Electronic fetal monitoring, cerebral palsy, and caesarean section: assumptions versus evidenceBMJ 2016; 355 doi: https://doi.org/10.1136/bmj.i6405 (Published 01 December 2016) Cite this as: BMJ 2016;355:i6405
All rapid responses
To the Editor:
As Dr. Lees indicates, children whose births were monitored electronically had significantly fewer seizures recognized in the newborn period.  A majority of the data about fetal monitoring and neonatal seizures come from the large Dublin study.  The meaning of this association is far from clear as there was no more cerebral palsy in children monitored by auscultation only. [1, 3] Examination at age one year of the 39 surviving Dublin infants who had had neonatal seizures found three abnormal children in each monitoring group, thus no difference in outcome according to method of monitoring in labor among those with neonatal seizures  or the total. [1, 3]
There are a great many potential causes of seizures in the neonate including infection, toxins, malformations, metabolic derangements, and perinatal stroke. We cannot accept Dr. Lees’ assumption that in the fetal monitoring trials “most of these seizures are hypoxic in origin and due to intrapartum events” because neonatal seizures that are due to acute intrapartum hypoxic-ischemic events are usually accompanied by low Apgar scores, cord blood acidosis, and need for special nursery care. None of these findings occurred more often in infants monitored by auscultation only, nor was perinatal mortality higher or long-term neurologic morbidity more frequent.
“The possible long-term effects of preventable neonatal seizures remain unknown,”  while the known effects of electronic fetal monitoring—more surgical deliveries with their associated risks, higher costs, and more litigation—are well established. 
Karin B. Nelson, Thomas P. Sartwelle, Dwight J. Rouse
1. 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.
2. MacDonald D, Grant A, Sheridan-Pereira M, Boylan P, Chalmers I. The Dublin randomized controlled trial of intrapartum fetal heart rate monitoring. Am J Obstet Gynecol. 1985;152:524-39.
3. Grant A1, O'Brien N, Joy MT, Hennessy E, MacDonald D.Cerebral palsy among children born during the Dublin randomised trial of intrapartum monitoring. Lancet. 1989 Nov 25;2(8674):1233-6.
4. Neonatal encephalopathy and neurologic outcome. 2nd ed. Washington DC: America College of Obstetricians and Gynecologists, American Academy of Pediatrics, 2014.
5. Nelson KB, Sartwelle TP, Rouse DJ. Electronic fetal monitoring, cerebral palsy, and caesarean section: assumptions versus evidence. BMJ. 2016 Dec 1;355:i6405. doi: 10.1136/bmj.i6405.
Competing interests: No competing interests
The article by Nelson et al 1 is a wake-up call for obstetricians and their professional organisations. Despite spending large sums of money for cerebral palsy (CP) litigation, the compensation remains a lottery for the sufferers.
CTG and Evidence based Medicine
Cardiotocography (CTG) has a 99.8% false positive rate in predicting CP, a very rare event. But, it is quite late to intervene when CP becomes a real and present danger. The main goal of CTG is to prevent birth asphyxia, potentially dangerous fetal acidaemia (pH <7.10 and base deficit >12 mEq/L) and hypoxic-ischemic-encephalopathy (HIE). For this, a false positive predictive value of 'abnormal' CTG of around 70% seems likely, reduced further by fetal scalp blood sampling. Although unproven, the practical experience of British Obstetricians in the past was not far from this.
A survey was conducted of the personal preferences of clinicians in our Institute with an existing liberal culture of “intermittent auscultation (IA) of fetal heart rate (FHR)”. They were reminded of the evidence that CTG is not reliable in preventing CP or intrapartum hypoxia even in the presence of risk factors but does increase operative delivery. All 14 Obstetricians and 11 out of 15 midwives still chose to have CTG for themselves or their partners in the presence of any risk factors. Thus, there seems a disconnect between the “evidence” and the beliefs/experience of birth-attendants themselves. Secondly, they seem to judge any harm from CTG in a different context/balance.
The limitations of evidence based medicine have been well described. 2,3 Although the gold standard,, systematic studies have failed to show a significant benefit from intrapartum CTG for several reasons.3 However, birth attendants have regularly observed in actual practice that CTG prevents birth asphyxia. CTG will remain a widely practised procedure in the near future despite mistakes and variability in interpretation. CTG abnormalities make a small contribution to overall increasing caesarean section rate. In fact in developing countries like Brazil and China (where CP litigation is very rare), the caesarean rate is two to three times that in developed countries.
