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Detecting ‘fetal distress’ in labour allows timely delivery, followed by effective resuscitation, if required, to restore or maintain adequate circulation with oxygenated blood to the baby. This should prevent or minimise brain damage from hypoxaemia or hypovolaemia. Nielso...
Detecting ‘fetal distress’ in labour allows timely delivery, followed by effective resuscitation, if required, to restore or maintain adequate circulation with oxygenated blood to the baby. This should prevent or minimise brain damage from hypoxaemia or hypovolaemia. Nielson et al (1) find the prevalence of cerebral palsy unchanged despite major changes in clinical care. This apparent failure of obstetric intervention and neonatal resuscitation should perhaps prompt a “back-to-basics” review of present paradigms. Morley’s excellent review (2) noted that “Newborn infants who do not breathe sufficiently need gentle assistance to make the transition from placental to pulmonary gas exchange” and “Current research is challenging widely held views about neonatal ’resuscitation’ and that a less aggressive, more gentle, approach may actually be more beneficial” but omitted the most aggressive intervention, of routine cord clamping.
Although a minute is recommended before initiating aggressive resuscitation - to assess the condition, count the heart rate and dry the newborn baby (3) - in practice decisions are made within seconds based on the CTG and first impressions. When the neonate is floppy, pale and does not establish breathing quickly, it seems obvious that the baby’s lungs should be ventilated with air. Nevertheless, this strategy does not seem to have delivered improvements. What if the journey to the resuscitaire to get air into the lungs, deprives the neonate of circulating blood to deliver oxygen to the brain? Sick neonates may be adversely affected by the abrupt interruption of the placental circulation and placental gas exchange. Back in 1981 it was advised that “There is … good reason in cases of resuscitation to keep the placental circulation intact.”(4) There is no logic in cutting off the functional, failing placental circulation before the pulmonary circulation is established. The pulmonary circulation could gently take over respiratory function as the placental circulation closes down. This happens gradually in nature with physiological management of the third stage. It could be replicated in medical practice, but somehow it is not convenient to combine the continuation of post-birth placental circulation with assessment of the neonatal condition, basic resuscitation and assisted ventilation.
The link between nuchal cord and two-fold increased risk for spastic cerebral palsy should give neonatologists food for thought (1). Iffy (5) also reported untoward sequelae when the nuchal cord was clamped before delayed delivery of the shoulders, considered to be due to the total loss of the placental circulation. However, as a result of cord compression, the return of oxygenated blood through the cord after delivery of the head but before delivery of the body is likely to be trivial. As cord compression leads to placental engorgement, and in consequence, fetal hypovolaemia, (6) clamping a nuchal cord may have little effect on the circulation before delivery is completed, but as soon as the baby is born the hypovolaemia then becomes critical as there is no opportunity for the blood backed up in the placenta to return. This is the “good reason” described to keep the placental circulation intact.(4)
Although early cord clamping clearly interrupts the physiological process of fetal adaptation to neonatal life, NICE recommends that the current practice is continued until there is conclusive evidence from RCTs that it is harmful.(7) A recent RCOG opinion paper also concluded that more evidence for effects (harm or benefit) on the neonate were required but that the timing of cord clamping had no impact on active third stage management.(8) All trials of cord clamping only address the issue in the baby not requiring resuscitation. Healthy babies usually cope with the sudden closure of the placental circulation, (9) so much so that it is generally considered part of normal transition. The impression that clamping a functioning placental circulation is normal is even promoted by physiology (10), paediatric (11) and cardiology (12) text books. In contrast, the first publication of its invention (13) instructed that the clamp should be applied “when pulsation in the cord has ceased”.
Clamping the cord before the placental circulation has been closed down naturally by the neonate has many significant and potentially adverse effects: there is a sudden increase in the afterload on the heart (9); the volume of blood required to fill the new pulmonary vascular bed must be “stolen” from the rest of the neonatal circulation (14), as the placental transfusion has been interrupted; this results in hypovolaemia which may be severe and unrecognised and could theoretically lead to the release of cytokines responsible for brain damage(15); it has been postulated that the acidaemia from accumulated lactic acid of labour may be exacerbated by early cord clamping (16); and lastly, a proportion of the baby’s stem cells, thought to be capable of repairing both brain and heart damage, will be lost within the clamped cord and placenta. (17) The opportunity to prevent asphyxia-related conditions, such as nuchal cord and occult cord compression, is lost: Firstly, division of a nuchal cord is rarely necessary (18); and secondly, there may indeed be other unidentified conditions (e.g. shoulder dystocia) where immediate cord clamping leads to greater disturbance in the neonatal vascular system and post-birth depression than is presently realised.
