376 SA MEDIESE TVDSKR1F

Intrapartum Fetal ResuscitationD. B. COWAN

30 Augustus 1980

a

-,

SUMMARY

Fetal distress is defined. The pathophysiology of fetaldistress is discussed and treatment is recommended. Theprinciples of intrapartum fetal resuscitation are proposed,with particular reference to the inhibiUon of uterineactivity.

5. AIr. med. J.. SS, 376 (1980).

The beneficial effects of maternal resuscitation duringlabour have been recognized for a long time, but theconcept of fetal intrapartum resuscitation is new. It is thepurpose of this article to review the ways in which thefetal condition can be improved when fetal distress occursin labour.

FETAL DISTRESS AND FETAL BLOODSAMPLING

Traditional teaching emphasizes the importance ofmeconium staining of the liquor and of fetal heart rateabnormalities as signs of fetal distress. Meconium in theliquor may be suggestive of fetal distress, but its signifi­cance is still debatabie. Understanding of the relationshipof the fetal heart rate to fetal condition has improved withthe introduction of cardiotocography, but Beard et al.'showed that complicated cardiotocographs could frequentlybe associated with a fetal scalp pH of >7,25, and anApgar score of >'7.

The most accurate way of correlating intrapartum con­dition with condition at birth is by fetal blood sampling.The technique was introduced by Saling' in the early1960s; in the hands of experienced obstetricians or mid­wives, good reproducibility of results can be achieved.

INTERPRETATION OF FETAL BWODSAMPLE pH

The hydrogen ions in the fetal scalp blood sample maybe either fetal or maternal in origin. Maternal acidosiscauses a transplacental infusion of hydrogen ions into thefetal circulation and may lower the fetal pH. It has beenstated that this occurs in approximately lOo~ of cases.3

Thus if the fetal pH is low, it is important to eliminatethe possibility of infusion acidosis.

Many studies have shown that during normal labourthe fetal scalp blood pH varies in parallel with the pHof maternal venous blood. usually taken from the ante-

Department of Obstetrics and G)'naecolog)', Universit)' ofNatal, Durban

D. B. COWAN, F.R.C.S., M.R.e.O.G.

cubital vein."" The normal maternofetal pH difference isapproximately 0,1 of a pH unit,"· and Rooth et al. definesthe difference in pH in fetal pre-acidosis as being 0,15 ­0,19, and that in fetal acidosis >'0,20.

Unfortunately the absolute values of maternal andfetal pH vary considerably between populations.... Thismay be due either to differences in labour managementor to physiological variations in the mechanism of labour.Thus if one relies only upon fetal scalp sampling to indi­cate fetal condition, the norms for the local populationhave to be ascertained.

Beard er al.,' Sating' and Lumley et al.' regard the lowerlimit of the J;lormal scalp sample pH as 7,25, and Table 1illustrates a practical (but conservative) interpretation offetal scalp sample pH results.

TABLE I. INTERPRETATION OF FETAL SCALP SAMPLE pH

pH range Fetal condition Action

>7,30 Good at present Repeat FBS 2 hlater

7,25 - 7,30 Pre-acidosis/asphyxia Repeat FBS 30min later

<7,25 Acidosis/asphyxia Repeat FBSimmediately

If the fetal scalp pH is >7,30, fetal condition is goodat that moment but a repeat sample should be taken 2hours later to ascertain whether there has been deteriora­tion. If the pH lies in the range 7,25 - 7,30 then pre­acidosis exists, and the test should be repeated 30 minuteslater. If the pH is <7,25 the result should be checkedimmediately, and if it is still <7,25 fetal distress isdiagnosed and delivery is indicated after intrapartum re­suscitation.

