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Chest shielding for prevention of a haemodynamically significant patent ductus arteriosus in preterm infants receiving phototherapy

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Authors

Kavita Bhola1, Jann P Foster2, David A Osborn3

Background - Methods - Results - Characteristics of Included Studies - References - Data Tables & Graphs


1Special care Nursery, Blacktown Hospital, Artarmon, Australia [top]
2School of Nursing and Midwifery, Western Sydney University, Penrith DC, Australia [top]
3Central Clinical School, Discipline of Obstetrics, Gynaecology and Neonatology, University of Sydney, Sydney, Australia [top]

Citation example: Bhola K, Foster JP, Osborn DA. Chest shielding for prevention of a haemodynamically significant patent ductus arteriosus in preterm infants receiving phototherapy. Cochrane Database of Systematic Reviews 2015, Issue 11. Art. No.: CD009816. DOI: 10.1002/14651858.CD009816.pub2.

Contact person

Kavita Bhola

Special care Nursery
Blacktown Hospital
5B-1 Francis Road
Artarmon
NSW
22050
Australia

E-mail: bholakavita@rediffmail.com

Dates

Assessed as Up-to-date: 31 March 2015
Date of Search: 31 March 2015
Next Stage Expected: 01 April 2017
Protocol First Published: Issue 4, 2012
Review First Published: Issue 11, 2015
Last Citation Issue: Issue 11, 2015

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Abstract

Background

Patent ductus arteriosus (PDA) is associated with mortality and morbidity in preterm infants. Phototherapy is a common treatment for jaundice in preterm infants. However, phototherapy has been associated with failure of closure of the ductus arteriosus in preterm infants.

Objectives

To determine if chest shielding of preterm infants receiving phototherapy reduces the incidence of clinically and/or haemodynamically significant PDA and reduces morbidity secondary to PDA.

Search methods

We searched the Cochrane Central Register of Controlled Trials (CENTRAL) (the Cochrane Library; 2015, Issue 3), MEDLINE, EMBASE, CINAHL, previous reviews, cross-references, abstracts, proceedings of scientific meetings, and trial registries through March 2015.

Selection criteria

Randomised controlled trials (RCTs), cluster-RCTs, or quasi-RCTs of chest shielding during phototherapy compared to sham shielding or no shielding for the prevention of a haemodynamically or clinically significant PDA in preterm infants.

Data collection and analysis

Three review authors independently assessed studies for eligibility and quality and extracted data. We defined a clinically significant PDA as the presence of a PDA with clinical signs of an effect on organ function attributable to the ductus arteriosus. We defined a haemodynamically significant PDA as clinical and/or echocardiographic signs of a significant ductus arteriosus effect on blood flow.

Main results

We included two small trials enrolling very preterm infants (Rosenfeld 1986; Travadi 2006). We assessed both as at high risk of bias. No study reported clinically significant PDA, defined as the presence of a PDA with clinical symptoms or signs attributable to the effect of a ductus arteriosus on organ function. Rosenfeld 1986 reported a non-significant reduction in haemodynamically significant PDA with left atrial to aortic root ratio greater than 1.2 (risk ratio (RR) 0.23, 95% confidence interval (CI) 0.05 to 1.01; 74 infants) but a statistically significant risk difference (RD -0.18, 95% CI -0.34 to -0.03; number needed to treat for an additional beneficial outcome (NNTB) 5, 95% CI 3 to 33). Rosenfeld 1986 reported a significant reduction in PDA detected by murmur (RR 0.50, 95% CI 0.29 to 0.88; RD -0.30, 95% CI -0.52 to -0.08; NNTB 3, 95% CI 2 to 12; 74 infants). Rosenfeld 1986 reported a significant reduction in treatment with indomethacin (RR 0.12, 95% CI 0.02 to 0.88; RD -0.21, 95% CI -0.35 to -0.06; NNTB 5, 95% CI 3 to 17; 74 infants), and only one infant had a ductal ligation in the no-shield group. There were no other significant outcomes, including mortality to discharge or 28 days, days in oxygen, days on mechanical ventilation, days in hospital, intraventricular haemorrhage, retinopathy of prematurity, or exchange transfusion.

Authors' conclusions

The available evidence is very low quality and insufficient to assess the safety or efficacy of chest shield during phototherapy for prevention of PDA in preterm infants. Further trials of chest shielding are warranted, particularly in settings where infants are not receiving prophylactic or early echocardiographic targeted cyclo-oxygenase inhibitors for PDA.

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Plain language summary

Chest shielding to prevent patent ductus arteriosus in preterm infants receiving phototherapy

 

Review question

Does the use of chest shielding in preterm infants receiving phototherapy reduce the incidence of clinically and/or haemodynamically significant patent ductus arteriosus (PDA) and reduce morbidity secondary to PDA?

Background

The ductus arteriosus is a fetal blood vessel that usually closes spontaneously after birth. However, in approximately 30% of infants born before 30 weeks gestation the vessel remains open (known as patent ductus arteriosus, or PDA), and the infant has problems with excess blood flow to the lungs, shunting of blood away from organs, and heart failure. Phototherapy is a common treatment for jaundice in preterm infants. However, phototherapy has been associated with failure of the closure of the ductus arteriosus in preterm infants.

Study characteristics

Two small randomised trials.

Results

We included two trials and reported conflicting evidence regarding the effect of shielding on the ductus arterious. They had substantial methodological differences.

The results of this review did not provide sufficient evidence to determine the effectiveness of chest shielding to prevent PDA in preterm infants receiving phototherapy.

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Background

Description of the condition

In term newborns, the ductus arteriosus functionally closes during the first few hours after birth. Failure to close results in a condition known as patent ductus arteriosus (PDA) (Bose 2007). A large PDA is present in approximately 50% of very preterm infants in the first day of life (Kluckow 2000). An early large ductus arteriosus is frequently clinically 'silent', without the characteristic clinical signs including murmur, hyperdynamic praecordium, and bounding pulses (Hammerman 1986; Skelton 1994; Davis 1995). Detection may be dependent on echocardiographic techniques including colour flow Doppler (Evans 1993). Although frequently clinically silent, an early large PDA has been associated with systemic hypotension and low systemic blood flow (Evans 1992; Kluckow 1996), which in turn has been associated with intraventricular haemorrhage (Kluckow 1996; Osborn 2003; Miletin 2008), neurodevelopmental impairment (Hunt 2004; Osborn 2007), necrotising enterocolitis, and mortality (Osborn 2003).

Approximately 30% of infants born before 30 weeks gestation will develop a clinically significant PDA after the first days of life (Kluckow 2000). A ductus may be confirmed as being clinically significant by the identification of clinical (hyperdynamic praecordium and bounding pulses) and/or echocardiographic signs (increased pulmonary blood flow, increased left atrial to aortic root ratio, or absent or reversed flow in the distal aorta or organ arteries) of haemodynamic significance (Evans 1993). The left-to-right shunting through the ductus arteriosus leads to overloading of the pulmonary circulation and reduced perfusion of the brain, gut, and kidneys, resulting in symptoms attributable to the PDA including respiratory distress, feed intolerance, and renal insufficiency. If left uncorrected, PDA can lead to pulmonary hypertension, congestive heart failure (Bose 2007), and reduced organ blood flows (ductal steal) (Shimada 1994). A clinically significant PDA has been associated with cystic periventricular leukomalacia (Pladys 2001; Chung 2005), chronic lung disease (Rojas 1995), necrotising enterocolitis (Gagliardi 2008), and mortality in very preterm infants (Noori 2009).

