Hypotensive Extremely Low Birth weight Infants Have Reduced Cerebral
Blood Flow.
Editor: This investigation illustrates many misconceptions and
unwarranted assumptions that the perinatal professions apply to the
preterm child. The first paragraph mentions conflicting CBF data in
“stable” preterm infants and in those with respiratory distress.
Abnormalities are noted in MAP and CBF in “well” preterm infants and
“sick” preterm infants; the authors aptly describe the evidence as
“confounding.” If abnormalities of autoregulation are found in sick and
comparatively well neonates, are abnormalities sometimes normal? What
differentiates the “well” from the “sick” preterm infant; is it infection,
metabolism, tumor, trauma, genetics or something else? The only process
that will correct this confusion is definition of the physiological norm.
An animal pseudo-model for the ELBW infant exists. A kangaroo
“Joey”, delivered in the immature post-embryonic state, weighing a few
grams, clamps and snaps its own cord, claws its way from the vulva into a
pouch-incubator, elongates a nipple into a feeding tube and produces the
next healthy kangaroo generation – physiologically. The human mother has
lost the marsupial pouch and nipple over evolutionary time, but has the 26
-week human preemie lost the genetic capability of normal pulmonary
respiration and physiological umbilical cord closure?
In this group of 17 ELBW infants, immediate intubation and
ventilation, presumably done after immediate cord clamping, prevented an
answer for that question, however, a very similar group of 17 infants, [1]
27-32 weeks gestation, that had delayed cord clamping with gravity
assisted placental transfusion (not quite physiological cord closure) had
remarkably normal lung function compared to the cohort of 19 that were
immediately clamped. The author, Kinmond, comments: “We did not time the
onset of respiration relative to cord clamping, but many infants in the
[delayed clamping] group were already crying.”
Indeed, initial pulmonary ventilation in the physiological neonate
(no cord clamp used) may be much more a functional result of placental
transfusion than contraction of the diaphragm and expansion of the rib
cage. Jaykka [2] demonstrated that perfusion of the fetal lung resulted
in “erection” and AERATION of alveoli. Gunther [3] demonstrated how
powerful that perfusion and erection could be – 100+ mls of blood forced
into the inferior vena cava, heart and lungs within 30 seconds by the
contracting (physiological) maternal uterus. Gunther also showed that the
neonate controls and terminates the placental transfusion reflexively,
with blood volume increasing in a stepwise manner with successive uterine
contractions until optimal transfusion has occurred; the umbilical vessels
then close permanently. One would expect ELBW infants to be similarly
endowed.
Respiratory distress syndrome (RDS) and hyaline membrane disease
(HMD) are manifestations of hypovolemia and hypovolemic shock – shock
lung. RDS occurs at any age and HMD can be induced in newborn rabbits and
puppies by withdrawing blood volume, and in foals and primates by
immediate cord clamping. [4, 5] The most frequent clinical manifestation
of RDS is retraction respiration (RR) (gasping, intercostal recession),
also termed “air hunger” in the exsanguinated adult.
The RR symptom is a reflex response to insufficient filling of the
right heart – low central venous pressure – and gasping creates intense
pulses of negative intra-thoracic pressure that pull venous blood into the
right heart. In the retracting preemie with low MAP, RR may also pull
arterial blood from peripheral arteries into the thoracic aorta, resulting
in almost tidal flow in the carotid arteries, pulses of negative blood
pressure, and very deficient CBF. This intermittent loss of CBF may
account for “conflicting CBF data” previously mentioned. Doppler flow in
any peripheral artery will demonstrate the phenomenon during RR.
On MRI, IVH is visualized as a hemorrhagic infarct of the germinal
matrix. Being the most metabolically active area of the preemie’s brain,
the germinal matrix is the first area to infarct from deficient perfusion.
Suarez [6] noted almost 100% correlation of RDS with IVH, and although IVH
occurred in both of Kinmond’s groups, [1] ventricular dilatation (visible
loss of brain tissue) occurred only in the immediately clamped group.
Recently, the Cochrane review has reported decreased incidence of IVH in
preemies with delayed cord clamping.
In this present group of ELBW infants, immediate intubation and
continuous positive pressure ventilation prevented pathogenic retraction
respiration, and apparently prevented IVH over a 48-hour period. If these
infants had been left attached to their placentas and subjected to the
physiological “Jaykka” effect of placental transfusion, would they have
escaped intubation by crying spontaneously like Kinmond’s group? In the
late clamped term infant, initial systolic BP is 80 mms Hg, in the
immediately clamped infant, 60 mm Hg. [7] With placental transfusion,
would the MAP of the ELBW control group have been 37 mms Hg? Would there
have been any ELBW infants in the pre and post dopamine groups? These
ELBW infants were not dopamine deficient; they were blood volume
deficient. The correct treatment of hypovolemic hypotension is blood
transfusion.
Late clamping (say after five minutes) is not the same as no
clamping. Gunther recorded cord pulsation lasting nearly 20 minutes after
birth, and in such cases, clamping at five minutes may have the “early-
clamp” effect of hypovolemia.
On the other hand, the clamp might coincide with a transfusing
uterine contraction. The result would be a child very “distended” with
blood, blood that otherwise (no cord clamp used) would have drained back
into the placenta during uterine diastole. Physiological cord closure
results in an optimal blood volume. When used before physiological cord
closure, the cord clamp is injurious; when used afterwards, it is
harmless, and superfluous.
Unfortunately, no study has ever been done on delivering term or
preterm babies physiologically without a cord clamp, but every other
mammal on the planet, including primates and marsupials, does so very
successfully. The reader is referred to an extensive review [8] on this
subject entitled, 'When Should We Clamp the Umbilical Cord?' In
conclusion to the review, there is no defined answer provided. (The
correct answer is, “almost never.”) A study on neonates, term, preterm
and ELBW that are sent to the nursery with cord and placenta intact, is
long overdue. It would answer the above question, and stop the current
epidemic of cord clamp injuries.
George Malcolm Morley, MB ChB FACOG
obgmmorley@aol.com
References:
Kinmond S et al. Umbilical Cord Clamping and Preterm Infants: a
Randomized Trial. BMJ 1993; 306: 172-175
Jaykka S. Capillary Erection and Lung Expansion. Acta Paediatr. 1965
[nppl] 109.
Gunther M. The transfer of blood between the baby and the placenta in
the minutes after birth. Lancet 1957;I:1277-1280.
Mahaffey Leo W. Rossdale, PD. CONVULSIVE SYNDROME IN NEWBORN FOALS
RESEMBLING PULMONARY SYNDROME IN THE NEWBORN INFANT; The Lancet 1959 1223-
1225.
Windle W. Brain Damage by Asphyxia at Birth. Scientific American.
1969 Oct;221(4):76-84.
Suarez RD et al. Indomethacin Tocolysis and Intraventricular
Hemorrhage. OBSTETRICS & GYNECOLOGY Vol. 97 No. 6 June 2001 921-925.
Peltonen T. Placental Transfusion, Advantage - Disadvantage. Eur J
Pediatr. 1981;137:141-146
Philip A.G.S. Saigal S. When Should We Clamp the Umbilical Cord?
Neonatal Reviews Vol.5 No.4 2004 e142 © 2004 American Academy of
Pediatrics
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