Early versus delayed initiation of continuous distending pressure for respiratory distress syndrome in preterm infants

Ho JJ, Henderson-Smart DJ, Davis PG

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

Dates

Date edited: 14/03/2007
Date of last substantive update: 12/02/2002
Date of last minor update: 04/12/2006
Date next stage expected 15/10/2008
Protocol first published: Issue 4, 2000
Review first published: Issue 2, 2002

Contact reviewer

Prof Jacqueline J Ho
Senior Lecturer
Dept Paediatrics
University of Kuala Lumpur Royal College of Medicine Perak
Greentown
Ipoh
MALAYSIA
30450
Telephone 1: +60 5 2532635 extension: 154
Telephone 2: +60 5 2533333 extension: 2441
Facsimile: +60 5 2432636
E-mail: jho@pc.jaring.my
Secondary address:
Hospital Ipoh
Ipoh
MALAYSIA
30990
Telephone: +60 5 2533333 extension: 2441
Facsimile: +60 5 2531541

Contribution of reviewers

JJH conducted the search with input from DHS. JJH and DHS independently evaluated the trials and extracted the data. JJH entered the data and wrote the paper with input from the other two reviewers.

Internal sources of support

Royal College of Medicine Perak, MALAYSIA
Dept Paediatrics, Hospital Ipoh, MALAYSIA
Centre for Perinatal Health Services Research, University of Sydney, AUSTRALIA
Royal Prince Alfred Hospital, Sydney, AUSTRALIA
Royal Womens Hospital, Melbourne, AUSTRALIA

External sources of support

None

What's new

This review updates the existing review "Early versus delayed initiation of continuous distending pressure for respiratory distress syndrome in preterm infants," first published in The Cochrane Library, Issue 2, 2002 (Ho 2002).

The literature search was repeated on October 1, 2006 and no further studies eligible for inclusion were found.

The overall conclusions of the review have not changed.

Dates

Date review re-formatted: / /
Date new studies sought but none found: 01/10/2006
Date new studies found but not yet included/excluded: / /
Date new studies found and included/excluded: / /
Date reviewers' conclusions section amended: / /
Date comment/criticism added: / /
Date response to comment/criticisms added: / /

Text of review

Synopsis

Premature babies often lack the substance, surfactant, a detergent like substance produced by the lung. This causes their lungs to fail to expand properly at birth, and breathing in requires a big effort. If left untreated, breathing difficulty progressively worsens and it may cause damage to the lung. Continuous distending pressure (CDP) improves the expansion of the lung making it easier for the premature baby to breath. It is applied through a face mask, or into the nostrils or by a partial vacuum outside the chest. When applied early, it may also reduce the lung damage that causes chronic lung disease. Different ways of using CDP were assessed in six controlled trials (four randomized), and it was found that fewer infants who received early CDP had to go on to be treated with intermittent positive pressure ventilation.

No adverse effect of early use of CDP was found in these trials. However, there were several limitations to information from the studies, as the number of infants was small and the mean age ranged from seven to eighteen hours old when CDP was applied. Practice has changed from when these studies were done. CDP interventions are applied earlier, and surfactants are commonly given as well. Corticosteroids are given to the fetus before birth (antenatally) to prepare their lungs for birth.

Abstract

Background

The application of continuous distending pressure (CDP) has been shown to have some benefits in the treatment of preterm infants with respiratory distress syndrome (RDS). CDP has the potential to reduce lung damage, particularly if applied early before atelectasis has occurred. Early application of CDP may better conserve an infant's own surfactant stores and consequently be more effective than CDP applied later in the course of RDS.

Objectives

To determine if early compared with delayed initiation of CDP results in lower mortality and reduced need for intermittent positive pressure ventilation in preterm infants with RDS.

Search strategy

Selection criteria

Trials which used random or quasi-random allocation to either early or delayed CDP in spontaneously breathing preterm infants with respiratory distress syndrome.

Data collection & analysis

Standard methods of the Cochrane Collaboration and its Neonatal Review Group were used, including independent assessment of trial quality and extraction of data by two authors.

Main results

In six studies on a total of 165 infants, early CDP was associated with a significant reduction in subsequent use of intermittent positive pressure ventilation (IPPV), (typical RR 0.55, typical RD -0.16, NNT 6), but there was no evidence of effect on overall mortality. There was no evidence of effect on the rates of pneumothorax (five studies) or bronchopulmonary dysplasia (one study). Early CDP resulted in a reduction in duration of oxygen therapy in the single study reporting this outcome.

