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| CASE REPORT |
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| Year : 2015 | Volume
: 12
| Issue : 2 | Page : 151-153 |
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Supraventricular tachycardia in a neonate with Wolff-Parkinson-White syndrome
Wilson E Sadoh, Ikechukwu R Okonkwo
Department of Child Health, University of Benin Teaching Hospital, Benin City, Nigeria
| Date of Web Publication | 30-Jul-2015 |
Correspondence Address:
Wilson E Sadoh
Department of Child Health, University of Benin Teaching Hospital, PMB 1111, Benin City
Nigeria
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/0189-7969.152036
Wolf-Parkinson-White syndrome (WPW) is an uncommon condition associated with rhythm disorder. Supraventricular tachycardia (SVT) is often the rhythm abnormality sufferers present with. The cardiovascular status with the SVT could be stable or unstable, dictating how aggressive the management of the arrhythmia should be. In this case, the presentation and management of a neonate with SVT, whose arrhythmia was first detected in utero and later confirmed postpartum is presented. Keywords: Adenosine, amiodarone, supraventricular tachycardia, Wolff-Parkinson-White syndrome
How to cite this article:
Sadoh WE, Okonkwo IR. Supraventricular tachycardia in a neonate with Wolff-Parkinson-White syndrome. Nig J Cardiol 2015;12:151-3 |
| Introduction | |  |
Wolf-Parkinson-White syndrome (WPW) is a pre-excitation condition characterized by the presence of accessary pathway (the bundle of kent) connecting the atria and ventricles and episodes of tachyarrhythmias. [1] The incidence is 0.9-3% of the general population. [2] WPW syndrome may be asymptomatic or could present with symptoms such as palpitations and exertional dyspnea. Supraventricular tachycardia (SVT) is a common mode of presentation which could cause heart failure. [1] This is particularly important in fetus where they could become hydropic from heart failure and suffer stillbirth. In the newborns and young infants who cannot communicate their complaints, attention may become drawn to the condition when heart failure ensues. Confirmation of WPW syndrome is done on electrocardiographic (ECG) evaluation. A short P-R interval, slurring of the initial QRS deflection called the delta wave and a widened QRS are typical findings. [1]
In a previous Nigerian report on WPW syndrome, a 24-year-old Nigerian woman with tuberous sclerosis and WPW syndrome was reported by Ijaola et al. [3] In the present case report, we present a neonate with SVT detected in utero on ultrasound scan and later confirmed on ECG post-natally to have WPW. The presentation and treatment of this case are highlighted.
| Case report | | |
Baby A is a 2.85-kg male baby delivered at 38 weeks of gestation to a booked 31-year-old Para 1 + 1 lady by emergency cesarean section. The indication for the delivery was persistent fetal tachycardia demonstrated during ultrasound scan (USS) and cardiotocograph (CTG) monitoring. The fetal heart rate was between 210 and 218 beat per minute (bpm). The pregnancy was supervised from the 12 th week of gestation in a tertiary center. Fetal tachycardia was noticed during an USS done at 35 th and 39 th weeks of gestation. The mother was referred to our center (which is better equipped) for delivery.
At delivery, he was vigorous at birth with an Apgar score of 9 in the first minute of life. The child remained pink in room air, had normal anthropometric indices (length of 46 cm and head circumference of 35 cm) and no obvious dysmorphic features. All the orifices were patent and in their normal anatomic positions.
The heart rate was 196 bpm and regular. The blood pressure (BP) was 70/32 mmHg while normal first and second heart sounds were heard. The examination of the other systems was unremarkable. A diagnosis of sinus tachycardia/SVT with stable rhythm was made and the baby was admitted into the neonatal unit and vital signs monitored on continuous multiple parameter monitor. The ECG showed supraventricular tachycardia with a heart rate of 220 bpm, regular. The P-R interval was 0.95 msec, the QRS initial upstroke was slurred (delta wave) in most leads, the delta wave was upright in the precordial leads with R/S ratio being approximately 1. Both R and S waves were prominent. The QRS duration was 0.75 msec. [Figure 1] The echocardiogram showed right atrial enlargement, a secundum type 7 mm atrial septal defect, the ventricles were normal but beating fast, the ventricular septum was intact and there was no patent ductus arteriosus. The diagnosis of SVT with type B WPW syndrome in a child with large ASD was made. | Figure 1: Electrocardiogram showing pre-excitation-short PR interval, slurred initial upstroke of the R wave, and widened QRS interval
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Ice packs were applied on the nose bridge for 15 minutes to induce the "dive reflex." This intervention failed to reduce the heart rate. Incremental adenosine therapy was then commenced, with the initial dose of 50 μg/kg which was ineffective. On the second dose (100 μg/kg) of adenosine, the rhythm was converted to atrial flutter [Figure 2] with reduction in ventricular rate to 112 bpm, the BP was 71/30 mmHg, the respiratory rate was 44 cycle per minute (cpm), the abdomen was unremarkable. The heart rate was noticed to have reverted to SVT some 24 hours later with an ECG showing SVT with heart rate of 220 bpm, the vital signs remained stable. He failed to respond to another course of adenosine and was then placed on intravenous amiodarone therapy with an intial dose of 5 mg/kg given in normal saline for over 30 minutes and subsequently maintained on 5 ug/kg/hour. The heart rate reduced to 150 bpm, regular with stable vitals. He was followed up for 9 months during which he was still on maintenance amiodarone. Currently, his ECG shows sinus rhythm, the heart rate range from 136 -150 bpm and there is no evidence cardiovascular instability. | Figure 2: Electrocardiographic (ECG) evaluation depicting the conversion to atrial flutter with lower ventricular rate
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| Discussion | | |
WPW syndrome is an uncommon condition associated with episodes of tachyarrhythmia. The tachyarrhythmia is often SVT with reentry tachycardia and it can be paroxysmal or incessant. Most cases are paroxysmal lasting for short periods of time and usually would not lead to heart failure and hydrops. [4],[5] In the present report, the SVT was incessant, but was not associated with unstable rhythm perhaps because the heart rate was less than 220/minute. Cardiovascular instability is unlikely when the heart rate is <220/minute in neonates. [6] The resulting cardiovascular collapse in cases with unstable rhythm draws attention to the presence of the condition. That the SVT was incessant was determined on continuous ECG monitor, on which this child was managed.
