Discussion
Fetal heart rate monitoring remains an important part of antenatal care,
and as seen in our case, the tachycardia was first detected by routine
fetal heart rate check.5 Fetal AF accounts for roughly
25-30 of all fetal tachyarrhythmias and is associated with variable AV
conduction. There are congenital structural anomalies that may occur
with AF including hypoplastic left heart syndrome, atrioventricular
septal defect, pulmonary atresia and Ebstein’s anomaly. Both SVT and
fetal AF have similar incidence of hydrops fetalis averaging 40% and
similar mortality rate of 10%. Studies have shown that hydropic
foetuses with fetal AF have higher ventricular rates than the
non-hydropic ones, but no difference in the atrial
rates.6
Most cases of fetal AF occur in the third trimester as seen in our case,
with the median age presentation of 32 weeks. The ventricles are
protected during fetal AF by the AV node which is not part of the
intra-atrial re-entrant circuit. This is achieved by variably blocking
the AV conduction, with 2:1 AV block present in over 80% of patients
with fetal AF.4,7 This finding is in keeping with our
patient who had 2:1 block. Fetal AF could easily be diagnosed by
clinicians using the M-mode ultrasound with the apical four-chamber
heart view. Both the atria and ventricles should be clearly identified
in relation to the spine and descending aorta as landmarks. The focus
should not be to get the ventricular rate only in fetal tachyarrhythmia
using the power Doppler button. With the M-mode across both either
atrium or ventricle, their respective rates could be measured and the
variable conduction pattern also. It is very important to make the right
diagnosis before proceeding to treatment especially in low resource
setting or general hospitals without paediatric cardiologist services.
In our case, the initial diagnosis was thought to be fetal SVT before
the patient was referred. This is because no simultaneous atrial reading
was taken. This is one of the major reasons of writing this report for
educational purposes. Secondly, it is known that up to 20% of fetal
tachyarrhythmia is associated with cardiac anomaly, hence the need to
perform fetal echocardiography before deciding on management
option.3,8 This informs the need of multidisciplinary
team management with neonatologists, paediatric cardiologist, and
obstetricians. At term pregnancies, the babies should not just be
delivered based on fetal distress without these considerations as the
outcomes may be untoward. This is well exemplified in this case.
Based on the points highlighted above, the antenatal management of fetal
AF depends on several factors including fetal gestational age, presence
of fetal hydrops or features of heart failure, and associated structural
heart disease. The risk of hydrops in fetal AF is said to be more with a
ventricular rate of over 210 bpm. There was no hydrops in our case even
though the ventricular heart rate was 260 bpm.6 The
development of associated cardiac anomaly is associated with poorer
neonatal outcome, hence the advantage of early detection and treatment.
Although prenatal treatment of fetal AF with transplacental
antiarrhythmic medications is the most common documented method of
treatment, this is not always the case.9 At term or
late preterm gestation, delivery of the foetus with postnatal treatment
is often considered as a better choice.3,10 This
obviates the adverse effects of the medication on the mother and the
risk of transplacental treatment on the foetus. This explains the basis
of our postnatal treatment modality.
The commonly used antiarrhythmic drugs include digoxin as first choice
and sotalol, flecainide, amiodarone, verapamil, procainamide as second
choice.2,11 Studies show that there is a significantly
better response to sinus rhythm prenatally when digoxin is used in
non-hydropic foetuses (80%), compared with 43% in hydropic
foetuses.8,12
It is important to remember that spontaneous conversion to sinus rhythm
does happen in fetal AF postnatally, although this was not observed in
our case.13 The ECG done postnatally confirmed the
neonate was still in AF (Figure 1), hence the use of synchronised
cardioversion which successfully resulted in sinus rhythm (Figure 2).
Digoxin was continued as an antiarrhythmic prophylaxis. After sinus
rhythm is achieved postnatally, one may monitor to see if there is
recurrence with AF before instituting prophylaxis, or electively treat
for 6 months to 1 year.10 However, the risk of AF
recurrence is very rare beyond the neonatal period. In our case, digoxin
was given for the first 28 days and to be continued for the first 6
months at least with follow up.