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Assessment of pulmonary function in resolving chronic lung disease of prematurity
1Department of Respiratory Paediatrics, Royal Hospital for Sick Children, Edinburgh.
Insights
Early measurements of alveolar-arterial difference in oxygen and PaCO2 in premature infants can predict long-term lung function. This helps assess chronic lung disease of prematurity (CLD) severity for early interventions.
Area of Science:
- Neonatology
- Pediatric Pulmonology
- Respiratory Physiology
Background:
- Chronic lung disease of prematurity (CLD) presents significant challenges in long-term respiratory health.
- Longitudinal assessment of interstitial and airway disease is crucial for understanding CLD progression.
Purpose of the Study:
- To investigate longitudinal changes in interstitial and airway disease in infants with resolving CLD.
- To identify early predictors of pulmonary dysfunction at one year of age in preterm infants.
Main Methods:
- Studied 33 infants from 35-40 weeks postconceptional age, with follow-ups for one year.
- Measured mean arterial oxygen saturation (MSaO2), its variability (delta MSaO2), PaCO2, PaO2, and calculated alveolar-arterial difference in oxygen ((A-a) DO2(50)).
- Assessed airway disease using partial forced expiratory flow volume curves (PEFC) to determine Vmax Frc.
Main Results:
- Significant improvements in all measured parameters were observed within the first three months.
- An (A-a) DO2(50) > 29 kPa and PaCO2 > 7 kPa at 35-40 weeks postconceptional age predicted an MSaO2 < 90% at one year with high sensitivity and specificity.
- Combined criteria demonstrated a perfect sensitivity and specificity for predicting pulmonary dysfunction at one year.
Conclusions:
- Alveolar-arterial difference in oxygen and PaCO2 measurements in early infancy can predict pulmonary dysfunction at one year.
- Quantifying CLD severity using these parameters can serve as a measurable endpoint for neonatal intervention studies.
Aim:
To investigate the longitudinal changes of interstitial and airways disease in resolving chronic lung disease of prematurity (CLD).
Methods:
Thirty three infants were studied between 35 and 40 weeks of postconceptional age, and then at three monthly intervals throughout their first year. Measurements of mean arterial oxygen saturation (MSaO2) and its variability (delta MSaO2) were recorded. PaCO2 and PaO2 were determined while the infants breathed steady state 50% oxygen via a hood. From these, the alveolar arterial difference (A-a) DO2(50) was calculated. Airway disease was assessed by the measurement of partial forced expiratory flow volume curves (PEFC) to give Vmax Frc.
Results:
The cohort mean +/- 95% confidence intervals measured between 35 and 40 weeks were for MSaO2 (89.25 +/- 1.87%, range 75-96.5%) and delta MSaO2 (4.79 +/- 0.8%, range 0.16-9.64%), PaCO2 (5.89 +/- 0.56 kpa, range 4.2-10.11 kpa), (A-a) DO2(50) (22.7 +/- 2.56 kpa, range 6.67-31.4 kpa) and VmaxFrc (41.5 +/- 8.65 mls/second, range 8.5-103.7 ml/second). The most significant improvement in all measurements occurred within the first three months (P = 0.05). An MSaO2 of less than 90% in room air at 1 year of age was predicted between 35 and 40 weeks postconceptional age by an (A-a) DO2(50) of greater than 29 kpa, with a sensitivity of 0.85 and a specificity of 0.88, and a PaCO2 greater than 7 kpa predicted a specificity of 0.78 and a sensitivity of 0.88. Predictions were strengthened by combining the above criteria and these then gave a sensitivity and specificity of 1.
Conclusion:
Measurements of (A-a) DO2(50) and PaCO2 taken between 35 and 40 weeks can be used to assess the degree of pulmonary dysfunction at 1 year. Quantification of the severity of CLD could be used as a measurable end point for early neonatal intervention studies.
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