Archives of Disease in Childhood - Fetal and Neonatal Edition Reviews

Designing the new UK-WHO growth charts to enhance assessment of growth around birth

Cole, T. J., Wright, C. M., Williams, A. F., RCPCH Growth Chart Expert Group — 2012-04-17T05:21:33-07:00

The decision to adopt the new WHO standard in the UK necessitated substantial changes to the neonatal section of the chart, including separation of the preterm UK birth weight reference from the WHO standard. The evidence-based design process has led to several novel features that could be generally applied in other chart designs, and revealed uncertainties leading to inconsistencies in charting. Failing to plot the birth weight of term infants at age 0 can lead to spurious centile crossing in the early weeks of life, particularly among infants at the extreme of gestation. Users will need training to use the charts, but this should improve overall understanding and the use of charts.

The management of neonatal pulmonary hypertension

Dhillon, R. — 2012-04-17T05:21:33-07:00

Most neonates with clinically significant pulmonary hypertension (PH) will have either persistent PH of the newborn (PPHN) or bronchopulmonary dysplasia. Cyanotic congenital heart disease must be actively ruled out as part of the differential diagnosis of PPHN. The maintenance of ductal patency with prostaglandins E1 or E2 in cases of doubt is safe and potentially beneficial given their pulmonary vasorelaxant properties. Specific tools in the treatment of PPHN include modern ventilatory strategies, inhaled nitric oxide, sildenafil, prostacyclin and extracorporeal membrane oxygenation.

Rarely will a cardiac lesion be primarily responsible for neonatal PH although pulmonary vein stenosis and the persistence of an arterial duct must be considered, particularly in the older preterm baby with bronchopulmonary dysplasia.

Management of posthaemorrhagic ventricular dilatation

Whitelaw, A., Aquilina, K. — 2012-04-17T05:21:33-07:00

Intraventricular haemorrhage and posthaemorrhagic ventricular dilatation remain an important challenge in the management of prematurity and are associated with significant permanent morbidity. Progressive ventricular dilatation causes white matter injury by pressure, distortion, free radical injury and inflammation. Therapeutic interventions include serial lumbar punctures, only useful when the ventricles remain in communication with the lumbar subarachnoid space, and repeated aspiration through a ventricular access device. Reduction of cerebrospinal fluid production by acetazolamide and frusemide in a large multicentre randomised trial showed a worse outcome in the treated arm. A trial of drainage, irrigation and fibrinolytic therapy did not demonstrate a reduced need for permanent cerebrospinal fluid diversion, but did show a significant reduction in severe cognitive disability at two years. Ventriculoperitoneal shunting is indicated when the ventricles continue to enlarge at a body weight of around 2.5 kg and cerebrospinal fluid protein levels are below 1.5 g /L.

This review summarises current concepts on the pathophysiology and management of posthaemorrhagic ventricular dilatation, underlining clinical challenges and ongoing research.

Although the percentage of small preterm infants developing intraventricular haemorrhage (IVH) has been greatly reduced in the last three decades, increased survival of very immature infants has meant that large IVH with subsequent posthaemorrhagic ventricular dilatation is still a serious unsolved problem.