Patent Ductus Arteriosus in the Neonate

Publication: 22/11/2010  --
Last review: 27/11/2018  
Next review: 27/11/2021  
Clinical Guideline
CURRENT 
ID: 2324 
Approved By: Trust Clinical Guidelines Group 
Copyright© Leeds Teaching Hospitals NHS Trust 2018  

 

This Clinical Guideline is intended for use by healthcare professionals within Leeds unless otherwise stated.
For healthcare professionals in other trusts, please ensure that you consult relevant local and national guidance.

Management of Patent Ductus Arteriosus in the Neonate

There is a parent information leaflet available at;
http://www.leedsth.nhs.uk/patients-visitors/our-hospitals/leeds-childrens-hospital/a-z-of-children-hospital-leaflets/

Background

In utero the ductus arteriosus connects the aorta and pulmonary artery allowing the majority of the right ventricular output to bypass the lungs and combine with the left ventricular output to supply blood to the body and the placenta. The ductus usually closes in the first few days of life but in the preterm infant this may be delayed. Failure of ductal closure leads to shunting of blood from the aorta to the pulmonary circulation as pulmonary vascular resistance falls. This may lead to pulmonary overcirculation and hypoperfusion (particularly during diastole) of the organs supplied by the systemic circulation. In very large PDAs there may be reverse flow in the descending aorta or mesenteric vessels during diastole. Clinical sequelae of this include chronic lung disease, pulmonary haemorrhage, renal hypoperfusion, necrotising enterocolitis, IVH and death.

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Clinical features

PDAs almost exclusively occur in preterm babies. It is useful to consider three different categories of PDA:

1. The “Clinically apparent PDA”- this baby has any of the following

  • easily palpable full pulses,
  • an active precordium
  • a systolic or continuous murmur, radiating to back
  • a wide pulse pressure (low diastolic pressure)

but is otherwise effectively asymptomatic.

2. The “symptomatic PDA”- this baby may have a range of symptoms arising from the patent ductus and associated abnormal blood flow:

  • respiratory distress
  • progressive cardiomegaly on CXR
  • pulmonary haemorrhage
  • frequent ‘swinging’ desaturations
  • failure to wean from respiratory support

3. The “haemodynamically significant PDA”- this baby is showing complications from the PDA and has clinical or echo evidence of congestive cardiac failure and organ dysfunction, with abnormal diastolic blood flow. (see below)

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Diagnosis and Investigation

1. Clinical examination: features as above

2. Echocardiogram-

  • should ideally be used to confirm a clinical diagnosis.
  • echo should be performed before medical closure of the duct is attempted (i.e. the use of ibuprofen) to exclude pulmonary hypertension or a duct dependent congenital heart defect.

Echocardiogram can  be used to assess the size and haemodynamic effect of a duct. The following are abnormal in a baby >12-24 hours old and suggest a haemodynamically significance duct3,4.

  • PDA with narrowest diameter (usually at pulmonary end) >2mm
  • PDA diameter> size of Left Pulomnary Artery
  • Aortal : Left atrial diameter > 1: 1.5
  • Unrestricted left to right flow pattern across PDA
  • Dilated left atrium and left ventricle due to PDA
  • Reverse diastolic flow in descending aorta or mesenteric vessels
  • Otherwise unexplained NEC, IVH or renal impairment  in a baby with a large PDA

3.  CXR - may show cardiomegaly  and pulmonary oedema

4. Cardiology opinion may be sought if clinically indicated.

5. ECG is not useful

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Treatment

1. Who to treat?

Clinically apparent but asymptomatic PDA: The natural history of the PDA is to close with time, provided the baby is haemodynamically stable without frequent periods of hypoxia. Many clinically apparent but not significant ducts will close with time. So a PDA murmur is a totally well baby does not need treatment.

Symptomatic PDA: Treatment is initially conservative. (conservative management) If these measures do not work treatment is escalated to medical closure of the PDA with a course of ibuprofen.

Haemodynamically significant duct in a baby who is unable to wean from respiratory support should have medical closure attempted, ideally within the first 14 days of life. Depending on the age of the infant a second course or extended course of ibuprofen can be tried if the first fails. If the duct does not close with medical management and is still felt to be a significant clinical issue referral for surgical closure should be considered.

2. How to treat?

  1. Conservative management
    • Fluids restricted 120-150ml/kg/day or stop increasing fluids if on less than this.
    • If signs of heart failure obtain an echo to assess haemodynamic effects of PDA.
    • Do not use frusemide as this may increase prostaglandin E2 levels, keeping the duct open. If diuretics are required use chlorthiazide +/- spironolactone.
  2. Medical closure
    • If PDA clinically significant i.e. preventing weaning of ventilatory support or affecting growth,  initiate medical closure of duct.
    • Echocardiogram mandatory before treatment begins
    • Ibuprofen is the first line treatment. Paracetamol may be considered as an alternative (see below)
    • Use with caution with other nephrotoxic drugs (e.g. gentamicin, vancomycin)
    • DOSE: (IV or oral if on full feeds)

Ibuprofen
Administered intravenously
1st dose:          10mg/kg
2nd dose:         5mg/kg 24 hours after first dose
3rd dose:         5mg/kg 24 hours after second dose

    • Contraindications to ibuprofen
      • thrombocytopenia (platelets less than 80 x 109/L)
      • poor renal function (creatinine greater than 125micromol/L)
      • Oliguria (urine output less than 0.5- 1ml/kg/hr)
      • Bleeding or coagulopathy (except pulomonary haemorrhage)
      • Necrotising enterocolitis or previous intestinal perforation
      • Marked unconjugated hyperbilirubuinaemia
      • Severe sepsis
      • If urine output less than 0.6ml/kg/hr or creatinine > 125micromol/L use with extreme caution and monitor renal function carefully. Ideally delay further doses until renal function returns to normal.
      • There is some evidence that ibuprofen may increase the risk of CLD

