Medicolegal aspects of intrapartum fetal monitoring
Obstetric litigations are on the rise worldwide and it is a major area of concern for maternity service providers. In United Kingdom, a study found 70% of all legal claims related to fetal brain damage to be based on abnormalities noted on FHR tracings (1).
Despite its low specificity for hypoxia, the CTG continues to be the central documentary evidence for all claims for fetal asphyxia (2). Other indicators including a low Apgar score at birth have been shown to be subjective and poor predictors of long-term neurological outcomes.Umbilical cord arterial blood gas analysis at birth has emerged as an important method, used to support or refute a diagnosis of intrapartum asphyxia. Many maternity units now routinely determine umbilical cord arterial and venous blood acid-base status on deliveries where there has been any concern during labour, for example, operative deliveries, cases where a FBS was done, pathological CTG trace, those with meconium-s tained amniotic fluid, bleeding in labour, preterm infants, multiple gestations, vaginal breech deliveries, and the depressed infant at birth. Although it is
clear that in some of the cases of newborns who later develop cerebral palsy interventions may have prevented or decreased the severity of cerebral palsy, it has been shown overall that FHR patterns are poor predictors of cerebral palsy (3, 4). The low specificity of CTG for fetal hypoxia therefore necessitates secondary or definitive tests to confirm fetal acid-base status in labour.
Patterns of intrapartum hypoxia and nature of birth injury
‘Hypoxaemia’ describes the condition where there is a reduction in the placental or cord blood flow causing a reduction in the level of oxygen in the peripheral arterial circulation of the fetus.
This can happen in a normal labour with uterine contractions and the majority of fetuses can cope well with such episodes for long periods of time without injury. ‘Hypoxia’ describes the condition where the blood flow is interrupted for more prolonged periods of time and results in a reduction in the delivery of oxygen to the peripheral tissues of the fetus. If hypoxia continues for prolonged periods, the fetus switches to anaerobic metabolism to create energy and metabolic acidosis starts developing. In early stages, buffering will allow a normal pH to be maintained for some time. In fetuses with compromised reserves such as preterm or growth-restricted fetuses, metabolic acidosis occurs earlier. Fetal infection also reduces the reserve to cope with hypoxia. ‘Asphyxia’ describes the extreme condition where the oxygen delivery to tissues fails, leading to metabolic acidosis in addition to hypoxia. This leads to critical organ damage which may cause brain injury or fetal death in utero.The nature of asphyxia can determine the type of brain injury and the neurological outcome as described by Myers in 1975 (32):
1. Total asphyxia causes damage to the brainstem and thalamus (athetoid or dyskinetic cerebral palsy).
2. Prolonged hypoxia with acidosis causes brain swelling and cortical necrosis (spastic quadriplegic cerebral palsy).
3. Prolonged hypoxia without acidosis causes white matter damage.
4. Total asphyxia preceded by prolonged hypoxia with mixed acidosis causes damage to the cortex, thalamus, and basal ganglia.
Acute hypoxia (Figure 27.4) is characterized by a sudden reduction in placental/cord blood flow and develops over minutes. Causes include acute accidents such as cord accident, abruption, hypertonic contractions, or uterine dehiscence and CTG often shows prolonged deceleration or bradycardia. Management demands rapid delivery or treatment of hyperstimulation to prevent death or long-t erm damage.
Gradually developing hypoxia (Figure 27.5): in gradually developing hypoxia accelerations do not appear, the baseline rate increases, and the variability reduces with progress of time.
