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Abstract Background--Monitoring activity on the neonatal unit is important for planning service provision and as part of monitoring quality of care. The dependency level of the patients cared for must [...]

Abstract Aims--To assess survival and neurodevelopmental outcome following prolonged ventilation beyond 27 or 49 days of postnatal life in neonates treated with antenatal steroids and surfactant. Methods--The medical records of [...]

AIM: To compare indices of respiratory failure in terms of their ability to predict adverse respiratory outcomes in preterm infants. The indices evaluated were: (a) the alveolar-arterial oxygen tension difference (A-aDO(2)); (b) the ratio of arterial to alveolar oxygen tension (a/A ratio); (c) the oxygenation index (OI); (d) the fractional inspired oxygen concentration (FIO(2)). METHODS: Details of respiratory support and arterial blood gas data in the first 24 hours of life were collected in ventilated infants below 34 weeks gestation. The worst single value of a particular index in the first 24 hours was chosen to quantify the severity of respiratory failure in each infant. Receiver operating characteristic curves were constructed and areas under the curve (AUC) calculated to compare the performance of the indices in predicting death from respiratory failure and/or the development of chronic lung disease (CLD). RESULTS: A total of 155 preterm infants were studied, of whom 35 (23%) died primarily from respiratory failure and 53 of the 120 survivors (44%) developed CLD. The overall performance of the four indices in predicting death from respiratory failure ranged from 0. 77 (AUC for maximum FIO(2)) to 0.88 (AUC for minimum a/A ratio). The corresponding AUCs for gestational age and birth weight were 0.75 and 0.76 respectively. In contrast, demographic variables tended to perform better than indices of respiratory failure in predicting CLD/death. CONCLUSIONS: There was no evidence of a significant difference between the performance of the a/A ratio, A-aDO(2), and OI in predicting adverse respiratory outcomes. Use of the OI is recommended because of its ease of calculation.

A prospective, blind study was carried out to determine: the amount of blood submitted for culture from neonates; whether small blood volumes resulted in false negative results; and whether there was a temporal relation between volume of blood cultured and time to positivity. Seventy three bottles were evaluated. They contained a median of 0.63 ml of blood. Twenty nine bottles (39.7%) contained less than 0.5 ml of blood; 21 bottles (28.8%) were positive. There were three false negative cultures, only one of which contained a blood volume below 0.5 ml. The median time to positivity was 22.4 hours. There was no correlation between blood volume cultured and time to positivity. Neonatal cultures frequently contain less than 0.5 ml of blood. False negative cultures are rare. Neonatal blood culture bottles need to be validated for blood volumes below 0.5 ml.

BACKGROUND: Pulmonary arterial pressure (PAP) is raised in preterm infants with respiratory distress syndrome who subsequently develop chronic lung disease. The natural history of pulmonary hypertension in infants with chronic lung disease is unknown. OBJECTIVES: To investigate changes in PAP, assessed non-invasively using Doppler echocardiography, in infants with chronic lung disease during the 1st year of life. METHODS: Serial examinations were performed in infants with chronic lung disease and healthy preterm infants. The Doppler derived acceleration time to right ventricular ejection time ratio (AT/RVET) was calculated from measurements made from the pulmonary artery velocity waveform. RESULTS: A total of 248 examinations were performed in 54 infants with chronic lung disease and 44 healthy preterm infants. The median AT/RVET was significantly lower in infants with chronic lung disease than in healthy preterm infants (0.31 v 0.37). AT/RVET significantly correlated with age corrected for prematurity in both infants with chronic lung disease (r = 0.67) and healthy infants (r = 0.55). There was no significant difference between the rate of change in AT/RVET between the two groups. In infants with chronic lung disease, multivariate analysis showed that AT/RVET was significantly independently associated with age and inversely with duration of supplemental oxygen treatment. Median AT/RVET was significantly lower in infants with chronic lung disease until 40-52 weeks of age corrected for prematurity. CONCLUSIONS: Although PAP falls with increasing age in both infants with chronic lung disease and healthy preterm infants, it remains persistently raised in infants with chronic lung disease until the end of the 1st year of life.