Reviewers' conclusions

Early application of CDP has a clinical benefit in the treatment of RDS in that it reduces subsequent use of IPPV and thus may be useful in preventing the adverse effects of this treatment. However, many of the trials were done in the 1970s and 1980s and re-evaluation of the strategy of early CDP in the era of antenatal steroid use and early surfactant administration is indicated focusing on administration methods.

Background

It is well known that primary surfactant deficiency is responsible for respiratory distress syndrome (RDS) in preterm infants (Avery 1959). This deficiency in surfactant results in low lung volumes, poor lung distensibility and atelectasis. The resulting hypoxia leads to increased pulmonary vascular resistance and right to left shunting (Gribetz 1959; Evans 1991). This exacerbates existing ventilation-perfusion abnormalities. The disease is also characterised by alveolar-capillary leakage, pulmonary oedema, and alveolar cell injury (Barter 1960). These lead to the formation of hyaline membranes seen on histological examination of diseased lungs.

Intermittent positive pressure ventilation (IPPV) without a positive end expiratory pressure was the first mode of assisted ventilation used for the treatment of RDS in preterm infants. When it became evident that low lung volume was a consequence of the disease, continuous distending pressure was developed as a means of increasing lung volume and improving oxygenation (Gregory 1971). Positive end expiratory pressure was also found to improve oxygenation in ventilated infants (Herman 1973; Cotton 1998).

The application of continuous distending pressure (CDP) either as continuous negative distending pressure (CNP) or continuous positive airway pressure (CPAP) has been shown to have some benefits in the treatment of preterm infants with RDS (Ho 2002). It was not clear whether the effectiveness of CDP is modified by birth weight or gestational age. However, in babies < 1000 g or < 28 weeks there may be insufficient respiratory drive for them to cope with CDP. Continuous distending pressure applied as nasal CPAP has been established in post-extubation care (Davis 2003). CDP improves lung function by reducing the work of breathing, normalizing lung volumes and improving ventilation-perfusion mismatch (Cogswell 1975; Saunders 1976; Richardson 1978; Cotton 1980; Field 1985; Harris 1996). CDP also conserves surfactant (Wyszogrodski 1975; Verder 1994). It splints the airways during expiration and thus reduces atelectasis in the surfactant-deficient lung (Miller 1990). It therefore has the potential to reduce lung damage seen in RDS, particularly if applied early before alveolar collapse occurs. Surfactant, a proven treatment for RDS, is more effective if applied early (Soll 2001; Yost 1999) suggesting the hypothesis that CDP by virtue of its properties may also be more effective if applied early.

The purpose of this review is to establish whether the early application of CDP has any benefit over later application in preterm infants with RDS. An earlier review on this subject has been done (Bancalari 1992).

Objectives

To determine if early compared with delayed initiation of CDP results in a lower mortality and reduced need for intermittent positive pressure ventilation in preterm infants with RDS.

Subgroup analyses were planned a priori on the basis of weight (with subdivisions at 1000 g and 1500 g) and gestation (with subdivisions at 28 and 32 weeks), the type of CDP (CPAP or CNP) and according to whether surfactant was used. Sensitivity analyses based on trial quality were also planned.

Criteria for considering studies for this review

Types of studies

Randomised or quasi-randomised controlled trials

Types of participants

Preterm infants (i.e. those < 37 weeks) with respiratory distress syndrome breathing spontaneously at trial entry prior to the application of any assisted ventilation other than for resuscitation at birth.

Types of interventions

Early CDP (commencing at randomization) delivered by nasal prongs, mask, single nasopharyngeal tube, endotracheal tube or a continuous negative pressure delivered via a pressure chamber enclosing the thorax, compared with a policy of delayed CDP [initiated at FiO2 (fraction of inspired oxygen) of approximately 0.6 or more] compared to standard care.