Phototherapy is the most widely used therapy for neonatal unconjugated hyperbilirubinaemia. Phototherapy leads to photoisomerisation of bilirubin into a water-soluble form that can be excreted by the kidneys (Wong 2006). In nearly all infants, phototherapy reduces the rise of serum bilirubin concentrations, Wong 2006, and the need for an exchange transfusion (Maisels 1998). Phototherapy may be delivered from sources including fluorescent tubes, light-emitting diodes, and fibreoptic sources. Phototherapy can be delivered by overhead lamps, lamps surrounding the infant, or a phototherapy 'blanket', at varying wavelengths and intensity. The American Academy of Pediatrics recommends phototherapy in the 430 nm to 490 nm wavelength spectrum and intensity of at least 30 uW/cm2/nm (American Academy of Pediatrics 2004).

The effect of light on the ductus arteriosus is not completely understood, but in vitro studies have shown that constricted arteries relax when exposed to light (Ehrreich 1968; Barefield 1993). More specifically, phototherapy has been associated with failure of closure of the ductus arteriosus in preterm infants (Scheidt 1987; Barefield 1993; Benders 1999).

Description of the intervention

It has been proposed that shielding the chest from phototherapy light may prevent a haemodynamically significant PDA (Clyman 1978). Chest shields are used for the duration the infant receives phototherapy. The chest shield may be made of any photo-opaque or reflective material designed to prevent phototherapy light from reaching the ductus. In theory, the photo-opaque material is taped over the left side of the chest, both front and back, to cover the area of the PDA. The shield should not cover more than 10% of the infant's body surface area, so as not to reduce the effectiveness of phototherapy, as determined by Rubaltelli 1978 and Hegyi 1981. The shield may be tested to block transmission of light by placing a radiometer directly underneath. Chest shields have been used to shield from phototherapy specifically, not ambient light, although this could be considered. Theoretical adverse effects of shielding with aluminium foil include burns and skin damage, although there are no current reports of this.

How the intervention might work

It is hypothesised that the skin of preterm infants permits transmission of light during phototherapy, causing photorelaxation of the musculature of the ductus arteriosus (Clyman 1978; Furchgott 1991). Chest shielding has the potential to prevent photorelaxation of the duct (Maisels 1992). Animal studies have shown that chest shielding blocks transmission of light and prevents photorelaxation of the ductus arteriosus. It has been shown that immature lambs are more sensitive to photorelaxation as compared to mature lambs (Clyman 1978). Hypotheses for this action include activation of photosensitive metabolites, alterations in membrane or receptor sites, or alteration in prostaglandin metabolism. It has been proposed that light may exert its effect through the nitric oxide pathway, accompanied with an increase in cyclic guanosine monophosphate, or may have a direct relaxation effect on arterial smooth muscle (Sisson 1973; Furchgott 1991; Barefield 1993). Light penetrates the skin, as shown in mice during phototherapy (Sisson 1973), with potential consequences on the ductus arteriosus. Front and back shielding may prevent the action of light.

Why it is important to do this review

PDA is a common problem of prematurity that is associated with significant morbidity and frequent treatment. Phototherapy is widely used in the first few days in preterm neonates when there is frequent ductal patency. Chest shielding is a simple intervention that has the potential to prevent a clinically and/or haemodynamically significant PDA in preterm babies treated with phototherapy.

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Objectives

To determine if chest shielding of preterm infants receiving phototherapy reduces the incidence of clinically and/or haemodynamically significant PDA and reduces morbidity secondary to PDA.

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Methods

Criteria for considering studies for this review

Types of studies

Randomised controlled trials (RCTs), quasi-RCTs, and cluster-RCTs.

Types of participants

Preterm infants (less than 37 weeks completed gestation) receiving phototherapy.

We intended to undertake separate comparisons of trials that enrolled the following infants:

  1. Unselected infants (not enrolled on the basis of a PDA detected clinically or echocardiographically); and
  2. Infants with a PDA (enrolled with clinical or echocardiographic signs of a PDA).

Types of interventions

Chest shielding with photo-opaque material versus no shielding, or chest shielding versus sham shielding (sham shielding defined as a simulated shield that is not photo-opaque).

Types of outcome measures

Primary outcomes
  1. Unselected infants (not enrolled on the basis of a PDA detected clinically or echocardiographically): presence of a clinically1 and/or haemodynamically2 significant PDA.
  2. Infants with a PDA (enrolled with clinical or echocardiographic signs of a PDA): persistence (at least seven days after enrolment) of a clinically1 and/or haemodynamically2 significant PDA.

1A clinically significant PDA is defined as the presence of a PDA (murmur and/or echocardiographically detected) with clinical signs of an effect on organ function attributable to the PDA (e.g. respiratory distress, feed intolerance, and renal insufficiency).

2A haemodynamically significant PDA is defined as clinical (hyperdynamic praecordium and bounding pulses) and/or echocardiographic signs (increased pulmonary blood flow, increased left atrial to aortic root ratio, or absent or reversed flow in the distal aorta or organ arteries) of a significant ductus arteriosus effect on blood flow.

Secondary outcomes
  1. Any PDA detected by presence of murmur and/or echocardiography after the first week.
  2. Treatment with cyclo-oxygenase inhibitors.
  3. Ductal ligation.
  4. Mortality prior to hospital discharge.
  5. Neonatal mortality (< 28 days of age).
  6. Congestive cardiac failure (defined as having respiratory distress, cardiomegaly and hepatomegaly, or medical treatment of clinically significant PDA with anti-cardiac failure therapy such as diuretics) (Mahajan 2006).
  7. Neurodevelopmental disability (after at least 18 months postnatal age) defined as neurological abnormality including cerebral palsy on clinical examination, developmental delay more than two standard deviations below population mean on a standardised test of development, blindness (visual acuity < 6/60), or deafness (any hearing impairment requiring amplification at any time after term corrected age).
  8. Number of days receiving oxygen.
  9. Number of days receiving mechanical ventilation (via an endotracheal tube).
  10. Number of days receiving respiratory support (including intermittent positive pressure ventilation, continuous positive airway pressure, or high-flow nasal cannula).
  11. Chronic lung disease, defined as a need for oxygen or respiratory support at 36-weeks postmenstrual age (Walsh 2003).
  12. Received home oxygen.
  13. Intraventricular haemorrhage (any grade) (Papile 1978).
  14. Periventricular leukomalacia (cystic lesions confirmed by ultrasound and/or magnetic resonance imaging).
  15. Necrotising enterocolitis (proven = Bell stage greater than/or equal to 2) (Bell 1978).
  16. Retinopathy of prematurity (Patz 1985).
  17. Postnatal growth failure (weight < 10th percentile near term or at discharge).
  18. Number of days in hospital.
  19. Number of days receiving phototherapy.
  20. Exchange blood transfusion.
  21. Adverse effects including skin damage.
  22. Other non-prespecified adverse events that are reported by the authors.

Search methods for identification of studies

We used the standard search strategy of the Cochrane Neonatal Review Group (CNRG) as outlined in the Cochrane Library. We attempted to identify all relevant studies regardless of language or publication status (published, unpublished, in press, and in progress).

Electronic searches

Two review authors independently performed the electronic database searches. This included electronic searches of the Cochrane Central Register of Controlled Trials (CENTRAL) Appendix 1, (the Cochrane Library; 2015, Issue 3), MEDLINE (1950 to March 2015), EMBASE (1980 to March 2015), and CINAHL (1982 to March 2015).

We searched MEDLINE (Appendix 2), EMBASE (Appendix 3,) and CINAHL for relevant articles using search terms: [Infant OR Newborn (explode) [MeSH heading] OR Ductus Arteriosus, Patent (explode) [MeSH heading] OR PDA OR ductus] AND [Phototherapy OR Phototherapy (explode) [MeSH heading]] AND [Chest Shield* OR Radiation Protection (explode) [MeSH heading]]. We searched clinical trials registries for current or recently completed trials (ClinicalTrials.gov External Web Site Policy, Controlled-Trials.com External Web Site Policy, and WHO International Clinical Trials Registry Platform (ICTRP) External Web Site Policy) through March 2015.

