30 Medico-legal Issues with CTG. Handbook CTG

 30

Medico-legal Issues with CTG

◈

K. Muhunthan and Sabaratnam Arulkumaran

Handbook of CTG Interpretation: From Patterns to Physiology, ed. Edwin Chandraharan.

Published by Cambridge University Press. © Cambridge University Press 2017.

Background

Key Facts

Medical negligence involves establishing the causation and liability.

Cardiotocography refers to the recording of fetal heart rate (FHR) and

contractions (tocography).

Continuous electronic fetal monitoring (EFM) has become a standard practice in

high-risk pregnancies and labour in the Western world.

Despite severely abnormal CTG changes, failure of timely action and

nonconsideration of the clinical situation leads to a compromised fetus.

In-utero fetal death in labour, neonatal death and cerebral palsy associated with

abnormal CTGs and asphyxia lead to medical litigation.

Presence of abnormal CTG, low Apgar score, low cord arterial pH, assisted

ventilation, admission to neonatal intensive care, moderate or severe neonatalKey Features on the CTG Trace

There are few key CTG patterns that are recognized to be associated with fetal

compromise and are described below with example CTGs.5

Acute Hypoxia

encephalopathy and subsequent neurological damage point to asphyxia as a

possible cause.

However, several intrinsic fetal disorders (e.g. severe hypoglycaemia) cause

neurological disability, and an abnormal CTG may have been coincidental.

Causation is best determined by neuroradiologist and paediatric neurologist. The

fetus born at term demonstrates certain areas of scarring within the brain on

MRI. The thalamus, basal ganglia injury show scarring, reflecting acute profound

hypoxia while prolonged partial hypoxia results in bilateral cortical atrophy.1

Paediatric neurologist supports these findings by demonstrating that the baby has

athetoid or dyskinetic cerebral palsy with acute profound hypoxia and spastic

quadriplegia with prolonged partial hypoxia.2

Liability is determined by demonstrating that appropriate and timey action was

not taken in the presence of an abnormal CTG in that clinical situation.3

Expert opinion is requested to judge whether care provided fell short of what

was expected (Bolam principle).4

Presents with profound deceleration with a heart rate <80 bpm (Figure 30.1).

The pH can drop on an average by 0.01 per minute.6,7 The outcome of the

fetus/newborn would depend on the physiological reserve of the fetus, actual

heart rate (whether it is 40 or 60 bpm), duration of prolonged deceleration

before delivery and cause for prolonged deceleration (e.g. abruption placentae,

cord prolapse or scar rupture).Figure 30.1 Acute hypoxia.

Subacute Hypoxia

An example of prolonged deceleration or bradycardia is given below. If

prolonged, it can cause fetal death, or if born asphyxiated, it may lead to

neurological injury associated with acute profound hypoxia.

The thalamus and basal ganglia region gets affected and leads to athetoid or

dyskinetic type of cerebral palsy.

An example of such a trace is shown in Figure 30.1.

Presents with prolonged decelerations (Figure 30.2).

The FHR is below baseline rate for a longer time (e.g. >60 to 90 seconds) than

at baseline rate (<30 seconds).8

With such FHR, there is less than optimal circulation through the placenta over a

given time, especially if the FHR drops to <80 bpm. With such a trace (Figure

30.2), some of the fetuses would get compromised with the progression of

acidosis of approximately 0.01 every 2–3 minutes.Figure 30.2 Subacute hypoxia.

Gradually Developing Hypoxia

The CTG trace usually starts with a normal baseline rate, normal baseline variability,

accelerations and no decelerations.

Once decelerations start due to cord compression (variable decelerations) or

reduced placental reserve (late decelerations), hypoxia can set in leading to

catecholamine surge and rise in the baseline rate.

With increasing hypoxia, accelerations do not appear and decelerations get deeper

and wider (i.e. longer duration).

The FHR reaches a peak rate beyond which it is unable to increase the FHR. Even

with this rate, if oxygenation to the autonomic system cannot be maintained, the baseline

variability tends to get gradually reduced to almost flat baseline variability (Figure

30.3).

In the presence of normal baseline variability, 97 percent of the times the pH is

likely to be >7.0.9

When acidosis gets worse, within a short period the heart rate comes down and

becomes asystolic and may end as a stillbirth.

