Non-steroidal anti-inflammatory drug (NSAID) treatment is known to cause premature closure of the fetal ductus arteriosus. The frequency of closure is dependent on gestational age, dose and length of treatment1, 2. Characteristic echocardiographic findings during closure of the ductus arteriosus include dilatation of the right ventricle with decreased fractional shortening during systole, and tricuspid regurgitation (TR). Blood flow velocity in the ductus is also increased, with a pulsatility index of less than 1.902. A case of normalization of fetal echocardiographic parameters following cessation of maternal use of NSAIDs is reported.
A pregnant woman at 31 weeks' gestation was admitted for inpatient care due to left-sided flank pain. She had no fever. Examination of her urine showed signs of blood on dipstick testing. The clinical diagnosis on admission was kidney stones, and she was started on hydromorphone–atropine sulfate (Dilaudid®) with good effect. Ultrasound examination the following day revealed a calcareous stone in the left renal pelvis with an average diameter of 4 cm. Moderate hydronephrosis was seen on the right side. After 3 days in the ward her symptoms became worse and NSAID administration was discussed. We opted to try the woman on sulindac tablets (Clinoril®) 200 mg twice daily because the risk of closure of the fetal ductus arteriosus has been reported to be lower than that for diclofenac (Voltaren®)3. During the following 7 days on treatment, there were no signs of constriction of the ductus arteriosus, but because of worsening of the patient's condition two rectal doses of 100 mg diclofenac were administered. The following day a fetal ultrasound examination revealed signs of severe constriction of the ductus arteriosus with very high velocities in the ductus (Figure 1) and a dilated right ventricle with decreased fractional shortening (15%) and TR (Figure 2). The NSAID treatment was stopped, but hydromorphone–atropine sulfate treatment was maintained. At the first follow-up ultrasound examination 3 days after discontinuing NSAID treatment, blood flow in the ductus had become normal. TR persisted and there was still decreased fractional shortening of the right ventricle during systole (21%). TR was still present 6 days from discontinuing treatment, but the fractional shortening had become normal (28%). After 10 days without treatment the TR had disappeared.
Three days later, at 34 weeks' gestation, a Cesarean section was performed and a girl weighing 2115 g, with normal Apgar scores and normal umbilical cord pH, was delivered. The baby was admitted for neonatal intensive care without complications. The mother was discharged 8 days later in good condition. The calcareous kidney stone in the left renal pelvis was later successfully treated non-invasively by ultrasound. At a follow-up visit 2 months later the patient was feeling well and was without symptoms.
The present case illustrates clearly the typical ultrasound findings during drug-induced constriction of the fetal ductus arteriosus. The follow-up examination also demonstrates a delay in recovery of right cardiac ventricle function, with normal function resuming after 10 days without NSAID treatment. The present case also emphasizes the need to restrict the use of NSAIDs during the second half of pregnancy. Whether this will affect long-term myocardial performance is unknown.