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I read this article by Bell with keen interest where author has
discussed about the need of blood transfusion in preterm babies. He has
suggested very practical and useful steps to minimise the number of the
blood transfusions in the preterm babies. The threshold for the blood
transfusion in preterm babies varies from centre to centre, within the
In one of my retrospective...
In one of my retrospective analysis study done in a regional tertiary
neonatal intensive care unit at St. Mary’s Hospital, Manchester had shown
that all (100% cases) the preterm babies requiring oxygen were transfused
when the haemoglobin level fell down < 12gm/dl. All these babies were
requiring respiratory support as well. Two of the well thriving babies
well transfused when haemoglobin level fell down < 8gm/dl.
While working in another regional tertiary neonatal intensive care
unit, Jessop Wing in Sheffield, we transfused all the extremely sick
preterm babies (with refractory hypotension, PPHN or requiring 100%
oxygen) when their haemoglobin level fell down < 13 gm/dl. We
transfused the babies if haemoglobin fell down < 12gm/dl and either
they required respiratory support or oxygen requirement was > 40% in
the first week of life. All oxygen dependent babies in the first week or
respiratory support with oxygen after first week get blood transfusion if
haemoglobin level fall < 11gm/dl. A well growing baby will get blood
transfusion if the haemoglobin level will fall < 7gm/dl.
A recent retrospective audit on the blood testing from unit clearly
showed that we do repeat blood tests far often than needed for these
extremely sick and fragile babies. Blood loss by the phlebotomy is one of
the most important reasons for a blood transfusion in small preterm
babies. Care providers for these preterm babies should make their local
guideline to minimise the blood loss by phlebotomy. Judicious individual
care plan should be made before ordering the blood tests.
Other methods as suggested by Bell like delayed cord clamping,
adequate nutrition by introducing total parenteral nutrition at an early
stage and further investigating importance of erythropoietin in preterm
babies can help in minimising the blood transfusion in the preterm babies.
We should stick to the single – donor transfusion programmes to minimise
the complications. In my experience we have been trying to transfuse the
preterm babies from the single donor whenever possible by using small
neonatal blood transfusion packs as suggested by Bell.
When to transfuse preterm babies
The SUMMARY begins by stating the false premises on which the article
is based: “The physiological anemia experienced by preterm babies is
exacerbated by the common practices such as early cord clamping … The need
for subsequent transfusion with red blood cells can be reduced by delaying
cord clamping … in infants who do not require immediate resuscitation.”
The cord clam...
The cord clamp is not a part of human anatomy or human physiology.
The logical conclusion deduced from the above statements is that early
clamping produces more anemia than late clamping; physiology is ignored.
Man is the only mammal that disrupts umbilical cord physiology with a cord
clamp; all mammals, including humans, close the umbilical cord
physiologically; the resultant physiological neonatal blood volume
contains blood that is moved from the placenta to the newborn after birth.
Blood counts following physiological cord closure are physiological. The
anemia of the author’s preterm babies is IATROGENIC and pathological; the
term “physiological anemia” is an oxymoron.
The statement “in infants that do not require immediate
resuscitation” implies that infants that DO require immediate
resuscitation MUST have immediate cord clamping (ICC) and must begin their
lives hypovolemic and anemic. The author does not elucidate the criteria
required for immediate resuscitation; however, the standard of care for
premature birth is ICC and removal to a resuscitation table. Thus preemies
are routinely compromised with hypovolemia and anemia produced by ICC –
NOT by physiology.
If the child is born with a pulsating cord, the placenta is supplying
the heart with oxygen. Whatever else may appear to be “at risk” for the
newborn requiring “immediate” resuscitation, could the author please
explain the resuscitation rationale for amputating the child’s existing
oxygen supply together with a major portion of its blood volume? Whatever
resuscitative measures are used immediately on the “at risk” newborn,
there is good reason to keep the placental circulation (oxygenation)
functioning and the blood volume intact during any resuscitation process.