Searching other resources

The search strategy included communication with expert informants, citations of reviews, and trials for references to other trials. We searched previous reviews, including cross-references, abstracts, and conferences and symposia proceedings of the Perinatal Society of Australia and New Zealand and Pediatric Academic Societies (American Pediatric Society, Society for Pediatric Research, and European Society for Paediatric Research) from 1990 to 2014. If we identified any unpublished trials, we intended to contact the corresponding investigator for information. We considered unpublished studies or studies only reported as abstracts as eligible for review, if the trial author could confirm the methods and data. We contacted the corresponding authors of identified trials for additional information about their studies when further data were required.

Data collection and analysis

We used the standard methods of the CNRG, as documented in the Cochrane Handbook for Systematic Reviews of Interventions (Higgins 2011).

Selection of studies

Review authors independently assessed for inclusion all the potential studies identified as a result of the search strategy. We resolved disagreements through discussion, or intended to consult a Cochrane review arbiter if needed.

Specifically, we:

  1. Merged the search results using Review Manager 5 software and removed duplicate records of the same report (RevMan 2012);
  2. Examined titles and abstracts to remove irrelevant reports;
  3. Retrieved the full text of potentially relevant reports;
  4. Linked together multiple reports of the same study;
  5. Examined full-text reports for compliance of studies with eligibility criteria;
  6. Corresponded with investigators, when appropriate, to clarify study eligibility;
  7. At all stages, noted the reasons for inclusion and exclusion of articles. (We resolved disagreements through consensus, or intended to refer them for arbitration to the editorial base of the CNRG if needed);
  8. Made final decisions on study inclusion and proceeded to data collection; and
  9. Resolved all discrepancies through a consensus process.

Data extraction and management

Each review author independently performed trial searches, assessments of methodology, and extraction of data with comparison and resolution of any differences found at each stage. We entered data into Review Manager 5 software and checked for accuracy (RevMan 2012). If information regarding any of the above was missing or unclear, we intended to attempt to contact authors of the original reports to provide further details.

Assessment of risk of bias in included studies

We used the standardised review methods of the CNRG (neonatal.cochrane.org/en/index.html External Web Site Policy) to assess the methodological quality of the included studies. Review authors independently assessed study quality and risk of bias using the following criteria documented in the Cochrane Handbook for Systematic Reviews of Interventions (Higgins 2011).

Random sequence generation (checking for possible selection bias)

We described for the included study the method used to generate the allocation sequence in sufficient detail to allow an assessment of whether it should produce comparable groups. We assessed the 'Risk of bias' methods as:

  • low risk (any truly random process, e.g. random number table; computer random number generator);
  • high risk (any non-random process, e.g. odd or even date of birth; hospital or clinic record number); or
  • unclear risk.
Allocation concealment (checking for possible selection bias)

We described for the included study the method used to conceal the allocation sequence in sufficient detail to determine whether intervention allocation could have been foreseen in advance of, or during recruitment, or changed after assignment. We assessed the 'Risk of bias' methods as:

  • low risk (e.g. telephone or central randomisation; consecutively numbered, sealed, opaque envelopes);
  • high risk (open random allocation; unsealed or non-opaque envelopes; alternation; date of birth); or
  • unclear risk.
Blinding (checking for possible performance bias)

We described for the included study the methods used, if any, to blind study participants and personnel from knowledge of which intervention a participant received. We judged the study to be at low risk of bias if it was blinded, or if we judged that the lack of blinding could not have affected the results. We assessed blinding separately for different outcomes and classes of outcomes. We assessed the 'Risk of bias' methods as:

  • adequate, inadequate, or unclear for participants;
  • adequate, inadequate, or unclear for personnel; or
  • adequate, inadequate, or unclear for outcome assessors.
Incomplete outcome data (checking for possible attrition bias through withdrawals, dropouts, and protocol deviations)

We described for the included study, and for each outcome or class of outcomes, the completeness of data including attrition and exclusions from the analysis. We stated whether attrition and exclusions were reported, the numbers included in the analysis at each stage (compared with the total randomised participants), reasons for attrition or exclusion where reported, and whether missing data were balanced across groups or were related to outcomes. Where sufficient information was reported, or could be supplied by the trial authors, we planned to re-include missing data in the analyses. We assessed the 'Risk of bias' methods as:

  • adequate (less than 20% missing data);
  • inadequate; or
  • unclear.
Selective reporting bias

We described for the included study how we investigated the possibility of selective outcome reporting bias and what we found. We assessed the 'Risk of bias' methods as:

  • low risk (where it was clear that all of the study’s prespecified outcomes and all expected outcomes of interest to the review were reported);
  • high risk (where not all of the study’s prespecified outcomes were reported; one or more reported primary outcomes were not prespecified; outcomes of interest were reported incompletely and so could not be used; study failed to include results of a key outcome that would have been expected to have been reported); or
  • unclear risk.
Other sources of bias

We described for the included study any important concerns we had about other possible sources of bias (e.g. early termination of trial due to data-dependent process, extreme baseline imbalance, etc.). We assessed other sources of bias as:

  • low risk;
  • high risk; or
  • unclear.
Overall risk of bias

We made judgements as to whether studies were at high risk of bias according to the criteria in the Cochrane Handbook for Systematic Reviews of Interventions (Higgins 2011). With reference to the above, we assessed the likely magnitude and direction of the bias and whether we considered it likely to impact on the findings.

Measures of treatment effect

We analysed the results of the studies using Review Manager 5 software (RevMan 2012). We summarised data in a meta-analysis if they were sufficiently homogeneous, both clinically and statistically.

Dichotomous data

For dichotomous data, we presented results as risk ratios (RRs) with 95% confidence intervals (CIs). If there was a statistically significant reduction, we intended to report risk differences (RDs) and calculate the number needed to treat for an additional beneficial outcome (NNTB) or number needed to treat for an additional harmful outcome (NNTH), and associated 95% CIs.

Continuous data

For continuous data, we used the mean difference (MD) if outcomes were measured in the same way between trials. We used the standardised mean difference (SMD) to combine trials that measured the same outcome but used different methods.

Unit of analysis issues

The unit of randomisation was the intended unit of analysis; as we expected, this was the individual infant.

Cluster-RCTs

We intended to include cluster-RCTs in the analyses along with individually randomised trials. We analysed cluster-RCTs employing the methods described in the Cochrane Handbook for Systematic Reviews of Interventions (Higgins 2011), using an estimate of the intracluster correlation coefficient (ICC) derived from the trial (if possible) or from another source. If we used ICCs from other sources, we intended to report this and conduct sensitivity analyses to investigate the effect of variation in the ICC. If we identified both cluster-RCTs and individually randomised trials, we planned to synthesise the relevant information. We considered it reasonable to combine the results from both if there was little heterogeneity between the study designs and we considered interaction between the effect of intervention and the choice of randomisation unit to be unlikely. We intended to acknowledge heterogeneity in the randomisation unit and perform a separate meta-analysis.

Dealing with missing data

We contacted the authors of one of the published studies when we required clarification or for additional information.

Assessment of heterogeneity

We used Review Manager 5.3 software to assess heterogeneity of treatment effects between trials using the following two formal statistics (RevMan 2012).

  1. The Chi2 test, to assess whether observed variability in effect sizes between studies was greater than would be expected by chance. Since this test has low power when the number of studies included in the meta-analysis is small, we set the probability at the 10% level of significance.
  2. The I² statistic to measure heterogeneity among the trials in each analysis. We graded the degree of heterogeneity as: < 25% no heterogeneity, 25% to 49% low heterogeneity, 50% to 74% moderate heterogeneity, and > 75% high heterogeneity.

Assessment of reporting biases

We contacted study authors asking them to provide further information when required.

