Human assisted delivery of thoroughbred foals
The Lancet published a letter from Mahaffey and
Rossdale (1957) describing their observations on a
convulsive syndrome affecting about 2 percent of
thoroughbred foals delivered with human
assistance. Their letter was in response to the
article by Gunther (1957) on postnatal transfusion
and an earlier paper by Bonham Carter et al. (1956)
on pulmonary problems and "cerebral irritation" in
human infants.
Mahaffey and Rossdale stated, "For a considerable
time we have been greatly concerned with the
possibility that the syndromes are associated with
very early severance of the umbilical cord." They
went on to suggest that this practice may deprive the
newborn foal of up to 1500 ml of placental blood,
which may be more than 25 percent of a normal
foal's blood volume, and then commented:
"It seems more than a coincidence that, as far
as we can verify, the syndromes do not occur in
thoroughbred foals which are born unattended
in open paddocks in Australia, but are well
known in France and Italy, where the cord is
always severed by attendants within seconds of
birth. Further, in Europe the disease seems to
be unkown in breeds of horses other than
thoroughbreds and these generally foal without
human 'interference.' Other domestic species
which give birth to their young alone, and
'naturally,' are similarly unaffected."
Mahaffey and Rossdale (1959) described the
pulmonary pathology associated with convulsive foal
syndrome along with the neonatal behavioral
disturbance. The condition was reported to follow an
apparently easy delivery, but when attempting to get
to his feet for the first time, the foal begins jerking his
head up and down, becomes unsteady on its feet,
and falls down. The animal may emit a barking noise
associated with rapid respirations and increased
heart rate, then go into violent convulsions. About
half of the foals recover without any apparent
residual effects, but may pass through a period of
seeming blindness, wandering aimlessly about
before learning to suck from their mother.
In foals that died, aeration of the lungs was found to
be incomplete. Lung tissue was described as dark
and dense, resembling fetal liver, as opposed to the
pink feathery appearance throughout the lungs of
foals that did not experience respiratory problems or
convulsions in the newborn period. Abnormalities of
lung tissue was noted to be comparable to that
described in human infants dying of pulmonary
syndrome. Mahaffey and Rossdale also noted that
the ductus arteriosus was patent to a marked degree
in the convulsive foals, an indication of incomplete
transition to normal postnatal circulation. They
attributed these abnormalities to the conduct of
human assisted parturition:
"Variable degrees of traction are usually
practised by attendants when the head and
forelegs are emerging from the vulva. The
amnion is prematurely ruptured by hand, the
legs are grasped and a pull is exerted upon
them... the umbilical cord is ruptured with such
haste that the newborn foal (weighing 100-120
lb.) is deprived of an average of 1020 ml. of
blood and often 1500 ml. -- probably about 30%
of its potential blood-volume.
Under normal conditions a mare usually rests
for period of up to half an hour after parturition,
during which the foal also is inactive. The cord
remains intact and is not broken until the mare
(sometimes the foal) attempts to get to its feet.
Meanwhile virtually all the blood in the placenta
has passed back into the circulation of the foal,
and it is difficult to collect even 50 ml. of blood
when the cord ruptures at this stage."
Dunn (1972) acknowledged the importance of
observations on the convulsive foal syndrome for
understanding respiratory distress in human infants,
which he described as a maladaptation to
extrauterine life, most frequently in preterm infants.
He discussed deficiency of surfactant in preterm
infants and frequent association with Caesarean
section as etiological factors. The child delivered by
Caesarean, "is often born in a state of blue asphyxia
-- apnoeic and cyanosed, yet with vigorous cord
pulsation... In most cases the pulsating umbilical
cord is clamped at once to allow the obstetrician to
complete the operation." Dunn commented further:
"In fact there is no reason why the cord should
be clamped at all and since 1961 I have been
advocating and practising delivery of the infant
and placenta together as one unit, both being
laid together at the same level and the cord
only ligated after respiration has been
established and all pulsation has ceased.
