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J Obstet Gynecol India Vol. 55, No.

2 : March/April 2005

Pg 115-117

The Journal of

EDITORIAL

Obstetrics and Gynecology


of India

Intrapartum fetal distress


Dr. Adi E. Dastur
asphyxos = without pulse (Greek)

Fetal distress in itself is a non-specific term as the various


parameters to determine the type and degree of distress are
themselves ill defined. The simplistic concept that fetal
dysfunction in labor can be considered as a single condition
and labelled as fetal distress is no longer tenable. The various
indicators such as an abnormal intrapartum FHR pattern,
meconium staining of the amniotic fluid, and low apgar scores
should be evaluated in terms of their individual significance
not expecting that an abnormality in one will necessarily be
reflected as an abnormality in the other. Use of a specific
and standardised terminology or the use of descriptive
terminology to characterize each case of fetal distress may
lead to uniformity and precise interpretation of data which
often seem contentious.
The original concepts of Little 1 and Haldane 2 that cerebral
palsy and fetal death are caused by hypoxia at the time of
delivery have been challenged by epidemiolgical data showing
that by the time labor begins most of the cerebral damage
has already taken place 3 . This does not mean that hypoxia
has no consequences in terms of cerebral palsy as a certain
number of patients do develop cerebral palsy due to hypoxia.
Fetal neuronal damage also depends on the degree of asphyxial
insult. The effects of a total cessation of fetal oxygenation
which is relatively rare are lesions in the pontine region of
the brainstem which almost invariably lead to fetal death.
Graded hypoxia leads predominantly to parietal subcortical
white matter and basal ganglia necrosis. Excitatory amino
acids, particularly glutamate and free oxygen radicals
released in response to a metabolic acidosis caused by
profound hypoxia, are concentrated in the watershed areas
of the brain due to the vasoconstriction associated with
the lactic acidosis 4 .
Evidence has been accumulating rapidly that FHR changes,
the blood acid - base status of the fetus / neonate and apgar
scores are very poor predictors of long term outcome. It is
now being suggested that birth asphyxia should only be
diagnosed when a baby goes on to develop hypoxic ischaemic encephalopathy (HIE). HIE has been shown to be

a much more reliable indicator of long term handicap than


any other perinatal measures 5-7.
.
Significance of meconium staining of amniotic fluid
The significance of the presence of meconium in labor is
controversial and likewise the necessity of rupturing the
membranes in an attempt to detect the presence of meconium.
The presence of thick meconium in labor particularly in
association with post-term pregnancy, oligo- or
anhydroamnios and poor fetal growth has been associated
with an increased risk of fetal acidemia which increases the
risk of meconium aspiration 8. There is some interaction
between meconium and cardiotocography (CTG) pattern
such that if the CTG is abnormal the presence of meconium
is associated with significantly higher chance of a baby being
acidotic, born in poor condition and needing resuscitation 9.
The presence of meconium stained amniotic fluid remains a
concern for both the obstetrician and the pediatrician because
of the high morbidity and mortality associated with meconium
aspiration syndrome. The finding of a normal pH does not
rule out the possibility of meconium aspiration and the
majority of babies suffering meconium aspiration may not
have acidosis 10.
A study by Usta et al 11 tried to identify potential predictors
of meconium aspiration syndrome in pregnancies
complicated by moderate or thick meconium stained amniotic
fluid. The authors identified six variables with independent
statistically significant effect on meconium aspiration
syndrome:
1) admission for induction with a non-reassuring fetal heart
rate (FHR) tracing, 2) need for endotracheal intubation and
suctioning below the vocal chords, 3) one minute apgar score
of 4 or less, 4) present cesarean delivery, 5) previous
cesarean delivery and 6) surprisingly cigarette smoking was
associated with a lower risk of meconium aspiration
syndrome.