The meta-analysis of randomised controlled trials (RCTs) of CTG versus IA is underpowered to show a small difference. Most studies were done in the USA, where the categorisation of FHR decelerations (centre-stage in interpretation) may have been inconsistent compared to the British practice before 2007. 4 Moreover, if IA suggests abnormality then CTG is required to confirm or rule out abnormality anyway. In the UK for low risk labours IA is the recommended method of fetal monitoring. However, there is a new risk that FHR decelerations limited to contractions may be used as an indication to switch over to CTG. These decelerations are common but benign (early). A large number of cases would be unnecessarily switched over to CTG or transferred to hospital obstetric units, with resultant disempowerment of patients and midwifery practice and increased medical intervention. 4 Hitherto they have been rightly disregarded based on sound pathophysiology, longstanding British obstetric and midwifery practice and experience. 4 A stance that it does not matter what label we attach to FHR decelerations is fallacious.
Cerebral Palsy litigation: Rarely, there are major mistakes in CTG interpretation which on balance of probability would account for CP. Barring that, the large scale proliferation of CP litigation and ever increasing legal expenses/claims are largely the fault of the legal system rather than CTG. Moreover, recently there have been many changes and even "U" turns in CTG interpretation guidelines, raising serious doubts about the validity of previous practice, and birth attendants have been left confused. However, this is no fault of the victims of intrapartum hypoxia. Thus for the time being a "no-fault" compensation (at a much lower monetary value) needs consideration. The International Cerebral Palsy Task Force report 5 remains valid in court-rooms but with one clarification. In defining neurological injury from acute intrapartum hypoxia, a sentinel hypoxic event in labour is not essential but rather one of the non-essential criteria.5
"More research is required" may be a benign "truism" but it should not detract us from critically examining the failure of previous 50 years of research and applying analytical methods to the validity of current CTG interpretation.4 The birth-related professional bodies have an imperative to undertake a fundamental re-think in CTG interpretation.
Declaration of interest: The author has no conflict of interest to declare.
Mr Shashikant L Sholapurkar, MD, DNB, MRCOG
Obstetrician and Gynaecologist,
Royal United Hospital Bath NHS Trust, Bath, UK
1. Nelson KB, Sartwelle TP, Rouse DJ. Electronic fetal monitoring, cerebral palsy, and caesarean section: assumptions versus evidence. BMJ 355:i6405. doi: 10.1136/bmj.i6405.
2. Greenhalgh T, Howick J, Maskrey N; Evidence Based Medicine Renaissance Group. Evidence based medicine: a movement in crisis? BMJ 2014; 348:g3725.
3. Sholapurakr SL. Intrapartum fetal monitoring: overview, controversies and pitfalls. The Health foundation, London, UK, 2015. Patient Safety Resource Centre. http://patientsafety.health.org.uk/resources/intrapartum-fetal-monitorin...
4. Sholapurkar SL. Categorization of Fetal Heart Rate Decelerations in American and European Practice: Importance and Imperative of Avoiding Framing and Confirmation Biases. J Clin Med Res 2015; 7: 672-680.
5. MacLennan A. A template for defining a causal relation between acute intrapartum events and cerebral palsy: international consensus statement. BMJ 1999; 319:1054-1059.
Competing interests: No competing interests
Nelson, Sartwelle and Rouse suggest that an impartial expert task force should consider the question "does electronic fetal monitoring in labour reduce the risk of cerebral palsy?". But that isn't really the question-nor has it been for at least three decades. We know that most cases of cerebral palsy are associated with antenatal, not intrapartum events, and are hence unlikely to be associated with fetal hypoxia/acidaemia in labour. The CTG detects, through fetal heart rate recording, hypoxia/acidaemia. Ergo, intrapartum CTG use won't reduce cerebral palsy rates-and the authors are quite right, it doesn't.
What the authors omit to mention or reference is that CTG use is associated with an approximate 50% reduction in neonatal seizures (2), that most of these seizures are hypoxic in origin and due to intrapartum events. The long term motor and cognitive outcome of hypoxic encephalopathic seizures is at best guarded and at worst poor (3,4,5,6). Paradoxically, hypoxic seizures may disproportionately affect the babies of 'low risk' women, as they undergo intermittent fetal heart auscultation rather than continuous CTG (7).
Notwithstanding this, the outcome that the vast majority of women want is a healthy baby whose later development is not overshadowed by events at the time of birth. Whether an increased Caesarean rate is an acceptable quid pro quo is surely a matter for the mother to be-informed by carefully weighed professional opinion.
