23 ST-Analyser. Handbook CTG

23

ST-Analyser

Case Examples and Pitfalls

Ana Piñas Carrillo and Edwin Chandraharan

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

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

Key Principles

ST-Analyser (STAN) is only validated for monitoring fetuses >36 + 0 weeks of

gestation and should not be used in fetuses <35 weeks + 6 days of gestation.

Contraindications to the application of fetal scalp electrode (e.g. any maternal

infection with increased risk of vertical transmission through a defect in the fetal

skin and fetal haemorrhagic disorders which may increase the risk of scalp

haemorrhage) should be excluded.

Fetus should retain the capacity to respond to evolving intrapartum hypoxic

stress (i.e. should have a stable baseline fetal heart rate (FHR) and a reassuring

variability indicative of good oxygenation of the central organs).

STAN should not be commenced in the presence of an unstable baseline FHR

(i.e. myocardial hypoxia), reduced baseline variability with preceding

decelerations (hypoxia to the central nervous system) or in the presence of a

preterminal trace indicative of total loss of the ability to respond to hypoxia.Table 23.1 STAN guidelines: classification of the CTG trace

Cardiotocographic

classification

Baseline heart

frequency

Variability

reactivity

Decelerations

Normal 110–150 bpm 5–25 bpm

accelerations

Early decelerations

Uncomplicated

variable

decelerations with

a duration of

<60 seconds and a

beat loss of

<60 bpm

Intermediary* 100–110 bpm

150–170 bpm

Short bradycardia

episode

>25 bpm

without

accelerations

<5 bpm for

>40

min

Uncomplicated

variable

decelerations with

a duration of

<60 seconds and a

beat loss of

>60 bpm

Abnormal 150–170 bpm

and reduced

variability

>170 bpm

<5 bpm for

>60

minutes

Sinusoidal

pattern

Repeated late

decelerations

Complicated variable

decelerations with

a duration of

>60 seconds

Preterminal Total lack of variability and reactivity with or without

decelerations or bradycardia

* Combination of several intermediary observations will result in an abnormal CTG.

STAN is a test to detect intrapartum hypoxia. However, other pathways of fetal

neurological damage (e.g. meconium aspiration syndrome, chorioamnionitis and

inflammatory brain damage) should be considered while using STAN.

CTG should be classified (Table 23.1) and STAN guidelines (Table 23.2) should

be used while using STAN in clinical practice. Algorithms such as the ‘6C’

approach (Figure 23.1) may aid in management.Table 23.2 STAN guidelines: interpretation of ST events

ST events Episodic T/QRS

rise

Baseline T/QRS

rise

Biphasic ST

Normal CTG Expectant management and continued observation

Intermediary

CTG

>0.15 >0.10 3 biphasic log

messages

Abnormal CTG >0.10 >0.05 2 biphasic log

messages

Preterminal CTG Immediate deliveryFigure 23.1 Suggested algorithm: 6C approach for use of STAN in clinical practice.

Case 1. Commencement of STAN

The CTG trace shows a stable baseline FHR and a reassuring baseline variability prior

to commencement of STAN. Appearance of ‘crosses’ or ‘x’ below the tocograph

indicates that the analysis of fetal ECG has commenced (Figure 23.2). The ‘event log’

indicates that the ‘baseline T/QRS was determined at 18:36 hours’. Therefore, it is

appropriate to rely on STAN from this time onwards.Each ‘x’ represents an average of 30 ECG complexes, and therefore, 4 ‘x’s are

seen in a box (1 minute) because baseline FHR is 140 bpm (30 × 4 = 120).

STAN requires approximately 120 ‘x’s (i.e. approximately 4 minutes if baseline

FHR is 120 bpm) to calculate a baseline T/QRS ratio for an individual fetus.

Subsequently, it compares the average of 30 ECG complexes with this original baseline

T/QRS ratio as well as the ST segment of the fetal ECG to determine whether there is a

significant change in the T/QRS ratio or the ST Segment.