PATHOPHYSIOLOGY OF FETALDISTRESS

Fetal distress occurs as a result of intrapartum hypoxiaand fetal acidosis. As a primary event, fetal well-beingdepends on adequate transplacental transfer of oxygenfrom mother to fetus (Fig. 1). If transfer is insufficientthe fetus will become progressively hypoxic and acidotic.Clearly, perfusion of intervillous spaces on the maternalside, together with the integrity of the maternal cardio­vascular system and adequate oxygenation of haemo­globin, will be determinants of transplacental oxygenavailability. On the fetal side perfusion of the chorionicvilli, umbilical blood flow, and distribution of oxygenatedfetal haemoglobin will determine fetal well-being. Whencontractions are superimposed on the situation shown inFig. 1 they will cause an increase in intra-uterine pressureand uterine blood flow will decrease concomitantly. Con-

-30 August 1980 SA MEDICAL JOUR AL 377

sequently perfusion of the intervillous space will decrease.It has been suggested that at pressures of >30 mmHgintervillous perfusion is drastically reduced, if not com­pletely abolished.;" Thus the effect of a uterine contrac­tion is to reduce maternal-placental perfusion, and totemporarily reduce oxygen availability to the fetu .

~;()'r!:t:R

oxygenat.ion

1Circulation

1Uterine Blood fIol<>'

1Perfusion of

Intervillou~

Space

PLACENTALOXYGEN

'i'R.;l\SFER

fETUS

Placental Perfusion

1Umbilical Blood rIm,'

Fetal Circulat.ion

Distribution

is mainly aortic, imple arterial compression will decreasecommon iliac blood flow. and thus dccrcase uterine arterialblood flow. This scheme of va cular comprcssion has ledSelwyn Crawford to label the entity 'the aortocaval com­pression syndrome' and its potentially harmful effect uponfetal condition at birth has been noted by many authors.Jt i recommended' that women hould lie in the lateralposition during most of the time pent in labour.

Aortocaval compression per se may worsen the feialcondition; when fetal distress occurs the patient shouldbe kept in the lateral position, or on a Sorbo rubberwedge providing 15 0 lateral tilt, so that aortocaval com­pression may be avoided. This applies to preparation fordelivery whether it be by forceps or caesarean section,transport io theatre, or as a part of intrapartum fetalresuscitation.

TABLE 11. OBVIOUS CAUSES OF FETAL DISTRESS

Fig. 1. Determinants of fetal well-being.

Maternal Position

MANAGEMENT OF FETAL DISTRESS

FetalP02

(mmHg)

15 (SO 7,5)21 (SO ± 7,9)

Maternal

P02

(mmHg)

86 (SO -+- 18)331 (SD -+- 123)

Room airOxygen by mask

TABLE Ill. EFFECT OF MATERNAL OXYGEN SUPPLEMEN­TATION ON THE MATERNAL AND FETAL

TRANSPLACENTAL OXYGEN TENSION (FROM HUCH9)

Supplementary Oxygen

When fetal distress has occurred it is possible to increasefetal oxygenation by raising the maternal arterial oxygentension. Table 111 shows the results obtained by HucheT al! with two transcutaneous oxygen electrodes. One wasapplied to the fetal scalp, and the other to the mother's skinbelow the clavicle. Huch et al. showed that the mean fetaltranscutaneous oxygen tension (Pteo,) could be raisedfrom 15 to 21 mmHg by giving upplementary oxygento the mother by face mask. This effect was demonstratedin 39 out of 40 women to whom oxygen was given. Inonly one case did the fetal Ptco, fall in response tomaternal supplemmtation. The mean fetal increase of 6mmHg shown in Table HI corresponds to an increase inoxygen saturation of 17o~. This small increase may meanthe diJer~nce between hypoxia and adequate tissue oxyge·nation. It has not been stated what the optimal oxygenconcentration is during fetal resusciiation, but Rorkeet al.'· have shown that the ideal inspired oxygen con::en­tration at caesarean section is 65 . 70o~ and that the acid­base status of babies delivered at this concentration of in·spired oxygen was superior to that in those born at 36%,60 0 {> , or even 100% oxygen.