If delivered at the ‘peak’ heart rate after 1 to 2 hours of the FHR baseline

variability becoming ‘flat’ (‘distress platform’), the baby may be born asphyxiated

(hypoxia in the tissues and metabolic acidosis) and may suffer neurological injury or

bilateral cortical injury leading to cerebral palsy with spastic quadriparesis due to

prolonged partial hypoxia.1Figure 30.3 gives an example of gradually developing hypoxia that has gone into

the stage of possible acidosis that may lead to an asphyxiated baby.

Figure 30.3 Gradually evolving hypoxia with loss of baseline variability.

Long-standing or Preexisting Hypoxia

A fetus that is hypoxic and with early evidence of acidosis may show a

nonreactive trace (no accelerations) with absent or markedly reduced baseline

variability and shallow decelerations (blunted CNS response) to hypoxic stress

produced by contractions.

A fetus with such a trace may withstand the stress of contractions for variable

number of hours without any change on the CTG trace before the fetus gets

severely acidotic and has a cardiovascular collapse.

Such a trace is shown in Figure 30.4. If delivered earlier, the fetus would be in a

better condition.

Not all the fetuses may be neurologically affected, and with such a trace, earlier

the delivery better the outcome.

Figure 30.4 is an example of a CTG trace where the fetus may be already

acidotic.Figure 30.4 Chronic or long-standing hypoxia.

Anaemia and Sinusoidal CTG Trace

Causes could be:10

Causes for fetal anaemia:

Physiological – sucking the thumb, smacking its lips – as demonstrated by

ultrasound examination.

Pathological – a severe anaemia causes a sinusoidal pattern although the

mechanism is not known.

Rhesus sensitization, Kell, Duff antibodies

ABO antibodies give rise to neonatal jaundice, not fetal anaemia

Lewis a and b and M and N antibodies usually do not cause fetal anaemia.

Parvo virus infection.

Fetomaternal transfusion.

Vasa praevia and bleeding due to the rupture of vessels.

Alpha thalassemia.Figure 30.5 Typical sinusoidal trace secondary to chronic fetal anaemia.

Key Pathophysiology behind Patterns Seen on

the CTG Trace

Acute hypoxia is due to reversible (hypotension due to epidural, vaginal

examination, artificial rupture of membranes and, at times, no cause may be

identified) and nonreversible causes (abruption, cord prolapse, scar rupture). To

maintain normal blood gases and pH, the FHR may be at 140 bpm, i.e. 1,400

circulations through the placenta per minute. When the FHR is 80 bpm, there are

only 800 circulations through the placenta, i.e. misses 600 circulations. This

causes a marked reduction in CO2 expulsion and accumulation in the fetus and

respiratory acidosis, and in addition, the reduction in oxygen intake promotes

anaerobic metabolism and metabolic acidosis. Hence the drop of pH is

approximately 0.01 per minute. In addition, there is impact of coronary filling as

well.

Subacute hypoxia is usually due to intermittent prolonged cord compression that

may be exaggerated by oxytocin infusion or posture. The more the FHR is below

baseline FHR and the lower the FHR, the higher is the lack of oxygen intake and

expulsion of CO2, i.e. suboptimal circulation which leads to build up of

acidosis.

Gradually developing hypoxia is due to ongoing cord compression interfering

with umbilical cord flow (variable decelerations) or due to a reduction of

retroplacental blood flow (late decelerations). With gradual reduction of oxygenRecommended Management

and hypoxia, there is catecholamine surge that increases baseline FHR and

peripheral vasoconstriction. Despite the increase in FHR, if there is time taken

for coronary filling is inadequate, then decelerations become deeper and of

longer duration. A further reduction of oxygen to the fetus affects the autonomic

system resulting in a marked reduction in baseline variability.

Long-standing hypoxia is due to nonrecognized intrauterine growth restriction,

infection, prolonged pregnancy, placental malfunction (i.e. usually placental

insufficiency). The central nervous system may be under the influence of

hypoxia, thus resulting in blunted response and shallow decelerations.

Additional contractions would cause further acidosis and sudden bradycardia

and collapse.

A sinusoidal pattern of concern is due to fetal anaemia. The exact mechanism by

which anaemia produces a sinusoidal pattern is not known. It is believed to be

due to acidosis to the brain centres.