BACKGROUND: There is controversy over whether improved survival of preterm infants has resulted in a higher incidence of severe (grade 3 or greater) retinopathy of prematurity (ROP). AIM: To compare survival rates and rates of > or = stage 3 ROP-that is, with a high risk of sequelae-in preterm infants in five English cities where, anecdotally, the incidence of ROP is reported to show considerable variation. METHODS: All infants of birth weight < 1500 g and or gestational age < 32 weeks, born in 1994 in one of the cities or transferred in within 48 hours, were studied. The populations were adjusted for case mix variation using CRIB (clinical risk index for babies, a disease severity scoring system). The incidence of severe ROP, the actual death rate, and that adjusted for disease severity were determined. RESULTS: The rate of severe ROP per 1000 births was higher in city 1 than in all the other cities. This increase in comparison with city 2 and city 4 was significant (city 1, 167 (95% confidence interval (CI) 96 to 260); city 2, 24 (6 to 59); city 4, 16 (1 to 84)). A significant difference was not seen between city 1 and cities 3 (23 (1 to 120)) and 5 (74 (21 to 79)). The relative risk of developing severe ROP in city 1 compared with all the other cities was 5.5 (2.5 to 11.9). The actual death rate per 1000 births in city 1 was significantly lower than that predicted by modelling death against CRIB score (city 1: actual 270; predicted 385 (95% CI 339 to 431)). In contrast, the other cities had actual death rates as predicted, or worse than predicted, by CRIB. INTERPRETATION: A significantly higher incidence of severe ROP was identified in one of the five cities studied. Variation in survival rates among high risk infants may explain this observation.

AIM: To compare patient triggered, with conventional fast rate, ventilation in a randomised controlled trial using the incidence of chronic lung disease as the primary outcome measure. METHODS: Three hundred and eighty six preterm infants with birthweights from 1000 to 2000 g, and requiring ventilation for respiratory distress syndrome within 24 hours of birth, were randomised to receive either conventional or trigger ventilation with the SLE 2000 ventilator. RESULTS: There were no significant differences in the incidence of chronic lung disease (28 day and 36 week definitions), death, pneumothorax, intraventricular haemorrhage, number of ventilator days, or length of oxygen dependency between groups. CONCLUSIONS: Patient triggered ventilation in preterm infants with respiratory distress syndrome is feasible. No significant differences, when compared with conventional fast rate ventilation in important medium and longer term outcome measures, were evident.

AIM: To determine whether individualised limits for arterial oxyhaemaglobin saturation by pulse oximetry (SpO(2)) are more effective for detecting hypoxia and hyperoxia in sick newborn infants than setting fixed limits. METHODS: Six hundred and ninety two simultaneous measurements of SpO(2) and partial pressure of oxygen in arterial blood (PaO(2)) were made in 95 infants. The sensitivity and specificity for predicting hypoxia and hyperoxia using various fixed SpO(2) limits and also individualised SpO(2) limits, calculated using a standard equation, were determined and compared. RESULTS: None of the fixed limits for SpO(2) was both sensitive and specific for predicting hypoxia and/or hyperoxia. There was no difference between these and individualised limits. CONCLUSION: Individualised SpO(2) limits are no more effective than fixed SpO(2) limits for predicting hypoxia and/or hyperoxia in sick newborn infants. SpO(2) monitoring is not an ideal method for assessing PaO(2).

AIM: To construct a reference range of SpO2 values in healthy preterm infants using a simple data logging device. METHODS: Thirty three healthy preterm infants were monitored for a continuous period of 4 hours at rest using an Ohmeda Biox 3700 E Pulse Oximeter and an electronic data logger (Rustrack Ranger). Stored data were downloaded and saved as individual files on a personal computer. RESULTS: The study group median and 5th and 95th percentiles were used to construct a cumulative frequency curve of time against SpO2 value, representing the normal reference range of SpO2 profiles in healthy preterm infants. CONCLUSION: Comparison of an infant's SpO2 profile against this curve may be more helpful in guiding supplemental oxygen treatment in that individual than a figure for a mean SPO2 and its standard deviation.

