27 Nonhypoxic Causes of CTG Changes. Handbook CTG

 27

Nonhypoxic Causes of CTG Changes

◈

Dovilé Kalvinskaité and Edwin Chandraharan

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

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

The fetal heart rate (FHR) is controlled through various integrated physiological

mechanisms, most importantly through an interaction of sympathetic and parasympathetic

nervous systems. Optimum functioning of the fetal heart requires an intact central

nervous system and a well-developed fetal heart to respond adequately. Thus, abnormal

CTG changes may be caused by congenital malformations or organic changes in the fetal

brain or heart, together with infection and other metabolic changes that might affect these

organs (Figures 27.1 and 27.2).Figure 27.1 Causes of nonhypoxic brain injuries.

Figure 27.2 Causes of nonhypoxic myocardial damage.

Key Facts

Various congenital, organic or metabolic changes in the fetus may cause an

abnormal FHR pattern, in the absence of hypoxia.

Up to 75 per cent of fetuses with nonhypoxic CNS damage represent changes in

CTG, even though there is no single unique feature on the CTG trace associatedKey Features on the CTG Trace

with such an abnormality.

‘Nonreassuring’ FHR patterns are more common in preterm fetuses because their

brain is less well developed. Such CTG abnormalities may occur in up to 60 per

cent of these cases.

Maternal administration with various medications may affect the fetus and

modulate the CTG changes.

Erroneous monitoring of MHR as FHR may also result in CTG changes (see

Chapter 6).

Fetuses with normal neurological state have quiet sleep and active periods

termed ‘cycling’. Absence of cycling may be due to major fetal brain

malformation or haemorrhage, fetal infection or medication.

Reduced or absent baseline variability is the most common feature seen in the

CTG when the CNS function is impaired due to congenital malformation or fetal

infection. It can also be caused by medications and occurs shortly after

administering them.

A persistently ‘flat’ baseline variability with normal baseline FHR and without

accelerations or decelerations may reflect a severe pre-existing neurological

damage (Figure 27.3). The fetus, therefore, is unlikely to be hypoxic if a

decreased variability develops in the absence of preceding decelerations. The

lack of baseline variability may also correlate with the severity of fetal brain

damage.

An increase in baseline FHR can be due to maternal infection, chorioamnionitis

or fetal infection. Other major causes of fetal tachycardia are cardiac

arrhythmias and maternal administration of sympathetic (e.g. terbutaline) or

parasympathetic (e.g. atropine) medications and maternal hyperthyroidism.The most common fetal tachyarrhythmia is supraventricular tachycardia (SVT),

which is characterized by a persistent tachycardia at FHR of 210 to 320 bpm

with reduced baseline variability. SVT usually appears around 28 to 30 weeks

of gestation, and if it is persistent at a rate of >230 bpm, it can lead to the

development of hydrops fetalis.

Baseline FHR bradycardia can be caused by maternal administration of drugs

(labetolol, atenolol), prolonged maternal hypoglycaemia or hypothermia,

connective tissue diseases, fetal cardiac conduction or anatomic defects. As long

as normal baseline variability is present, fetal bradycardia may be considered

benign in such cases. Intermittent fetal bradycardia frequently is due to

congenital heart block. Even in cases of complete heart block, the FHR does not

go below 55–60 bpm (ventricular rate); if it does, a coexisting fetal hypoxia

should be excluded. The baseline variability will be lost within deceleration in

cases of hypoxia due to a reduction in cerebral circulation.

Pseudo-sinusoidal fetal heart pattern may be observed following the

administration of meperidine, morphine, and it should resolve within 30 minutes.

A true sinusoidal trace may occur with fetal intracranial haemorrhage,

chorioamnionitis or severe maternal diabetes.

Unsteady baseline rate or ‘wandering’ baseline can be due to a severe brain or

cardiac malformation and may appear as a preterminal event.Figure 27.3 CTG trace of a fetus with a massive intracranial haemorrhage in the antenatal

period. Note the total absence of baseline variability and absence of preexisting

decelerations.