The rest of the summary pertains to indications for iatrogenic
transfusion – liberal or constrictive guidelines – but the main indication
for transfusion remains “anemia.” The transfusion consists of red blood
cells. The author acknowledges that small preterm babies are anemic from
loss of blood VOLUME at birth. They are not anemic at the time of blood
loss; anemia is diagnosed from hemoglobin and /or hematocrit readings that
become pertinent many days AFTER the causative injury – that remains
undiagnosed and untreated. No evidence is presented that anemia per se is
pathogenic, or that correction with red cells is beneficial.
“Should I transfuse this baby today, or would it be better to wait?
This question has perplexed neonatologists for decades!” It has perplexed
perinatologists for decades! They all have been indoctrinated with the
false concept of a cord-clamped neonate having a physiological / normal
blood volume. The ICC neonate (preemie or otherwise) is routinely
HYPOVOLEMIC, and routinely becomes anemic depending on the amount of blood
volume clamped in the placenta. With loss of blood volume, various organs
become ISCHEMIC, and ischemic lesions (infarcts) may develop.
Ischemic encephalopathy results in infarction of the basal ganglia
and the cerebral cortex. In the preemie, cerebral ischemia results in
hemorrhagic infarction of the germinal matrix – with intra-ventricular
hemorrhage, (IVH). Necrotizing entero-colitis (bowel infarction) occurs
in these ICC babies. They develop “hypovolemic shock lung” – hyaline
membrane disease – pulmonary infarction.  All the above pathologies
have nothing to do with anemia, oxygenation or the capacity of blood to
carry oxygen; they are all caused by INADEQUATE BLOOD FLOW through the
tissues. With copious blood flow, tissues can survive on anaerobic
“Should I transfuse this baby today, or would it be better to wait?”
The correct answer is, “IT DOESN’T MATTER EITHER WAY!” By the time the
child corrects its blood volume with plasma to the point of anemia, the
ischemic infarcts are permanent damage. The correct QUESTION AT BIRTH is:
“Should I clamp the cord now, or would it be better to wait until after
physiological placental transfusion is complete?”
During physiological birth, (without a cord clamp) the placental life
support functions are transferred to the newborn in the form of a massive
blood transfusion totaling from 30% to 50% of the child’s final blood
volume. [3,4] This additional blood volume is used to initiate the
pulmonary circulation, to convert the fetal circulation to the adult
circulation, and to establish active function in the gut, kidneys,
skeletal muscles, (diaphragm) CNS and all other life support systems
needed for atmospheric existence.
Gravity, maternal intra-abdominal pressure and / or uterine
compression of the placenta generate this “placental transfusion,” and
they can force 75 ccs of blood into the newborn within 20 to 30 seconds.
[3, 4] The timing of this transfusion can occur immediately after birth
 or it may take more than ten minutes to occur.  The transfusion is
regulated and terminated reflexively by the newborn.
The uterine arteries / arterioles close in response to high oxygen
tension that releases prostaglandin from their vessel walls.  Placental
oxygenation / respiration are thus maintained until pulmonary respiration
is well established. The uterine vein (in the abdomen) is closed by
sphincters controlled by pressor receptors in the atria in response to
high central venous pressure.
After physiological cord closure, the term child has obtained a
maximal, optimal, physiological blood volume, and has received enough iron
to prevent anemia for the first year of life. [6, 7] This is also true for
babies born at 34 to 36 weeks.  The marsupial mammals routinely deliver
at a very early gestational age, equivalent to 14 weeks of human
gestation. The kangaroo “Joey” is almost post-embryonic; it clamps its
own cord and claws its way into a pouch (incubator) and swallows a long
nipple into its stomach (feeding tube.) The immature kangaroo Joey’s
lungs are mature and function perfectly; development proceeds without
pathology and without a cord clamp. There is no evidence to contradict
that a human preemie could survive similarly.
“Should I transfuse this 26 weeks gestation baby today, or would it
be better to wait?” “Should I clamp this 26 week pulsating cord now, or
would it be better to wait until after physiological placental transfusion
has provided enough blood volume to initiate function in all the child’s
life support systems, to prevent ischemic infarctions, to prevent anemia
and obviate any need for red cell transfusion later?”
This particular baby (26 weeks gestation) has delivered normally. It
is not yet breathing, and the cord is pulsating vigorously at 130 bpm.