3. When to treat? 5,6,7

  • Prophylactic treatment of all babies <28 days is no longer erecommended as the long term outcomes were no different.
  • A clinical trial (Baby OSCAR) is underway looking at the benefits of very early (72 hrs of life) targeted medical closure.
  • Ibuprofen is most effective in the first 14 days and less likely to be effective beyond 21 days of age.
  • In Leeds our approach is to move from conservative to medical treatment with ibuprofen at the point that a PDAs if felt to be both haemodynamically and clinically significant (see above)
  • DURATION: Usually for three doses over three days as above. If duct not closed can consdide extending course for a further 3 days as long as no contraindications and the duct has been re-evaluated by echo.
  • Second course of medical treatment.  If the first course of ibuprofen treatment fails a second course can be considered. Surgical ligation should also be considered if baby >21 days old.

4. Alternative treatment options

PARACETAMOL8

  • There is currently insufficient evidence to recommend replacing ibuprofen with paracetamol. Early trials suggest in a group of babies paracetamol was as effective as ibuprofen at closing the duct, but many were more mature babies in whome the duct may have closed spontaneously. However if ibuprofen is contraindicated or not tolerated , paracetamol may be considered  in individual cases. Dose = 15mg/kg/tds for 3 days.

SURGERY

  • There is no evidence that early surgical closure has long term benefits over conservative treatment or medical treatment. Surgery carries a significant risk of short and medium term complications, but is effective at closing the duct.
  • If medical treatment fails and the ductus is considered a significant problem (Significant ventilator/oxygen dependency) referral for surgical opinion should be considered. A cardiologist-performed echo will be required.

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Summary of Evidence2

Key Point

 Level of Evidence

Risk of PDA increases with lower gestation, lack of antenatal steroids and hyaline membrane disease.

 Level of Evidence 2A

Early diagnosis requires cardiac ultrasound

 Level of Evidence 2A

Larger ductal diameter is associated with lower systemic blood flow in the first 12 hours after birth.

 Level of Evidence 2B

Ibuprofen is the first line treatment.
Consider surgery only if medical treatment has failed or is contraindicated and there are persisting cardiopulmonary symptoms that are probably due to ductal shunting.

Level of Evidence 1A

Grade of Recommendation B

There is no evidence that prophylactic indomethacin (now withdrawn) improves long term neurodevelopmental outcomes.

 Level of Evidence 1A

Early prophylactic or targeted treatment of ducts may reduce the risk of early pulmonary haemorrhage.

 Level of Evidence 1B
Grade of Recommendation B

If the duct has significantly constricted 24 hrs after the first dose, consideration should be given to not giving further doses.

Level of Evidence 1B
Grade of Recommendation B

Oral ibuprofen appears to be as effective as intravenous ibuprofen in babies treated after 48 hrs of age.

 Level of Evidence 1B
Grade of Recommendation B

Provenance

Record: 2324
Objective:

Aims
To streamline the management of patent ductus arteriosus (PDA) in the neonatal population

Objectives
To understand

  • the physiology of PDA in the preterm infant
  • the clinical signs and symptoms of PDA
  • the indications and contraindications for treatment of PDA
  • the non medical management of PDA
  • the mechanism of action and choice of medical treatments
Clinical condition: Patent ductus in the newborn
Target patient group: Neonates
Target professional group(s): Secondary Care Doctors
Secondary Care Nurses
Adapted from:

Evidence base

1. UpToDate:  Joseph B Phillips. Management of PDA in preterm infants (Accessed 20.1.16) http://www.uptodate.com/contents/management-of-patent-ductus-arteriosus-in-
premature-infants?source=search_result&search=patent+ductis+arteriosus&selectedTitle=4%7E150

2. Evans, N et al. Royal Prince Alfred Hospital, Syndey Guideline on Patent Ductus Arteriosus. (accessed Jan 2016) (this contains excellent images of how to assess significance using Doppler flow patterns. http://www.slhd.nsw.gov.au/rpa/neonatal%5Ccontent/pdf/guidelines/pda.pdf

3.  Evans N. Diagnosis of patent ductus arteriosus in the preterm newborn. Arch Dis Child 1993;68:58-61.

4. Condo M. Evans N. Bellu R. Kluckow M. Echocardiographic assessment of ductal significance: retrospective comparison of two methods. Archives of Disease in Childhood Fetal & Neonatal Edition. 2012;97(1):F35-8,

5 Benitz WE. Treatment of persistent patent ductus arteriosus in preterm infants: time to accept the null hypothesis? Journal of Perinatology. 2010;30(4):241-52

6. Bose CL. Laughon MM. Patent ductus arteriosus: lack of evidence for common treatments. Archives of Disease in Childhood Fetal & Neonatal Edition. 2007;92(6):F498-502

7. Knight DB. The treatment of patent ductus arteriosus in preterm infants. A review and overview of randomised trials. Seminars in Neonatology 2000;6:63-74

8. Hammerman C. Bin-Nun A. Markovitch E. Schimmel MS. Kaplan M. Fink D. Ductal closure with paracetamol: a surprising new approach to patent ductus arteriosus treatment. Pediatrics. 2011;128(6):e1618-21

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Approved By

Trust Clinical Guidelines Group

Document history

LHP version 1.0

Related information

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