12 Role of Chorioamnionitis and Infection. Handbook CTG

Role of Chorioamnionitis and

Infection

◈

Jessica Moore and Edwin Chandraharan

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

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

Key Facts

Chorioamnionitis is a significant cause of non-hypoxic fetal compromise.

It may occur prior to the onset of labour or during the intrapartum period.

Clinical chorioamnionitis is characterized by maternal pyrexia (≥38°C) and at

least one of the following parameters: fetal tachycardia, maternal tachycardia,

uterine tenderness, and/or offensive smelling liquor or purulent vaginal

discharge.

Meconium-stained liquor may also be a feature of chorioamnionitis.

Once clinical chorioamnionitis is evident, it is likely that the infective process is

well established in the fetoplacental unit.

Histological chorioamnionitis is a presence of inflammatory cell infiltrates in the

membranes of the placenta and in severe cases in the umbilical cord (funisitis).

The presence of funisitis demonstrates the presence of a fetal systemic

inflammatory response syndrome (FSIRS).The term subclinical chorioamnionitis is used when there are no overt signs of

clinical chorioamnionitis but the placental histopathological examination reveals

histological evidence of chorioamnionitis. This may manifest as preterm rupture

of membranes or preterm labour or term pre-labour rupture of membranes

(PROM).

The term ‘subclinical chorioamnionitis’ may also refer to cases where

intrauterine infection is suspected – such as maternal and fetal tachycardia with

meconium-stained liquor. However, the criteria for clinical chorioamnionitis are

not met. In addition, subclinical chorioamnionitis may present as preterm rupture

of membranes or preterm labour.

Adverse maternal outcomes with chorioamnionitis include postpartum

haemorrhage from uterine atony, sepsis and postpartum endometritis.

Adverse outcomes for the fetus include stillbirth, premature birth, neonatal

infection, respiratory disease and brain injury and longer term sequelae such as

learning difficulties and cerebral palsy.

The presence of intrauterine infection is associated with a significantly

increased risk of cerebral palsy. Clinical chorioamnionitis is associated with a

fivefold increase in the risk of cerebral palsy, and histological chorioamnionitis

an even higher risk of brain injury.

Coexistence of intrauterine infection and hypoxia further increases the risk of

cerebral palsy as compared to hypoxia alone (78- vs 5-fold as compared to

background risk).

The relationship between severity of maternal disease in clinical

chorioamnionitis and outcome for the fetus is unpredictable. In some cases, the

mother may have significant signs of sepsis and yet the fetus may be born in good

condition. Conversely, a mother may have no signs of clinical chorioamnionitis

and yet the fetus may be born with significant systemic inflammation.

It is vital to appreciate that chorioamnionitis is a fetal disease, and therefore,

occurrence of maternal symptoms and signs may indicate an advanced fetalRisk factors and associations with chorioamnionitis include:

Key Pathophysiology of Infection and CTG

infection with poor neonatal outcome.

Emerging scientific evidence suggests that inflammatory mediators per se can

cause fetal neurological damage due to poor development of fetal blood–brain

barrier without the presence of organisms within the amniotic cavity.

Premature rupture of membranes and labour. It is likely that subclinical

chorioamnionitis plays a role in the pathophysiology of premature rupture of

membranes. However, once this occurs, there is an increased risk of clinical

chorioamnionitis due to ascending infection.

Prolonged rupture of membranes.

Group B streptococcal colonization in the mother.

The understanding of CTG changes in the presence of fetal infection is poor.

Chorioamnionitis may lead to FSIRS.

It is possible that fetal inflammatory response may cause neurological injury

through different mechanisms to those caused by hypoxia although there may be

common synergetic pathways. Although it is possible that with infection there is

no protective upregulation of anti-inflammatory cytokines which occurs in fetal

hypoxic ischaemia.

The possible mechanisms of fetal brain injury include a reduction in oxygen

transfer across inflamed fetal membranes or a reduction in fetal cardiac output

secondary to myocardial dysfunction causing a reduction in cerebral blood flow.

