Intra-partum Fetal Monitoring – Cardiotocograph

IntroduCtIon The course of labour is the first challenge one ever undertakes. The uterine contractions during labour exposes the fetus to a possible risk of hypoxic brain injury due to repeated cord compression or reduction of utero-placental perfusion1. Intrapartum fetal surveillance evolved with the principal aim of preventing adverse perinatal outcomes arising from fetal metabolic acidosis / cerebral hypoxia related to labour. However, the severity of an asphyxial injury is influenced by many factors (e.g. tissue perfusion, tissue substrate availability, fetal condition prior to the insult, duration of the insult and the severity of the insult). Therefore, the relationship between metabolic acidosis and cerebral injury is complex. Furthermore, it is clear that very often damage is actually sustained during pregnancy, prior to labour, rather than arising de novo during labour and delivery2 . In spite of this, intrapartum fetal surveillance for early detection of fetal hypoxia has become a key component of modern maternity care. Intrapartum fetal surveillance was traditionally carried out by intermittent auscultation (IA) of the fetal heart rate (FHR). This approach would be adequate to monitor a fetus at low risk of compromise, but may be inadequate for high-risk pregnancies. Therefore, the use of intrapartum electronic fetal monitoring (EFM) with cardiotocography (CTG), has steadily increased over the last three decades in an attempt to reduce the incidence of intrapartum fetal morbidity and mortality.


IntroduCtIon
The course of labour is the first challenge one ever undertakes.The uterine contractions during labour exposes the fetus to a possible risk of hypoxic brain injury due to repeated cord compression or reduction of utero-placental perfusion 1 .Intrapartum fetal surveillance evolved with the principal aim of preventing adverse perinatal outcomes arising from fetal metabolic acidosis / cerebral hypoxia related to labour.However, the severity of an asphyxial injury is influenced by many factors (e.g.tissue perfusion, tissue substrate availability, fetal condition prior to the insult, duration of the insult and the severity of the insult).Therefore, the relationship between metabolic acidosis and cerebral injury is complex.Furthermore, it is clear that very often damage is actually sustained during pregnancy, prior to labour, rather than arising de novo during labour and delivery 2 .In spite of this, intrapartum fetal surveillance for early detection of fetal hypoxia has become a key component of modern maternity care.Intrapartum fetal surveillance was traditionally carried out by intermittent auscultation (IA) of the fetal heart rate (FHR).This approach would be adequate to monitor a fetus at low risk of compromise, but may be inadequate for high-risk pregnancies.Therefore, the use of intrapartum electronic fetal monitoring (EFM) with cardiotocography (CTG), has steadily increased over the last three decades in an attempt to reduce the incidence of intrapartum fetal morbidity and mortality.
For low-risk women in labour, it has a Consultant Obstetrician and Gynaecologist, District Base Hospital, Rikillagaskada, Sri Lanka b J.M.S.W Jayasundara, Registrar in Obstetrics  and Gynaecology, Castle Street Hospital for  Women, Colombo 8, Sri Lanka   Correspondence: Dr. C. G. A. Gunasena MD  MRCOG   E mail -asankagunasena@gmail.comCompeting interests: The authors report no conflict of interest

Leading articLe
www.slcog.lk/sljogbeen suggested that the only clinically significant benefit from the use of routine continuous EFM in comparison to IA was in the reduction of neonatal seizures but with no statistically significant improvement in long-term outcomes such as cerebral palsy, although it increased the caesarean section and operative vaginal delivery rates 3 .Therefore, the use of continuous CTG for low risk pregnancies is not recommended 4 .It is also widely appreciated that there are still shortcomings in interpretation of CTG which is evident by the reviews of cases with poor perinatal outcomes 5 .
In order to improve the interpretation of CTG, it is important to understand the control of the fetal heart rate by the sinoatrial node, sympathetic and para-sympathetic autonomic nervous systems, baroreceptors, chemoreceptors, catecholamines and cardio-regulatory center.In addition to that, the physiology of fetal oxygenation and how the fetus reacts to hypoxia, the types of intra partum hypoxia (gradual, subacute, acute, chronic), the pathophysiological basis for CTG abnormalities, and the principles of EFM should also be clearly understood for decision making on intrapartum CTG
Although its pathophysiology is poorly understood, it is thought to be due to a hyperactive fetal autonomic nervous system.It may be seen in fetal hypoxia associated with decelerations (10).

