Kernicterus and the blood-brain-barrier (BBB)
Lou et al. (1977) addressed what appeared to be
the primary concern over "delayed" cord clamping
allowing placental transfusion [1].  Citing the paper
by Lucey et al. (1964) [2] they stated:

    "Asphyxiated infants are especially susceptible
    to kernicterus, even if their plasma-bilirubin
    levels are low.’ Furthermore, it is very difficult to
    produce clinical and pathological signs of
    kernicterus by injection of bilirubin intravenously
    in normal infant monkeys, while kernicterus was
    readily produced in previously asphyxiated
    monkeys." [1, p1062]

Mossakowski et al. (1968) used Evans blue dye to
investigate the blood-brain barrier in newborn
monkeys subjected to asphyxia by clamping the
umbilical cord and obstructing the airway [3].  Lou et
al. also used Evans blue dye in fetal lambs subjected
to oxygen insufficiency for 1-2 hours:

    "The fetuses were asphyxiated by partially
    inflating a cuff around the umbilical cord.
    Asphyxia developed over a period of 1-2 h (pH
    about 690)." [1, p1062]

The initial response of the fetal lambs was a slowing
of heart rate and increased blood pressure during
the first half- to one-hour period of umbilical cord
blood flow restriction.  After that the blood pressure
declined and remained low.  Twinning is frequent in
lambs, and Lou et al. used the twin as a control for
the fate of Evans blue dye, and reported:

    "We have found, in experimental asphyxia
    lasting 1-2 h, a striking discoloration throughout
    cortex and basal ganglia after intravenous
    injection of 3 ml/kg of a 2% solution of Evans
    blue in eight non-exteriorised fetal lambs, in
    contrast to the uncoloured brain tissue in non-
    asphyxiated twins acting as controls." [1, p1062]

In conclusion they commented:

    "We suggest that the breakdown of the fetal
    blood/brain barrier to albumin is due to a
    combination of the initial moderate hypertension
    and severe vasodilation during asphyxia.7 The
    permeability of the blood/brain barrier to
    albumin in asphyxiated babies would facilitate
    the transport of bilirubin from plasma to
    neurones and thus explain the increased
    susceptibility to kernicterus." [1, p1063]

If a baby does not breathe right away at birth, should
the umbilical cord be clamped off right away?  
Respiratory depression in infants born alive is a
current concern and topic for research [4, 5].  If an
infant is born alive, it has been receiving oxygen
through the umbilical cord up to the time of birth.  
Shouldn't that lifeline be left intact until the lungs
become functional?

Breakdown of the blood brain barrier by asphyxia
has been shown to allow bilirubin and other
substances in the circulation to enter the brain.  High
levels of bilirubin won't affect the brain if the blood-
brain barrier has not been breached.  Immediate
clamping has been too long defended as a means to
avoid circulatory overload and hyperbilirubinemia.

Lou et al. (1979) reported results of more research
on the vulnerability of the blood-brain barrier to
circulatory insufficiency in fetal lambs [6].

(in progress)
References
  1. Lou HC et al. (1977)
    Breakdown of blood/brain
    barrier in kernicterus.
  2. Lucey JF et al. (1964)
    Kernicterus in asphyxiated
    newborn monkeys.
  3. Mossakowski MJ et al.
    (1968) The early
    histochemical and
    ultrastructural changes in
    perinatal asphyxia.
  4. Baskett TF et al. (2006)
    Predictors of respiratory
    depression at birth in the
    term infant.
  5. Milsom I et al. (2002)
    Influence of maternal,
    obstetric and fetal risk
    factors on the prevalence of
    birth asphyxia at term in a
    Swedish urban population.
  6. Lou HC et al. (1979)
    Pressure passive cerebral
    blood flow and breakdown of
    the blood-brain barrier in
    experimental fetal asphyxia.
Full References
  1. Lou HC, Tweed WA, Johnson G, Jones M, Lassen NA. Breakdown of
    blood/brain barrier in kernicterus. Lancet. 1977 May 14;1(8020):1062-3.
  2. Lucey JF, Hibbard E, Behrman RE, Esquival FO, Windle WF. Kernicterus in
    asphyxiated newborn monkeys.  Exp Neurol 1964 Jan; 9(1):43-58.
  3. Mossakowski MJ, Long DM, Myers RE, DeCuret HR, Klatzo I. The early
    histochemical and ultrastructural changes in perinatal asphyxia. J
    Neuropathol Exp Neurol. 1968 Jul;27(3):500-516.
  4. Baskett TF, Allen VM, O'Connell CM, Allen AC. Predictors of respiratory
    depression at birth in the term infant. BJOG. 2006 Jul;113(7):769-74.
  5. Milsom I, Ladfors L, Thiringer K, Niklasson A, Odeback A, Thornberg E.
    Influence of maternal, obstetric and fetal risk factors on the prevalence of
    birth asphyxia at term in a Swedish urban population. Acta Obstet Gynecol
    Scand. 2002 Oct;81(10):909-17
  6. Lou HC, Lassen NA, Tweed WA, Johnson G, Jones M, Palahniuk RJ.
    Pressure passive cerebral blood flow and breakdown of the blood-brain
    barrier in experimental fetal asphyxia. Acta Paediatr Scand. 1979 Jan;68(1):
    57-63.
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