Why early cord clamping at birth must stop now !

How can it be safe to suddenly clamp the cord within a few seconds of birth and when it is full of blood
and still circulation 40% of the babies combined cardiac output ?
Learn more below

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BMJ article about why cord early cord clamping must stop

Letter about neonatal resuscitation in Archives of Disease in Childhood

Clamping the umbilical cord at birth is not necessary although it has been convenient so that the baby can be removed from its mother before delivery of the placenta, usually 5 to 10 minutes after the birth of the baby. We now clearly recognise that taking the baby away from its mother at birth is harmful to both the baby and the mother. Some years ago it was thought that early cord clamping was an important element in active management of the third stage of labour to prevent post partum haemorrhage. This is now known not to be the case. RCOG Greentop guideline 52 page 4 addendum

ILCOR also recognise just how important it is for the newborn baby to transiton naturally from placetnal respiration to pulmonary respiration. European Resuscitation Guidelines Page 1222Clamping and cutting the cord at birth is an intervention which has no purpose. Withdrawal of such an intervention does not require proof of harm. There is however plenty of evidence of harm ! The latest in a long line of trials showing harm is in a recent BMJ study from Sweden

Why do so many intelligent, caring obstetricians and neonatologists not stop routine cord clamping at birth? Part of it may be complacency. (Some are also very concerned like myself) Many think the harm that cord clamping may do is very minor and pressure of time prevents them from looking into it more carefully. However I will show you that the harm of cord clamping can sometimes be very serious.

Perth (Austrialia) professor tells of serious risks of cord clamping

RCM to recommend delayed cord clamping

International conference on transition and cord clamping at birth April 2013

It is increasingly recognised that the circulatory changes involved in transition at birth cannot occur within a few seconds of birth. While the healthy fetal circulation and the healthy neonatal circulation are moderately well understood, the underlying triggers, the precise sequence and speed of the changes in the circulation are not. (How can we interefere in something we do not understand ?)

Nearly all textbooks and journals which include the physiological transition of the neonate at birth describe a marked change in the peripheral vascular resistance and an increase in the afterload of the heart. One notable exception is Gray's Anatomy. Gray's Anatomy describes inflation of the neonatal lungs as the first change after birth and does not describe any changes in the afterload of the heart. Afterload is the force that the myocardium generates during ejection against systemic and pulmonary vascular resistances. Reductions in afterload increase stroke volume if other variables remain constant. Gray's Anatomy also describe the release of bradykinins from the pulmonary vascular epithelium which are vasoconstrictors to the umbilcal arteries. A high oxygen tension in the blood reaching the umbilcal arteries also has a vasoconstrictor effect on these vessels. Those texts that describe the sudden increase in afterload of the heart, explain that this is the result of withdrawal or closure of the placental circulation. Although Hofmeyer did demonstrate a sudden increase in arterial pressure in the healthy neonate in response to the application of a clamp on the umbilical cord 35 seconds after birth there have been no other investigations of the arterial effects of clamping the umbilical cord. On the other hand the effects of the cord clamp on the venous circulation has been investigated in some detail very recently by Farrar et al showing that sometimes as much as 40% of the neonatal blood volume is permanently trapped in the placenta by early cord clamping.

There is enough understanding of the fetal and neonatal circulation to build a computer simulation and determine whether or not the marked rise in afterload of the heart is likely to occur during a physiological transition. This is what it shows. Although the transition of the neonate has not been well investigated, it occurs successfully in the vast majority of births and has been observed by thousands of midwives. There is no question that a healthy baby will start to breathe soon after birth and the umbilical cord will stop pulsating and become white and empty a few minutes later. In animals it is well established that the high vascular resistance of the fetal lung falls quickly after the lungs are inflated with air. Thus the cardiac output will be partly redirected into the pulmonary circulation when the baby starts to breath and this has the effect of reducing the placental blood flow. (see above) In reality it is likely that the rate of fall in vascular resistance of the lungs will be closely matched by the rate of rise in vascular resistance of the placental circulation. Since the two most clearly understood triggers for closure of the umbilical arteries will not be present in the umbilical arterial blood until the after the lungs start to function. There have been no longitudinal studiesto measure the circulation in the fetus and neonate. In the fetal circulation the right ventricular output (250mls/min/kg) is slighly greater than that of the left. (200mls/min/kg) After transition and closure of the ductus arteriosus the outputs must equalise. How this is achieved by the neonatal heart is not understood and failure to equalise could be a consequence of a sudden increase in afterload at birth. Heart loads are also thought to have a considerable influence on the active adaption of the heart after birth.(18) This model shows no evidence to support the idea that a physiological transition is accompanied by any significant change in the after load of the heart, nor any significant change in the systemic vascular resistance as has been described. Tit shows that there is no need for any change in the cerebral circulation. This is of considerable importance as our investigation indicates that the sudden rise in afterload of the heart is the result of early cord clamping, which will result in a marked increase in the cerebral circulation and in the cerebral vascular pressure. The neonatal brain cannot be expected to cope with a sudden increase in the cerebral blood flow by a factor of 2.2 without some risk of injury. Studies of the venous effects of early cord clamping show the result is hypovolaemia, which can be severe, (10) and will lead to a subsequent fall in cardiac output and fall in cerebral circulation. This could account for the findings of Meyer and Mildenhall (19) who showed a fall in the superior vena cava blood flow (a surrogate measure for cerebral blood flow) in preterm babies who had immediate cord clamping from 20% to 12% of the CCO. Baenziger et al (20) showed a similar fall in cerebral circulation with early cord clamping. Until respiration is well established the pulmonary vascular resistance will remain high leading to a high afterload of the heart. In cases 4,5,6 and 8, after physiological transition, the cerebral blood flow fell from the fetal level by up to 16%. This is the result of the pulmonary circulation taking a greater proportion of the cardiac output in the neonatal model than did the placental circulation before transition. The vascular resistance of the placenta was adjusted in these cases to provide a placental flow down to 20%. Given the importance of maintaining a consistent cerebral circulation this seems an unlikely physiological pattern, but could have implications in intra-uterine growth restriction when the placental blood flow is reduced. Most investigations measured the normal placental blood flow at 40% of the CCO. Simulation might be the only way of demonstrating these marked changes which early cord clamping imposes on the neonatal circulation. Clinical studies of the short and long term consequences of cord clamping have shown evidence of harmful effects on the brain particularly in preterm babies.(21) It would be extremely difficult and may be unethical with the current evidence and guidelines, to carry out direct measurements in the newborn baby. The model indicates that the description of a marked rise in afterload of the heart does not occur in a physiological transition.

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