BRONCHOALVEOLAR LAVAGE FLUID CHARACTERISTICS OF EARLY INTERMEDIATE AND LATE PHASES OF ARDS - ALTERATIONS IN LEUKOCYTES, PROTEINS, PAF AND SURFACTANT COMPONENTS

Objective: To determine the concentration of proteins and phospholipid s, markers of inflammatory reaction such as platelet-activating factor (PAF), and cell alterations in bronchoalveolar lavage (BAL) fluid dur ing the evolution of the acute respiratory distress syndrome (ARDS). D esign: Prospective controlled study. Setting: 14-bed medical-surgical intensive care unit in a 750-bed university teaching hospital. Patient s: 19 mechanically ventilated patients, 9 patients with ARDS and 10 pa tients without cardiopulmonary disease (controls), were eligible for t his study. Interventions: BAL was performed during the early, intermed iate, and late phases of ARDS. Measurements and results: Total phospho lipids and individual phospholipid classes of the surfactant, proteins , PAF, and cells were measured. High levels of PAF, an increase in neu trophils and proteins, and quantitative as well as qualitative alterat ions in phospholipids in BAL fluid were observed in ARDS patients comp ared to the control group. PAE proteins, and neutrophils were higher i n early ARDS than in intermediate or late ARDS. The surfactant pool in creased in the early phase and decreased in the intermediate or late p hase of the syndrome. The qualitative alterations of surfactant consis t of reduced phospholipid content in the surfactant structures with go od surface properties; moreover, there was a considerable decrease in the percentage of phosphatidylcholine and phosphatidylglycerol, follow ed by an increase in phosphatidylethanolamine, phosphatidylserine, pho sphatidylinositol, and sphingomyelin in all three phases of ARDS compa red to the control group. Lysophosphatidylcholine was detectable only in late ARDS. Conclusion: Total surfactant phospholipids, surfactant c omponents, and inflammatory markers such as PAF, cells, and proteins w ere affected in patients with ARDS, These factors, undergoing quantita tive alterations during the course of ARDS, could have a significant r ole in the pathogenesis and evolution of ARDS.