Here we present a case of non-immune hydrops with in utero CCF.

A 32 year old female with 8 months of ammenorrhoea, third gravida and two live issues visited our hospital for antenetal checkup. One month before the visit she had a History of mildgrade fever for which she took some treatment, fever subsided within 2 to 4 days. Her blood group was A Rh Positive. First antenatal sonological evaluation revealed a single live fetus with heart rate of 253/min. regular with right atrial enlargement. There was pleural, pericardial effusion, slight polyhydromnios and bilateral hydrocoele.

Repeat USG done a week apart showed similar findings twice.

Mother had no history of toxemia, thyrotoxicosis. Intravenous digoxin to mother was advised but could not be given due to some petty reasons.

Patient was delivered at Gestational age approx. 36 wks.

At birth baby cried well immediately after birth heart rate was 234 / min. Respiratory rate 52/min. no significant sign of respiratory distress, subcutaneous oedema was present along with hydrocoele. Gestational age was approx. 36wks. Auscultation revealed decreased air entry bilaterally with gallop rhythm and no murmurs. There was no dysmorphism or obvious congenital anomaly.

Patients blood group was A positive and Haemoglobin was 13.6 gm per dl. X – Ray Chest at birth showed bilateral pleural effusion with subcutaneous oedema. While ECG was suggestive of Supraventricular tachycardia (SVT) with no WPW syndrome. USG abdomen showed ascites and normal kidneys, patient was put on Intravenous lasix and digoxin.

Within 72 hours patient improved with heart rate reducing to 120 /min. absent gallop, improved activity, improved air entry bilaterally and third day X-ray chest showed complete clearance of pleural effusion and decrease subcutaneous oedema. ECG was within normal limits. Echo study revealed marked reduction in size of right atrium and no other structural anomaly.

Baby was discharged on long term digoxin therapy after one week. After 1½ month follow up there was normal cardio respiratory status, normal growth and normal ECG and Echo.

This is a thus a case of decompensated in utero SVT. Such cases are considered as high risk with mortality approx. 30%, and so aggressive transplacental therapy is advisable. But in this case transplacental therapy could not be given and though in decompensated phase fetus survived and later responded well to digoxin after birth.

The other interesting finding was relative enlargement of right atrium without any associated cardiac anomaly, which started regressing after 1-2 days of birth and at 2 month shows absolutely normal structured heart.

Drugs used for transplacental therapy are Digoxin, Flecainide (more effective in hydropic cases)⁽⁵⁾, Adenosin (direct foetal administration)⁽⁶⁾. Delivery should be done by ceaserean section and prematurely if required.

All neonates with SVT should be subjected to vagal manoeuver like application of ice cold cloth overface. Unstable patients (with CCF, shock) should be subjected to DC conversion while stable patients can be given IV Adenosin (preferred) or Digoxin (contraindicated in WP syndrome), Propranolol, amidarone or edrophonium. Verapamil should be avoided in infancy.

Chronic management consist of long term drugs therapy or RFA depending on age of patient and type and characteristic of SVT.

For neonatal arrhythmias adenosine is a preferred drug, but its short half life and as it requires adequate monitoring, digoxin is still being used as first drug in many centres in absence of WPW syndrome.

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