Home oxygen for children: who, how and when?

A review of the specific requirements of home oxygen therapy in children which attempts to offer guidance to clinicians and service providers

Secondary Surfactant Dysfunction and Deficiency

Based on literature in Adult Respiratory Distress Syndrome in humans and evidence of surfactant activation in vitro and vivo, and our clinical observations of secondary respiratory decompensation in premature infancies recovering from RDS, a study was designed to look at the possibility of benefit from secondary surfactant administration in premature infancies with secondary decompensation after recovery from respiratory distress syndrome (RDS). A prospective pilot study was performed to study the effects of secondary surfactant administration on oxygenation, ventilation and pulmonary function of neonates who had respiratory decompensation after recovery from RDS. A secondary data analysis was performed looking at pulmonary function related to ventilatory efficiency index (VEI), modified ventilatory index (MVI) and respiratory severity score (RSS). Entry criteria included infants admitted with RDS who were 7 days to 3 months of age, with birth weights ≥ 500 grams. Infants qualified if they demonstrated recovery from RDS with a secondary respiratory decompensation defined prospectively as an acute pulmonary decompensation after 6 days of age, which was non-cardiac in origin and accompanied by diffuse parenchymal lung disease on chest x-ray, in conjunction with sustained increase in fraction of inspired oxygen (FiO2; ≥20%) and mean airway pressure (MAP; ≥2 cm) above base-line for at least 4 hours prior to surfactant administration. Infants meeting all enter criteria received surfactant within four hours of the qualifying decompensation and again 12 hours later. Oxygenation, ventilation and pulmonary function were compared before and after administration at 12 and 24 hours. Twenty neonates qualified for secondary surfactant administration. The PCO2, pH, MAP, FiO2, MVI and RSS all improved significantly at 12 and 24 hours after surfactant administration. Infants who received Curosurf had improvement in pH and PCO2 within 2 hours of surfactant administration. The rates of adverse events were low. These findings suggest that secondary surfactant administration may be effective in reducing short term oxygen and ventilatory requirements and improving pulmonary function in neonates who have a respiratory decompensation after recovery from initial RDS. Secondary surfactant replacement may improve outcomes in this subset of patients and further randomized controlled trials are needed to confirm these preliminary findings

Origins of neonatal intensive care in the UK

Chaired by Professor Robert Boyd, this seminar reviewed the development and changes in care of the newborn in the UK over the past 50 years. Advances in techniques were described, such as mechanical ventilation, total parenteral nutrition and continuous monitoring of vital signs, to care for ill or vulnerable newborn infants. Diagnostic techniques that were developed and introduced in the 1970s and early 1980s were discussed, such as ultrasound imaging, magnetic resonance spectroscopy and imaging and near infrared spectroscopy, for the non-invasive investigation of the brain, as well as the setting up of neonatal intensive care units. Witnesses include: Professor Eva Alberman, Dr Herbert Barrie, Professor Richard Cooke, Dr Beryl Corner, Dr Pamela Davies, Professor John Davis, Professor David Delpy, Professor Victor and Dr Lilly Dubowitz, the late Professor Harold Gamsu, Professor David Harvey, Professor Colin Normand, Professor Tom Oppé, Professor Osmund Reynolds, Dr Jean Smellie, Professor Maureen Young and nurses, including Miss Anthea Blake, Miss Caroline Dux and Miss Mae Nugent. Introduction by Professor Peter Dunn, viii, 84pp, 1 chart, glossary, subject and name index

A Model Analysis of Arterial Oxygen Desaturation during Apnea in Preterm Infants

Rapid arterial O2 desaturation during apnea in the preterm infant has obvious clinical implications but to date no adequate explanation for why it exists. Understanding the factors influencing the rate of arterial O2 desaturation during apnea () is complicated by the non-linear O2 dissociation curve, falling pulmonary O2 uptake, and by the fact that O2 desaturation is biphasic, exhibiting a rapid phase (stage 1) followed by a slower phase when severe desaturation develops (stage 2). Using a mathematical model incorporating pulmonary uptake dynamics, we found that elevated metabolic O2 consumption accelerates throughout the entire desaturation process. By contrast, the remaining factors have a restricted temporal influence: low pre-apneic alveolar causes an early onset of desaturation, but thereafter has little impact; reduced lung volume, hemoglobin content or cardiac output, accelerates during stage 1, and finally, total blood O2 capacity (blood volume and hemoglobin content) alone determines during stage 2. Preterm infants with elevated metabolic rate, respiratory depression, low lung volume, impaired cardiac reserve, anemia, or hypovolemia, are at risk for rapid and profound apneic hypoxemia. Our insights provide a basic physiological framework that may guide clinical interpretation and design of interventions for preventing sudden apneic hypoxemia