Types of outcome measures

Primary

Failure - death or use of intermittent positive pressure ventilation (IPPV) prior to hospital discharge
Mortality (first 28 days of life and prior to discharge)
Use of IPPV prior to discharge

Secondary

Air leak (pneumothorax, pneumomediastinum, or pulmonary interstitial emphysema).
Intraventricular haemorrhage (IVH) (any or grades 3 or 4)
Necrotising enterocolitis (NEC) (Bell criteria stage 2, (Bell 1978))
Retinopathy of prematurity (ROP) (any or stage 3 and greater)
Bronchopulmonary dysplasia (BPD) (oxygen dependency at 28 days)
Chronic lung disease (CLD) (oxygen dependency at 36 weeks postmenstrual age)
Long-term growth and neurodevelopmental outcome (cerebral palsy and abnormal mental development < 2 SD below the mean on a standardised score)

Search strategy for identification of studies

The standard search strategy of the Cochrane Neonatal Review Group was used. This included searches of the Oxford Database of Perinatal Trials, Cochrane Central Register of Controlled Trials (CENTRAL, The Cochrane Library, Issue 3 2006), MEDLINE (1966 to September week 4, 2006), all languages), previous reviews including cross-references and abstracts. The MEDLINE search terms used were newborn, neonate, respiratory distress syndrome, hyaline membrane disease, continuous distending pressure, continuous distending airway pressure, continuous positive airway pressure, continuous positive transpulmonary pressure, continuous transpulmonary pressure, continuous inflating pressure, continuous negative distending pressure, continuous negative pressure or continuous airway pressure.

Methods of the review

Identified trials were reviewed independently by each reviewer for methodological quality. Criteria used for assessment of quality were blinding of randomization, blinding of treatment, completeness of follow-up and blinding of assessment of outcomes. Agreement was reached by consensus. Two reviewers extracted the data independently.

Data were synthesised using the standard method of the Cochrane Neonatal Review Group. Relative risk (RR), risk difference (RD), and number needed to treat (NNT) or number needed to harm (NNH) derived from 1/RD were used for categorical outcomes, and weighted mean difference (WMD) was used for continuous outcomes. For each measure of effect the 95% confidence interval was calculated. A fixed affects model was applied for the meta-analysis. Heterogeneity was examined using the I-squared statistic.

Description of studies

Eight studies involving a total of 251 infants were identified. One of these studies identified was the quasi-random study of John 1976 and co-workers that excluded patients after allocation who died or required mechanical ventilation. Data on excluded patients were not available; thus, treatment effects on none of the primary outcomes specified in this review are available from this study. This study was excluded. One further study, (Tooley 2003), involving 42 infants was excluded as infants were randomised after intubation and administration of surfactant to extubation and application of nasal CPAP or continued conventional ventilation.

The included studies were all carried out in the pre-surfactant era (Allen 1977,Gerard 1975, Hegyi 1981, Krouskop 1975, Mockrin 1975, Rowe 1978). All infants required clinical and radiological evidence of RDS for trial entry. The FiO2 required at entry ranged from 0.3 or more to 0.7 or more. Early CDP was initiated at trial entry and late CDP was initiated if further deterioration occurred at an FiO2 ranging from 0.5 up to 1.0. This FiO2 was given to maintain the partial pressure of oxygen of 50 mm Hg in four studies, 60 in one study and 100 in one study. Thus there was considerable variation and overlap in the criteria used for initiating early and late CDP.

Of the six studies included in the review, two used CNP (Gerard 1975; Mockrin 1975), one used face mask CPAP (Allen 1977) and three used binasal CPAP (Hegyi 1981; Krouskop 1975; Rowe 1978). One study (Hegyi 1981) addressed the overall objectives and was included although the criterion for delayed CDP was based on an FiO2 of 0.5 rather than the strict 0.6 prespecified. Post hoc the protocol has been altered to make the criteria less narrow by inserting approximately 0.6 or more in the criteria for delayed CDP.

The primary outcome measure for all studies was use of IPPV and mortality. The point in time at which mortality was measured was not specified in any of the studies, although the age of death for each individual death was given in two of the trials. The combined outcome of death before discharge or subsequent use of IPPV was not given in any of the trials. Five studies reported the incidence of pneumothorax (Allen 1977, Gerard 1975, Hegyi 1981, Mockrin 1975, Rowe 1978), one reported bronchopulmonary dysplasia (undefined) (Rowe 1978), and one reported retinopathy of prematurity (Krouskop 1975) as secondary outcomes. One study did a subgroup analysis of mortality on very low birth weight infants (Krouskop 1975). Duration of oxygen therapy in survivors (time period of survival not stated) was reported in one study (Allen 1977). This was not a prespecified outcome measure but was included post hoc as it was considered an important secondary outcome.