In addition, to ensure adequate ECG signals, crosses (‘x’) should not be absent

continuously for >4 minutes and there should be a minimum of 10 ‘x’s in any 10-minute

period.

Figure 23.2 Stable baseline and reassuring baseline variability at the commencement of

STAN monitoring. Note the event log.

Case 2. STAN Events on a Normal CTG Trace

Repeated fetal movements can result in fetal catecholamine surge as a part of ‘startle

response’ leading to glycogenolysis in the myocardium to release extra energy. This

results in the release of potassium ions stored within glycogen into the myocardial cells

as glycogen is broken down to glucose to provide extra energy substrate for the

myocardial cell. Increased intracellular myocardial potassium level leads to tall ‘T’

waves on the ECG complexes and the generation of ST event (Figure 23.3).

Such false-positive ST events are common with repeated fetal movements,

especially if there is a confluence of accelerations (Figure 23.3). No intervention isrequired as the CTG trace is entirely normal with no evidence of ongoing hypoxia

(Table 23.2).

Figure 23.3 ‘Episodic’ ST events secondary to repeated fetal movements. Note the

abrupt increase in ‘x’s coinciding with the ST events confirming that there was an abrupt

in

crease in the height of ‘T’ wave of fetal ECG due to intracellular release of potassium

secondary to catecholamine-mediated glycogenolysis.

Case 3. Nonsignificant ‘Episodic’ STAN Events

Even if the STAN generates ST events, no action is needed if the magnitude of the event

does not meet the threshold for intervention (Table 23.2). Therefore, every ST event that

is noted on the monitor does not require an intervention.

The onset of maternal active pushing may result in the development of hypoxia

within 10 minutes, leading to the generation of an ST event (Figure 23.4). However,

even if the magnitude of episodic T/QRS event is 0.10, if the CTG trace is not abnormal,

no intervention is required. In an intermediary CTG, a higher threshold (>0.15) would

be required to warrant an intervention (Table 23.2).Figure 23.4 Worsening decelerations with the onset of maternal active pushing and

transient increase in the ‘x’ in response to the release of intracellular potassium ions

secondary to catecholamine-mediated myocardial glycogenolysis. The ECG complex also

shows an elevation of the ST segment. However, no intervention is required as the type and

magnitude of ST event is not significant for the observed CTG changes.

Case 4. Abnormal CTG without Significant ST

Events

If the CTG remains abnormal despite absence of any significant ST events, a careful

assessment should be made to ensure that the signal quality is adequate. In the presence

of meconium staining of amniotic fluid and/or ongoing infection (i.e. chorioamnionitis),

coexisting hypoxia can significantly worsen perinatal outcomes. Therefore, in the

presence of deep prolonged decelerations and baseline tachycardia (Figure 23.5) and/or

loss of baseline FHR variability, asphyxia-mediated intrapartum meconium aspiration

syndrome and fetal inflammatory brain damage may occur, despite the absence of ST

events.

Clinicians should appreciate the fact that STAN is a test of hypoxia and would not

predict or diagnose meconium aspiration syndrome or diagnose ongoing inflammatory

brain damage secondary to clinical or subclinical chorioamnionitis. Therefore,

management decisions should be made based on the degree of CTG abnormalities noted,parity, cervical dilatation, progress of labour, need for augmentation with oxytocin and

fetal reserve.

If other risk factors are absent and the CTG is abnormal, it is appropriate to

continue labour in the absence of ST events, and conservative measures such as

changing maternal position to avoid umbilical cord compression may be attempted to

improve the CTG. However, in the presence of other risk factors such as thick

meconium staining of amniotic fluid or clinical chorioamnionitis, intrapartum

management should not depend on the absence of significant ST event alone. It is

recommended that in the presence of clinical chorioamnionitis, an intermediary CTG

should be upgraded to an abnormal CTG while interpreting ST events to recognize the

fact that coexisting inflammation lowers the threshold at which hypoxia can damage the

brain cells.