Key Pathophysiology behind Patterns Seen on

the CTG Trace

Decreased or absent variability occurs when the autonomic nervous system,

which is responsible for the modularity function of the CNS, is impaired. Hence,

severe malformations or organic changes (e.g. large cerebral haemorrhage) in

the midbrain or cortex (Figure 27.1) – or when central neural pathways are

disorganized because of chromosomal or other genetic abnormalities – abnormal

features may be observed on the CTG trace.

Increase in sympathetic or decrease in parasympathetic nervous system tone

causes fetal tachycardia. It can be due to a direct fetal infection or as a

secondary fetal response due to transplacental passage of pyrogens in the

presence of maternal infection, as well as due to fetal cardiac electrical

abnormalities, medications or maternal anxiety (release of adrenaline).

Fetus exposure to an infection may cause a fetal inflammatory response

syndrome which leads to the development of cytokine-mediated white matter

injury in the fetal brain and, therefore, changes in the CTG (Figure 27.4).

Fetal heart conduction defects usually are associated with maternal connective

tissue diseases, because maternal SS-A/Ro and SS-B/La antibodies cause

inflammatory myocarditis and disrupts fetal cardiac conduction system.

If there is a derangement or a virtual absence of CNS control over the FHR, a

sinusoidal pattern is observed.

Intrauterine convulsions may result in repeated accelerations with the absence of

cycling (Figure 27.5). Repeated ‘low-amplitude’ accelerations secondary to

disorganized fetal movements during convulsions with absence of cycling should

alert clinicians to ongoing intrauterine convulsions (Figure 27.5). In this case,Figure 27.4 Total loss of baseline variability due to a severe fetal CNS infection.

Figure 27.5 CTG trace in intrauterine fetal convulsions. Note the absence of cycling and

repeated ‘low-amplitude’ accelerations secondary to disorganized fetal movements during

convulsions.

Recommended Management

the umbilical cord gases would be entirely normal, but the neonate may continue

to have neonatal convulsions. An MRI scan may not show any evidence of

hypoxic injury.Key tips to Optimize the Outcome

Hypoxic causes and maternal or fetal infection that may have resulted in

nonreassuring CTG changes must be excluded.

If the fetus is unlikely to be hypoxic and there are no other causes to explain

nonreassuring features observed on the CTG trace, a further detailed

investigation should be performed (e.g. ultrasound to confirm congenital

malformations, fetal echocardiography).

SVT and fetal heart block require an active management and may be associated

with fetal compromise and/or maternal disease. Most other cardiac arrhythmias,

although, are considered as benign and do not require immediate delivery or

other than management targeted at a specific condition (e.g. sympatholytic drugs

to correct supraventricular tachycardia).

In cases of complete fetal heart block, a search for autoimmune antibodies in

mother’s blood should be performed even if she is asymptomatic.

FHR changes which develop after administration of drugs can be managed

expectantly.

The whole clinical picture and previous CTG traces have to be considered to

exclude ongoing nonhypoxic causes of fetal injury.

One has to make sure that the CTG trace is normal with no evidence of hypoxia

before giving any medications.

If a nonhypoxic cause (e.g. intrauterine infection, intrauterine convulsions or

cardiac rhythm abnormality) is suspected, the neonatal team should be informed

in advance to optimize outcome after birth.

Women should be counselled regarding the prognosis of the suspected/diagnosed

nonhypoxic cause of fetal injury as well as the role and limitations of electronic

FHR monitoring.Pitfalls

Figure 27.6 CTG trace in a fetus with severe cardiac conduction defects.

Consequences of Mismanagement

Failure to recognize the absence of cycling on the CTG trace. In the absence of

ongoing hypoxia, decelerations may be absent.

The changes observed on the CTG trace may be misdiagnosed as due to hypoxia

leading to unnecessary interventions such as fetal scalp blood sampling or

unnecessary emergency caesarean section.

In the presence of abnormal CTG trace with a confirmed fetal anomaly (Figure

27.4), a true ongoing fetal hypoxia and acidaemia may not be recognized, which

may worsen neurological damage to the fetus.

The use of fetal ECG (STAN) in the presence of cardiac conduction defects

(Figure 27.6) as these may influence the waveforms observed on the fetal ECG

leading to unnecessary operative interventions.

Antepartum fetal death.

Fetal neurological impairment or higher neonatal morbidity rate due to a failure

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