Methodological quality of included studies

All the studies were controlled trials. Five studies were randomized. Of these five, one (Gerard 1975) used concealed allocation (sealed envelopes). It was not clear whether the allocation was concealed in the other four studies. One study used random numbers (Mockrin 1975) and in two other studies the method of randomisation was not stated (Allen 1977; Rowe 1978). Hegyi 1981 used hospital number to randomize, but the way in which this was done is not clear. The remaining study (Krouskop 1975) was quasi-random in part. They used a sequential design where the first eight matched pairs were randomized to treatment group using sealed envelopes but subsequent infants were allocated alternately.

There was no blinding of the intervention or the outcome assessment in any of the studies. There was complete follow-up of randomised patients in all studies. Only two studies stated how many of the potentially eligible infants were entered (Gerard 1975, Hegyi 1981).

Results

Six studies (Allen 1977; Gerard 1975; Hegyi 1981; Krouskop 1975; Mockrin 1975; Rowe 1978) involving 165 infants met the entry criteria and were included in the analysis.

PRIMARY OUTCOMES

Use of IPPV (Outcome 01-01):
None of the six individual trials showed that early vs delayed CDP caused a significant reduction in the requirement for IPPV. However, the meta-analysis of all six trials supports a reduction in use of IPPV in the early CDP group that was statistically significant and clinically important [typical RR 0.55 (0.32, 0.96), RD -0.16 (-0.28, -0.03), NNT 6 (4, 33)].

Subgroup analyses by type of CDP was done for the four studies using CPAP and the two studies using CNP. Early CDP caused a significant reduction in use of IPPV in the two studies using CNP [typical RR 0.12 (0.02, 0.85), RD -0.36 (-0.58, -0.14), NNT 3 (2, 7)], but not in the four studies using CPAP [typical RR 0.77 (0.43, 1.38), typical RD -0.08 (-0.23, 0.08)].

Mortality (Outcome 01-02):
Mortality (explicitly specified as mortality prior to discharge) prior to discharge was not reported in any of the studies. For mortality (time not specified) there was no significant effect of early CDP in any of the six individual trials or in the pooled estimate [typical RR 0.68 (0.34, 1.38), typical RD -0.07 (-0.18, 0.04)]. In the subgroup analysis by type of CDP there was no evidence of effect on mortality.

Mortality at 28 days (Outcome 01-03):
There was no significant effect of early CDP on mortality at 28 days in the two studies that reported this [typical RR 0.93(0.13, 6.81)].

Failure
None of the trials reported failure as we defined it, i.e. death or subsequent use of IPPV.

SECONDARY OUTCOMES

There was no significant effect of early CDP on the rate of pneumothorax (outcome 01-04) (five trials) or BPD (Outcome 01-10) at 28 days (one trial, Rowe 1978). The number of days on oxygen (Outcome 01-05) in survivors, assessed in one trial (Allen 1977), was reduced in the early CDP group [MD -1.70 (-3.27, -0.13)]. A further study (Rowe 1978) found no difference in the time spent in FIO2 > 0.3 or > 0.7. The outcomes IVH, NEC, and CLD at 36 weeks were not reported in any of the studies nor was there follow up assessment of physical growth, neurodevelopmental outcome or cerebral palsy in any of the studies. One study (Krouskop 1975) reported no cases of ROP (Outcome 01-11) in either group. In subgroup analysis by type of CDP there was no evidence of effect on pneumothorax.

Subgroup Analysis by Birthweight (Outcome 01-08):
One study (Krouskop 1975) did a subgroup analysis by birthweight using subgroups < 1500 g and 1500 g or more. There were no deaths in either group for infants 1500 g or more. Among infants <1500 g there was no significant effect of early CDP in use of IPPV [typical RR 1.00 (0.45, 2.23)] or mortality [typical RR 1.00 (0.45, 2.23)], but only a very small number of patients were analysed.

Sensitivity Analysis
Excluding the quasi-random study of Krouskop did not change the conclusion that early compared with delayed CDP reduces use of IPPV.

Discussion

The results of this review suggest that in preterm infants with RDS, early compared with delayed application of CDP is effective in reducing subsequent use of IPPV. This is clinically important, as IPPV is associated with increased costs and adverse effects.