Data synthesis

We carried out statistical analysis using Review Manager 5.3 software (RevMan 2012). We used a fixed-effect Mantel-Haenszel method meta-analysis for combining data where trials were examining the same intervention and we judged the trials population and methods to be similar. We assessed possible source(s) of heterogeneity using subgroup and sensitivity analysis. If there was not sufficient similarity of populations, interventions, and methods, we did not conduct a meta-analysis.

Subgroup analysis and investigation of heterogeneity

If sufficient data were available, we planned to explore potential sources of clinical heterogeneity through the following a priori subgroup analyses.

  1. Ductus arteriosus status at enrolment: given prophylactically (all infants); infants with a clinically and/or haemodynamically significant ductus arteriosus; and infants with a clinically insignificant PDA.
  2. Gestational age (< 28 weeks, 28 to 32 weeks, and 33 to 37 weeks).
  3. Timing of initiation of chest shielding (early: one to three days; intermediate: four to seven days; late: > 7 days).
  4. Intensity of phototherapy (4 цW/cm2/nm to 10 цW/cm2/nm, 10 цW/cm2/nm to 20 цW/cm2/nm, and > 20 цW/cm2/nm).
  5. Wavelength of phototherapy (430 nm to 460 nm, 460 nm to 490 nm).
  6. Type of phototherapy (fluorescent, light-emitting diode, and fibreoptic).
  7. Site of phototherapy (chest, back, and chest and back).
  8. Area of chest shielding (5%, 10%, and 20% of body surface area).

Sensitivity analysis

If sufficient data were available, we planned to explore methodological heterogeneity through the use of sensitivity analyses. We planned to perform these through including trials of higher quality, based on the presence of any of the following: adequate sequence generation, allocation concealment, and less than 10% loss to follow-up.

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Main results

Description of studies

Results of the search

The search of CENTRAL, MEDLINE, EMBASE, CINAHL, and clinical trials registries March 2015 found three studies that we assessed for eligibility. We identified no ongoing trials.

Included studies

Two RCTs met our inclusion criteria (Rosenfeld 1986; Travadi 2006); see Characteristics of included studies.

Participants

Rosenfeld 1986 enrolled 74 preterm infants with birth weight 539 g to 1500 g and gestation 26 to 32 weeks. No exclusion criteria were reported. Infants were not enrolled according to ductus status. Infants had prophylactic phototherapy for hyperbilirubinaemia from day one of life.

Travadi 2006 enrolled 54 preterm infants with birth weight 705 g to 1165 g and gestation 25 to 28 weeks. PDA was present in 74% on baseline echocardiogram. Indomethacin treatment of haemodynamically significant PDA reported as at similar median time as phototherapy. Exclusion criteria included if phototherapy started before randomisation, congenital heart disease, major congenital abnormalities, hydrops fetalis or rhesus isoimmunisation, and infants requiring exchange transfusion.

Interventions
Chest shield group

Rosenfeld 1986: Infants had their "left chests covered with a folded (doubled) piece of standard aluminium foil. The foil was covered with a gauze pad and taped over the left chest continuously while receiving phototherapy".

Travadi 2006: The left side of the chest (front and back) was shielded during the entire duration of phototherapy using a double piece of aluminium foil with gauze underneath. The resultant non-irradiated area did not exceed 10% of the infant's body surface area.

Control group

Rosenfeld 1986 and Travadi 2006 reported no chest shield. Sham treatment was not used.

Outcomes measures

Rosenfeld 1986 reported incidence of PDA (clinical presence of a murmur consistent with a ductus). Those infants with a murmur consistent with a PDA were assessed by echocardiography; left atrial to aortic root (LA/Ao) ratio greater than 1.2 was considered haemodynamically significant. The study also reported mortality, use of fluid restriction, furosemide, indomethacin, surgery (ductal ligation), exchange blood transfusion, intraventricular haemorrhage, retinopathy of prematurity, and days in hospital.

Travadi 2006 reported incidence and severity of PDA assessed by serial echocardiographic examinations at 48 hours after commencement or cessation of phototherapy. Significant PDA requiring treatment was defined as echocardiographic-confirmed PDA with LA/Ao ratio greater than 1.4 or a ductal diameter greater than 1.5 mm with a left-to-right shunt. The study also reported mortality to discharge, intraventricular haemorrhage Papile grade 3 or 4, days in hospital, days respiratory support (continuous positive airway pressure), days ventilation, and days phototherapy.

Excluded studies

We excluded one historical control study (Kim 1997); see Characteristics of excluded studies.

Risk of bias in included studies

We assessed both studies as being at risk of bias; see 'Risk of bias' summary (Figure 1). We assessed Rosenfeld 1986 as at high risk of selection, performance, and detection bias and as at unclear risk of attrition bias. We assessed Travadi 2006 as at low risk of detection bias and attrition bias but at high risk of performance bias and bias due to some clinically but not statistically important baseline differences and premature stopping. We assessed neither trial as eligible for inclusion in sensitivity analysis for trials of higher quality.

Allocation (selection bias)

Both studies used methods of random sequence generation at low risk of bias. We assessed Travadi 2006 as maintaining allocation concealment. However, we considered Rosenfeld 1986 as at high risk of selection bias as informed parental consent was only obtained from the parents of infants in the shielded group. The study had unbalanced group numbers for weight strata at baseline.

Blinding (performance bias and detection bias)

We assessed both studies as being at high risk of performance bias due to lack of blinding of intervention (no use of sham treatment) (Rosenfeld 1986; Travadi 2006).

Rosenfeld 1986 reported that the study was "unblinded", and so we assessed it to be at high risk of detection bias. Travadi 2006 reported that the cardiologist was "blinded" to intervention at time of ductal assessment, and so we considered it to be at low risk of detection bias for the primary outcomes.

Incomplete outcome data (attrition bias)

Rosenfeld 1986 did not report outcomes in 8 of 74 infants (11%) who died prior to completion of phototherapy (four in each group), and so we considered it to be at unclear risk of attrition bias. We assessed Travadi 2006 as at low risk of attrition bias with no reported losses.

Selective reporting (reporting bias)

Both studies were designed to assess the effect of phototherapy on the incidence of PDA, and so we assessed them as at low risk of reporting bias (Rosenfeld 1986; Travadi 2006).

Other potential sources of bias

Rosenfeld 1986 had unbalanced groups at baseline (treatment group had 15 infants less than/or equal to 1000 g and 21 infants > 1000 g; control group had 21 infants less than/or equal to 1000 g and 15 infants > 1000 g). Travadi 2006 reported some clinically but not statistically significant differences in groups for sex at baseline and reported premature stopping after an interim analysis reported the study was unlikely to find any difference between groups. In addition, 40.7% (11 infants in each of the two groups) were treated with indomethacin pre-phototherapy. Seventy per cent of infants in the chest shield group and 77% in the no-chest shield group were diagnosed with a patent ductus pre-phototherapy. The analyses were substantially underpowered to detect important clinical effects.

Effects of interventions

Chest shielding versus no treatment in unselected preterm infants (Comparison 1)

Primary outcomes

Presence of a clinically significant PDA: not reported.

Haemodynamically significant PDA (Outcome 1.1): Haemodynamically significant PDA defined as clinical (hyperdynamic praecordium and bounding pulses) and/or echocardiographic signs (increased pulmonary blood flow, increased LA/Ao ratio, or absent or reversed flow in the distal aorta or organ arteries) of a significant ductus arteriosus effect on blood flow.

Rosenfeld 1986 reported no significant difference in infants with an echocardiographically confirmed PDA with an LA/Ao ratio greater than 1.2 (RR 0.23, 95% CI 0.05 to 1.01; 74 infants) but a statistically significant RD (RD -0.18, 95% CI -0.34 to -0.03; NNTB 5, 95% CI 3 to 33; 74 infants).

Secondary outcomes

Any PDA (echocardiography detected) (Outcome 1.2): Travadi 2006 reported no significant difference in echocardiographically detected PDA (RR 0.92, 95% CI 0.52 to 1.64; RD -0.04, 95% CI -0.30 to 0.23; 54 infants).