Severe fetal infection may result in a metabolic acidosis although often the cord

pH may be normal despite the fetus being born in poor condition.

Fetal infection in the presence of ongoing hypoxic stress will result in a worse

outcome for the fetus. This is because inflammatory mediators lower the

threshold at which hypoxia can cause fetal neurological damage.Key Features on the CTG Trace

It must be remembered that CTG monitoring is a test for fetal hypoxia and that

the role of CTG in chorioamnionitis is less clear.

There is a lack of evidence that specific features on the CTG trace can identify

cases of clinical or subclinical chorioamnionitis. However, understanding the

pathophysiology of hypoxia and FSIRS may help in recognizing ongoing clinical

or subclinical chorioamnionitis based on the features observed on the CTG

trace.

It is probably important to consider the features of a term CTG separately to

those in a preterm CTG.

Studies that have looked at the role of CTG in the identification of systemic fetal

infection have often applied the definitions used for hypoxia, and it is possible

that intra-amniotic infection exerts an effect on the fetus through different

pathways. This may explain why many of the studies evaluating the CTG in fetal

infection have not been conclusive.

CTG features seen in the presence of intrauterine infection include fetal

tachycardia, reduced variability, lack of accelerations, presence of decelerations

and lack of cycling (Figure 12.1), but none of these features have been seen

consistently.

‘Saltatory pattern’ (variability >25 bpm) may be seen in maternal pyrexia due to

the dysregulation of fetal thermoregulatory centre.

One study estimated that fetal tachycardia at term was associated with an

increased risk of systemic fetal inflammation of 9 times the odds of a term fetus

with no tachycardia. There is also evidence that fetal tachycardia increases the

incidence of cerebral palsy.

If fetal tachycardia and reduced variability are seen without preceding or ongoing decelerations, then consideration should be given to infection as the

primary cause. This is because fetal tachycardia will be almost always preceded

by decelerations in cases of intrapartum hypoxia.Figure 12.1 CTG features associated with chorioamnionitis at term. Note the absence of

cycling and accelerations with the baseline FHR at or above the upper limit of normal.

Recommended Management

It is important to compare FHR with any previously recorded FHR as a

significant rise in FHR should prompt the question of infection.

Ongoing baseline fetal tachycardia on admission or in early labour in a term

fetus may be suggestive of underlying subclinical chorioamnionitis. This should

prompt a clinician to look for other signs of maternal inflammatory response. In

the absence of a diagnosis of clinical chorioamnionitis, the patient should be

observed closely for evolving signs (maternal tachycardia, maternal pyrexia,

meconium staining of amniotic fluid or an offensive vaginal discharge).

Other causes of fetal tachycardia such as maternal hypotension, dehydration,

chronic hypoxia and medications (e.g. salbutamol) should be excluded.

If clinical chorioamnionitis is diagnosed, then a full septic screening of the

mother should be undertaken along with the administration of broad-spectrum

intravenous antibiotics and antipyretics.

One should not rely on the CTG as a test of fetal well-being when clinical

chorioamnionitis is present. However, evidence of coexisting intrapartum

hypoxia (i.e. presence of repetitive atypical variable or late decelerations) is a

bad prognostic indicator.

Consider expediting delivery. It is difficult to give exact timing for when

delivery should occur. However, if subclinical chorioamnionitis is suspected,care should be taken to avoid further hypoxic stress on the fetus due to the

synergistic damaging effect of hypoxia and infection on the fetal brain.

If a diagnosis of clinical chorioamnionitis is made prior to delivery,

consideration should be given to delivery by caesarean section to avoid any

additional hypoxic stress from labour (e.g. primigravida with cervical dilatation

<6 cm, or if there is evidence of failure to progress requiring oxytocin

augmentation).

Avoidance of additional hypoxic stress (e.g. repetitive cord compression or

increased uterine activity leading to reduced utero-placental oxygenation) is

paramount (Figure 12.2). This means oxytocin should be used with great caution,

and it is prudent to avoid a prolonged labour or a complicated delivery.