The decelerations get deeper and wider with increasing hypoxia. One needs to consider the clinical picture of parity, cervical dilatation, rate of progress, and high-risk factors, and either perform FBS or consider delivery.The natural response for the fetus with hypoxic stress that previously had a reactive CTG would be the appearance of decelerations (variable due to cord compression or late due to placental insufficiency), the disappearance of accelerations (fetal response to conserve energy), a gradual rise in the baseline rate (due to hypoxia and catecholamine surge), deepening and widening of the decelerations (with increasing hypoxia to the myocardium), and finally progressive reduction of the baseline variability (after a maximum baseline rate has been achieved and with further lack of oxygen there is depression of the autonomic nervous system). Within a reasonable time (60-90 minutes) of no baseline variability in the CTG (i.e. flat baseline variability with tachycardia and repeated late or atypical variable decelerations) (Figure 27.5), delivery should be carried out in order to avoid a baby with a low Apgar score and cord blood metabolic acidosis. An alternative would be to perform a FBS for determination of the acid-base balance and then to decide the management based on the FBS results.
Long-standing or chronic hypoxia (Figure 27.6) happens due to a reduction in placental blood flow over a long period of time and is associated with underlying conditions such as pre-eclampsia or fetal growth restriction. In the antenatal period the fetus will cope for a significant period of time by redistribution of the blood flow to vital organs, reduction in growth or activity, and buffering against lactic acid. Surveillance with Doppler ultrasound can detect the point where decompensation is likely so that delivery can be recommended. In labour, it may present with a CTG trace with no baseline variability and shallow late decelerations.
Subacute hypoxia (Figure 27.8): this may occur due to recurrent cord compression in labour. It may be particularly worsened in situations such as oligohydramnios or prolonged pregnancies.
The CTG in this situation is characterized by prolonged decelerations where the FHR spends more time below the baseline rate (>90 seconds) and a shorter duration at the baseline rate (palsy. N Engl J Med 1996;334:613-18.5. Haverkamp AD, Thompson HE, McFee JG, Cetrulo C. The evaluation of continuous fetal heart rate monitoring in high risk pregnancy. Am J Obstet Gynecol 1976;125:310-20.
6. Haverkamp AD, Orleans M, Langendoerfer S, McFee J, Murphy J, Thompson HE. A controlled trial of the differential effects of intrapartum fetal monitoring. Am J Obstet Gynecol 1979;134:399-412.
7. Renou P, Chang A, Anderson I, Wood C. Controlled trial of fetal intensive care. Am J Obstet Gynecol 1976;126:470-76.
8. Kelso IM, Parsons RJ, Lawrence GE, Arora SS, Edmonds DK, Cooke ID. An assessment of continuous fetal heart rate monitoring in labor: a randomized trial. Am J Obstet Gynecol 1978;131:526-32.
9. Wood C, Renou P, Oates J, Farrell E, Beischer N, Anderson I. A controlled trial of fetal heart rate monitoring in a low-risk population. Am J Obstet Gynecol 1981;141:527-34.
10. McDonald D, Grant A, Sheridan-Pereira M, Boylan P, Chalmers I. The Dublin randomized control trial of intrapartum fetal heart rate monitoring. Am J Obstet Gynecol 1985;152:524-39.
11. National Institute for Health and Care Excellence (NICE). Intrapartum Care for Healthy Women and Babies. Clinical guideline [CG190]. London: NICE; 2014. Available at: https://www. nice.org.uk/guidance/cg190.
12. National Institutes of Health. Antenatal Diagnosis. Report of a Consensus Development Conference. NIH Publication No. 791973. Bethesda, MD: National Institutes of Health; 1979.
13. Alfirevic Z, Devane D, Gyte GM. Continuous cardiotocography (CTG) as a form of electronic fetal monitoring (EFM) for fetal assessment during labour. Cochrane Database Syst Rev 2013;5:CD006066.
14. Centre for Maternal and Child Enquiries (CMACE). Perinatal Mortality 2008: United Kingdom. London: CMACE; 2010.
15. Department of Health. Intrapartum-related deaths: 500 missed opportunities. In: On the State of Public Health: Annual Report of the ChiefMedical Officer2006., pp. 41-48. London: Department of Health; 2007.
16. Lieberman Richardson DK, Lang J, Frigoletto FD, Heffner LJ, Cohen A. Intrapartum maternal fever and neonatal outcome. Pediatrics 2000;105:8-13.