1. BMJ 2016;355:i6405
2. Alfirevic Z, Devane D, Gyte GML. Continuous cardiotocography (CTG) as a form of electronic fetal monitoring (EFM) for fetal assessment during labour. Cochrane Database of Systematic Reviews 2013, Issue 5. Art. No.: CD006066.
3. Temple CM, Dennis J, Carney R, Sharich J. Neonatal seizures: long-term outcome and cognitive development among ‘normal’ survivors. Dev Med Child Neurol1995;37:109-18
4. Marlow N, Rose AS, Rands CE, Draper ES. Neuropsychological and educational problems at school age associated with neonatal encephalopathy. Arch Dis Child Fetal Neonatal Ed2005;90:F380-7.
5. Lindström K, Lagerroos P, Gillberg C, Fernell E. Teenage outcome after being born at term with moderate neonatal encephalopathy. Pediatr Neurol2006;35:268-74.
6. Van Handel M, Swaab H, de Vries LS, Jongmans MJ. Long-term cognitive and behavioral consequences of neonatal encephalopathy following perinatal asphyxia: a review. Eur J Pediatr2007;166:645-54.
7. Dyson C, Austin T, Lees C. Could routine cardiotocography reduce long term cognitive impairment? BMJ. 2011 May 31;342:d3120.
Competing interests: I occasionally act as an expert witness in civil litigation and Coronial cases.
I read the authors' article (1) with great interest but I disagree with the concept that experts should develop consensus ''Whether electronic fetal monitoring reduces risk of cerebral palsy '' or move toward "intermittent auscultation". It is not about re-visiting the scientific facts which are already established in the literature regarding use of electronic fetal monitoring in labour or its predictive value. It is not about developing consensus over scientific evidence but rather about changing public perception and expectations.
We obstetricians need to realise that it is the time to change our approach in monitoring and assessing fetal well-being during labour. For this we use additional tools like fetal blood sampling (not used widely in theUSA) and other methodologies like STAN machines, K2 MS Guardian systems so that we can intervene early in case of fetal distress. It is established that lactate is an early marker of acidosis in labour as compared to pH measurement, but still in the UK, even after the publication from RCOG UK (2), NICE guideline CG 190 and the FIGO guideline,(3) not all units have implemented lactate measurement in their guidelines to assess fetal acidosis and hypoxia.
Obstetricians face the challenge of keeping a balance between maintaining a target of low caesarean section rates without compromising perinatal outcome. This task is hard to achieve and sadly obstetricians get the blame if they intervene early--labelled as "Interventionist''-- and if they avoid early intervention in cases of poor outcome.
Labour is a dynamic process. Acid-base physiology and equilibrium (acidosis) in the intrauterine environment is a challenging subject and studied in humans and animal models but still some questions remain unanswered. Since pH monitoring developed in 1970, scientists are still not sure which indicator is best to be used (Lactate vs pH vs Base deficit) as a good predictor of fetal outcome. All that obstetricians are doing is practising whatever the best data available show in their present times.
I totally agree with the authors that "Our current high rate of caesarean births is an important women’s health issue" but to support my argument of the need to change public perception and realistic expectation from clinicians, I would like to quote here an example of an extraordinary clinician (Dr Kieran O'Driscoll) who faced undue criticism for low caesarean section rate. Historically when the caesarean section rate was 5% in Ireland it was 15% in the UK. The publication from the National Perinatal Reporting System shows that the Caesarean Section rate, which was 10.6% in 1990, rose to 25.9% in 2008 (4) and there were multiple factors but one of the factor was criticism in the media and literature of clinicians at the Maternity Hospital, Dublin.
The comments from newspapers and other publications highlight this issue, and some examples are here:
One woman wrote, "I had a drip of what the nurses called 'jungle juice' inserted into my arm" (5); again in the same article it was commented, "Male-dominated labour practices are disempowering women"(5). Similarly the criticism on active management of labour did not stop here, and one of the authors in a publication '"ACTIVE MANAGEMENT OF LABOUR - A FEMINIST CRITIQUE" commented, ''The masculinist nature of the literature is evident'' (6).
Dr O'Driscoll who was the author of the book "Active management in Labour" and was criticised for this approach although low caesarean section rate or instrumental delivery was not the main goal of active management of labour.' Dr O’Driscoll emphasised that the word “active” referred to more involvement of the obstetrician during labour, as opposed to more active surgical intervention'' (7). This is an example where unfortunately a great obstetrician of his time was criticised as "interventionist" and his intention was completely lost.