If labour is progressing quickly and vaginal delivery is anticipated within the

next 3–4 hours, it is appropriate to continue with labour if the CTG trace is

entirely normal suggestive of no ongoing hypoxic stress.

Partogram should be carefully scrutinized to monitor the progress in labour

closely as well as any signs of deterioration in the condition of mother or fetus.

Consider the mode of delivery. There is a lack of evidence that caesarean

section at the time of diagnosis of clinical chorioamnionitis will improve the

neonatal outcome. However, there is a significant association between duration

of chorioamnionitis and 5-minute Apgar score <3 and mechanical ventilation

within 24 hours.

Ensure a neonatologist is present at delivery.

Take umbilical cord gases in confirmed or suspected clinical chorioamnionitis.

The placenta should have a swab taken for microscopy and culture and the

placenta should be sent for histopathological examination.Figure 12.2. Onset of atypical variable decelerations on the background of fetal

tachycardia secondary to clinical or subclinical chorioamnionitis. Such a combination of

hypoxia and infection can potentiate fetal neurological injury.

Key Tips to Optimize Outcome

Consider infection as a cause for fetal tachycardia especially in the absence of

decelerations and look for other signs to confirm this.

Consider infection as a cause of loss of cycling in the CTG suggestive of

depression of the central nervous system.

Consider delivery by caesarean section especially if vaginal delivery is not

imminent (i.e. if cervix <6 cm in a primigravida, or if there is evidence of failure

to progress).

Remember to look at the whole clinical picture when managing a labour with

suspected infection.

Remember that infection will cause morbidity and mortality in mother and fetus.

The correlation between severity of maternal disease and neonatal outcome is

not clear.

Avoid coexisting intrapartum hypoxia as it will have a synergistic effect with

infection.

Consider other causes of maternal pyrexia such as use of epidural medications

and drugs. However, be aware that pyrexia of any cause is associated with an

increased incidence of neonatal seizures.Pitfalls

Consequences of Mismanagement

Exercises

Meconium may be associated with ongoing clinical and subclinical

chorioamnionitis as it may indicate ongoing fetal stress secondary to infection.

Conversely, meconium may reduce the antibacterial activity of the amniotic fluid

and may predispose to chorioamnionitis. Therefore, presence of meconium with

ongoing fetal tachycardia is an ominous sign and delivery should be expedited.

A failure to consider infection as a cause of abnormal CTG which does not fit

into a hypoxic pattern (i.e. absence of repetitive decelerations).

A failure to appreciate that even mild hypoxia in the context of clinical

chorioamnionitis will have worse prognosis.

Failure to incorporate the whole clinical picture, e.g., primparous, early labour,

thick meconium, pyrexia and fetal tachycardia may lead to poor outcomes and

these cases are likely to benefit from an early delivery by a caesarean section.

Performing additional tests of fetal well-being such as fetal scalp blood

sampling (FBS), fetal scalp lactate or fetal ECG (ST-Analyser). None of these

tests designed to diagnose intrapartum hypoxia are reliable in fetal infection.

Intrapartum fetal death

Early neonatal death

Severe neonatal sepsis

Long-term sequelae such as learning difficulties and cerebral palsy1. A primigravida was admitted for induction of labour at 41 weeks + 3 days of

gestation. She had no antenatal risk factors. CTG trace was commenced (Figure 12.3).

Figure 12.3

a. How would you classify the CTG trace?

b. What is your management plan?

A plan was made for expectant management and the maternal pulse rate was noted to

be 108 bpm.

c. What is the likely diagnosis?

d. What is your management plan?

What are the signs and symptoms you would be anticipating in this case?

A plan was made to continue with labour. Three hours later, maternal temperature

was recorded as 38.2°C. Paracetamol and intravenous antibiotics were administered.

Six hours later, cervix was found to be 4 cm dilated and artificial rupture of membranes

was carried out and meconium staining of amniotic fluid was noted.

g. What is your diagnosis?

h. What is your management plan and why?

ObGyncases (Healthcare Touch)

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