However, caution is required in interpreting these results as the sample size is small and the studies were all performed in the pre-surfactant era when the use of antenatal steroids was not common. These interventions could reduce baseline risk and hence the effect size that CDP may have on RDS. The mean birth weight and gestation of the treatment groups ranged from 1545 to 2113 g and 31 to 34 weeks, considerably higher than the major group of infants receiving treatment for RDS in current practice. The age at application of early CDP ranged from a mean of 7.1 to 18 hours, later than what would currently be considered early intervention for the treatment of RDS (Narendran 2003; Tooley 2003). In addition there was wide variation in the criteria used for initiating early and late CDP and some overlap between the intervention and control groups as well as no blinding of treatment or outcome assessment.

We have included any type of CDP irrespective of the mode of delivery. Included trials used CNP and CPAP delivered by face mask or nasal prongs. In this review the studies using CNP showed a reduction in treatment failure but this was not seen in the studies using CPAP. Airway resistance is increased with CPAP compared with CNP so this difference may be plausible. Indeed recently differences in efficacy between CPAP devices have been described (De Paoli 2003) and direct comparison of CNP with other methods of applying CDP may be warranted.

Pneumothorax occurred in more than 10% of infants in the CDP subgroup. This is higher than would be expected today (Verder 1999). There was no evidence of effect of early CDP on the rate of pneumothorax. The one small study that looked at BPD did not find any effect but there is insufficient evidence to draw any conclusion. The rates of ROP, NEC and post discharge outcomes were not reported in any study.

Reviewers' conclusions

Implications for practice

There is some evidence that early application of CDP has a clinical benefit in the treatment of RDS in that it reduces subsequent use of IPPV and thus may be useful in preventing the adverse effects of this treatment.

However the applicability of these findings to the current practice of neonatal intensive care is uncertain given that the trials in this review were all conducted in the pre-surfactant era when antenatal steroid usage was uncommon and infants were higher birth weights, gestations and older than those currently treated for RDS.

Implications for research

Revaluation of the strategy of early CDP in the era of antenatal steroid and surfactant administration is indicated. However, as CDP is now a standard practice the main thrust for research in this area should be towards establishing the preferred mode, level of pressure and timing of CDP use. These studies should also attempt to answer the question about the preferred timing, dose and mode of administration of surfactant when used in conjunction with CDP.

Acknowledgements

Potential conflict of interest

None

Characteristics of included studies

Study	Methods	Participants	Interventions	Outcomes	Notes	Allocation concealment
Allen 1977	Concealment of allocation unclear, no blinding of intervention or outcome assessment, follow-up complete	24 infants with clinical and radiological RDS not previously ventilated and PaO2 < 60 mm Hg on FIO2 > 0.6	Face mask CPAP 5-10 cm H2O at allocation vs CPAP or IPPV for PaO2 < 50 mm Hg in FIO2 > 0.95	Use of IPPV, mortality (time not specified), pneumothorax, days in O2		B
Gerard 1975	Allocation concealed using sealed envelopes, no blinding of intervention or outcome assessment, complete follow-up	23 infants > 1000 g, with clinical & radiological RDS, spontaneously breathing, PaCO2 < 70 mm Hg and FIO2 >0.4 but < 0.8 to maintain PaO2 above 40 mm Hg	CNP 5-12 cm H2O at allocation vs CNP for PaO2 < 100 mm Hg in FIO2 1.0	Use of IPPV, mortality (time not specified), pneumothorax		A
Hegyi 1981	Randomised by hospital number, concealment of allocation unclear. No blinding of intervention or outcome assessment. Complete follow-up	38 (13 study & 25 control) preterm infants with clinical & radiological RDS requiring FIO2 0.3 or greater to maintain PaO2 > 50 mm Hg	Nasal prong CPAP at 6 cm H20 at allocation vs CPAP at FIO2 0.5 or more to maintain PaO2 > 50 mm Hg	Use of IPPV, mortality (time not specified), mortality at 28 days, pneumothorax	Reason for inequality in group sizes not stated. The way in which the hospital number was used for randomization was not clear.	B
Krouskop 1975	Matched on admission for birthweight and age. Allocation randomized for first 8 pairs (sealed envelope), but alternate allocation for rest. No blinding of intervention or outcome assessment. Follow-up complete	21 infants with clinical and radiological RDS, PaO2 < 60 mm Hg in FIO2 0.4 on 2 occasions within 1 hour	8-14 cm H20 nasal prong CPAP on allocation vs nasal prong CPAP for PaO2 < 60 mm Hg in FIO2 0.7	Use of IPPV, required use of IPPV < 1500 g, required use of IPPV >= 1500 g, mortality (time not specified), mortality < 1500 g, mortality >= 1500 g		C
Mockrin 1975	Random numbers used in allocation, concealment of allocation unclear. No blinding of intervention or outcome assessment. Complete follow-up	23 infants (10 early and 13 late) with RDS diagnosed on clinical, blood gas and xray evidence), < 24 hours of age, spontaneously breathing and PaO2 between 50 and 100 mm Hg on 70% oxygen	CNP starting at 8 and increasing as required to 15 cm H2O at allocation vs for PaO2 < 50 mm Hg in FIO2 0.7	Use of IPPV, mortality (time not specified), mortality at 28 days, pneumothorax		B
Rowe 1978	Concealment of allocation not clear. No blinding of intervention or outcome assessment. Complete follow-up.	36 infants with RDS and PaO2 < 50 mm Hg in FIO2 >0.4	Nasal prong CPAP at allocation vs at PaO2 < 50 mm Hg in FIO2 > 0.7	Use of IPPV, mortality (time not specified), pneumothorax, bronchopulmonary dysplasia	Data from conference abstract. Author clarification sought re definition of BPD	B