IV fluids with or without

ephedrineLateral positionTransfusionTransfusion with or without

exchange transfusionStop oxytocin; tocolytic therapy

Treatment

Secure normotension

Excessive uterine activity

Cause

Maternal circulatory col­lapseExcessive hypotensive

therapyEpidural/spinal hypoten-

sionSupine hypotensionHaemorrhageAnaemia

The cause of fetal distress is usually not apparent andmanagement will be discussed under the followingheadings: (i) maternal position; (ii) oxygen supplementa­tion; (iii) hypoventilation; (i\') glucose infusion; and (v)tocolytic therapy.

From Fig. 1 it is apparent that fetal oxygen deficiencycan originate at a variety of stages along the path offetal oxygen supply. Table 11 summarizes causes andremedies of fetal distress which may be apparent to theattending obstetrician, and requires no further comment.

When a gravid woman lies in the dorsal posItIOn, heruterus may compress the great vessels of the posteriorabdominal wall. This may cause a partial aortic and/orcaval compression with reduction in blood flow throughthese vessels. If the effect is mainly caval then the venousreturn to the heart will be reduced, which will reducecardiac output, cause hypotension and result in a reduc­tion of the transplacental perfusion pressure. ]f the effect

Hypoventilation

Hypoventilation should be avoided in labour. particu­larly when fetal distress is present. Huch eT at." observedthat in 2 patients hyperventilation was followed by com­pensatory hypoventilation. During the compensation phasethe maternal Ptca, fell, whereupon the fetal Po, also felland a late fetal heart rate deceleration pattern resulted.

3'70/0 SA MEDIESE TYDSKRIF 30 Augustus 1980

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TABLE IV. EFFECT OF OACIPAENALlNE ON THE FETAL HAEMOGLOBIN SATURATION (-+- 1 SO) (FROM FAIABROTHERAND KAMBARAN UNPUBLlSH~D DATA)

No. of Before 40 min afterGroup patients orciprenaline orciprenaline Significance·

No distress 8 31 % (-+- 12,62) 36% (-+- 10,17) 0,05 > p> 0,02Distress 10 17;0 (-+- 5,74) 18% (-+- 10,51) NS

With resumption of normal ventilation the maternal Ptc0, rose arid the fetal Po, accordingly increased. When thefetal Ptca, was high, maternal hypoventilation did not re­sult in significant fetal deterioration, but when the fetalPo, was low (as it is with fetal distress) a reduction in ma­ternal Ptca, values to less than 70 mmHg produced latefetal heart rate decelerations.

Glucose

There is a theoretical place for giving intravenous glu­cose as part of intrapartum fetal resuscitation, but whetherit is of value or illot has not been ascertained, and it maybe potentially harmful to the fetus. Theoretical calcula­tions" indicate that when a fetus is distressed approxi­mately 60% of the oxygen deficit is supplied from the fetaloxygen stores (i.e. in the fetal erythrocytes), while 40%is derived from anaerobic metabolism of glycogen. It hasbeen calculated that in a well-grown fetus subjected to a4°~ oxygen deficit the oxygen stores will be depleted in 36minutes whereas the glycogen stores will last much longer.In other words, the speed at which the oxygen stores aredepleted is much faster than the speed at which the gly­cogen stores are depleted. There are, however, two excep­tions to this. The glycogen stores are reduced in both theasymmetrically growth-retarded fetus and the prematureinfant. In these two situations glucose may prolong fetalsurvival time.

However, Shelley and Bassett" showed that an elevationof the fetal blood glucose level may be deleterious in thepresence of hypoxia. These authors found, in chronicallycatheterized fetal lambs subjected to a 9% oxygen mixturefor 60 minutes, that as the fetal plasma glucose level rose(whether this was by direct fetal or maternal infusion) thefinal total arterial pH after 60 minutes of hypoxic insultfell dramatically, and that the fall in pH was mirrored bya rise in fetal plasma lactate levels.

