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Low-dose prostaglandin E1 is safe and effective for critical congenital heart disease: is it time to revisit the dosing guidelines?

Authors
  • Vari, Daniel1
  • Xiao, Wendi2
  • Behere, Shashank3
  • Spurrier, Ellen3
  • Tsuda, Takeshi3
  • Baffa, Jeanne M3
  • 1 Department of Pediatrics, Nemours/Alfred I. duPont Hospital for Children, Wilmington, DE, USA.
  • 2 Department of Biostatistics, Nemours/Alfred I. duPont Hospital for Children, Wilmington, DE, USA.
  • 3 Nemours Cardiac Center, Nemours/Alfred I. duPont Hospital for Children, Wilmington, DE, USA.
Type
Published Article
Journal
Cardiology in the Young
Publisher
Cambridge University Press
Publication Date
Jan 01, 2021
Volume
31
Issue
1
Pages
63–70
Identifiers
DOI: 10.1017/S1047951120003297
PMID: 33140712
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

Prostaglandin E1 is used to maintain ductal patency in critical congenital heart disease (CHD). The standard starting dose of prostaglandin E1 is 0.05 µg/kg/minute. Lower doses are frequently used, but the efficacy and safety of a low-dose regimen of prostaglandin E1 has not been established. We investigated neonates with critical CHD who were started on prostaglandin E1 at 0.01 µg/kg/minute. We reviewed 154 consecutive patients who were separated into three anatomical groups: obstruction to systemic circulation, obstruction to pulmonary circulation, and inadequate mixing (d-transposition of the great arteries). Treatment failure rates and two commonly reported side effects, respiratory depression and seizure, were studied. A total of 26 patients (17%) required a dose increase in prostaglandin E1. Patients with pulmonary obstruction were more likely to require higher doses than patients with systemic obstruction (15/49, 31% versus 9/88, 10%, p = 0.003). Twenty-eight per cent of patients developed respiratory depression and 8% of patients needed mechanical ventilation. Prematurity (<37 week gestation) was the primary risk factor for respiratory depression. No patient required dose escalation or tracheal intubation while on transport. No patient had a seizure attributed to prostaglandin E1. Prostaglandin E1 at an initial and maintenance dose of 0.01 µg/kg/minute was sufficient to maintain ductal patency in 83% of our cohort. The incidence of respiratory depression requiring mechanical ventilation was low and was mostly seen in premature infants. Starting low-dose prostaglandin E1 at 0.01 µg/kg/minute is a safe and effective therapy for critical CHD.

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