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  1. Ben Stenson, Associate editor

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CHRONIC LUNG DISEASE SYMPOSIUM

Promises alone do not seduce Professor Greenough. In the first of four articles on management issues in chronic lung disease of prematurity she provides a concise review of the evidence base for the many new ventilation modes available and concludes that we shouldn't adopt them into routine practice until they are proven to be efficacious. Likewise pulmonary function testing. Schibler and Frey describe the currently available techniques and the complexities of their interpretation. Measurements are getting easier and this offers new insights into neonatal ventilator care but there are many pitfalls and we await evidence that we can use them to improve outcomes. Kotecha and Allen nail their colours to the mast over supplemental oxygen treatment, recommending that infants with established chronic lung disease who are not at risk of further progression of retinopathy of prematurity should have their saturations maintained above 94%. Abman discusses the monitoring of cardiovascular function and the potential to influence hypoxia associated pulmonary hypertension and also recommends target saturations of 94–96%. There is widespread variation in practice and adopting this guidance in all units would place large numbers of additional infants in oxygen and increase substantially the use of home oxygen. Results from a prospective, blinded randomised multicentre trial (BOOST) may soon put their beliefs to the test. See p 2

LINE MANAGEMENT

Do you know what proportion of percutaneously inserted long lines in your unit are removed because of concerns about infection? How many of them are eventually shown to have been infected? What about antibiotics through the line—do they work? Hodge and Puntis review the evidence and offer some recommendations. See p 21

SHAKING UP TROUBLE

Williams and Sutherland remind us of the background to the hypothesis that vigorous chest physiotherapy in extreme preterm infants may provide a mechanism for severe brain injury if excessive head movement is not avoided. No new data are provided and in an accompanying commentary, Rosenbloom and Ryan provide forceful criticism of the hypothesis. See p 29 and p 30

MORE ON POSTNATAL STEROIDS

Nicholl and colleagues randomised 16 infants with chronic lung disease to receive either systemic dexamethasone or inhaled budesonide for 10 days. Budesonide treated infants did not demonstrate the shrinkage in leg length that was observed with dexamethasone. They didn't demonstrate shrinking oxygen requirements either. Romagnoli and colleagues add to the follow up data from randomised controlled trials of postnatal dexamethasone treatment. No excess morbidity was apparent in their 30 infants. Many trials have not reported follow up outcomes so the risk estimates for later impairments remain uncertain. Beresford and colleagues observed no positive effect on the incidence of respiratory symptoms in infants with chronic lung disease during a year of treatment with inhaled fluticasone in a small placebo-controlled trial that was stopped early because of poor recruitment. See p 55, p 59, and p 62

RESISTANCE WORK

There is not yet an adequate clinical evidence base for selecting one nasal continuous positive airway pressure device over another. One factor which may be important is the resistive work of breathing imposed by the device. De Paoli and colleagues measured the resistance of a series of devices and found substantial variations between devices. See p 42

POSTHAEMORRHAGIC HYDROCEPHALUS

Most neonatologists encounter few infants with posthaemorrhagic ventricular dilatation. Heep and colleagues demonstrate increased collagen turnover in the cerebrospinal fluid of affected infants suggesting that the pathogenesis may in part relate to arachnoid fibrosis. Because the results of early intervention are disappointing clinicians tend to avoid intervention in the hope the problem will arrest. Murphy and colleagues describe the natural history of the condition in those infants who are still alive at 14 days of age. Of 221 VLBW infants who developed intraventricular haemorrhage (IVH) between 1994 and 1997, 56 (25%) developed progressive ventricular dilatation (PVD). Spontaneous arrest occurred in 21/56 and arrest after non-surgical treatment in a further eight. Surgical intervention was considered necessary in 19/56 and took place on median day of life 35 (range 4–147). Death occurred in 10/56. Most PVD (80%) occurred in infants with grade 3/IV IVH and no infant with lesser IVH required surgery. See p 34 and p 37

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