Any PDA (murmur detected) (Outcome 1.3): Rosenfeld 1986 reported a significant reduction in PDA detected by murmur (RR 0.50, 95% CI 0.29 to 0.88; RD -0.30, 95% CI -0.52 to -0.08; NNTB 3, 95% CI 2 to 12; 74 infants).

Treatment with cyclo-oxygenase inhibitors (Outcome 1.4): Rosenfeld 1986 reported a significant reduction in treatment with indomethacin (RR 0.12, 95% CI 0.02 to 0.88; RD -0.21, 95% CI -0.35 to -0.06; NNTB 5, 95% CI 3 to 17; 74 infants).

Ductal ligation (Outcome 1.5): Rosenfeld 1986 reported one control infant had a surgical ligation (RR 0.35, 95% CI 0.01 to 8.36; RD -0.03, 95% CI -0.10 to 0.04; 74 infants).

Neonatal mortality prior to hospital discharge (Outcome 1.6): Neither study reported a significant difference in mortality before discharge. Meta-analysis of the two studies found no significant difference (typical RR 1.68, 95% CI 0.75 to 3.78; typical RD 0.08, 95% CI -0.04 to 0.21; 128 infants) (Rosenfeld 1986; Travadi 2006).

Neonatal mortality (< 28 days of age) (Outcome 1.7): Rosenfeld 1986 reported no significant difference (RR 1.06, 95% CI 0.16 to 7.10; RD 0.00, 95% CI -0.10 to 0.11; 74 infants).

Number of days receiving oxygen (Outcome 1.8): Rosenfeld 1986 reported no significant difference (MD -2.80, 95% CI -14.11 to 8.51; 74 infants).

Number of days receiving mechanical ventilation (Outcome 1.9): Rosenfeld 1986 reported no significant difference (MD -5.10, 95% CI -14.94 to 4.74; 74 infants).

Number of days in hospital (Outcome 1.10): Meta-analysis of two studies found no significant difference (MD -8.05, 95% CI -18.04 to 1.94; 128 infants) (Rosenfeld 1986; Travadi 2006).

Intraventricular haemorrhage (any grade) (Outcome 1.11): Rosenfeld 1986 reported no significant difference (RR 0.53, 95% CI 0.10 to 2.71; RD -0.05, 95% CI -0.17 to 0.07; 74 infants).

Intraventricular haemorrhage grade 3 or 4 (Outcome 1.12): Meta-analysis of two studies found no significant difference (typical RR 0.64, 95% CI 0.22 to 1.85; typical RD -0.04, 95% CI -0.15 to 0.06; 128 infants) (Rosenfeld 1986; Travadi 2006).

Retinopathy of prematurity (Outcome 1.13): Rosenfeld 1986 reported no significant difference (RR 0.53, 95% CI 0.10 to 2.71; RD -0.05, 95% CI -0.17 to 0.07; 74 infants).

Number of days receiving phototherapy: Neither study reported an effect on duration of phototherapy. Rosenfeld 1986 reported mean duration shielding group 8.3 days and control group 8.5 days. Travadi 2006 reported median duration shield group 46 hours and control group 46 hours (P = 0.42).

Exchange blood transfusion (Outcome 1.14): Rosenfeld 1986 reported no significant difference (RR 0.70, 95% CI 0.12 to 3.97; RD -0.02, 95% CI -0.14 to 0.09; 74 infants).

Secondary outcomes not reported by studies: neonatal mortality (< 28 days of age); congestive cardiac failure; neurodevelopmental disability; number of days receiving respiratory support; chronic lung disease; received home oxygen; periventricular leucomalacia; necrotising enterocolitis; and adverse effects including skin damage.

Chest shielding versus no treatment in unselected preterm infants: Sensitivity analysis (Comparison 2)

We assessed both studies as being at high risk of bias, and so they are ineligible for a sensitivity analysis.

Subgroup analyses

Given that there are only two similar studies and we have considered both studies to be at high risk of bias, we have not reported formal subgroup analysis separately. The assessments below report the potential eligibility for the two studies for the prespecified subgroup analyses.

  1. Ductus arteriosus status at enrolment: Both studies enrolled unselected infants. Rosenfeld 1986 did not report PDA status at baseline. Travadi 2006 reported that 40 of 54 infants (74%) had PDA on initial echocardiogram. Both studies used targeted indomethacin treatment of echocardiographically confirmed and haemodynamically significant PDA. No separate subgroup analysis is reported.
  2. Gestational age: Rosenfeld 1986 enrolled infants 26 to 32 weeks gestation, 539 g to 1500 g, and reported the outcome of infants born less than/or equal to 1000 g and those born > 1000 g separately. However, the subgroups had substantial imbalances in numbers. Travadi 2006 enrolled infants < 29 weeks gestation.
  3. Timing of initiation of chest shielding: Both studies initiated chest shielding early (one to three days): Rosenfeld 1986 reported that infants received prophylactic phototherapy. Travadi 2006 reported infants commenced phototherapy at a median (interquartile range, range) age in hours: shield group 31 hours (15, 100) and control group 27 hours (1, 271).
  4. Intensity of phototherapy: Rosenfeld 1986 reported spectral intensity was always > 4.00 uW/cm2 and mean flux was 4.77 uW/cm2. Travadi 2006 reported using Medela phototherapy lamp or the Micro-Lite phototherapy system, which have reported irradiance of 2.06 mW/cm2 and 2.50 mW/cm2 respectively, placed 45 cm away from the body surface. The two studies are probably applicable to the lower subgroup analysis for spectral intensity of phototherapy 4 цW/cm2 to 10 цW/cm2.
  5. Wavelength of phototherapy: Neither study reported the wavelength of phototherapy. The devices used are likely to have wavebands from 400 nm to 550 nm, overlapping prespecified subgroup analyses criteria.
  6. Type of phototherapy: Rosenfeld 1986 used a fluorescent phototherapy system. Travadi 2006 used both a fluorescent phototherapy system and a halogen bulb system.
  7. Site of phototherapy: Rosenfeld 1986 reported covering the anterior chest but not the positioning of the infant receiving phototherapy. Travadi 2006 reported covering anterior and posterior chest and alternating the infant between prone and supine.
  8. Area of chest shielding: Rosenfeld 1986 did not report area of chest covered, although it is likely to represent 5% to 10% of the infant's surface area. Travadi 2006 reported covering 10% of infant's surface area.

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Discussion

Summary of main results

There is inconsistent evidence regarding the effectiveness of chest shielding of infants receiving phototherapy for prevention of PDA. Both studies were small and have methodological concerns. They both enrolled very preterm infants and used a double piece of aluminium foil over gauze to shield the left side of the chest of infants undergoing phototherapy in the first few days after birth. Rosenfeld 1986 enrolled infants with unknown ductal status in the first day undergoing prophylactic phototherapy. The trial reported that anterior chest shielding resulted in a significant reduction in PDA detected by presence of a murmur and confirmed echocardiographically. There was a significant reduction in haemodynamically significant PDA and treatment with indomethacin. The trial reported no other significant clinical effects. However, the trial had substantial methodological concerns, particularly with regard to the lack of allocation concealment and blinding. Travadi 2006 enrolled infants at the initiation of phototherapy who were undergoing echocardiographic surveillance of the ductus. The majority of the infants had an echocardiographic PDA detected at baseline and targeted treatment with indomethacin at the same median time as phototherapy was commenced. The trial reported that there was no effect of chest shielding on echocardiographic parameters of ductal patency and haemodynamic status, or use of indomethacin treatment. The trial reported no other significant clinical effects. The trial was of higher methodological quality, being assessed as at low risk of selection bias and blinding echocardiographic assessment. However, a substantial proportion of infants were treated with indomethacin at a similar median time as the commencement of phototherapy, suggesting the effect of the intervention could have been modified by early indomethacin treatment. Neither study reported a significant effect of chest shielding on treatment of jaundice.