FetAl tAChyCArdIA
A

VArIAble deCelerAtIons
Variable decelerations represent a baroreceptor-mediated response to increased arterial pressure, as occurs with umbilical cord compression.They are variable in shape, depth, duration and timing with the contractions and exhibit a good variability within the deceleration.They typically have a rapid onset (onset to nadir < 30 seconds) and a rapid recovery to baseline.Variable decelerations constitute the majority of decelerations during labour.They are seldom associated with an important degree of fetal hypoxia/acidosis.Increases in FHR immediately before and after a variable deceleration have been referred to as "shoulders."These increases can be visually similar to accelerations, and this led to speculations that they had a similar predictive value.However, there is inadequate evidence to support the notion that "shoulders" have the same predictive value as accelerations 12 .
Variable decelerations were formerly categorized as 'typical' if they were considered to be normal and not indicating fetal hypoxia and 'atypical' if they were considered to be abnormal and indicating probable fetal hypoxia.Although the terms 'typical' and 'atypical' are not currently used, the non-reassuring features in variable decelerations which require appropriate action, as they indicate the likelihood of fetal hypoxia, have been clearly described 2,6,11 .These nonreassuring features which are also referred to as 'complicated variable decelerations' include a persistently large amplitude (> 60 bpm in depth) and / or long duration (> 60 seconds duration), a slow return to the baseline after the contraction, smooth (with no baseline variability) postdeceleration shoulders ("overshoots") often associated with a rising baseline or a baseline tachycardia and a reduced baseline variability 6 .

lAte deCelerAtIons
Late decelerations are caused by contractions in the presence of fetal hypoxia.These are uniform and repetitive.Late decelerations start after the start of the contraction and the nadir of the deceleration is more than 30 seconds after the peak of the contraction.They return to the baseline after the contraction has finished.Late decelerations of any depth are significant and should be immediately attended to.In fact shallow decelerations (with decreases of < 10 bpm ) with reduced baseline variability are particularly dangerous and indicate significant fetal hypoxia.These can even be detected with careful IA of FHR immediately after uterine contractions, but not in between uterine contractions when the FHR has returned to its normal baseline

prolonGed deCelerAtIons
Decelerations lasting > 3 minutes are defined as prolonged decelerations.They may indicate chemoreceptor-mediated hypoxaemia.Decelerations exceeding 5 minutes, with FHR less than 80 bpm and reduced variability within the deceleration are frequently associated with acute fetal hypoxia/acidosis and require urgent intervention 10 .

sInusoIdAl pAttern
This is an oscillating pattern resembling a sine wave (very smooth with a regular cycle rate).It has a relatively fixed period of 3-5 cycles per minute and typically an amplitude of 5-15 beats.Its pathophysiology is poorly understood but it may be seen with severe fetal anemia (fetal-maternal haemorrhage, twinto-twin transfusion syndrome, anti-D alloimmunization and vasa previa) It has also been described in cases of acute fetal hypoxia, infection, cardiac malformations, hydrocephalus, and gastroschisis 10 .
There is agreement about baseline FHR and fetal tachycardia, with FIGO describing a time frame too .Although NICE Guidelines describe FHR of 160-180 bpm as non-reassuring and FHR > 180 bpm as pathological, FIGO Guidelines do not sub categorize fetal tachycardia in this manner.A fetal tachycardia (FHR > 160 bpm) may be secondary to fetal compensatory response to evolving hypoxia.A mere increase in  The FIGO Guidelines consider FHR < 100 bpm as pathological and RANZCOG Guidelines also describe prolonged bradycardia of FHR < 100 bpm for more than 5 minutes as a likely feature of fetal compromise.It has been suggested that a stable baseline fetal heart rate between 90 and 99 bpm with normal baseline variability (having confirmed that this is not the maternal heart rate) may not be pathological 11 .However, it is essential that patients with such CTGs are evaluated properly by an experienced senior obstetrician.
There is no significant difference in the definitions of normal baseline variability and reduced variability, between the different guidelines.However, the NICE Guidelines further categorize reduced baseline variability being non-reassuring or abnormal according to the duration, which would be more useful in clinical decision making.