Characteristics of excluded studies

Study	Reason for exclusion
John 1976	Quasi-random study of 42 infants 29 weeks or more with RDS. Deaths and those requiring mechanical ventilation were excluded post-allocation.
Tooley 2003	The study of 42 infanats included infants of 25 to 28 weeks gestation who were all intubated at birth, given a single dose of surfactant and positive pressure ventilation then randomised at about one hour of age to extubation to nasal CPAP or to continued conventional IPPV. No criteria for the diagnosis of RDS were given.

References to studies

References to included studies

Allen 1977 {published data only}

Allen AP, Reynolds EOR, Rivers RPA, Le Souef PN, Wimberley PD. Controlled trial of continuous positive airway pressure given by face mask for hyaline membrane disease. Archives of Disease in Childhood 1977;52:373-8.

Gerard 1975 {published data only}

Gerard P, Fox WW, Outerbridge EW, Beaudry PH, Stern L. Early versus late introduction of continuous negative pressure in the management of the idiopathic respiratory distress syndrome. Journal of Pediatrics 1975;87:591-5.

Hegyi 1981 {published data only}

Hegyi T, Hiatt IM. The effect of continuous positive airway pressure on the course of respiratory distress syndrome: The benefits of early initiation. Critical Care Medicine 1981;9:38-41.

Krouskop 1975 {published data only}

Krouskop RW, Brown EG, Sweet AY. The early use of continuous positive airway pressure in the treatment of idiopathic respiratory distress syndrome. Journal of Pediatrics 1975;87:263-6.

Mockrin 1975 {published data only}

Mockrin LD, Bancalari EH. Early versus delayed initiation of continuous negative pressure in infants with hyaline membrane disease. Journal of Pediatrics 1975;87:596-600.

Rowe 1978 {unpublished data only}

Rowe JC, Guthrie RD, Hinkes P, Prueitt J, Murphy J, Woodrum DZ, Hodson WA. Time of initiation of CPAP in HMD (Abstract ). Pediatric Research 1978;12:533.

References to excluded studies

John 1976 {published data only}

John E, Thomas DB, Burnard ED. Influence of early introduction of continuous postive pressure breathing on the course of hyaline membrane disease. Australian Paediatric Journal 1976;12:276-80.

Tooley 2003 {published data only}

Tooley J, Dyke M. Randomized study of nasal continuous positive airway pressure in the preterm infant with respiratory distress syndrome. Acta Paediatrica 2003;92:1170-4.

* indicates the primary reference for the study

Other references

Additional references

Avery 1959

Avery ME, Mead J. Surface properties in relation to atelectasis and hyaline membrane disease. American Journal of Diseases of Children 1959;97:517.

Bancalari 1992

Bancalari E, Sinclair JC. Mechanical ventilation. In: Sinclair JC, Bracken MB, editor(s). Effective Care of the Newborn Infant. Oxford: Oxford University Press, 1992:200-20.

Barter 1960

Barter RA, Maddison TG. The nature of the neontal pulmonary hyaline membrane. Archives of Disease in Childhood 1960;25:460.

Bell 1978

Bell MJ, Ternberg JL, Feigin RD, Keating JP, Marshall R, Barton L, Brotherton T. Neonatal necrotizing entercolitis. Therapeutic decisions based upon clinical staging. Annals of Surgery 1978;187:1-7.