Overall completeness and applicability of evidence

The two trials included in the review enrolled a total of 128 very preterm infants receiving prophylactic (74 infants born 26 to 32 weeks gestation) and early (54 infants born less than 29 weeks gestation) phototherapy. The infants in both trials were relatively immature. They had different average exposures to phototherapy, suggesting a potentially modifying effect. Rosenfeld 1986 reported using prophylactic phototherapy, and the infants had an average exposure of 8.3 to 8.5 days. The infants had initial clinical assessment for a murmur, with the timing of appearance between days one to 15. Travadi 2006 used enrolled infants receiving phototherapy treatment for hyperbilirubinaemia, and the infants had an average exposure of 46 hours. The infants had blinded echocardiographic monitoring and targeted treatment of the ductus with indomethacin initiated at a similar time as phototherapy. This is a potentially modifying intervention, especially given the relatively short duration of which phototherapy was administered. Neither trial reported the incidence of clinically significant PDA. Both trials reported echocardiographically confirmed and haemodynamically significant PDA and treatment with indomethacin.

The intensity of phototherapy used was in the lower range. Aluminium foil was used to shield the left side of the chest, which has been demonstrated to nearly eliminate direct spectral intensity, although the effect on reflected or transmitted light is unclear.

Quality of the evidence

We assessed both studies as being at high risk of bias. We assessed Rosenfeld 1986 as at high risk of selection, performance, and detection bias, and at unclear risk of attrition bias. We assessed Travadi 2006 as at low risk of attrition bias, detection bias, and attrition bias, but at high risk of performance bias and bias due to some clinically but not statistically important baseline differences and premature stopping. Eleven infants in each of the two groups (40.7%) were treated with indomethacin before the intervention commenced. The analyses are substantially underpowered to detect important clinical effects.

Potential biases in the review process

There were no apparent biases in the review process outside the quality of the available evidence. There was no suggestion of publication bias.

Agreements and disagreements with other studies or reviews

Currently there are no recommendations regarding the use of chest shielding in infants receiving phototherapy for prevention of PDA. One excluded historical control study also reported a significant reduction in incidence of PDA (18% in shield group and 41% in control group; P < 0.05) after introduction of a similar chest shield (Kim 1997). There is no current reported data on prevalence of use of chest shielding during phototherapy.

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Authors' conclusions

Implications for practice

The available evidence is very low quality and insufficient to assess the safety or efficacy of chest shielding during phototherapy for the prevention of PDA in preterm infants.

Implications for research

Further trials of chest shielding are warranted, particularly in settings where infants are not receiving prophylactic or early echocardiographic targeted cyclo-oxygenase inhibitors for PDA. It is recommended that future studies use Doppler flow echocardiography to diagnose PDA. It is possible that a sham shield could be developed with limited photoabsorption properties to ensure blinding of the intervention. However, given the difficulty of blinding the intervention, it is important that outcome measurement is blinded to allocation.

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Acknowledgements

Dr Travadi for providing additional data and clarification.

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Contributions of authors

KB, JF, and DO collaborated on the protocol and review. All review authors assessed eligibility and risk of bias, extracted data, and agreed on conclusions.

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Declarations of interest

None declared.

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Differences between protocol and review

None.

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Characteristics of studies

Characteristics of included studies

Rosenfeld 1986

Methods

Parallel-group, randomised controlled trial

Participants

Inclusion criteria: preterm infants admitted to the NICU (not enrolled into study on basis of a PDA detected clinically or echocardiographically):

  • birth weight between 539 g and 1500 g (mean 1034 g);
  • gestational age between 26 to 32 weeks (mean 29.4 weeks)

Exclusion criteria: none reported

Interventions

Chest shielding (n = 36): Infants had their "left chests covered with a folded (doubled) piece of standard aluminium foil. The foil was covered with a gauze pad and taped over the left chest continuously while receiving phototherapy. Whenever the foil had to be removed for examination, treatment, or cleaning of the patient, the phototherapy was discontinued", versus

Control (n = 38): No chest shield

Co-interventions: All infants were nursed under radiant warmers, received mechanical ventilation for respiratory distress syndrome, and prophylactic phototherapy for hyperbilirubinaemia from day 1 of life. Standard Air Shields phototherapy units were used (model PTU 78-1) for all infants. Light intensity was measured with a Minolta Fluorolite meter 451. Flux was always > 4.00 uW/cm2/nm, and mean flux was 4.77 uW/cm2/nm

PDA status at baseline: Ductal status was not reported at baseline. No indomethacin use reported prior to enrolment in study

Outcomes

Primary outcome: Incidence of PDA: the clinical presence of a murmur consistent with a ductus. Those infants with a murmur consistent with a PDA were assessed by echocardiography; left atrial to aortic root ratio > 1.2 was considered haemodynamically significant

Reported: fluid restriction, furosemide, indomethacin, surgery (ductal ligation), exchange blood transfusion, retinopathy of prematurity, days in hospital

Notes  
Risk of bias table
Bias Authors' judgement Support for judgement
Random sequence generation (selection bias) Low risk

"Consecutive patients were first separated according to sex and then according to a previously constructed randomisation chart and assigned to either the treatment group ....or a control group...."

Allocation concealment (selection bias) High risk

Post allocation consent for 1 group only. "Written, informed, parental consent was obtained from the parents of all infants in the shielded group".

Blinding of participants and personnel (performance bias) High risk

Parents unblinded. Blinding of staff not reported and unlikely

Blinding of outcome assessment (detection bias) High risk

Reported "unblinded"

Incomplete outcome data (attrition bias) Unclear risk

Excluded infants who died before finish of phototherapy. However, number of enrolled infants excluded from analysis not reported

Selective reporting (reporting bias) Low risk

Reported primary outcome incidence PDA

Other bias High risk

Unbalanced groups at baseline (treatment group had 15 infants less than/or equal to 1000 g and 21 infants > 1000 g; control group had 21 infants less than/or equal to 1000 g and 15 infants > 1000 g). No power calculation reported

Travadi 2006

Methods

Parallel-group, randomised controlled trial

Participants

Inclusion criteria: preterm infants < 29 weeks gestation admitted to the NICU (not enrolled into study on basis of a PDA detected clinically or echocardiographically):

  • birth weight between 705 g and 1165 g;
  • gestational age between 25 to 28 weeks;
  • required phototherapy due to hyperbilirubinaemia (not prophylactic)

Exclusion criteria:

  • phototherapy started before randomisation
  • infants with congenital heart disease
  • major congenital abnormalities
  • hydrops fetalis or rhesus isoimmunisation
  • infants requiring exchange transfusion
Interventions

Chest shielding (n = 27): The left side of the chest (both front and back) was shielded during the entire duration of phototherapy using a double piece of aluminium foil with gauze underneath. The resultant non-irradiated area did not exceed 10% of the infant's body surface area. The shield was tested to block all transmission of light by placing a radiometer directly underneath the double piece of shield placed 45 cm away from the phototherapy source and noting zero spectral irradiance

Control (n = 27): No chest shield

Co-interventions: Phototherapy was administered using a Medela phototherapy lamp (Medela AG, Switzerland) or the Micro-Lite system (Hill-Rom, Hatboro, PA, USA) placed 45 cm away from the body surface. The median spectral irradiance of light received by each infant was: chest shield group 553 μW and control group 490 μW. Infants were nursed spending equal time alternating between the prone and supine position

PDA status at baseline: 40/54 (74%) had PDA on initial echocardiogram. Indomethacin treatment (40.7%) commenced at similar median time as phototherapy in both groups

Outcomes

Primary outcome: Incidence and severity of PDA assessed by serial echocardiographic examinations at 48 hours after commencement of phototherapy or cessation of phototherapy. Significant PDA requiring treatment defined as echocardiographic-confirmed PDA with left atrial to aortic root ratio > 1.4 or a ductal diameter > 1.5 mm with a left-to-right shunt

Indomethacin treatment reported as being pre-phototherapy

Reported: Mortality, intraventricular haemorrhage, days in hospital, days on respiratory support (continuous positive airway pressure), days of ventilation, days of phototherapy

Notes  
Risk of bias table
Bias Authors' judgement Support for judgement
Random sequence generation (selection bias) Low risk

"Randomisation was accomplished by a computer-generated random sequence. Infants stratified into < 27 weeks gestation and 27-28 weeks gestation..."

