Is it safe to allow a placental transfusion?
By the 1970s the practice of clamping the cord was
so widespread, at least in obstetric practice
associated with academic institutions, that whether a
placental transfusion should be allowed became a
major topic for research. Thus the opening
comment of the highly influential report of Saigal et
al. (1972) states:
"In full-term infants placental transfusion
increases the blood volume of the newborn
by 40% to 60% within 5 minutes of
birth. Most of the excess blood volume is
eliminated within 4 hours by an extravasation
of plasma from the circulation. For the
remainder of the neonatal period, such infants
retain a 50% larger red cell volume
dispersed through a slightly enlarged blood
volume, with higher hematocrit values than
are found in infants whose umbilical cords
are clamped immediately at birth." [1, p406]
Saigal et al. proceeded to note that the placenta is
proportionately larger than fetal weight of a child
born prematurely. They question how the circulation
of a premature infant responds to the "volume
overload" if a placental transfusion is allowed, and
whether the immature liver is prepared to handle the
greater amount of bilirubin produced by breakdown
of red blood cells.
Saigal et al. note that research to date had dealt with
the question of immediate versus delayed cord
clamping, but not "intermediate" cord clamping.
They thus designed the study reported to look at the
effects of clamping immediately and at 1 and 5
minutes after birth. A randomizing protocol was used
to assign infants to clamping of the cord at each of
the time points. Blood volume was measured in 125
premature and 45 full-term infants using radioactive
iodine.
Bilirubin levels greater than 15mg/100ml were
viewed as dangerous, and exchange transfusions
were therefore required for 7 premature infants, 5 of
whom had cord clamping at 5 minutes after birth.
Exchange transfusions were thought necessary for 2
infants with immediate clamping of the cord. None of
the full-term infants had bilirubin levels greater than
14mg/100ml, but small increases were documented
for infants with cord clamping at 1 and 5 minutes.
Respiratory distress occurred in 22 of the premature
infants, 8 in the immediate clamping group, and 7
each in the 1- and 5-minute clamping groups.
Presence or absence of respiratory problems was
not associated with increased bilirubin levels, but
Saigal et al. concluded their discussion with the
statement:
"If delayed cord clamping is adopted as
a means to reduce the incidence of respiratory
distress syndrome in premature births,
there will be accompanying augmentation
of hyperbilirubinemia to deal with." [1, p 418]
This paper, with its single focus of bilirubin danger,
has been one of the most influential in adopting
immediate clamping of the umbilical cord at birth as a
standard protocol.
Five years later Saigal and Usher (1977) described
"symptomatic neonatal plethora" in 8 premature and
3 full-term infants with the suggestion that these
conditions were caused by "large placental
transfusions associated with delayed clamping of the
umbilical cord" [2, p62]. These infants were noticed
during an investigation of the effect of placental
transfusion on respiratory distress syndrome. Again
radioactive iodine was used to measure blood
volume, with acknowledgement by Saigal and Usher
that this was controversial.
The 8 premature children who exhibited symptoms of
"plethoric" skin color, rapd respirations, and
neurologic depression were hypervolemic, the 3 full-
term infants with these symptoms had elevated
hematocrits. Saigal and Usher stated implications of
their findings as follows.
"After many years of controversy, the question
of when to clamp the umbilical cord seems to be
resolving towards a middle course. Excessive
delay (more than 2 min) in cord clamping
produces hyperbilirubinemia and sometimes
symptomatic hypervolemia or polycythemia.
Immediate cord clamping in premature infants
tends to increase mortality from respiratory
distress syndrome. It seems advisable,
therefore, to delay cord clamping for 1 to 1 1/2
min in premature infants, with less delay in full-
term infants." [2, p70]
Thus clamping the cord soon after delivery had
become the norm. There seemed to be no memory
of the traditional teaching of textbooks, or research
like that of Gunther (1957) only 20 years earlier [3].
Treatment of mothers in premature labor with
betamethasone began in the 1970s to prevent
respiratory distress syndrome and hyaline
membrane disease of the lungs [4-6]. The
association of lung pathology with clamping of the
umbilical cord had become irrelevant, but placental
transfusion was now regarded as a potential hazard.
(in progress)
- Saigal S et al. (1972)
Placental transfusion and
hyperbilirubinemia in the
premature.
- Saigal S, Usher RH (1977)
Symptomatic neonatal
plethora.
- Gunther M (1957) The
transfer of blood between
baby and placenta in the
minutes after birth.
- Liggins GC, Howie RN
(1972) A controlled trial of
antepartum glucocorticoid
treatment for prevention of
the respiratory distress
syndrome in premature
infants.
- Avery ME (1972). Prevention
of hyaline membrane
disease.
- Avery ME (2000) Surfactant
deficiency in hyaline
membrane disease: the
story of discovery.
- Saigal S, O'Neill A, Surainder Y, Chua LB, Usher R. Placental transfusion
and hyperbilirubinemia in the premature. Pediatrics. 1972 Mar;49(3):406-
19.
- Saigal S, Usher RH. Symptomatic neonatal plethora. Biol Neonate. 1977;32
(1-2):62-72.
- Gunther M. The transfer of blood between baby and placenta in the
minutes after birth. Lancet. 1957 Jun 22;272(6982):1277-80.
- Liggins GC, Howie RN. A controlled trial of antepartum glucocorticoid
treatment for prevention of the respiratory distress syndrome in premature
infants. Pediatrics. 1972 Oct;50(4):515-25.
- Avery ME. Prevention of hyaline membrane disease. Pediatrics. 1972 Oct;
50(4):513-4.
- Avery ME. Surfactant deficiency in hyaline membrane disease: the story of
discovery. Am J Respir Crit Care Med. 2000 Apr;161(4 Pt 1):1074-5.