal Encephalopathy.(NE) Lancet 2003 Cowan's clinical definition of NE is:
1. Abnormal tone pattern Weaker than it ought to be
2. Feeding difficulties Not vigorous
3. Altered alertness Apathetic
4. Late decelerations Cord compression in utero
5. Delayed respirations Not red
6. Arterial cord blood pH > 7.1 Immediate Cord Clamping to obtain blood
7. Apgar >7 at 5 mins Pale and apathetic, not active
8. multi-organ failure Hypovolemic shock
The clinical definition of NE is an accurate clinical description of the immediately clamped newborn. (ICC)
2004 N A
Infant anemia correlates strongly
with ADHD, autism, ASD, learning and behavioral
disorders and mental deficiency in grade school
children. Lozoff B. (
2004 Delayed cord clamping (DCC) prevents brain damage (hemorrhagic
infarction, IVH) and anemia in preterm infants: Cochrane Report. DCC is advocated on term infants to
prevent infant anemia (and childhood mental deficiency:)
2001-2005 Successful routine prevention of infant anemia,
respiratory distress and HIE by routine cord clamping after delivery
of the placenta.
2005 Dec. Green Journal: Experimental attempt to prevent HIE by hypothermia – cooling newborn brains; editorial and article. No informed parental consent offered for amputation of the functioning placenta.
The mother of the above red infant is not anemic; the red infant is not at risk for anemia or for hypoxic ischemic encephalopathy; delivered Jan 14, 2006.
This paper was presented at:
The 5th International Symposium for the use of Hyperbaric Oxygen in Neurosciences
July 21, 2006,