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Adi E Dastur

The presence of atleast one of the first five risk factors had
a sensitivity of 92%, a specificity of 56%, a positive predictive
value of 8%, and a negative predictive value of 99% for
meconium aspiration syndrome.
Analyses of data from the Collaborative Perinatal Study, a
prospective study of nearly 59,000 pregnancies found that
14% of the risk for quadriplegic cerebral palsy was associated
with meconium stained amniotic fluid. Logistic regression
analyses found this risk to be independent of other risk factors
for cerebral palsy. This does not prove that meconium in the
amniotic fluid sometimes caused cerebral palsy, only that
the possibility exists. Although only suggestive, the evidence
that meconium induced vasoconstriction sometimes produces
severe fetal ischemia, hypoxemia and cerebral palsy requires
further corroborating evidence for final conclusions to be
drawn.
Intrapartum fetal monitoring
The objective of monitoring the fetus in labor is to detect
fetal abnormalities at a stage where they are reversible. The
current modalities for the monitoring of the fetus are
intermittent auscultation, CTG, color and quantity of amniotic
fluid, and fetal blood sampling. Biophysical profile, moulding
of the fetal head and caput formation serve as accessories to
monitor the fetus.
We have unfortunately not yet achieved a stage where we
can predict with accuracy which fetus would develop
hypoxia in labor and the degree of hypoxia the baby would
undergo. Therefore careful monitoring and early detection
of fetal compromise seem to be the sine qua non of preventing
an unfavourable perinatal outcome. The controversy over
which modality of monitoring and which patients to use it
for, is a reflection of our inability to devise the ideal
monitoring tool.
Management of fetal distress
The first response when fetal distress is detected or suspected
is that of intrauterine resuscitation which will improve the
condition of the fetus and may help to avoid unnecessary
intervention.
Alteration of maternal position
Only a minority of laboring women exhibit hypotension when
they are in the supine position 12. But in the majority of women
there is reduced venous return due to the pressure of the
pregnent uterus on the inferior vena cava and increased
intraabdominal pressure. This can cause a drop in the cardiac
output which leads to diminished uterine flow. Thus when
there are late decelerations in the FHR tracing indicating

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reduced perfusion in the retroplacental area the position of


the woman should be taken into consideration. The position
of the woman also plays an important role when she recieves
epidural analgesia. Such women are subject to peripheral
vasodilatation and therefore along with the supine position
are prone to a reduced venous return. Altering the position
may be adequate management in some cases of late
decelerations provided they do not reappear. Variable
decelerations due to cord compression usually found in cases
of oligohydroamnios may disappear by changing the position
and preventing pressure on the cord.
Hydration
Hydration should constitute an integral part of intrauterine
resuscitation unless there is a contraindication for infusing
reasonable amounts of 180 - 200 mL of fluid per hour. In
conditions where hypotension is expected e.g. epidural
analgesia, maternal bleeding, etc it is important to hydrate
the women well to prevent FHR changes. Inadequate
uteroplacental perfusion or umbilico-placental perfusion in
some cases is responsible for fetal hypoxia and acidosis.
Thus hydration is an important component of labor
management.
Oxygen
It must be stressed that the oxygen transfer at the placental
interphase is more dependent upon the perfusion rather than
on the lack of oxygen in most of the cases. It is therefore of
primary importance to increase the perfusion on either sides
of the placenta in order to increase the amount of oxygen
available to the fetus. Some workers have suggested that
administration of 100 % oxygen to severely growth retarded
fetuses may do more harm than good. Bekadam et al 13
showed that there were decelerations in the FHR after
hyperoxia was stopped in such babies. This might divert the
oxygen from the brain to other areas. Thus it appears that
oxygen therapy may result in some improvement in selected
cases and no improvement in severely growth retarded
fetuses. It is important to note that the fetus does not benefit
in any way if decelerations persist inspite of oxygen.
Intravenous hypertonic dextrose
In the past bolus doses of hypertonic dextrose were used
for the management of fetal distress. But the use of dextrose
and many other substrates has been shown to be of little
value 14. There is however no risk of neonatal lactoacidosis
or hypoglycemia in the normoxemic normally grown fetus
when 5% dextrose is given at a rate of 180 mL/hour 15. In
severe IUGR however it is thought that the lack of insulin
response to hyperglycemia may block the cellular glucose
uptake and promote an anerobic metabolism with subsequent
acidosis.