The color is purple pink, tone is normal, reflexes are normal. It is in a
warm blanket and a rectal thermometer records 36.5 deg. C. The child is
very healthy on placental life support – as it was in utero.
As the uterus contracts around the placenta, blood is forced into the
child, through the heart and into the pulmonary vessels; this produces the
“Jaykka effect” – erection and aeration of the alveoli.  [10, 11, 12]
Blood flow (high colloid osmotic pressure [COP]) around alveoli absorbs
amniotic fluid (low COP) from the alveoli and the lungs are dried out.
Left ventricular blood becomes oxygenated and breathing / crying reflexes
are stimulated.  Placental transfusion has initiated pulmonary
Oxygenated blood in the umbilical arteries closes them with release
of prostaglandin; further uterine contractions force more blood into the
child who responds to high central venous pressure by closing the
umbilical vein with “pressure valve” sphincters until the placenta is
delivered and an optimal blood volume achieved.  After full placental
transfusion, some hemo-concentration usually occurs with increased blood
pressure forcing fluid into the extra-cellular space; hemoglobin and
hematocrit readings RISE as does albumin concentration, (COP) further
drying out the preemie’s lungs.
The child, cord and placenta can then be placed in an incubator for
In Kinmond’s study,  MANY of the preemies delivered with delayed
cord clamping (30 seconds delay with GRAVITY PRESSURED placental
transfusion) WERE CRYING WHEN THE CORD WAS CLAMPED (Jaykka effect); 
this was less likely in the ICC group (no Jaykka effect). When a preemie
is crying, is immediate resuscitation needed? When a preemie is NOT
breathing soon after birth, the rational resuscitation procedure is to
have the mother PUSH; maternal intra-abdominal pressure will achieve
placental transfusion and the Jaykka effect will initiate respiration -
A cord pulsating at >100 bpm indicates normal newborn oxygenation
and full placental life support; it contradicts iatrogenic interference
with the cord and the ongoing physiological transition to establish the
newborn’s life support systems.
The rational management of all preterm births thus becomes NON-
INTERFERENCE in the physiological closure of the umbilical cord after
birth. Airway clearance and open placental circulation should be ensured.
The cord clamp should not be used. The child, cord and placenta should
arrive intact in the NICU.
1. Peltonen T. Placental Transfusion, Advantage - Disadvantage. Eur J
2. Landau DB. Hyaline membrane formation in the newborn: hematogenic
shock as a possible etiological factor. Missouri Med1953; 50: 183.
3. Gunther M. The transfer of blood between the baby and the placenta
in the minutes after birth. Lancet 1957;I:1277-1280.
4. Diaz Rossello JL. Cord clamping for Stem Cell Donation: Medical
Facts and Ethics. Neoreviews 2006;7;e557-e563. DOI: 10.1542/neo.7-11-e557
5. McGrath JC, McClennan SJ. Contraction of umbilical artery, but nor
vein, by oxygen. J. Physiology 1986;380;513-519
6. Wilson, Windle, Howard. Deprivation of Placental Blood as a Cause
of Iron Deficiency in Infants. Amer. Jour. Child. Diseases 1941
7. Chaparro CM, Neufield NM, Effect of timing of umbilical cord
clamping on iron status in Mexican infants. Lancet 2006 June 17; 367(9527)
8. Ultee J, Swart K, Delayed Cord Clamping in Preterm Infants
delivered at 34 to 36 weeks gestation. Arch. Dis. Child. Online Feb 2007.
9. Kinmond S et al. Umbilical Cord Clamping and Preterm Infants: a
Randomized Trial. BMJ 1993; 306: 172-175
10. Jaykka S. Capillary Erection and Lung Expansion. Acta Paediatr.
1965 [nppl] 109.
11. Jaykka S. An experimental study of the effect of liquid pressure
applied to the capillary network of excised fetal lungs, Acta Paediatr.
1957; Supp 112:2-91.
12. Avery ME et al. The inflationary pulmonary force produced by
pulmonary vascular distension in excised lungs. The possible relation of
this force to that needed to inflate the lungs at birth. J. Clin. Invest.
1959; 38: 456-460
G. M. Morley, MD