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Indian Pediatr 2012;49: 611-612 |
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Patent Ductus Arteriosus: Looking for the
Right Approach of Management
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Deepak Chawla
Department of Pediatrics, Government Medical College
and Hospital, Sector 32, Chandigarh, India.
Email:
[email protected]
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I n majority of healthy preterm neonates, ductus
arteriosus closes spontaneously by 3-7 days after birth [1]. However,
three-fourth of very preterm neonates with respiratory distress may
continue to have a patent ductus arteriosus (PDA) at end of first week
of life. Persistent patency of ductus arteriosus increases blood flow
through pulmonary vascular bed and decreases blood flow through
cerebral, mesenteric and renal vascular beds. PDA has been associated
with decreased survival and increased incidence of pulmonary hemorrhage
and bronchopulmonary dysplasia. Ever since initial reports of effect of
indomethacin in inducing ductal closure were published in 1970s, impact
of prophylactic and therapeutic administration of prostaglandin
inhibitors on short- or long-term outcomes of preterm neonates has been
an active research issue [2]. During the last decade, acquisition of
basic echocardiographic skills by neonatologists has led to earlier
recognition and treatment of PDA before the associated clinical features
make their appearance. However, questions on selecting appropriate
biomarker of hemodynamic significance, optimal timing (prophylactic,
pre-symptomatic or symptomatic) of administration of prostaglandin
inhibitors, and even necessity of inducing PDA closure remain largely
unanswered.
In this issue of Indian Pediatrics, Popat,
et al. [3] present their data on closure rate of PDA with
indomethacin. PDA was treated on appearance of clinical symptoms and up
to three course of indomethacin were administered. Two-thirds of
neonates born at less than 29 weeks gestation had significant PDA.
Although, 90% responded to multiple courses of indomethacin, treatment
of PDA was not associated with improved neonatal morbidities. Neonates
who did not respond to multiple courses of indomethacin were more likely
to be females, born at earlier gestation, and tended to have higher
sickness severity scores and culture-proven sepsis.
Indomethacin is the drug of choice for inducing PDA
closure in preterm neonates. However, non-response or reopening of PDA
after single course of indomethacin administration is not uncommon. Lack
of exposure to antenatal steroids, small-for-gestation status,
significant respiratory distress, lower gestation age, liberal fluid
intake and a shorter duration of indomethacin treatment are associated
with a decreased probability of treatment response [4]. Once
indomethacin treatment fails to induce ductal closure, options include
ductal ligation, repeated courses of indomethacin or conservative
management waiting for spontaneous closure. Surgical ligation of PDA has
its own set of associated morbidities (vocal cord paralysis,
pneumothorax, chylothorax, scoliosis and infection) and may lead to
impaired lung growth and increased incidence of BPD [4]. Indomethacin
administration has not only been unsuccessful in improving survival or
decreasing incidence of BPD and pulmonary hemorrhage, its infusion
induces vasoconstriction in different vascular beds leading to decreased
end-organ perfusion. Repeated courses may have cumulative detrimental
effect. As a result, advocacy for investigating the third option of
conservative watch of PDA is now gaining more voice [5].
Prophylactic administration of indomethacin within 24
h of birth has been associated with decreased incidence of
intraventricular or pulmonary hemorrhage and risk of developing
symptomatic PDA [6]. Although no improvement in survival without
disability was reported at 18 months, gender-specific effect on
neurological outcome has been proposed [1]. The need and length of
subsequent courses of therapeutic indomethacin may also influence the
neurological outcome.
Preterm neonates constitute a heterogenous group in
which PDA may close spontaneously, respond to prostaglandin inhibitors
or remain open despite multiple attempts of medical closure. Search
continues for a select subgroup of neonates, who, identified through a
suitable biomarker, will benefit from prophylactic, early therapeutic or
repeated administrations of prostaglandin inhibitors.
Funding: Nil; Competing interests: None
stated.
References
1. Hamrick SE, Hansmann G. Patent ductus arteriosus
of the preterm infant. Pediatrics. 2010;125:1020-30.
2. Heymann MA, Rudolph AM, Silverman NH. Closure of
the ductus arteriosus in premature infants by inhibition of
prostaglandin synthesis. N Engl J Med. 1976;295:530-3.
3. Popat H, Kapoor V, Travadi J. Patent ductus
arteriosus in infants <29 weeks gestation outcomes and factors Affecting
closure. Indian Pediatr. 2012;49:615-20.
4. Clyman RI, Couto J, Murphy GM. Patent ductus
arteriosus: are current neonatal treatment options better or worse than
no treatment at all? Semin Perinatol. 2012;36:123-9.
5. Benitz WE. Patent ductus arteriosus: to treat or
not to treat? Arch Dis Child Fetal Neonatal Ed. 2012;97:F80-2.
6. Fowlie PW, Davis PG, McGuire W. Prophylactic
intravenous indomethacin for preventing mortality and morbidity in
preterm infants. Cochrane Database Syst Rev. 2010:CD000174.
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