The concept of maintaining placental circulation during resuscitation is gaining some recognition (19) though the practicalities of bringing the resuscitation to the baby, rather than the baby to the resuscitaire, are still to be realised. At normal delivery it is relatively simple to move to the bedside. (Mercer J, personal communication) (20) Ironically, resuscitation with an adequately long intact cord at caesarean section is also straightforward. (21) Vaginal instrumental delivery may present the greater challenge and require some innovative design and thinking. The strategy may be even more important in preterm babies. (22)
There is no physiological sense in clamping the umbilical cord before resuscitation, which can only exacerbate the risks of hypoxia and ischaemia, thought to be causes of cerebral palsy.
1. Nielson LF, Schenedel D, Grove J, Hvidtjorn D, Jacobsson B, Josiassen T, Vestergaard M, Uldall P, Thorsen P. Asphyxia related risk factors and their timing in spastic cerebral palsy. BJOG 2008;115:1518-1528
2. Morley CJ, Davis PG. Advances in neonatal resuscitation: supporting transition Arch Dis Child Fetal Neonatal Ed 2008;93:F334–F336
3. Richmond S. Newborn Life Support. London; Resuscitation Council (UK):2005
4. Peltonen T. Placental transfusion - advantage and disadvantage. Eur J Pediatr 1981;137:141-146
5. Iffy L, Varadi V. Cerebral palsy following cutting of the nuchal cord before delivery. Med Law 1994;13:323–30
6. Dunn PM. Tight nuchal cord and neonatal hypovolaemic shock. Arch Dis Child 1988;63:570–1
7. NICE intrapartum care guideline http://www.nice.org.uk/nicemedia/pdf/CG55FullGuideline.pdf
8. RCOG opinion paper http://www.rcog.org.uk/resources/public/doc/draftearlylatecordclamping.doc
9. Gardiner HM. Response of the fetal heart to changes in load: from hyperplasia to heart failure. Heart 2005;91:871–873
10. Keel CA & Neil E (Eds.) Sampson Wright’s Applied Physiology 12th Edition. London, Oxford University Press 1971:551
11. Campbell AGM & McIntosh N. Forfar and Arneil’s Textbook of Pediatrics 5th Edition Churchill Livingstone New York, Edinburgh. 1998:106-107
12. Braunwald E, Zipes DP, Libby P. Heart Disease. In: A Textbook of Cardiovascular Medicine 6th edition Saunders Philadelphia 2001:1512
13. Magennis E. Analytical records – new inventions. A midwifery surgical clamp. Lancet 1899;May 20th:1373
14. Linderkamp O. Placental transfusion: determinants and effects. Clin Perinatol 1982;9:559–92
15. Rajnik, M., et al. Salkowski, CA. Thomas, KE. ; Li, Y; Rollwagen, F M. Vogel, SN., Induction of early inflammatory gene expression in a murine model of nonresuscitated, fixed-volume hemorrhage. Shock, 2002;17(4):322-8
16. Hutchon DJR. Immediate cord clamping may increase neonatal acidaemia. BJOG 2008;115(9):1190-1
17. Cord Blood for Neonatal Hypoxic-Ischemic Encephalopathy NCT00593242 http://clinicaltrials.gov/ct2/show/NCT00593242
18. Mercer JS, Skovgaard RL, Peareara-Eaves J, Bowman TA. Nuchal cord management and nurse-midwifery practice. J Midwifery Womens Health 2005;50:373–9
19. Wyllie J & Niermeyer S. The role of resuscitation drugs and placental transfusion in the delivery room management of newborn infants. Seminars in Fetal and Neonatal Medicine 2008;13:416-23
20. Mercer J. Potential effects of immediate cord clamping at birth. Seminar “Hypovolaemia and resuscitation – is the timing of cord clamping relevant?” Royal Hospital for Sick Children, Glasgow 5th June 2008
21. Hutchon DJR. How to resuscitate the neonate with the cord intact at caesarean section. British International Congress of Obstetrics and Gynaecology, 6 July 2007, London
22. Bell EF. When to transfuse preterm babies. Arch Dis Child Fetal Neonatal Ed 2008;93:F469–F473
David J R Hutchon
Consultant Obstetrician, Guy’s & St Thomas’ NHS Foundation Trust,
10th floor North Wing
St Thomas’ Hospital
Westminster Bridge Road
London SE1 7EH
Northwick Park Hospital,
North West Hospitals NHS Trust,
Harrow HA1 3UJ