Cogswell 1975

Cogswell JJ, Hatch DJ, Kerr AA. Effects of continuous positive airway pressure on lung mechanics of babies after operation for congenital heart disease. Archives of Disease in Childhood 1975;50:799-804.

Cotton 1980

Cotton RB, Lindstrom DP, Kanarek KS, Sundell H, Stahlman MT. Effect of positive-end-expiratory-pressure on right ventricular output in lambs with hyaline membrane disease. Acta Paediatrica Scandinavica 1980;69:603-6.

Cotton 1998

Cotton RB. Pathophysiology of hyaline membrane disease (excluding surfactant). In: Polin RA, Fox WW, editor(s). Fetal and Neonatal Physiology. 2nd edition. Philadelphia: WB Saunders, 1998:1165-74.

Davis 2003

Davis PG, Henderson-Smart DJ. Nasal continuous positive airways pressure immediately after extubation for preventing morbidity in preterm infants. Cochrane Database of Systematic Reviews 2003, Issue 2.

De Paoli 2003

De Paoli AG, Davis PG, Faber B, Morley CJ. Devices and pressure sources for administration of nasal continuous airway pressure (NCPAP) in preterm neonates. Cochrane Database of Systematic Reviews 2003, Issue 3.

Evans 1991

Evans NJ, Archer LN. Doppler assessment of pulmonary artery pressure and extrapulmonary shunting in the acute phase of hyaline membrane disease. Archives of Disease in Childhood 1991;66:6-11.

Field 1985

Field D, Milner AS, Hopkins EK. Effects of positive end expiratory pressure during ventilation of the preterm infant. Archives of Disease in Childhood 1985;60:21-68.

Gregory 1971

Gregory GA, Kitterman JA, Phibbs RH, Tooley WH, Hamilton WK. Treatment of the idiopathic respiratory distress syndrome with continuous positive airway pressure. New England Journal of Medicine 1971;284:1333-40.

Gribetz 1959

Gribetz I, Frank NR, Avery ME. Static volume-pressure relations of excised lungs of infants with hyaline membrane diesase, newborn and stillborn infants. Journal of Clinical Investigation 1959;38:2168-75.

Harris 1996

Harris TR, Wood ER. Physiologic principles. In: Goldsmith JP, Karotkin EH, editor(s). Assisted ventilation. 3rd edition. Philadelphia: WB Saunders, 1996:21-68.

Herman 1973

Herman S, Reynolds EOR. Methods of improving oxygenation in infants mechanically ventilated for severe hyaline membrane disease. Archives of Disease in Childhood 1973;48:612-7.

Ho 2002

Ho JJ, Subramaniam P, Henderson-Smart DJ, Davis PG. Continuous distending pressure for respiratory distress syndrome in preterm infants. Cochrane Database of Systematic Reviews 2002, Issue 2.

Miller 1990

Miller MJ, DiFiore JM, Strohl KP, Martin RJ. Effects of nasal CPAP on supraglottic and total pulmonary resistance in preterm infants. Journal of Applied Physiology 1990;68:141-6.

Narendran 2003

Narendran V, Donovan EF, Hoath SB, Akinbi HT, Steichen JJ, Jobe AH. Early bubble CPAP and outcomes in ELBW preterm infants. Journal of Perinatology 2003;23:195-9.

Richardson 1978

Richardson CP, Jung AL. Effects of continuous positive airway pressure on pulmonary function and blood gases of infants with respiratory distress syndrome. Pediatric Research 1978;12:771-4.

Saunders 1976

Saunders RA, Milner AD, Hopkin IE. The effect of CPAP on lung mechanics and lung volumes in the neonate. Biology of the Neonate 1976;29:178-81.

Soll 2001

Soll RF, Morley CJ. Prophylactic versus selective use of surfactant for preventing morbidity and mortality in preterm infants. Cochrane Database of Systematic Reviews 2001, Issue 2.

Verder 1994

Verder H, Richardson B, Griesen G, Ebbesen F, Albertsen P, Lundstrom K, Jacobsen T. The Danish-Swedish multicentre study group. Surfactant therapy and respiratory distress syndorme. New England Journal of Medicine 1994;331:1051-5.

Verder 1999

Verder H, Albertson P, Ebbesen F, Griesen G, Robertson B, Bertelsen A, Agertoft L, Djernes B, Natha E, Reinholdt J.. Nasal contiuous positive pressure and early surfactant therapy for respiratory distress syndrome in newborns less than 30 weeks gestation. ePediatrics 1999:http//www.pediatrics.org/cgi/content/full/103/2/e24.