Tocolytic Therapy

Uterine contractility and fetal well-being are often hap­pily associated, but this is not always the case. As intra­uterine pressure increases with each contraction, maternal­placental perfusion falls because the difference between theperfusing maternal arterial pressure and the intraplacental(or intra-uterine) pressure is reduced. With a pressure of> 30 mmHg placental blood flow is grossly reduced or itmay cease. The net result of reduced or arrested placentalperfusion should be to cause fetal hypoxia, dependingupon the functional capacity of the placenta:' Huch andHuch'" have shown that there is often a relationship be­tween an individual uterine contraction and a period ofhypoxia following the contraction. It should therefore be

",

possible to improve placental oxygen transfer by inhibitinguterine contractions.

Many agents are capable of causing uterine relaxationand they have a theoretical place in the management offetal distress. These include ethanol, amyl nitrite, mag­nesium sulphate, certain anaesthetic gases and the /3,­agonists. The latter have found popularity with obstetri­cians and have been used as a temporary measure for fetaldistress."'" Their use is based. upon the presence of j3­adrenoreceptors in the myometrium'· and in the smoothmuscle of the uterine arterioles. Stimulation of these causesmuscular relaxation. The rationale of use of the j3-agonistsis: (a) inhibition of uterine activity will increase placentalblood flow through its effect on the myometrium andcause arteriolar vasodilatation which reduces peripheralresistance and facilitates increased venous return to theheart, thus increasing cardiac output," (b) maternal bloodglucose levels may be increased, thereby increasing glucosetransfer to the fetus;'" (c) the progressive fetal respiratoryacidosis which occurs in the second stage of labour maybe blocked. I'

Although it was suggested by Caldeyro-Barcia" in 1969that /3-agonists might have a place in the management ofthe distressed fetus, this practice has not been commonlyimplemented.

Fairbrother and Kambaran (unpublished data) showedin a controlled study in 1976 that orciprenaline wouldmaintain the efficiency of maternofetal exchange in thepresence of fetal distress, while orciprenaline infusioncaused an improvement in gaseous exchange in labourswhich were not complicated by fetal distress (Table IV).

Lipshitz" described improvement of fetal condition insix situations of fetal distress when a bolus intravenousdose of 10 ,p.g of hexoprenaline was given. Arias" describedthe cardiotocographic response of 15 distressed fetuses toa bolus dose of terbutaline, which is a selective /3-agonist.

Which tocolytic agent should one use? Studies on thecomparative tocolytic and cardiovascular effects of fourj3,-agorusts (hexoprenaline, salbutamol, ritodrine and feno­terol), given as either a bolus dose or as an intravenousinfusion, showed that hexoprenaline had the greatest selec­tive /3,-agonistic effect, and is the j3-sympathomimetic agentof choice in the resuscitation of the distressed fetus."'"

However, a word of caution is necessary, as the j3,-ago­nistic agents may cross the placenta to the fetal circulationand some have been shown to be capable of inducing myo­cardial necrosis after prolonged administration.""" Theyhave also been shown to alter the conductance of bloodvessels"" and to modify the distribution of blood flow inboth maternal and fetal circulation.

-30 August 1980 SA MEDICAL 10 R 'AL 379

The effect that the f1"-agonists may have on the fetalautonomic nervous system has not been established. Thismay be important as it may determine the fetal response tohypoxia. Only when the stimulus to the onset of labourha been identified may it be possible to physiologicallyarrest uterine contractility and improve fetal oxygenationwithout worrisome side-effects.

REFERENCES

1. Beard, R. W., Filshie, G. M., Knight, C. A. et al. (1971): J. Obstet.Gynaec. Brit Cwlth, 78, 865.

2. Saling, E. (1965): J. int. Fed. Gynec. Obstet., 3. 101.3. Edingron, P. T., Sibanda, J. and Beard, R. W. (1975): Brit. med. J.,

3. 341.4. Rooth, G., McBride, R. and Ivy, B. J. (1973): Acta obstet. gynec.

scand .• 52, 47.5. Lumley, J., McKinnon, L. and Wood, C. (1971): J. Obstet. Gynec.

