Prophylaxis of early adrenal insufficiency did not improve survival without BPD in the overall study population; however, treatment of chorioamnionitis-exposed infants significantly decreased mortality and improved survival without BPD. Low-dose hydrocortisone therapy did not suppress adrenal function or compromise short-term growth. The combination of indomethacin and hydrocortisone should be avoided.

The severity of NEC and its systemic signs and symptoms are not due to a deficiency of counterregulatory cytokines. In fact, mean concentrations of IL-1ra in NEC are higher than what has been reported in other populations. The cytokines IL-8, IL-1ra, and IL-10 are released later or more slowly after a stimulus and may be more useful in identifying, within hours of symptom onset, which infant will develop significant NEC.

BACKGROUND. Low cortisol concentrations in premature infants have been correlated with increased severity of illness, hypotension, mortality, and development of bronchopulmonary dysplasia. A total of 360 mechanically ventilated infants with a birth weight of 500 to 999 g were enrolled in a randomized, multicenter trial of prophylaxis of early adrenal insufficiency to prevent bronchopulmonary dysplasia. Mortality and bronchopulmonary dysplasia were decreased in the hydrocortisone-treated patients exposed to chorioamnionitis. We now report outcomes at 18 to 22 months' corrected age.

End-tidal CO2 monitoring in NICU patients is as accurate as capillary or transcutaneous monitoring but less precise than the latter. It may be useful for trending or for screening patients for abnormal arterial CO2 values.

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Ventilator-induced lung injury in children and adults is characterized by an initial inflammatory phase. To investigate whether the inflammatory cytokine, IL-1, plays a role in this process, a rabbit model of ventilator-induced injury was created. Animals maintained under pentobarbital anesthesia were primed for injury by undergoing lung lavage with 22 mL/kg of saline and then ventilated for 8 h with either FIO2 0.21 and normal pressures or FIO2 1.0 and high ventilator pressures. The animals exposed to hyperoxia/hyperventilation demonstrated a greater increase in lung lavage neutrophil counts and a higher histological injury score, as well as a faster decline in oxygenation compared to the control animals. A third group of rabbits received 800 micrograms of recombinant IL-1 receptor antagonist after lung lavage and prior to the exposure to FIO2 1.0 and high ventilator pressures. These animals had significantly lower concentrations of albumin and elastase and lower neutrophil counts in their lungs after the 8-h ventilatory period compared to hyperoxia/hyperventilation rabbits. IL-1 blockade had no effect on the decline in dynamic compliance and oxygenation seen in saline-treated hyperoxic/hyperventilated rabbits. IL-1 is a mediator of acute inflammation due to ventilator-induced lung injury.

Summary. Tracheobronchomalacia (TBM) is increasingly recognized in infants, children, and adults with acquired chronic lung diseases as the use of flexible bronchoscopy has become widely established in spontaneously breathing patients. However, the lack of a reliable method to quantify the severity of the airway collapse has made serial studies, evaluation of therapies, and comparisons between patients difficult. The purpose of this study was to describe a method of quantifying airway collapse in TBM. The degree of airway collapse was quantitated by measuring the ratio of the smallest to the largest airway area during a respiratory cycle. The videotape of flexible bronchoscopy was run through a video monitor and frozen at the appropriate times. The airway circumference was then traced onto plastic overlays and the area measured. The videotapes of seven infants and children with TBM and eight with normal airways were reviewed by investigators who did not know the diagnosis. Intra-observer variability was 2.2%, and interobserver variability was 1.4%. The mean smallest/largest airway ratio was 0.34 ? 0.14 (SD) in the subjects with known TBM, compared with a ratio of 0.82 2 0.08 (SD) in children with a normal airway (P < 0.0001). The range in the children with TBM was 0.22-0.61, whereas for the control children it was 0.73-0.93. In this series, there was no overlap in the ratios between affected and unaffected patients. In addition to the manual method of calculating airway area ratios, a computer-assisted method is described that could be adapted to real-time use. This way of analyzing the degree of airway collapse could be used to assess patients with TBM quantitatively and reproducibly.

Objectives: To determine if tracheal lavage concentrations of the transcription factor NF-kB, which is activated by risk factors associated with bronchopulmonary dysplasia (BPD) and induces expression of cytokines associated with BPD, is related to BPD in premature infants. Design: Serial tracheal lavage samples from intubated premature infants were analysed for cell count and concentrations of interleukin (IL)8 and NF-kB, corrected for dilution by secretory component concentrations. Setting: Level III university hospital neonatal intensive care unit. Patients: Thirty three intubated infants (mean (SD) birth weight 903 (258) g, median gestation 27 weeks (range 24-31)) in the first 14 days of life. Main outcome measures: Tracheal effluent NF-kB, IL8, and cell counts, corrected for dilution by secretory component measurement. Results: Square root transformed NF-kB concentrations were significantly related to signs of inflammation (cell count, p = 0.002; IL8, p = 0.019) and to simultaneous fraction of inspired oxygen in samples from the first 3 days of life (r = 0.512, p,0.003). Of the 32 subjects with samples in the first 3 days of life, the half who either died or had BPD had higher NF-kB concentrations than those without BPD (square root concentration 0.097 (0.043) v 0.062 (0.036) mg/mg protein/mg secretory component, p = 0.018). Conclusions: Tracheobronchial lavage NF-kB concentrations are related to lung inflammation, oxygen exposure, and pulmonary outcome in intubated preterm infants. NF-kB activation may be an early critical step leading to BPD. B ronchopulmonary dysplasia (BPD) occurs primarily in premature infants who are mechanically ventilated and exposed to oxygen early in their life. It is associated with early inflammation of the airways and lung interstitium, ), which are raised in tracheobronchial lavage obtained from patients who progressed to BPD. Expression of these mediators is partially controlled through the activation of transcription factors. These are proteins that, on appropriate stimulation, attach to a recognition sequence in the promoter region of specific genes.6 One of these transcription factors is nuclear factorkappa B (NF-kB).NF-kB, a ubiquitous transcription factor, promotes the expression of many genes, including proinflammatory cytokines associated with the development of BPD. It is activated by a variety of factors, including infectious stimuli, inflammatory cytokines, deformation, oxidants, and other causes of cell stress.7 8 It has roles in controlling apoptosis and cell proliferation and differentiation 9 and may be involved in lung development. 10Activation of NF-kB occurs in many inflammatory conditions both in vivo and in vitro. Lung macrophages from adults at risk of acute respiratory distress syndrome had significantly more activated NF-kB than from those who did not develop acute respiratory distress syndrome.11 NF-kB activation was higher in monocytes and neutrophils in adults with fatal systemic inflammatory response than in those who survived. 12As NF-kB is activate...