Intraalveolar fibrin deposition is a prominent histologic feature of neonatal respiratory distress syndrome (RDS). We hypothesized that in infants in whom RDS progresses into CLD, chronic inflammation of the airway would derarrange alveolar-capillary integrity and lead to prolonged fibrin deposition in the alveolar spaces. To test this hypothesis, we determined concentrations of inflammatory cells (neutrophils,N, and macrophages, M,) and products of fibrin turnover (D-dimers) in the bronchoalveolar lavage (BAL) fluid of infants who initially had RDS and developed CLD than infants who had uncomplicated RDS. Methods: twenty-three preterm infants who required mechanical ventilation because of RDS underwent BAL on day 1 of life and thereafter every other day during endotracheal intubation. The samples collected on dexamethasone admninistration were not included. After cell counts were made, BAL fluids were centrifuged and D-dimers measured (ELISA).Results: Fourteen patients (EG: 27wks±2, BW:805g±187) developed CLD (02≥28 days) and 9 did not (EG:28wks±2, BW: 899g±166). Median values ± SD of N and D-dimers are shown below. M counts did not statistically differ between the two groups of infants.*p<0.05 Table
We conclude that extravascular fibrin deposition and degradation occurs beyond the early stage of RDS in infants who develop CLD, in association with inflammation of the airways. Because fibrin and its degradation products may modulate the tissue repair by altering vascular tone, impairing surfactant function, stimulating fibroblast and neutrophil migration, we speculate that persistent fibrin turover in the airways can be a mechanism that contributes to the development of CLD.
