Immediate Cord Clamping: the Primary Injury


Immediate clamping of the umbilical cord before the child has breathed (ICC) has been condemned in obstetrical literature for over 200 years. [1] [2] In the 1970s, primate research [A][3][4] using ICC to produce neonatal asphyxia resulted in brain lesions similar to those of human “neonatal asphyxia.”  Two extensive review papers on placental transfusion and the time of cord clamping [5,6] both condemned the practice of ICC:

·                    Linderkamp ‘82 [5]: “… immediate cord clamping can cause hypovolemia, hypotension and anemia …”

·                    Peltonin ’81 [6]: “Thus [clamping before the first breath] is unphysiological and should be avoided under certain unfavourable circumstances the consequences may be FATAL.”


Peltonen described the effect of ICC on cardiac ventricle filling visualized under fluoroscopy – there was momentary “cardiac arrest.”  This effect is seen in [A] when a normal neonate is subjected to ICC: the heart rate (AND CARDIAC OUTPUT) fall immediately by about 50%.  The umbilical vein is comparable to the vena cava.  Sudden removal of this large venous return to the heart has major effects on tissue perfusion of the neonate, as does sudden removal of a very large volume of placental blood from the general circulation.


However, in the early 1980’s, ICC use increased, as neonatologists demanded ICC for instant neonatal transport to the resuscitation table to correct and prevent neonatal asphyxia.  Neonatal deaths decreased markedly; the incidence of cerebral palsy stayed constant.  Lives were saved; brains were not saved.


By the early 1990’s, medico-legal advice encouraged obstetricians to send an immediately excised portion of cord for blood analysis [9] to prove that the child was not asphyxiated at birth.  By 2000, ICC was standard practice.  In August 2003, ACOG quietly revoked publication of Practice Bulletin 138; obstetricians, perinatologists and neonatologists continue to think that ICC is harmless.


Today, very few neonates are allowed to close the cord physiologically and to achieve a blood volume that is optimal for survival; however, the actual amount of individual blood loss from ICC varies enormously.  The child with intra-partum cord compression (a tight nuchal cord is the most common cause) combined with ICC [10] is usually critically hypovolemic and prone to HIE, whereas the child that cries when the head is born, and is delivered with the next uterine contraction may receive a very adequate (uterine generated) blood volume before the cord can be clamped.


In general, most vaginally delivered neonates that breathe before the cord is clamped attain a functional blood volume.  Those neonates clamped before the first breath have less than an optimal blood volume, and preemies, c-section babies, and depressed babies in this category are prone to severe compromise from hypovolemia / hypotension.


The pathology generated by ICC also varies widely – from severe ischemic brain damage and death to none – a normal child.  The incidence of cerebral palsy has remained constant at about 1 per 1000 births over the past 30 years, but an epidemic of autism, ASD, ADD, ADHD, behavioural and achievement disorders is raging in the Western World.  The specific ischemic brain lesions related to these “minor” neurological disorders have been addressed by Eileen Simon [11] and similar disorders have been produced in primates by birth asphyxia.  [3] Relatively small ischemic lesions at birth in the nuclei of the brain stem that disrupt function in the auditory / speech circuits may not be apparent until the child is in school.


In the 1980s, Lozoff published the first correlations between infant anemia and mental disorders in grade school children. [7] Multiple publications have confirmed her initial findings.  In 1999, Hurtado showed, in grade school children, a direct relationship between objective assessments of the degree of mental deficiency (IQ testing) and the degree of anemia (hemoglobin levels) in infancy. [8] Non-use of the cord clamp at birth (full placental transfusion) provides the neonate with enough iron to prevent anemia during the first year of life.  Whether the brain damage occurs sooner (at birth from hypo-perfusion of the brain) or later (by affecting brain development), it is preventable by not clamping the cord.


Intra-ventricular hemorrhage (IVH) in preemies is seen on MRI as a hemorrhagic infarct of the germinal matrix – the most metabolically active part of the premature brain, manufacturing neurons that build the cerebral cortex; it is thus the area most susceptible to ischemic damage.  IVH is frequently associated with IRDS (shock lung) [12] Preemies have routine ICC.