Wyszogrodski 1975

Wyszogrodski I, Kyei-Aboagye K, Taeusch HW Jr, Avery ME. Surfactant inactivation by hyperventilation: conservation by end-expiratory pressure. Journal of Applied Physiology 1975;38:461-6.

Yost 1999

Yost CC, Soll RF. Early versus delayed selective surfactant treatment for neonatal respiratory distress syndrome. Cochrane Database of Systematic Reviews 1999, Issue 4.

Other published versions of this review

Ho 2002b

Ho JJ, Henderson-Smart DJ, Davis PG. Early versus delayed initiation of continuous distending pressure for respiratory distress syndrome in preterm infants. Cochrane Database of Systematic Reviews 2002, Issue 2.

Ho 2005

Comparisons and data

Comparison or outcome	Studies	Participants	Statistical method	Effect size
01 Early vs late CDP
01 Use of IPPV	6	165	RR (fixed), 95% CI	0.55 [0.32, 0.96]
02 Mortality (time not specified)	6	165	RR (fixed), 95% CI	0.68 [0.34, 1.38]
03 Mortality at 28 days	2	61	RR (fixed), 95% CI	0.93 [0.13, 6.81]
04 Pneumothorax	5	144	RR (fixed), 95% CI	0.84 [0.37, 1.91]
05 Duration of oxygen in survivors (days)	1	20	WMD (fixed), 95% CI	-1.70 [-3.27, -0.13]
06 Use of IPPV below 1500 g	1	8	RR (fixed), 95% CI	1.00 [0.45, 2.23]
07 Use of IPPV 1500 g or more	1	13	RR (fixed), 95% CI	Not estimable
08 Mortality (time not specified) below 1500 g	1	8	RR (fixed), 95% CI	1.00 [0.45, 2.23]
09 Mortality (time not specified) 1500 g or more	1	13	RR (fixed), 95% CI	Not estimable
10 Bronchopulmonary dysplasia	1	36	RR (fixed), 95% CI	1.12 [0.08, 16.52]
11 Retinopathy of prematurity	1	21	RR (fixed), 95% CI	Not estimable
02 Early vs late CDP - excluding Krouskop 1975 (quasi-random)
01 Use of IPPV	5	144	RR (fixed), 95% CI	0.49 [0.26, 0.90]
02 Mortality (time not specified)	5	144	RR (fixed), 95% CI	0.59 [0.26, 1.36]

01 Early vs late CDP

01.01 Use of IPPV

01.01.01 CPAP

01.01.02 CNP

01.02 Mortality (time not specified)

01.02.01 CPAP

01.02.02 CNP

01.03 Mortality at 28 days

01.03.01 CPAP

01.03.02 CNP

01.04 Pneumothorax

01.04.01 CPAP

01.04.02 CNP

01.05 Duration of oxygen in survivors (days)

01.06 Use of IPPV below 1500 g

01.07 Use of IPPV 1500 g or more

01.08 Mortality (time not specified) below 1500 g

01.09 Mortality (time not specified) 1500 g or more

01.10 Bronchopulmonary dysplasia

01.11 Retinopathy of prematurity

02 Early vs late CDP - excluding Krouskop 1975 (quasi-random)

02.01 Use of IPPV

02.01.01 CPAP

02.01.02 CNP

02.02 Mortality (time not specified)

02.02.01 CPAP

02.02.02 CNP

Contact details for co-reviewers

Dr Peter G Davis
Department of Obstetrics and Gynaecology
Royal Women's Hospital
132 Grattan Street
Carlton
Victoria AUSTRALIA
3053
Telephone 1: +61 3 93442151
Facsimile: +61 3 93471761
E-mail: pgd@unimelb.edu.au

Prof David J Henderson-Smart
Director
NSW Centre for Perinatal Health Services Research
Queen Elizabeth II Research Institute
Building DO2
University of Sydney
Sydney
NSW AUSTRALIA
2006
Telephone 1: +61 2 93517318
Telephone 2: +61 2 93517728
Facsimile: +61 2 93517742
E-mail: dhs@perinatal.usyd.edu.au

This review is published as a Cochrane review in The Cochrane Library, Issue 2, 2007 (see http://www.thecochranelibrary.com 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 version of the review.