Editorial

Amnioinfusion
Amnioinfusion has recently received considerable attention
in medical literature. Although several permutations of the
technic have been described, the common therapeutic goal
is expansion of the amniotic fluid volume. Amnioinfusion is
not justified in all types of deceleration patterns. Because
late decelerations result from a different pathophysiological
mechanism than variable decelerations amnioinfusion is
contraindicated in their presence. In fact by increasing
intrauterine pressure amnioinfusion may further compromise
uteroplacental blood flow. Amnioinfusion has also been used
for dilution and lavage of meconium. Meconium lavage may
theoretically reduce the potential for chorioamnionitis as a
few in vitro studies suggest that meconium may enhance
bacterial growth in amniotic fluid in a dose dependent fashion.
The absolute contraindications for this procedure include
active maternal genital herpes infection, diminished FHR
variability or reactivity, fetal scalp pH below 7.20, late
decelerations in the FHR, placenta previa, and placental
abruption. The relative contraindications are fetal anamolies,
impending delivery, multiple gestations, and prior cesarean
delivery.
Although hypothetically a number of complications are
possible the literature shows that they rarely occur.
Complications like uterine overdistension and hyperactivity,
amniotic fluid embolism, placental abruption, uterine rupture,
cord prolapse, amnionitis, and maternal cardiopulmonary
compromise are theoretically possible but none of the studies
have reported a rise in the incidence of these eventualities.
Tocolysis
Inhibition of uterine activity is useful in abnormal uterine
activity, fetal distress related to uterine hyperactivity and
prolonged bradycardia. It could also be useful during
complicated cesarean sections, external cephalic version at
term, during the transport of a laboring woman and, when
operation theater or anesthetist is unavailable for cesarean
section. The use of terbutaline, ritodrine, salbutamol and
magnesium sulphate have all been documented. A bolus dose
of a tocolytic drug produces maternal tachycardia (mostly
from peripheral vasodilatation) and increased cardiac output,
and thus increases uteroplacental perfusion. In addition,
inhibition of uterine contractions reduces the interruption of
blood flow to the placental bed.
The decision to delivery interval
Medical litigation is on the rise in our country particularly
with relation to obstetrics. The day is not far when premiums
for malpractice insurance rise parallel to the rise in the
compensation offered for these cases. Majority of the cases

seem to be due to the delay in the decision to delivery interval


rather than the problems with diagnosis. Although there is
poor correlation between FHR patterns and long term
outcome a significant association has been noted between
the decision to delivery interval and admission to the neonatal
intensive care unit for neonatal asphyxia 16. An effort must
be made to reduce the decision to delivery interval and restrict
it to not more than 30 minutes. It should be the norm to keep
the women and her relatives apprised of the situation of the
labor at all times and involve them in the decision making. In
some cases of fetal distress immediate operative delivery
may be the only option to ensure a healthy neonate. Even in
these situations intrauterine resuscitation can play a role in
enhancing the perinatal outcome.
Ultimately, efficient management and a good outcome in cases
of fetal distress reflects a strong infrastructure and good
coordination between the obstetrician, the nursing staff, the
staff in the operation room and the neonatologist.
References
1. Little WJ. On the influence of abnormal parturition, difficult labour,
premature birth and asphyxia neonatorum on the mental & physical
conditions of the child, especially in relation to deformities. Trans Obstet
Soc London 1862;3 :293.
2. Haldane JS. Respiration. New Haven Yale University Press . 1992 ;23-4.
3. Nelson KB. Ellenberg J.H Antecedents of cerebral palsy. N Eng J Med
1986;315:81-96.
5. Hall DB. Birth asphysia and cerebral palsy. BMJ 1989; 299: 279-82.
6. Levene M, Sands C, Grindulis H et al. Comparison of 2 methods of
predicting outcome in perinatal asphyxia. Lancet 1986;1:67-9.
7. Hull J, Dodd KL. Falling Incidence of hypoxic ischaemic encephelopathy
in term infants. Br J Obstet Gynecol 1992;99: 386-91.
8. Bochner CJ, Medearis AL, Ross MG et al. The role of antepartum
testing in the management of post term pregnancies with heavy meconium
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cardiotocograms in labour meconium staining of the amniotic fluid,
arterial cord blood PH and apgar scores. Obstet Gynecol 1989;74:71521.
10. Yeomans ER, Gilstrap LC, Leveno KJ et al. Meconium in the amniotic
fluid an fetal acid-base status. Obstet Gynecol 1989;73: 175-8.
11. Usta IM, Mercer BM, Sibai BM . Risk factors for meconium aspiration
syndrome. Obstet Gynecol 1995;86:230-4.
12. Howard BK, Goodson JH, Mengert WF. Supine hypotensive syndrome in
late pregnancy. Obstet Gynecol 1953;1:371 - 7.
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hyperoxia on fetal breathing movements, body movements and heart
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14. Mann U, Prichand JW, Symmes D. The effect of glucose loading on the
fetal response to hypoxia. Am J Obstet Gynecol 1970;107 : 610-8.
15. Nordstorm L, Arulkumaran S. Lactate in fetal suveillance. Sing J Obstet
Gynecol 1993;24:87-97.
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