In acute hypoxia, the 3, 6, 9, 12, 15 rule is useful.11 Three minutes of low FHR

makes it a CTG of concern. If it is due to irreversible causes of abruption, cord

prolapse or scar rupture, steps should be taken for immediate delivery. If the

CTG is abnormal prior to bradycardia/prolonged deceleration or if there is

evidence of clinical compromise (e.g. IUGR, thick meconium), steps for

delivery should be taken by 6 minutes and in others by 9 minutes if conservative

measures of postural change, stopping oxytocin and tocolytics when needed do

not reverse bradycardia/prolonged deceleration. Earlier the delivery, better the

condition and aim for delivery within 15 to 30 minutes.

In subacute hypoxia, conservative measures of change of posture, hydration,

stopping oxytocin and tocolytics should be considered as needed, but if the FHR

does not return to near normality, operative delivery is advised unlessKey Tips to Optimize Management

spontaneous vaginal delivery is imminent. Caesarean or instrumental delivery

should be undertaken depending on the stage of labour within 30 to 40 minutes.12

In gradually developing hypoxia, delivery should be undertaken when there is

maximal rise in baseline rate with increasing depth and duration of decelerations

with reduction of interdeceleration intervals and marked reduction in baseline

variability for a period of 1 hour unless fetal scalp pH shows that further

observation is safe.

In long-standing hypoxic patterns, early delivery (40–60 minutes) should be

undertaken in the presence of significant meconium, absence of fetal movements,

bleeding per vagina, IUGR or prolonged pregnancy. In the absence of such

symptoms, observation could be continued for up to 90 minutes before

consideration of delivery.

In sinusoidal patterns, if fetal anaemia is suspected by blood group antibody

testing, Kelihauer–Betke test for fetomaternal transfusion, or increased blood

flow velocity of fetal middle cerebral artery, then delivery should be undertaken.

In addition to sinusoidal, if late decelerations are present with contractions,

early delivery is advised.

Better understanding of the significance of CTG patterns based on

pathophysiology (attending master classes, appropriate e-learning programs,

books, in-hospital case reviews with CTG).

CTG is an investigation, and hence management decision should be based on the

clinical situation in addition to CTG.

Requesting a senior person to review CTGs when in doubt.

Central monitoring systems that help other people also to observe the CTG

(‘neighbourhood watch’) and discuss it with the caregiver.Pitfalls

Based on the Fourth Confidential Enquiry into Stillbirths and Deaths in Infancy (CESDI)

and reports from the National Health Services Litigations Authority (NHSLA),13,14 the

common pitfalls are:

Failure to incorporate the clinical feature can be due either to a preexisting situation

making the fetus at risk where acidosis can develop faster with an abnormal CTG

compared to an appropriately grown fetus at term with clear liquor or to injudicious

management that puts the fetus at risk. They are listed below:

Fetus at Risk

Where possible and appropriate to use adjunct methods – fetal ECG (STAN

monitoring) or fetal scalp blood sampling (FBS) for pH or lactate.

Appropriate and timely intervention when conservative measures do not reverse

the CTG pattern.

Adequate staffing including senior staff and ready availability of theatre

facilities.

Inability to interpret the CTG trace

Failure to incorporate the clinical picture

Delay in taking action

Poor communication between team members

Preterm

Postterm

Intrauterine growth restriction

Thick meconium with scanty fluid

Intrauterine infectionFetus at Possible Risk Due to Injudicious Management

Consequences of Mismanagement

Mismanagement leads to a situation from normoxaemia to hypoxaemia (lack of oxygen in

blood) to hypoxia (lack of oxygen in tissue) and asphyxia (lack of oxygen in tissue and

metabolic acidosis).

Hypoxia and metabolic acidosis leads to cell dysfunction in various tissues and

may present as:

1. Heart failure

2. Pneumocytes type 2 injury lead to less surfactant factor

3. GI system ‘necrotizing enterocolitis’

4. Renal failure

5. Endothelial damage leads to DIC (disseminated intravascular coagulation)

6. CNS – cerebral oedema, seizures or coma (grades II and III neonatal

encephalopathy). Cell death could lead to cerebral palsy.

