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Indian Pediatr 2014;51: 227 -228 |
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Ventricular Tachycardia due to Perinatal
Asphyxia
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Nilay Nirupam, Sushma Nangia and Arvind Saili
From Department of Pediatrics, Division of
Neonatology, LHMC and Kalawati Saran Children’s Hospital, New Delhi,
India.
Correspondence to: Dr Nilay Nirupam, Senior Resident,
Department of Pediatrics, Lady Hardinge Medical College,
New Delhi 110001, India.
Email: [email protected]
Received: November 17, 2013;
Initial review: December 18, 2013;
Accepted: January 21, 2014.
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Background: Perinatal asphyxia is known to precipitate myocardial
dysfunction, rhythm abnormalities and congestive cardiac failure.
Case characteristics: A 2-day old neonate with perinatal asphyxia.
Observation: He developed shock secondary to ventricular
tachycardia, and required synchronized cardioversion for reversion of
abnormal rhythm. Outcome: Reversal of arrhythmia leading to
recovery. Message: Early identification and management of
ventricular tachycardia in neonate with perinatal asphyxia can be
life-saving.
Keywords: Arrythmia, Cardioversion, Neonate.
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Symptomatic neonatal arrhythmias are rare in
neonates; most are secondary to underlying congenital heart defects,
metabolic disturbances, septicemia and primary rhythm abnormalities. We
report ventricular tachycardia and cardiogenic shock secondary to
perinatal asphyxia in a neonate.
Case Report
A male neonate (birth weight 2.7 kg) was born to a
primigravida mother at term gestation, and required positive pressure
ventilation in delivery room for 15 minutes. The Apgar scores were 1, 3
and 5 at 1, 5 and 10 minutes of life, respectively. The cord pH was 6.64
with evidence of mixed acidemia. Subsequently baby received mechanical
ventilation. He developed multiple episodes of clonic seizures at 7
hours of life. Phenobarbitone (40 mg/kg) and phenytoin (20 mg/kg) were
administered for control of seizures.
At 26 hours of life, the baby developed tachycardia
(220/min) and irregular heart rate. The electrocardiograph showed broad
QRS complexes (duration 0.12) suggestive of monomorphic ventricular
tachycardia. His capillary refill time (CRT) was around 2 seconds with
good volume pulses and mean blood pressure of 39 mmHg with oxygen
saturation (SpO 2) of 92%.
The central venous pressure was 8 cm of water.
His hemoglobin was 19.2 g/dL, total leucocyte count
17,300/mm 3 and platelet
count was 1.0×109 L. The
arterial blood gas revealed a PaO2
of 59 mmHg and pH of 7.33: dextrose was 73 mg/dL, serum sodium 142 meq/L,
serum potassium 5.3 meq/L, ionized calcium 4.6 mg/dL, serum magnesium
2.3 mg/dL, blood urea 47 mg/dL, and serum creatinine of 1.2 mg/dL. The
serum bilirubin was 2.7 mg/dL with alanine transaminase of 213 U/L,
aspartate transaminase of 247 U/L and alkaline phosphatase of 312 U/L.
The CPK-MB was 479 U/L (Normal 20-80 U/L) and troponin–T by card test
was positive. Serum phenytoin levels were 3.2 mcg/mL (Normal 10-20 mcg/mL).
The chest roentgenogram was normal.
Child did not improve to a loading dose of lidocaine
(1 mg/kg) followed by infusion (25 g/kg/min), and signs of poor
peripheral perfusion with shock developed. Synchronized cardioversion
was given with 1 joule/kg and the heart rate reverted to 170 min. The
peripheral perfusion and capillary refill time improved with return of
normal sinus rhytm. Subsequently vasopressor support was tapered off. An
echocardiography on day 2 of life was suggestive of right ventricular
and left ventricular hypokinesia with mild tricuspid regurgitation. A
repeat electrocardigram obtained on day 4 did not reveal evidence of
Brugada syndrome or WPW syndrome. There was T wave inversion in leads V4
and V5, indicating ischemia.
Discussion
Perinatal asphyxia is a common problem, with the
incidence varying from 0.5-2% of live births [1]. The hypoxic-ischemic
insult leads to organ dysfunction affecting kidney, central nervous
system, heart and lungs. The incidence of clinical cardiac dysfunction
in perinatal asphyxia varies from 24-31% [2]. The cardiac manifestations
described include myocardial dysfunction with shock, valvular
dysfunction, rhythm abnormalities and congestive cardiac failure.
Symptomatic neonatal arrhythmias are rare [3], and
supraventricular tachycardia (SVT) is the commonest. Ventricular
arrhythmias are often secondary to metabolic disturbances and hence
potentially treatable. In a case series, nine neonates reporting to a
tertiary care centre in India were identified to have arrhythmias over a
3 year period [4]. Four had primary rhythm disorder and five had
secondary arrhythmias of ventricular origin, 3 attributable to metabolic
disturbances, 1 to septicemia and 1 to left atrial mass lesion. Another
case report highlighted the occurrence of hyperkalemia and ventricular
tachycardia in an extremely low-birth-weight neonate [5]. Neonates with
congenital adrenal hyperplasia/hypoglycemia with ventricular tachycardia
have been described in literature [6,7]. In one case report, neonatal
tachycardia associated with maternal bupivacane block was reverted with
cardioversion [8]. Studies evaluating ECG and echocardiographic changes
in perinatal asphyxia have reported the occurrence of ECG abnormalities
in around 40% of neonates [9,10].
We attribute the occurrence of monomorphic
ventricular tachycardia in present child to perinatal asphyxia. The
secondary causes like hypoglycemia, hypothermia, hyperkalemia, acidosis
and hypovolemia were ruled out with relevant tests. His PaO 2
was low. There was no evidence of structural heart disease and abnormal
conduction pathway. Phenytoin levels were within therapeutic range. The
elevated CPK-MB and troponin–T levels suggested presence of myocardial
ischemia. The severe hypoxic-ischemic injury to myocardium could have
precipitated a fatal arrhythmia in our neonate.
We report this case to highlight the need to screen
neonates with perinatal asphyxia for rhythm irregularities, especially
when they develop shock. Early identification and prompt management of
any precipitating cause can be life-saving.
Contributors: All the authors were involved in
management of the patient. NN: reviewed the literature and drafted the
manuscript. SN: and AS: critically reviewed the manuscript. All authors
approved the final version of the manuscript.
Funding: none; Competing interests: None
stated.
References
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