This debate of intervention versus no intervention or continuous electronic fetal monitoring versus intermittent auscultation is not going to resolve the issue. All that obstetricians need to do is to focus on early intervention with the best methodology available to indicate early hypoxia, acidosis or fetal distress. If this approach comes along with the baggage of increased intervention then it should not be criticised and should be accepted in the light of the fact that an obstetrician is intervening in the best interest of mum and the un-born baby. Any stillbirth or any case of cerebral palsy (intrapartum related fetal distress) is a sad and unwanted outcome which may not be completely preventable because we have no diagnostic or predictive tool with high sensitivity or specificity. Hence it is unfair to blame clinicians for the poor outcomes even when they have intervened in their best intention. The paradigm shift needed is to accept that "Electronic fetal monitoring should not be used as a predictive tool (already established fact as can’t prevent cerebral palsy) but should be used as tool to tell us whether to intervene early or not". One should not be blamed for an early intervention.
1: Nelson Karin B, Sartwelle Thomas P, Rouse Dwight J. Electronic fetal monitoring, cerebral palsy, and caesarean section: assumptions versus evidence BMJ 2016; 355:i6405
2: Is it Time for UK Obstetricians to Accept Fetal Scalp Lactate as an Alternative to Scalp pH? (Scientific Impact Paper No. 47)
3: G.H. Visser, D. Ayres-de-Campos . FIGO consensus guidelines on intrapartum fetal monitoring.Adjunctive technologiesnternational Journal of Gynecology and Obstetrics 131 (2015) 25–29
7: Thomas F. Baskett. A Tribute to Kieran O’Driscoll (1920–2007).J Obstet Gynaecol Can 2007;29(8):672–673
Competing interests: No competing interests
Nelson et al raise the thorny issue of continuous, electronic fetal monitoring and cerebral palsy (1). They present a clear case that continuous EFM causes additional Caesarean sections though there may be many intangible benefits in contemporary intrapartum care.. However intrapartum care has moved on considerably since 1989; we are dealing with a new set of biological problems that we are ill-equipped to manage (2).
Many primigravid women now enter induced labour (40-50% in some units) with damaged uteri and complex medical problems e.g. obesity, impaired glucose tolerance, hypertension, etc. They have had surgical or medical evacuations of their uteri for miscarriage or abortion, or they have pelvic neurological injuries associated with persistent physical efforts during defaecation. Their uteri work less well than their mothers uteri as exemplified by increased CS rates, and, the high rates of postpartum haemorrhage that have increased by 500-1000% over the past decade. These uteri do not respond well to high-dose oxytocin regimens (2-4-8-16-32 mU per minute). Mis-management of intravenous oxytocin to cause excessive uterine activity is the single largest contributor to medicolegal claims for fetal injuries e.g .cerebral palsy, in the UK (3). Many senior, UK obstetricians believe that dosage should be reduced to 2-4-6-8-10-12mU, or, abolished altogether. However, up to 40% of these women will suffer decades of chronic pelvic pain, menstrual disturbances, painful sex, irritative bladder and bowel symptoms, vulval pain and recurrent infections i.e. gynaecology, commencing five years after their first delivery (4). Traumatic injuries sustained during childbirth through prolonged labours, big babies, operative vaginal delivery, etc injure pelvic nerves that re-grow to cause pain. Evidence of this future morbidity are the high rates of parous women with “pelvic girdle pain” that starts at 16-20 weeks and continues until induction of labour at 38 weeks. The same obstetricians that provide the advice that causes the intractable, neuropathic pain, are the gynaecologists that will treat this pain. This will be a fertile field for litigation in coming years.
There is a crisis on UK labour wards because there are no clear objectives for clinical care. Caesarean section rates are, at best, process indicators whose circumscribed morbidity women need to take into account. But it has to be set against the avalanche of later, gynaecological morbidity that they prevent. At present women are unaware of this morbidity. In 2016, the EFM debate is not top of the intrapartum agenda; there are more pressing problems ?
(1) Nelson K, Sartwelle T, Rouse D.
Electronic fetal monitoring, cerebral palsy, and, caesarean section: assumptions versus evidence.
BMJ 2016; 355:i6405-7.
(2) Grant A, O’Brien N, Joy MT, Hennessy E, MacDonald D.
Cerebral palsy among children born during the Dublinn randomised trial of intrapartum monitoring.
Lancet 1989: 2 1233-6.
(3) Steer P
Oxytocin should not be used to augment labour; there is too much risk for too little benefit.
BJOG 2015; 122(11): 1543.
(4) Quinn, MJ
Endometriosis: the consequence of uterine denervation-reinnervation.
Arch Gynecol Obstet. 2011; 284(6):1423-9.
Competing interests: No competing interests