Allocation concealment (selection bias) Low risk

The investigators obtained informed written parental consent once the clinical team caring for the infant had determined that phototherapy was required. Allocation determined by selection of sequentially numbered, opaque envelopes

Blinding of participants and personnel (performance bias) High risk

Unlikely, did not report using 'sham' treatment. On-duty neonatologist made all management decisions, including decision to treat a PDA, independent of the research team

Blinding of outcome assessment (detection bias) Low risk

The ductal assessment was blinded by temporary cessation of phototherapy and removal of the chest shield immediately prior to the arrival of echocardiographers. The cardiologist reporting the scan was blinded to study group allocation

Incomplete outcome data (attrition bias) Low risk

No losses reported

Selective reporting (reporting bias) Low risk

Study was designed to assess whether chest shielding during phototherapy reduces the incidence and severity of PDA, as assessed by serial echocardiographic examinations. Ligation of PDA not reported as an outcome in publication

Other bias High risk

Some statistically non-significant but potentially clinically important baseline differences in sex (chest shield group: male 70% versus no shield: male 44%).

Premature stopping: initial sample size of 80 infants in each group was needed (ά = 0.05 and β = 0.2) to show a reduction in incidence of PDA by 33% after phototherapy. An interim analysis was planned at 1 year when approximately half this number was predicted to have enrolled. "The interim analysis showed that we were unlikely to find any difference between the groups and recommended that the study be stopped."

Footnotes

NICU: neonatal intensive care unit
PDA: patent ductus arteriosus

Characteristics of excluded studies

Kim 1997

Reason for exclusion

Historical control study

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References to studies

Included studies

Rosenfeld 1986

Rosenfeld W, Sadhev S, Brunot V, Jhaveri R, Zabaleta I, Evans H. Phototherapy effect on the incidence of patent ductus arteriosus in premature infants: prevention with chest shielding. Pediatrics 1986;78(1):10-4.

Travadi 2006

Travadi J, Simmer K, Ramsay J, Doherty D, Hagan R. Patent ductus arteriosus in extremely preterm infants receiving phototherapy: does shielding the chest make a difference? A randomised, controlled trial. Acta Paediatrica 2006;95(11):1418-23.

Excluded studies

Kim 1997

Kim HS, Kim EK, Lee HE, Lee YK, Park CH, Park KR, et al. Influence of phototherapy on incidence of patent ductus arteriosus in very low birth weight infants. Journal of Korean Pediatric Society 1997;40:1410-8.

Studies awaiting classification

None noted.

Ongoing studies

None noted.

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Other references

Additional references

American Academy of Pediatrics 2004

American Academy of Pediatrics Subcommittee on Hyperbilirubinemia. Management of hyperbilirubinemia in the newborn infant 35 or more weeks of gestation. Pediatrics 2004;114(1):297-316.

Barefield 1993

Barefield ES, Dwyer MD, Cassady G. Association of patent ductus arteriosus and phototherapy in infants weighing less than 1000 grams. Journal of Perinatology 1993;13(5):376-80.

Bell 1978

Bell MJ, Ternberg JL, Feigin RD, Keating JP, Marshall R, Barton L, et al. Neonatal necrotising enterocolitis. Therapeutic decisions based on clinical staging. Annals of Surgery 1978;187(1):1-7.

Benders 1999

Benders MJ, Van Bel F, Van de Bor M. Cardiac output and ductal reopening during phototherapy in preterm infants. Acta Paediatrica 1999;88(9):1014-9.

Bose 2007

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

Chung 2005

Chung MY, Fang PC, Chung CH, Huang CB, Ou Yang MH, Chen CC. Risk factors for hemodynamically-unrelated cystic periventricular leukomalacia in very low birth weight premature infants. Journal of the Formosan Medical Association 2005;104(8):571-7.

Clyman 1978

Clyman RI, Rudolph AM. Patent ductus arteriosus: a new light on an old problem. Pediatric Research 1978;12(2):92-4.

Davis 1995

Davis P, Turner-Gomes S, Cunningham K, Way C, Roberts R, Schmidt B. Precision and accuracy of clinical and radiological signs in premature infants at risk of patent ductus arteriosis. Archives of Pediatrics and Adolescent Medicine 1995;149(10):1136-41.

Ehrreich 1968

Ehrreich SJ, Furchgott RF. Relaxation of mammalian smooth muscles by visible and ultraviolet radiation. Nature 1968;218(5142):682-4.

Evans 1992

Evans N, Moorcraft J. Effect of patency of the ductus arteriosus on blood pressure in very preterm infants. Archives of Disease in Childhood 1992;67(10):1169-73.

Evans 1993

Evans N. Diagnosis of patent ductus arteriosis in the preterm newborn. Archives of Disease in Childhood 1993;68(1):58-61.

Furchgott 1991

Furchgott RF. Endothelium-dependent relaxation, endothelium-derived relaxing factor and photorelaxation of blood vessels. Seminars in Perinatology 1991;15(1):11-5.

Gagliardi 2008

Gagliardi L, Bellu R, Cardilli V, De Curtis M; Network Neonatale Lombardo. Necrotising enterocolitis in very low birth weight infants in Italy: incidence and non-nutritional risk factors. Journal of Pediatric Gastroenterology and Nutrition 2008;47(2):206-10.

Hammerman 1986

Hammerman C, Strates E, Valaitis S. The silent ductus: its precursors and its aftermath. Pediatric Cardiology 1986;7(3):121-7.

Hegyi 1981

Hegyi T, Brantley V, Hiatt IM. The effects of shielding the hepatic area on the clinical response to phototherapy. European Journal of Pediatrics 1981;137(3):303-5.

Higgins 2011

Higgins JPT, Green S (editors). Cochrane Handbook for Systematic Reviews of Interventions Version 5.1.0 [updated March 2011]. The Cochrane Collaboration, 2011. Available from www.cochrane-handbook.org.

Hunt 2004

Hunt RW, Evans N, Rieger I, Kluckow M. Low superior vena cava flow and neurodevelopment at 3 years in very preterm infants. Journal of Pediatrics 2004;145(5):588-92.

Kluckow 1996

Kluckow M, Evans N. Relationship between blood pressure and cardiac output in preterm infants requiring mechanical ventilation. Journal of Pediatrics 1996;129(4):506-12.

Kluckow 2000

Kluckow M, Evans N. Ductal shunting, high pulmonary blood flow, and pulmonary hemorrhage. Journal of Pediatrics 2000;137(1):68-72.

Mahajan 2006

Mahajan T, Chang A. Heart failure in the neonate. In: Chang A, Towbin J, editor(s). Heart Failure in Children and Young Adults. Philadelphia: Saunders Elsevier, 2006.

Maisels 1992

Maisels MJ. Neonatal jaundice. In: Sinclair JC, Bracken MB, editor(s). Effective Care of the Newborn Infant. Oxford University Press, 1992:515.

Maisels 1998

Maisels MJ, Kring EA, Klarr J. Comparison of the efficacy of two fibreoptic phototherapy blankets. Pediatric Research 1998;43(4):183A.