The earliest sign of the condition is fetal tachycardia, found during fetal echocardiography/USS, where heart rate ≥220 bpm and 1:1 atrio-ventricular conduction is suggestive of SVT. [7] In the present report, SVT was suspected because of the rapid heart rate detected on USS at 32 nd week although fetal echocardiography was not done. There however was no hydrops detected on USS. It is noteworthy that fetal echocardiography should have been done at this stage (which facility is available in the referred hospital) to confirm SVT and to have more frequent evaluations to detect the presence of hydrops early should heart failure from unstable rhythm occur. The presence of hydrops has been associated with mortality in cases with SVT. [8]
In an effort to closely monitor the high risk pregnancy during labor, cardiotocography was done which also showed fetal tachycardia. The diagnosis of WPW syndrome was made in this patient postpartum because of the evidence of pre-excitation on ECG. At birth, the infant was promptly evaluated for the tachyarrhythmia which was subsequently managed.
In stable cardiovascular state, there is time to initiate non-pharmacologic and short-term pharmacologic cardioversion as was done in this case. Non-pharmacologic measures such as vagal maneuvers are the first line of treatment. The application of ice pack on the forehead or immersion of the patient's face into iced water for young children and valsava maneuver in children old enough to comply may induce cardioversion. Digital ocular pressure which may also induce cardioversion should be avoided in infants. [1] Failure to stop the SVT with these non-pharmacologic measures as was the case in the present report is an indication to commence intravenous adenosine. Adenosine is an endogenous nucleotide that slows conduction through the atrio-ventrcular node (AV), atrium, and the sinus node. [9] The AV block breaks the re-entry tachycardia and revert to sinus rhythm. Treatment with adenosine may be ineffective necessitating the use of other antiarrhythmic medications such as amiodarone and propranolol or use of electrical cardioversion. In this report, adenosine failed to convert to sinus rhythm, converting instead to atrial flutter. Failure of adenosine to convert the arrhythmia has been similarly described. [10] It is said to be commonly seen in long standing cases of SVT which allows for increase in sympathetic tone and has been reported in a variant of SVT with a permanent junctional reciprocating tachycardia. [10] It is possible that the longstanding nature of the SVT in this case having been noticed at the 32 nd week of gestation may have contributed to the poor response to adenosine. The patient in the present case is currently on medications for the SVT. Some worker have reported that patients with SVT and stable rhythm may remain on medications in the first months of life but however tend not to require the medications beyond the first year of life. [11]
The treatment of SVT with unstable cardiovascular status is more aggressive inconverting to sinus rhythm. Synchronized direct cardioversion often convert the SVT to sinus rhythm and prevent death from shock. The pharmacologic and electrical treatment modalities are mostly unavailable in resource limited settings leading to needless death of affected children. It is possible that in resource constrained settings, the diagnosis may not even be made either because the diagnosis is missed completely or there is no ECG machine to facilitate the daignosis. The WPW syndrome may be associated with cardiovascular abnormality notably Ebstein's anomaly and L-transposition of the great arteries. [9] In this case, it was associated with atrial septal defect.
The diagnosis and type of WPW syndrome can be made on electrocardiographic tracing. Type A WPW syndrome can be identified by the dominant R wave and inverted T wave in in VI. The R/S ratio is greater than 1. While in type B, S wave is prominent in VI and VII. At this age, R wave is usually dominant in VI because of the right ventricular dominance. The prominent S wave in the right chest leads may support a type B WPW syndrome in this patient.
In conclusion, a case of a neonate with WPW syndrome and stable SVT diagnosed in utero who failed to respond to non-pharmacologic measures and adenosine therapy but however responded to intravenous amiodarone which he is currently being maintained on after 9 months on follow-up.
| References | | |
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| 3. | Ijaola O, Festus-Abibo LC, Lawani O, Kuku SF. Cardiac involvement (Wolff-Parkinson-White syndrome) in tuberous sclerosis. Postgrad Med J 1994;70:124-7. |
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| 7. | Campbell RM, Dick M, Rosenthal A. Cardiac arrhythmias in children. Ann Rev Med 1984;35:397-405. |
| 8. | Boldt T, Enomen M, Anderson S. Long term outcome in fetuses with cardiac arrhythmias. Obstet Gynaecol 2003;112:1372-9. |
| 9. | Perry JC. Supraventricular tachycardia. In: Garson A Jr, Bricker J, Fisher D, Neish SR, editors. The science and practice of pediatric cardiology.2 nd ed. Baltimore: Williams and Willkins; 1998. p. 2059-101. |
| 10. | Waisman Y, Berman S, Fogelman R, Zeevi B, Mimouni M. Failure of adenosine to convert a subtype of supraventricular tachycardia. Israel J Emerg Med 2003;3:4-7. |
| 11. | 11 Hahurij ND, Blom NA, Lopriore E, Aziz MI, Hagel HT, Rozendaal L, el al. Perinatal management and long-term cardiac outcome in fetal arrhythmias. Early Hum Dev 2010;87:83-7. |
[Figure 1], [Figure 2]
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