IntrApArtuM Fhr InterpretAtIon And MAnAGeMent; A step-wIse physIoloGIC ApproACh
An

step 1-the norMAl And the AbnorMAl InItIAl CtG
If the CTG is normal the fetus is very likely to be neurologically intact, normoxic, without acidaemia or acidosis, at low risk of intrapartum asphyxia, and is able to react and defend itself against intrapartum hypoxia.Surveillance may continue depending on the situation or the woman may be monitored by IA 13 .

step 2-reCoGnItIon oF the CoMpensAted And the deCoMpensAtInG Fetus
An intact fetus with a previously normal CTG will exhibit predictable patterns of FHR responses if exposed to hypoxic ischaemic insults during labour.Based on the intensity and duration of hypoxic stress during labour, three types of intrapartum hypoxia had been described, namely: gradually evolving hypoxia; subacute hypoxia; and acute hypoxia.The management should be tailed according to the type of hypoxia to optimize fetal outcome 7 .

GrAduAlly eVolVInG hypoxIA
The hypoxic stress evolves over time (hours) giving the fetus time to use its compensatory mechanisms effectively in order to prevent hypoxic damage.The first feature on CTG is the presence of decelerations with contractions.If the hypoxic insult continues, the decelerations will be followed by ABCDE.

Compensated stress decompensation end stage
The accelerations disappear in order to conserve oxygen and energy substrates in the fetus.The catecholamine release increases the FHR and cardiac output to maintain perfusion to the vital organs.Therefore, a sustained FHR tachycardia in association with uterine contractions is a sensitive marker of a compensatory Leading articLe www.slcog.lk/sljogincrease in fetal cardiac output.If the hypoxic insult continues, depending on the fetal reserve and the intensity and duration of hypoxia, fetal decompensation may ensue.When the perfusion to the brain is compromised, loss in the baseline variability would be observed in the CTG trace.Finally, myocardial hypoxia and acidosis may lead to a terminal bradycardia resulting in the 'step-ladder pattern to death' 7 .
The management should be tailored according to the level of hypoxia.In the presence of a stable baseline in between decelerations and normal baseline variability, labour can be continued with continuous CTG monitoring.If raised baseline and or abnormal variable or late decelerations appear on the CTG, care should be taken to improve fetal environment (intrauterine resuscitation) which may include stopping or reducing oxytocin, iv fluids and placing patient in the left lateral position.If baseline variability is reduced despite conservative measures, immediate delivery should be considered 7 .

ACute hypoxIA
This is characterized by a sudden drop in the baseline heart rate, which is also known as a 'single prolonged deceleration'.This could be either suspicious (lasting for < 3 minutes and returning to the normal baseline with good variability) or abnormal (lasting for > 3 minutes ) First, it is essential to exclude three major intrapartum accidents (placental abruption, umbilical cord prolapse and uterine rupture) and two iatrogenic causes (hyper-stimulation due to oxytocin or prostaglandins and maternal hypotension usually secondary to supine hypotension or epidural analgesia).In case of intrapartum accidents, delivery should be expedited via the safest and quickest way to save the fetus.
If acute hypoxia is considered to be due to an oxytocin infusion, 'intrauterine resuscitation' should be initiated immediately.In the presence of normal variability prior to deceleration and within the first three minutes of deceleration and the three accidents mentioned above are absent, unto 90% of the prolonged decelerations have been reported to recover by 6 minutes and 95% by 9 minutes 14 .
In case of acute hypoxia occurring in the absence of intrapartum accidents or iatrogenic causes, the '3, 6, 9, 12 and 15-minute' rule , which includes the following ,should be applied: if a normal baseline variability has been noted before the onset of deceleration and within the first 3 min of the deceleration , appropriate intrauterine resuscitation by 6 min, moving the patient to a theatre by 9 min, and if the CTG shows no signs of recovery, commencing delivery by 12 min with the aim of delivering the baby by 15 min 15 .
Reduced baseline variability before or within the first 3 min of the deceleration, repetitive late decelerations before the onset of the prolonged deceleration or a drop in the heart rate to >60 bpm are associated with a poor outcome.In these circumstances, the '3, 6, 9, 12 and 15minute' rule should not be applied, and immediate delivery should be undertaken 7 .