Brit. CWllh, 78, 13.6. Jacobson, L. and Rooth, G. (197t): Ibid., 78, 971.7. Towell, M. E. (1966): Pediat. Clin. N. Amer., 3, 575.8. Novy, M. J., Thomas, C. L. and Lees, M. H. (1975): Amer. J.

Obstet. Gynec., 122, 419.9. Huch, A., Huch, R., Schneider, H. et al. (1977): Brit. J. Obslet.

Gynaec., 84. suppl. 1.10. Rorkt:. M. J .. D3Vl:Y. D. A. and Du Toil, H. J. U96S): An<lcsthl:si:.t,

23. 5~5.

11. ROOlh. G .(1973): J. painat. Med., I, 7.12. Shelley, H. 1. and Basset!, J. M. (1975): Brit. med. Bull., 31, 37.13. Huch, A. and Huch, R. (1977): III Proceedings of the Scientific

Meeting of the Royal College of Obstetricians and Gynaecologists.Vienna,2 December. p. 51.

14. Lipshitz, 1. (1977): Amer. J. Obslet. Gynec., 129, 31.15. Arias, F. (1978): Ibid., 131. 39.16. Lands, A. M., Ludnena, F. R. and Bullo, H. Y. (1967): Life Sci ..

6. 2241.17. Coleman, A. and Leary, W. P. (1973): S. Afr. med. 1.. 47. 621.18. Gamissans, 0., Carreras, M., Duran, P. er of. (1973): Proceedings of

the International Symposium, Vienna. p. 145.19. Humphrey. M., Chang, A .. Gilbert, M. " al. (1975): Brit. J. Obstet.

Gynaec., 82, 234.20. Caldeyro-Ba,cia, R. (1969): In Perillatal Factors Affectillg Humall

Development (Scientific Publication No. 185). p. 24. Washington,DC: Pan American Health Organization.

21. Lipshitz, J., Baillie, P. and Davey, D. A. (1976): S. Afr. med. J .• 50,1969.

22. Lipshitz, J. and Baillie, P. (1976): Ibid., 50. 1973.23. Rona, G., Chappel, C. 1., Balazs, T. et al. (1959): Arch. Path., 67,

443.24. Weidinger, H., Weist, W., Schleich, A. et al. (1976): J. perinat.

Med., 4, 280.25. Meyers, R. E., Joelsson, 1. and Adamson, K. (1978): Acta obste!.

gynec. scand., 57, 317.

Amniotic Fluid .Infection SyndromeS. M. ROSS

SUMMARY

Inflammatory changes in the extraplacental fetal mem­branes and subchorionic plate of the placenta lire acommon cause of perinatal mortality and morbidity incertain communities if associated with fetal pneumonia,and may also interfere with long-term psychomotor de­velopment. This latter complication is particularly likelyto occur if there has been a moderate degree of hyper­bilirubinaemia in the 'neonate. The pathway of infectionis by ascent through the cervical os and the organismsinvolved are usually bacteria.

S. Afr. med. l., 58, 379 ~1980).

Department of Obstetrics and Gynaecology, University ofatal, Durban

S. M. ROSS. F.R.C.O.G., D.L'.!. & H.

The amniotic fluid infection syndrome is the conditionin which intra-uterine infection of the extraplacental fetalmembranes and plate of the placenta occurs before theonset of labour and in the presence of intact membranes.Congenital pneumonia may develop as part of this syn­drome. The diagnosis is based on microscopic evidenceof acute inflammation of the extraplacental membranesand subchorionic plate of the placenta together with, insome instances, fetal pneumonia. Most of these infectionsare not recognized on clinical grounds.' They may beginas early as the first trimester, but are much morecommon towards the end of pregnancy.'"

The pathway for infection may either be through thematernal circulation or by ascent through the cervical os.The evidence in favour af the latter route being the com­moner source of infection is that: (a) bacterial culturesfrom the vagina and those from the infant's respiratorytract are usually identical;' (b) infection starts at the pointof break in the membrane, as evidenced by more ad­vanced inflammation and necrosis of tis ue; (c) in a twin