17. Impey L, Greenwood C, MacQuillan K, Reynolds M, Sheil O. Fever in labour and neonatal encephalopathy: a prospective cohort study. Br J Obstet Gynecol 2001;108:594-97.
18. Fleischer A, Schulman H, Jagani N, Mitchell J, Randolph G. The development of fetal acidosis in the presence of an abnormal fetal heart rate tracing. I. The average for gestational age fetus. Am J Obstet Gynecol 1982;144:55-60.
19. Phelan JP, Ahn MO. Perinatal observations in forty- eight neurologic- ally impaired term infants. Am J Obstet Gynecol 1994;171:424-31.
20. Gibb D, Arulkumaran S. Fetal Monitoring in Practice, 3rd edn. Oxford: Elsevier Ltd. 2008.
21. Bailey RE, Hinshaw K. Intrapartum fetal monitoring. In: ALSO Provider Manual, 3rd edn. Leawood, KS: AAFP; 2001.
22. Leslie K, Arulkumaran S. Intrapartum fetal surveillance. Obstet Gynaecol Reprod Med 2011;21:59-66.
23. Wiberg-Itzel E, Lipponer C, Norman M, et al. Determination of pH or lactate in fetal scalp blood in management of intrapartum fetal distress: randomised controlled multicentre trial. BMJ 2008;336:1284-87.
24. East CE, Begg L, Colditz PB, Lau R. Fetal pulse oximetry for fetal assessment in labour. Cochrane Database Syst Rev 2014;10:CD004075.
25. Skupski DW, Rosenberg CR, Eglinton GS. Intrapartum fetal stimulation tests: a meta-analysis. Obstet Gynecol 2002;99:129-34.
26. East CE, Smyth R, Leader LR, Henshall NE, Colditz PB, Tan KH. Vibroacoustic stimulation for fetal assessment in labour in the presence of a nonreassuring fetal heart rate trace. Cochrane Database Syst Rev 2013;1:CD004664.
27. Amer-Wahlin I, Hellsten C, Noren H, et al.
Cardiotocography only versus cardiotocography plus ST analysis of fetal electrocardiogram for intrapartum fetal monitoring: a Swedish randomised controlled trial. Lancet 2001;358:534-38.28. Amer- Wahlin I, Kjellmer I, Marsal K, Olofsson P, Rosen KG. Swedish randomized controlled trial of cardiotocography only versus cardiotocography plus ST analysis of fetal electrocardiogram revisited: analysis of data according to standard versus modified inten- tion-to-treat principle. Acta Obstet Gynecol Scand 2011;90:990-96.
29. Luzietti R, Erkkola R, Hasbargen U, Mattsson LA, Thoulon JM, Rosen KG. European Community multi-Center Trial ‘Fetal ECG Analysis During Labor’: ST plus CTG analysis. J Perinat Med 1999;27:431-40.
30. Neilson JP. Fetal electrocardiogram (ECG) for fetal monitoring during labour. Cochrane Database Syst Rev 2012;4:CD000116.
31. Ojala K, Vaarasmaki M, Makikallio K, Valkama M, Tekay A. A comparison of intrapartum automated fetal electrocardiography and conventional cardiotocography—a randomised controlled study. BJOG 2006;113:419-23.
32. Myers RE. Four patterns of perinatal brain damage and their conditions of occurrence in primates. Adv Neurol 1975;10:223-34.
33. ISRCTN Registry. A multicentre randomised controlled trial of an intelligent system to support decision making in the management of labour using the cardiotocogram (INFANT). ISRCTN98680152. Prof. Peter Brocklehurst, University of Oxford, UK. Available at: http://www.isrctn.com/ISRCTN98680152.
34. Keith RD, Westgate J, Ifeachor EC, Greene KR. Suitability of artificial neural networks for feature extraction from cardiotocogram during labour. Med Biol Eng Comput 1994;32 Suppl 4:S51-57.
35. Ugwumadu A, Steer P, Parer B, et al. Time to optimise and enforce training in interpretation of intrapartum cardiotocograph. BJOG 2016;123:866-69.