Figure 23.5 Ongoing complicated (or atypical) variable decelerations and increasing

baseline FHR secondary to evolving hypoxia. Although the CTG is ‘abnormal’ according

to STAN guidelines, there are no ST events and the signal quality is good (‘x’s are absent

only for 2 minutes).

Case 5. Abnormal CTG with a Significant STAN

EventsAny significant ST event requires an immediate intervention to improve utero-placental

circulation (changing maternal position, stopping oxytocin infusion with or without

administration of tocolytics and/or administration of intravenous fluids,) and if this is

not possible, an urgent delivery should be accomplished within 20 minutes of the

significant ST event. This holds true during first stage of labour and passive second

stage of labour. A significant ST event on an abnormal CTG (Figure 23.6) requires an

urgent intervention. The ‘event log’ would highlight the type and magnitude of the ST

event (Figure 23.6).

During active second stage of labour (i.e. after the onset of active maternal

pushing), immediate operative delivery (within 20 minutes) should be carried out,

unless a spontaneous vaginal delivery is imminent within the next 10 minutes. This is

because the evolution of hypoxia could be very rapid during active second stage of

labour. If a delay in delivery is anticipated, maternal pushing should be stopped to

rapidly improve fetal oxygenation.

If CTG has improved with conservative measures, it is appropriate to continue

labour with close observation. If there are repeated ST events, the timing of the very

first ST event should be considered in formulating a management plan. Worsening

magnitude of ST events (e.g. baseline T/QRS ratios of 0.06, 0.09, 0.11, etc.) over time

would indicate a progressively worsening hypoxic insult to the fetus, and urgent action

should be taken to improve utero-placental oxygenation, and if this is not possible or

appropriate (e.g. placental abruption or uterine rupture), an immediate operative

delivery should be undertaken.

Figure 23.6 Abnormal CTG trace with repeated complicated (or atypical) variable

decelerations lasting >60 seconds. The event log highlights baseline T/QRS ratio of 0.06,

which is significant for an abnormal CTG according to STAN guidelines.Pitfalls with the Use of STAN

Human error with regard to CTG interpretation and appropriate classification remains

the main concern. In addition, failure to incorporate the wider clinical picture such as

presence of thick meconium staining of amniotic fluid or evidence of clinical

chorioamnionitis also may lead to poor outcomes.

Failure to adhere to STAN guidelines (commencing STAN monitoring in preterm

fetuses or fetuses with known cardiac malformations), failure to accomplish delivery

within 20 minutes in the presence of a significant ST event or commencement of STAN

monitoring in the presence of preterminal CTG or chronic hypoxia (i.e. loss of baseline

FHR variability) may also lead to poor outcomes.

Conclusions

STAN determines oxygenation of the fetal myocardium and the capacity of the

myocardium to deal with ongoing hypoxic stress via the onset of anaerobic metabolism,

catecholamine-mediated cardiac glycogenolysis and consequent release of potassium

ions within the myocardial cell. If the T/QRS ratio is significantly higher than the ratio

calculated within the first 4 minutes of commencement of STAN monitoring, an ST event

will be generated.

Intervention should be based on the type and magnitude of ST event as well as the

classification of the CTG. Additional risk factors such as the presence of meconium

staining of amniotic fluid, evidence of ongoing chorioamnionitis, lack of progress of

labour, reduced physiological reserve of the fetus etc., should also be considered, and

one should not merely rely on STAN alone.

It should be noted that if a fetus has exhausted all its reserves and does not have the

capacity to mount a compensatory response to ongoing hypoxic stress (i.e. preterminal

CTG trace), ST events may not be seen. This is because of depletion of myocardial

energy stores (i.e. glycogen) and the resultant absence of catecholamine-mediated

glycogenolysis and consequent absence of any further changes in ST segment or T/QRS

ratio.Further Reading

1. Chandraharan E. STAN: an introduction to its use, limitations and caveats. Obs Gyn

Midwifery Prod News; 2010.

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