This short blog posts shares new considerations of thought around the mechanism of placental transfusion and onset of breathing and introduces some of the very latest research.
Is spontaneous breathing the driver for placental transfusion?
Placental transfusion is a widely accepted benefit of delaying cord clamping, as described in many scientific publications. Waiting to clamp the cord results in a net shift of blood volume from the placenta to the neonate and with that, improves iron stores during infancy and supports health and development for the growing child. Nevertheless, the exact underlying physiological mechanisms of placental transfusion still remain unclear, making placental transfusion a topic of many scientific debate.
What about the influence of gravity or uterine contraction?
The effect of gravity may be less than many people assume. In the human study by Nestor Vain (Vain at al 2014[1]), he found that the position of the newborn baby before cord clamping does not affect the volume of placental transfusion. Experimental studies with lambs by Stuart Hooper show that the umbilical venous flow is closely related to the umbilical arterial flow, suggesting that what goes into the placenta largely determines what goes out, regardless of the position of the baby in relation to the placenta (Hooper et al 2017[2]).
Experimental studies have shown that uterine contractions reduce rather than increase umbilical venous blood flow (Westgate et al 2007[3], Hooper et al 2017 [2], Stenning et al 2021[4]).
How about spontaneous breathing?
In the 1960s, studies have found that infants who breathe spontaneously prior to umbilical cord clamping, have less residual placental blood volume (Redmond et al 1965[5], Kjeldsen et al 1967[6]).
In a study by Isabelle Boere, published in 2015, it was observed that venous and arterial umbilical flow occur for much longer than previously described and is unrelated to the cessation of pulsations in the umbilical cord.
In many babies, the umbilical cord flow does not stop within 3 min and continues after the cord is white and stops pulsating.
It was also observed that there is a large influence of the infants’ first spontaneous breaths on the venous flow patterns, suggesting that spontaneous breathing could play an important role in placental transfusion (Boere et al 2015[7]).
What’s new?
Last month, on September 22nd, Dr. Emma Brouwer successfully defended her PhD thesis; “Physiological measurements of the effect of cord clamping strategies”[8]. Her work includes interesting new findings and suggestions on the mechanism that may be responsible for placental transfusion.
One of these findings is the effect of spontaneous breathing on venous return in healthy term infants during DCC (Brouwer et al 2021[9]). Emma found that inspiration was associated with a collapse of the inferior vena cava and an increased ductus venous flow and hepatic vein flow. Inspiration therefore appears to preferentially direct blood flow from the ductus venosus into the right atrium. In her thesis, Emma suggests that spontaneous breathing generates a negative intrathoracic pressure, drawing air into the lungs, but also possibly creating a greater influx of venous umbilical blood flow, while restricting arterial outflow. This results in a net increase in blood volume (Sommers et al 2012[10]). This theory could also explain why experimental studies failed to simulate this effect when using positive pressure ventilation to aerate the lungs, generating positive intrathoracic pressure.
And just hot of the press: KC Ashish from Uppsala[11] published an observational study among 2563 stimulated non-crying neonates, where he found that stimulation with the cord intact may help establish spontaneous breathing in apnoeic neonates; among neonates stimulated with the cord intact, 81.1% took spontaneous breaths.
Moreover, neonates with intact cord had a 84% increased odds of spontaneous breathing compared with those stimulated with the cord clamped.
What does this imply?
These findings suggest that spontaneous breathing could possibly be an important driving force for placental transfusion. This raises the thought though, that infants who do not breathe spontaneously at birth and receive (positive pressure) mechanical ventilation, may not benefit from placental transfusion.
Although this may be a concerning thought, Stuart Hooper actually teaches us that the key to delaying cord clamping is not placental transfusion but is to maintain cardiac output; to maintain the cardiac output, you’ll need the cardiac input to the left side of the heart which is provided by venous return from the placenta. Or, to flip this argument around, the decrease in cardiac output when clamping the cord before the baby is breathing, increases the risk of bradycardia and hypoxia and is probably an important cause of harm.
[1] https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(14)60197-5/fulltext
[2] http://dx.doi.org/10.1136/archdischild-2016-311159
[3] https://www.ajog.org/article/S0002-9378(07)00429-2/fulltext
[4] https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0253306
[5] https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(65)91403-0/fulltext
[6] https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(67)91823-5/fulltext
[7] https://fn.bmj.com/content/100/2/F121
[8] https://scholarlypublications.universiteitleiden.nl/handle/1887/3213482
[9] https://fn.bmj.com/content/early/2021/06/08/archdischild-2020-321431
[10] https://pediatrics.aappublications.org/content/129/3/e667.short
[11] https://bmjpaedsopen.bmj.com/content/5/1/e001207
Rianne Rotink
This blogpost is written by Rianne Rotink, CEO of Concord Neonatal. In her blogposts, Rianne will be sharing her latest personal insights and knowledge about stabilization with intact cord and physiological based cord clamping.