NUEVOS ESTUDIOS SOBRE EL CORTE TARDÍO DEL CORDÓN UMBILICAL

Hutchon, D J R; Thakur, I  Resuscitate with the placental circulation intact Archives of Disease in Childhood.  Volume  93(5), May 2008, p 451

Reynolds, in common with the majority of neonatologists and obstetricians, would be unable to keep his nerve and delay three minutes before clamping and cutting the cord to be able to proceed with resuscitation. However, maintaining a placental circulation may sometimes be all that is required as Aristotle observed, “Frequently the child appears to be born dead, when it is feeble and when, before the tying of the cord, a flux of blood occurs into the cord and adjacent parts. Some nurses who have already acquired skill squeeze (the blood) back out of the cord (into the child’s body) and at once the baby, who had previously been as if drained of blood, comes to life again”.

We do not recommend the practice described by Aristotle but some lateral thinking is required. When reversal of tracheal occlusion, performed in cases of severe congenital diaphragmatic hernias, is needed at birth an ex utero intrapartum treatment (EXIT) procedure is used. Essentially a functional placental circulation is maintained until the tracheal occlusion can be removed and the neonate ventilated.

Resuscitation before the placental circulation has ceased allows some warm oxygenated blood to return to the neonate to supplement oxygenation from the newborn’s lungs. Indeed as the pulmonary vasculature opens up, drawing blood from the rest of the body, the deficit is replaced by redistribution of the returning placental blood. This effect is recognised as the placental transfusion that occurs in a physiological third stage.

Resuscitation before the cord is clamped and cut takes a little preparation and thought. We have developed a procedure for use during a caesarean section to provide all the normal equipment for resuscitation without compromising the facilities for the neonate or the mother, so that ventilation and pulmonary respiration can be established while the cord remains intact. Precise arrangements may need to be modified according to different theatre layouts. Essentially it involves bringing the resuscitaire up to the side of the operating table. Other approaches are possible. Preparation and cooperation between obstetrician, paediatrician and theatre staff are the keys to success. There are likely to be substantial benefits for babies with significant hypoxia. When fetal distress is caused by cord compression such as with a nuchal cord, the fetus may already be hypovolaemic at birth. Delayed clamping allows time for the placental transfusion to correct the hypovolaemia.

N Wiberg,  K Källén,  P Olofsson   Delayed umbilical cord clamping at birth has effects on arterial and venous blood gases and lactate concentrations.  BJOG Volume 115 (6) Mayo 2008, p 697-703

ABSTRACT

Objective: To estimate the influence of delayed umbilical cord clamping at birth oarterial and venous umbilical cord blood gases, bicarbonate , base excess (BE) and lactate in vigorous newborns.

Setting: University hospital.

Design: Prospective observational.

Sample: Vaginally delivered term newborns.

Material and methods: Umbilical cord arterial and venous blood was sampled repeatedly every 45 seconds (T₀= time zero; T₄₅= 45 seconds, T₉₀= 90 seconds) until the cord pulsations spontaneously ceased in 66 vigorous singletons with cephalic vaginal delivery at 36–42 weeks. Longitudinal comparisons were performed with the Wilcoxon signed-ranks matched pairs test. Mixed effect models were used to describe the shape of the regression curves.

Main outcome measures: Longitudinal changes of umbilical cord blood gases and lactate.

Results: In arterial cord blood, there were significant decreases of pH (7.24–.21), (18.9–8.1 mmol/l) and BE (−4.85 to −6.14 mmol/l), and significant increases of PaCO₂ (7.64–8.07 kPa), PO₂ (2.30–2.74 kPa) and lactate (5.3–5.9 mmol/l) from T₀ to T₉₀, with the most pronounced changes at T₀–T₄₅. Similar changes occurred in venous blood pH (7.32–7.31),  (19.54–19.33 mmol/l), BE (−4.93 to −5.19 mmol/l), PaCO₂ (5.69–5.81 kPa) and lactate (5.0–5.3 mmol/l), although the changes were smaller and most pronounced at T₄₅–T₉₀. No significant changes were observed in venous PO₂.

Conclusion:  Persistent cord pulsations and delayed cord clamping at birth result in significantly different measured values of cord blood acid–base parameters.

DJR Hutchon Immediate cord clamping may increase neonatal acidaemia BJOG Volume 115 (9) Julio 2008, p 1190-1191

Sir,

Wiberg et al.1 have identified another likely risk of immediate cord clamping and a reason to routinely delay cord clamping at birth. They explain the fall in pH during the first 90 seconds after birth by a ‘tissue trapping’ phenomenon that leads to a flood of accumulated anaerobic metabolites in nonpriority organs reaching the general circulation of the baby after birth.

When the cord is clamped immediately after birth, these anaerobic metabolites are distributed into a smaller volume of blood (that of the baby alone) leading to a lower pH from which the baby will need to recover. As they point out, by delaying clamping, the blood volume of the baby is greater by up to 30% and these metabolites are then diluted into a larger volume of blood. If the cord is not clamped, there will also be

the opportunity for the metabolites to be distributed into the whole of the fetal–placental blood volume. Although the results did not suggest a large ability of the placenta to transport fixed acids in the few minutes after birth, there is the potential for a further improvement in the acid–base balance of the newborn baby through this mechanism.

Measuring acid–base balance at birth reflects the degree of hypoxia during labour and this information is valuable largely for medico-legal purposes. The acidaemia is a consequence of hypoxia but acidaemia itself also has a number of other effects. One adverse effect is in compromising the integrity of the blood–brain barrier.2 The integrity of the blood–brain barrier is critical for normal brain function and development.

Any reduction in neonatal acidaemia could help to keep the blood–brain barrier intact.

Only three of the babies in this study had significant acidaemia and none needed active resuscitation. Until the pulmonary circulation is open, the baby will remain hypoxic and the anaerobic metabolites will remain in the nonpriority organs only to be released after oxygen levels improve. When active resuscitation is necessary, it is common practice to clamp the cord before resuscitation commences. After successful resuscitation, therefore, these babies will have these anaerobic metabolites distributed into a much reduced circulating blood volume. Resuscitation with the cord intact overcomes the problems described above.3 The baby will have a normal blood volume and the anaerobic metabolites will be diluted as much as possible. There is the additional advantage of a complimentary supply of oxygen from the placenta as shown in this study. While the arterial oxygen going into the placenta was about 2.5 kPa, the blood returning to the baby has an oxygen level of about 3.7 kPa during the first 90 seconds after birth. Ways to avoid immediate cord clamping and allow resuscitation if necessary at all births must be explored.

References

 1 Wiberg N, Kallen K, Olofsson P. Delayed umbilical cord clamping at birth has effects on arterial and venous blood gases and lactate concentrations. BJOG 2008;115:697–703.

2 Lou HC, Tweed WA, Johnson G, Jones M, Lassen NA. Breakdown of blood/brain barrier in kernicterus. Lancet 1977;14:1062.

3 DJR Hutchon, Thakur I. Resuscitate with the placental circulation intact. Arch Dis Child 2008;93:451.