It is of interest that this practice was widely
followed throughout most of the world until the
recent spread of Western civilisation. Even
today it is still adhered to in many isolated and
primitive communities. It is of course practised
by many animals.
In this context it was with tremendous interest
that I read of Mahaffey and Rossdale's (1959)
observation that "barkers" were never found
among foals born in the open field but only
among those delivered indoors with human
supervision, including early ligature and division
of the umbilical cord."
In 1976 Palmer and Rossdale reported
neuropathological changes found in 18 foals that
had exhibited signs of the "convulsive foal
syndrome." A spectrum of changes in the brain were
observed, including ischemic necrosis within the
cerebral cortex in nine of the foals, with involvement
of the diencephalon and brainstem in three of
these. Hemorrhagic damage of the cerebrum, and
sometimes the brainstem and cerebellum, was
observed in the other nine foals.
Palmer and Rossdale compared their findings with
the two patterns of damage described by Myers in
1972 seen in monkeys subjected to hypoxia and or
asphyxia shortly before or after birth. Myers
subjected monkeys to partial hypoxia late in
gestation, which resulted in damage of the cerebral
cortex similar to that seen in human cases of
cerebral palsy. On the other hand, when he inflicted
catastrophic total asphyxia at birth for several
minutes, damage was restricted to the brainstem.
Palmer and Rossdale found brainstem damage in
foals who suffered apnea at birth, including lesions
of the inferior colliculi as had been the case in
monkeys subjected to asphyxia.
- Mahaffey LW, Rossdale PD (1957) On the newborn infant's oxygen supply.
Lancet 1957 Jul 13, ii:95.
- Gunther M (1957) The transfer of blood between baby and placenta in the
minutes after birth. Lancet. 1957 Jun 22;272(6982):1277-80.
- Bonham-Carter R E, Bound J P, Smellie J M. (1956) Mean venous
pressures in the first hours of life. Lancet i: 1320–1323
- Mahaffey LW, Rossdale PD (1959) A convulsive syndrome in newborn
foals resembling pulmonary syndrome in the newborn infant. Lancet. 1959
Jun 13;1(7085):1223-5.
- Bound JP, Harvey PW, Bagshaw HB (1962) Prevention of pulmonary
syndrome of the newborn. Lancet. 1962 Jun 9;1:1200-3.
- Myers RE (1972) Two patterns of perinatal brain damage and their
conditions of occurrence. American Journal of Obstetrics and Gynecology
112:246-276.
- Dunn PM (1972) Human "barkers". Equine Vet J. 1972 Jul;4(3):128-34.
- Palmer AC, Rossdale PD. (1975) Neuropathology of the convulsive foal
syndrome. J Reprod Fertil Suppl. 1975 Oct;(23):691-4.
- Palmer AC, Rossdale PD. (1976) Neuropathological changes associated
with the neonatal maladjustment syndrome in the thoroughbred foal. Res
Vet Sci. 1976 May;20(3):267-75.
- Mahaffey LW, Rossdale PD
(1957) On the newborn
infant's oxygen supply.
- Gunther M (1957) The
transfer of blood between
baby and placenta in the
minutes after birth.
- Bonham-Carter R E et al.
(1956) Mean venous
pressures in the first hours of
life.
- Mahaffey LW, Rossdale PD
(1959) A convulsive
syndrome in newborn
foalsresembling pulmonary
syndrome in the newborn
infant.
- Bound JP et al. (1962)
Prevention of pulmonary
syndrome of the newborn.
- Myers RE (1972) Two
patterns of perinatal brain
damage and their conditions
of occurrence.
- Dunn PM (1972) Human
"barkers".
- Palmer AC, Rossdale PD.
(1975) Neuropathology of the
convulsive foal syndrome.
- Palmer AC, Rossdale PD.
(1976) Neuropathological
changes associated with the
neonatal maladjustment
syndrome in the
thoroughbred foal.