“Sick neonates are one of the most heavily transfused groups of patients in modern medicine.” [13] “At risk” – sick neonates have routine ICC.  The symptoms and signs of nearly every child admitted to an NICU – pallor, weakness, inability to suckle, oliguria / anuria, hypotension, hypothermia, metabolic acidosis, anemia and hypoglycemia are those of hypovolemia and hypovolemic shock.  The retraction respirations (RR) of an ICC neonate are the same as those of an adult dying in hypovoelmic shock (air hunger).  RR fills the right heart with blood; it is in response to a very low central venous pressure.  Hyaline membranes form in adult shock lung and neonatal shock lung, IRDS, and in foals, puppies and newborn rabbits that lose blood volume at birth. [14]


The sequence of intra-partum Asphyxia-to-HIE-to-Cerebral Palsy has been widely reported, [10] [15] all under the misconception that hypoxia causes brain damage.  The hypoxia resulting from cord compression inevitably entails fetal hypovolemia – the oxygenated blood engorges the placenta while the fetus becomes exsanguinated.  ICC finalizes and accentuates the hypovolemic state.  Ischemic encephalopathy then begins and progresses after birth regardless of the oxygenation of the newborn.  Macroscopic ischemic neuron necrosis is readily visualized on MRI.  Minor lesions in small brainstem nuclei are more difficult to define.  Physiological neonatal cerebral blood flow (the MRI norm) following physiological placental transfusion has yet to be reported.


In summary, ICC may be harmless in the child that receives a large placental transfusion before the cord is clamped, but ICC compromises all other neonates to varying degrees by loss of blood volume.  Tissue damage results from deficient tissue perfusion with permanent injury occurring mainly in the brain and lungs, although multi-organ dysfunction is often seen as well.


The newborn child, premature or otherwise, is very capable of closing its own cord vessels.  It has had millions of years of natural selection to perfect the required reflexes that ensure survival.  Very basically, blood volume from the placenta is used to initiate function of the child’s own life support organs and systems, after which the placental vessels close reflexively.  The use of a cord clamp during this process disrupts physiology and causes injury.






1.                  "A Treatise on the Management of Pregnant and Lying-In Women" by Charles White, published in 1773.


2.                  Erasmus Darwin,  Zoonomia, 1801; Vol. III page 321


3.                  Windle WF (1969) Brain damage by asphyxia at birth.  Scientific American 221(#4): 76‑84.

4.                  Myers RE (1972) Two patterns of perinatal brain damage and their conditions of occurrence.  American Journal of Obstetrics and Gynecology 112:246-276.30.

5.                  Linderkamp O. Placental transfusion: determinants and effects. Clinics in Perinatology 1982;9:559-592

6.                  Peltonen T.  Placental Transfusion, Advantage - Disadvantage. Eur J Pediatr. 1981;137:141-146


7.                  Lozoff B. Jimenez E. Wolf AW.  Long Term Development Outcome in Infants with Iron Deficiency. N Eng J Med 1991; 325: 687-94.


8.                  Hurtado EK et al.  Early childhood anemia and mild to moderate mental retardation.  Am J Clin Nut. 1999; 69(1): 115-9.


9.                  ACOG Committee Opinion Number 138 - April 1994, published in the International Journal of Gynaecology and Obstetrics 45:303-304 [54], reaffirmed 2000, and listed as current in OBSTETRICS & GYNECOLOGY, February 2002,


10.             Frances Cowan et al. Origin and Timing of Brain Lesions in Term Infants with Neonatal Encephalopathy.  The Lancet, Vol.361, Issue 9359,1 March, 2003 pages 736-742


11.             Simon E.  Brainstem Lesions in Autism: Birth Asphyxia and Ischemia as Causative Factors IMFAR presentation October 2002


12.             Suarez RD et al. Indomethacin Tocolysis and Intraventricular Hemorrhage. OBSTETRICS & GYNECOLOGY Vol. 97 No. 6 June 2001 921-925.


13.             N A Murray and I A G Roberts.  Neonatal transfusion practice Arch. Dis. Child. Fetal Neonatal Ed., Mar 2004; 89: F101 – 107




15.             Hankins G.D.V.  et al.  Neonatal Organ System Injury in Acute Birth Asphyxia Sufficient to Result in Neonatal Encephalopathy.  OBSTETRICS & GYNECOLOGY, May 2002. Vol. 99, No. 5, part 1. Pages 688-691



Figure 1. Myers RE (1972) Two patterns of perinatal brain damage and their conditions of occurrence.  American Journal of Obstetrics and Gynecology 112:246-276.30.


Copyright September 2004 G. M. Morley MB ChB FACOG