subACute hypoxIA
This is characterized by complicated variable decelerations, with the amplitude of the deceleration > 60 bpm and lasting for > 90 seconds.When the FHR returns to its baseline in subacute hypoxia, it spends less than 30 seconds at the baseline level before the onset of the next deceleration 7,16 .Therefore, the time available at the baseline to wash off the acid and carbon dioxide and to obtain fresh oxygenated blood from the placenta becomes progressively shorter.Therefore, a rapidly cumulative build up of CO2 takes place which results in an initial respiratory acidosis and a subsequent metabolic acidosis.The baseline FHR may remain within the normal range (110-160 bpm) as the fetus is unable to raise its baseline heart rate because of the short duration of time spent at the baseline in between two decelerations.Subacute hypoxia is associated with a rapid decline Leading articLe www.slcog.lk/sljog in pH, usually at the rate of 0.01 every 2-4 minutes, in contrast to the gradually evolving hypoxia 16 .
Once subacute hypoxia is established, there is likely to be insufficient time to obtain, analyze and react to a fetal blood sample result without the risk of severe acidaemia.Therefore, in clinical practice, it is crucial to recognize this pattern 16 .
The management involves in utero resuscitation and discouraging active maternal pushing for the next few contractions to ensure oxygenation of placental venous sinuses.Immediate delivery should be considered if changes are not reversed with conservative measures 7 .

ChronIC hypoxIA
In this situation, the fetus has been exposed to a prolonged period of hypoxia with or without resultant neurological injury during the antenatal period before the onset of labour.This happens usually secondary to chronic utero-placental insufficiency.The fetus adapts several compensatory mechanisms for survival including reduction in growth, movements and diversion of oxygenated blood and nutrients from non-vital organs to supply the vital organs 7 .
The affected fetus may be identified by the features observed on the CTG; increase in the baseline rate with reduced variability and the presence of shallow decelerations.Even though some degree of cerebral damage may have already taken place, the presence of this CTG pattern requires immediate delivery.This is because, there will be further reduction in oxygenation of the fetus with the onset of labour due to uterine contractions, intermittent umbilical cord compression and reduction in utero-placental circulation.This will eventually lead to hypoxic ischaemic encephalopathy, terminal bradycardia and fetal death 7 .

FetAl sCAlp blood sAMplInG (Fbs)
This is a test to assess the acid-base status of the fetus.The units employing EFM are encouraged to have access to FBS facilities to aid in the management of labours where fetus shows equivocal CTG changes.FBS can be assessed for pH and lactate levels.The incidence of false positives from an abnormal CTG can be reduced with FBS.A reduction in the total caesarean section rate from 18% to 11% and caesarean section indicated by fetal distress from 7% to 3%, when fetal scalp blood sampling was allowed, has been reported 17 .
The most important question is the identification of the appropriate clinical situation for FBS.Delivery must be expedited and FBS should not be undertaken, if there is clear evidence of serious and/or sustained fetal compromise.Delivery also needs to be expedited if CTG abnormalities are of a degree requiring further assessment, but FBS is unavailable or contraindicated.

ContrAIndICAtIons to Fbs
< 110 bpm lasting > 10 minutes is considered as fetal bradycardia.However a baseline FHR between 100 and 109 bpm with normal baseline variability and no variable or late decelerations should not prompt any further action 11 .The causes of fetal bradycardia include low inherent rate, medications (e.g.local anesthetics

table 1 : Antenatal risk factors which would justify continuous intrapartum cardiotocography -adapted from rAnZCoG Guidelines 2014 (2)
Hyperglycaemia in pregnancy requiring medication, or if it is poorly controlled, or if associated with macrosomia Current or previous conditions which constitute a risk of fetal compromise e.g.cholestasis, isoimmunisation, substance abuse Significantly reduced fetal movements preceding labour Morbid obesity BMI ≥ 40 Maternal age ≥ 40