Miletin 2008

Miletin J, Dempsey EM. Low superior vena cava flow on day 1 and adverse outcome in the very low birthweight infant. Archives of Disease in Childhood. Fetal and Neonatal Edition 2008;93(5):F368-71.

Noori 2009

Noori S, McCoy M, Friedlich P, Bright B, Gottipati V, Seri I, et al. Failure of ductus arteriosus closure is associated with increased mortality in preterm infants. Pediatrics 2009;123(1):e138-44.

Osborn 2003

Osborn DA, Evans N, Kluckow M. Effect of early targeted indomethacin on the ductus arteriosus and blood flow to the upper body and brain in the preterm infant. Archives of Disease in Childhood. Fetal and Neonatal Edition 2003;88(6):F477-82.

Osborn 2007

Osborn DA, Evans N, Kluckow M, Bowen JR, Rieger I. Low superior vena cava flow and effect of inotropes on neurodevelopment to 3 years in preterm infants. Pediatrics 2007;120(2):372-80.

Papile 1978

Papile LA, Burstein J, Burstein R, Koffler H. Incidence and evolution of subependymal and intraventricular hemorrhage: a study of infants with birth weight less than 1500 grams. Journal of Pediatrics 1978;92(4):529-34.

Patz 1985

Patz A. The new international classification of retinopathy of prematurity. International Ophthalmology 1985;8(1):11-2.

Pladys 2001

Pladys P, Beuchee A, Wodey E, Treguier C, Lassel C, Betremieux P. Patent ductus arteriosus and cystic periventricular leukomalacia in preterm infants. Acta Paediatrica 2001;90(3):309-15.

RevMan 2012

Review Manager (RevMan) [Computer program]. Copenhagen: The Nordic Cochrane Centre, The Cochrane Collaboration, 2012.

Rojas 1995

Rojas MA, Gonzalez A, Bancalari E, Claure N, Poole C, Silva-Neto G. Changing trends in the epidemiology and pathogenesis of neonatal chronic lung disease. Journal of Pediatrics 1995;126(4):605-10.

Rubaltelli 1978

Rubaltelli FF, Zanardo V, Granati B. Effects of various phototherapy regimens on bilirubin decrement. Pediatrics 1978;61(6):838-41.

Scheidt 1987

Scheidt PC, Bryla DA, Hoffman HJ. Phototherapy and patent ductus arteriosus. Pediatrics 1987;80(4):593-4.

Shimada 1994

Shimada S, Kasai T, Konishi M, Fujiwara T. Effects of patent ductus arteriosis on left ventricular output and organ blood flows in preterm infants with respiratory distress syndrome treated with surfactant. Journal of Pediatrics 1994;125(2):270-7.

Sisson 1973

Sisson TR, Wickler M. Transmission of light through living tissue. Pediatric Research 1973;7:316.

Skelton 1994

Skelton R, Evans N, Smythe J. A blinded comparison of clinical and echocardiographic evaluation of the preterm infant for patent ductus arteriosus. Journal of Paediatrics and Child Health 1994;30(5):406-11.

Walsh 2003

Walsh MC, Wilson-Costello D, Zadell A, Newman N, Fanaroff A. Safety, reliability, and validity of a physiologic definition of bronchopulmonary dysplasia. Journal of Perinatology 2003;23(6):451-6.

Wong 2006

Wong RJ, DeSandre GH, Sibley E, Stevenson DK. Neonatal jaundice and liver disease. In: Martin RJ, Fanaroff AA, Walsh MC, editor(s). Neonatal-Perinatal Medicine: Diseases of the Fetus and Infant. 8th edition. Philadelphia: Elsevier, 2006:1419-65.

Other published versions of this review

Classification pending references

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Data and analyses

1 Chest shielding versus no treatment in unselected preterm infants

Outcome or Subgroup Studies Participants Statistical Method Effect Estimate
1.1 Haemodynamically significant PDA 1 74 Risk Ratio (M-H, Fixed, 95% CI) 0.23 [0.05, 1.01]
1.2 Any PDA - Echocardiographically detected 1 54 Risk Ratio (M-H, Fixed, 95% CI) 0.92 [0.52, 1.64]
1.3 Any PDA - Murmur detected 1 74 Risk Ratio (M-H, Fixed, 95% CI) 0.50 [0.29, 0.88]
1.4 Treatment with indomethacin 1 74 Risk Ratio (M-H, Fixed, 95% CI) 0.12 [0.02, 0.88]
1.5 Ductal ligation 1 74 Risk Ratio (M-H, Fixed, 95% CI) 0.35 [0.01, 8.36]
1.6 Mortality before discharge 2 128 Risk Ratio (M-H, Fixed, 95% CI) 1.68 [0.75, 3.78]
1.7 Mortality (<28 days of age) 1 74 Risk Ratio (M-H, Fixed, 95% CI) 1.06 [0.16, 7.10]
1.8 Days in oxygen 1 74 Mean Difference (IV, Fixed, 95% CI) -2.80 [-14.11, 8.51]
1.9 Days mechanical ventilation 1 74 Mean Difference (IV, Fixed, 95% CI) -5.10 [-14.94, 4.74]
1.10 Days in hospital 2 128 Mean Difference (IV, Fixed, 95% CI) -8.05 [-18.04, 1.94]
1.11 Intraventricular haemorrhage (any) 1 74 Risk Ratio (M-H, Fixed, 95% CI) 0.53 [0.10, 2.71]
1.12 Intraventricular haemorrhage grade 3 or 4 2 128 Risk Ratio (M-H, Fixed, 95% CI) 0.64 [0.22, 1.85]
1.13 Retinopathy of prematurity 1 74 Risk Ratio (M-H, Fixed, 95% CI) 0.53 [0.10, 2.71]
1.14 Exchange blood transfusion 1 74 Risk Ratio (M-H, Fixed, 95% CI) 0.70 [0.12, 3.97]
 

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Figures

Figure 1

Refer to Figure 1 caption below.

Risk of bias summary: review authors' judgements about each risk of bias item for each included study (Figure 1).

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Sources of support

Internal sources

  • No sources of support provided

External sources

  • Australasian Satellite of the Cochrane Neonatal Review Group, Australia
  • Editorial support of the Cochrane Neonatal Review Group has been funded with Federal funds from the Eunice Kennedy Shriver National Institute of Child Health and Human Development National Institutes of Health, Department of Health and Human Services, under Contract No. HHSN275201100016C, USA

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Appendices

1 CENTRAL search strategy

Searched March 2015, Retrieved = 5

  1. Patent ductus arteriosus (all text)
  2. Ductus (all text)
  3. #1 OR #2
  4. Shield
  5. #3 AND #4

2 MEDLINE search strategy

Searched March 2015, Retrieved = 3.

  1. exp Infant, Newborn/
  2. newborn.mp
  3. neonat$.mp
  4. #1 OR #2 OR #3
  5. patent ductus arteriosus.mp.
  6. exp Ductus Arteriosus, Patent/
  7. PDA.mp
  8. ductus.mp
  9. #5 OR #6 OR #7 OR #8
  10. Phototherapy.mp
  11. exp Phototherapy/
  12. #10 OR #11
  13. exp Radiation Protection/
  14. Chest Shield.mp
  15. #13 OR #14
  16. #4 AND #8 AND #9 AND #10

3 EMBASE search strategy

Searched March 2015, Retrieved = 5

  1. 'newborn'/exp
  2. neonat* AND [humans]/lim
  3. #1 OR #2
  4. chest'/exp
  5. shield
  6. #5 OR #6
  7. Phototherapy/exp8. Phototherapy 9. #8 OR #910. #3 AND #6 AND #9

This review is published as a Cochrane review in The Cochrane Library, Issue 11, 2015 (see http://www.thecochranelibrary.com External Web Site Policy for information). Cochrane reviews are regularly updated as new evidence emerges and in response to feedback. The Cochrane Library should be consulted for the most recent recent version of the review.