J Obstet Gynecol India Vol. 55, No.

2 : March/April 2005

Pg 115-117

EDITORIAL

The Journal of 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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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

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.

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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 in early labour. Obstet Gynecol 1987; 69:903-7. 9. Steer PJ, Eigbe F, Lissaeur TJ et al. Interelationships among abnormal 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. 13. Bekadam DJ, Muller EJH, Snijders RJM et al. The effects of maternal hyperoxia on fetal breathing movements, body movements and heart rate variation in grown retarded fetuses. Early Hum Dev 1991;27:223 32. 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. 16. Dunphy BC, Robinson JM, Sheil OM et al. Caserean section for fetal distress, the interval from decision to delivery and the relative risk of poor neonatal condition. J Obstet Gynecol 1991;11:241-4.

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