7. Stillbirth or neonatal death

Intrapartum bleeding

Injudicious use of oxytocin

Epidural in advanced labour and with a CTG showing abnormal pattern

Difficult instrumental delivery, shoulder dystocia, vaginal breech delivery

Acute events (cord prolapse, abruption, scar rupture)

Suspicious/abnormal admission FHR on CTG or auscultation

Needless to say, mismanagement leads to medical litigation. Litigation can

also be an unpleasant experience and have significant long-term consequences

for the working lives for healthcare staff involved.Exercise

A 28-year-old gravida 2 is in spontaneous normal labour. She has no high-risk factors

and she is in the active second stage of labour. She was monitored for audible

abnormality of the FHR. Abdominally the fetus was estimated to be 3.8 kg and the head

was 0/5th palpable. Vaginally there was clear amniotic fluid, she was fully dilated, and

the occiput was in left occipito transverse position at station 0 to +1. There is ++ caput

and ++ moulding. The CTG trace is shown in Figure 30.6.

Figure 30.6

Escalating costs of claims and insurance premiums have led to a major

concern for maternity service providers across most of the countries.14

Malpractice fears are also believed to have contributed, in small part, to the

rising defensive practice in obstetrics.15

Anyhow, most malpractice claims seem to be unrelated to the incompetence of

an individual provider but to systemic failures that overwhelm competent

people working in a highly imperfect and complex environment.

Report published by NHSLA in October 2012 provides an analysis of the

various clinical situations that have led to maternity claims. In a 10-year

analysis of maternity claims (between 1 April 2000 and 31 March 2010),

there were 5,087 claims with a total value of £3.1 billion.14

This amounts to <0.1 percent of births, indicating that the vast majority of

births do not result in a clinical negligence claim.1. Describe your plan of action.

a. Observe for another hour

b. Perform FBS

c. Perform caesarean section

d. Perform instrumental delivery

e. Give acute tocolysis and await further descent

References

1. Myers RE. Four patterns of perinatal brain damage and the conditions of occurrence in

primates. Advances in neurology. Vol. X. Eds. BS Meldrum and CD Marsden. Raven Press,

New York. 1975; pp. 223–34.

2. MacLennan A. A template for defining a causal relation between acute intrapartum events

and cerebral palsy: international consensus statement. BMJ 1999;319:1054–9.

3. Williams B, Arulkumaran S. Cardiotocography and medico-legal issues. Best Pract Res

Clin Obstet Gynaecol 2004;18(3):457–66.

4. Electronic fetal monitoring: medico-legal issues. Fetal monitoring in practice. Second

edition. Eds. G Donald and S Arulkumaran. Butterworth Heinemann, Oxford. 2008; pp.

225–9.

5. Arulkumaran S. Fetal surveillance in labour. Munro Kerr’s operative obstetrics. Twelfth

edition. Eds. TF Baskett, AA Calder and S Arulkumaran. Saunders Elsevier, Ediburgh. 2014;

pp. 41–56.

6. Ingemarsson I, Arulkumaran S, Ratnam SS. Single injection of terbutaline in term labor.

Effect on fetal pH in cases with prolonged bradycardia. Am J Obstet Gynecol

1985;153:859–65.

7. Leung TY, Chung PW, Rogers MS, et al. Urgent caesarean delivery for fetal bradycardia.Obstet Gynecol 2009;114(5):1023–8.

8. Cahill AG, Kimberly AR, Odibo AO, Maconaes GA. Association and prediction of

neonatal acidaemia. Am J Obstet Gynecol 2012;207:206–8.

9. Williams KP, Galerneau F. Intrapartum fetal heart rate patterns in the prediction of neonatal

acidemia. Am J Obstet Gynecol 2003;188:820–3.

10. Cardiotocographic interpretation: more difficult problems. Sinusoidal pattern. Fetal

monitoring in practice. Third edition. Eds. G Donald and S Arulkumaran. Butterworth

Heinemann, Oxford. 2008; pp. 159–88.

11. Intrapartum care. Care of healthy women and their babies during childbirth. NICE clinical

guideline 190, December 2014, pp 39–57.

12. The role of scal pH. Fetal monitoring in practice. Third edition. Eds. G Donald and S

Arulkumaran. Butterworth Heinemann, Oxford. 2008; pp. 189–203.

13. Confidential enquiry into stillbirths and deaths in infancy. Fourth annual report. 1997.

Maternal and Child Health Research Consortium.

14. Ten years of maternity claims. An analysis of NHS Litigation Authority data. NHS

Litigation Authority. October 2012.

15. Schifrin BS, Cohen WR. The effect of malpractice claims on the use of caesarean

section. Best Pract Res Clin Obstet Gynaecol 2012:S1521-6934(12)00165-4.