AIM: To determine if pulmonary artery pressure (PAP) in ventilated preterm infants is independently associated with the development of chronic lung disease (CLD) and whether early assessment has any prognostic value. METHODS: Two cohorts (development n = 55; and validation n = 28) of preterm infants were studied at 24 hours of age. PAP was assessed non-invasively using its inverse correlation with the corrected acceleration time to right ventricular ejection time ratio (AT:RVET(c)), calculated from the pulmonary artery Doppler waveform. Clinical and respiratory variables were also collected. Using logistic regression analysis to identify factors independently associated with CLD, a prognostic score was developed to predict CLD. The ability of the score to predict CLD was described using receiver operating characteristic (ROC) curves. RESULTS: Birthweight, inspired oxygen concentration, and AT:RVET(c) were independently predictive of CLD. The area under the ROC curve was 0.96 for the development and 0.89 for the validation cohort. Exclusion of AT:RVET(c) resulted in a reduction to 0.88 and 0.73, respectively. CONCLUSION: PAP is independently associated with CLD. An early assessment of PAP using AT:RVET(c) may permit the early prediction of CLD as part of a multifactorial scoring system.

AIM: To investigate changes in various cardiorespiratory variables with inhaled nitric oxide (NO), as part of a randomised controlled trial. METHODS: Infants were treated with inhaled NO for 72 hours. Changes in oxygenation were assessed using the oxygenation index (OI). Serial changes in pulmonary artery pressure (PAP) were assessed using the Doppler derived acceleration time to right ventricular ejection time ratio (AT:RVET). Doppler measurements of right ventricular output, pulmonary blood flow, and systolic PAP was performed in a subset of infants. RESULTS: Twenty infants received inhaled NO and 22 acted as controls. Infants were treated at a median dose of 5 (range 5 to 20) ppm. There was a fall in median OI by 17% in treated infants within 30 minutes of treatment. The fall in OI in treated infants was significantly different from the response in controls until 96 hours. Infants treated with inhaled NO showed a rapid response with a median rise in AT:RVET of 0.04 (range -0.06 to 0.12) within 30 minutes. The change in AT:RVET was significantly different from controls until 4 hours. Median systolic PAP also fell in treated infants by 6.1 (range -14.4 to -4.4) mm Hg within 1 hour. Changes in OI were significantly associated with changes in PBF (r = 0.44), but not with changes in AT:RVET. CONCLUSION: Treatment with inhaled NO rapidly improves oxygenation and lowers PAP in preterm infants. However, these effects are transient and treatment does not influence long term outcome.

AIM: To determine whether treatment with inhaled nitric oxide (NO) and/or dexamethasone reduces the incidence of chronic lung disease (CLD) and/or death in high risk preterm infants. METHODS: Infants below 32 weeks of gestation were recruited at 96 hours of age if they were deemed to be at high risk of developing CLD. Infants were randomly assigned to one of four treatment groups using a factorial design: (1) 5-20 parts per million inhaled NO for 72 hours; (2) 0.5-1 mg/kg/day intravenous dexamethasone for 6 days; (3) both drugs together; (4) continued conventional management. RESULTS: Forty two infants were randomised: 10 infants received inhaled NO alone; 11 dexamethasone alone; 10 both treatments; and 11 neither treatment. There was no difference in the combined incidence of CLD and/or death before discharge from hospital between either infants treated with inhaled NO and controls (RR 1.05, 95% CI 0.84-1.25), or those treated with dexamethasone and controls (RR 0.95, 95% CI 0.79-1.18). CONCLUSIONS: At 96 hours of age, neither treatment with inhaled NO nor dexamethasone prevented CLD or death.

AIM: To determine the consequences of renal calcification in preterm infants. METHODS: A cohort of 11 preterm babies was studied at the age of 4 to 5 years. They had had renal calcification as neonates. Seventeen matched controls were also studied. Each child had a renal ultrasound scan, a calcium load test, and a desmopressin test for renal concentrating ability (RCA). The study group also had glomerular filtration rate (GFR) estimated, using the height:creatinine ratio, and tubular phosphate reabsorption, without phosphate load, per glomerular filtration rate (Tp/GFR) calculated, RESULTS: In the study group the median GFR was 61 ml/min/1.73m2 (range 46-79 ml/min/1.73m2) and the median calculated Tp/GFR SD score was -0.94 (range -2.8-0.68). Five children out of the study group had ultrasonic evidence of renal calcification. There was no significant difference between the two groups in renal size, calciuria, before or after calcium load, or RCA. Eight children (three patients, five controls) had an abnormal calcium load test. The RCA of the children in the study and control groups combined was below that of published values, with a median calculated SD score -0.71 (95% CI -1.21 to -0.23). CONCLUSIONS: There was evidence of renal dysfunction in children who had been born preterm. Renal calcification detected in the neonatal period does not seem to be a major predisposing factor for the abnormalities of renal function subsequently observed in these infants.