Hydrostatic mechanisms may contribute to the pathogenesis of human re-expansion pulmonary edema.

Abstract

The primary objective was to test the hypothesis that clinical re-expansion pulmonary edema is predominantly due to increased permeability of the alveolar-capillary barrier. A secondary objective was to determine if the alveolar epithelium was functionally intact in patients with re-expansion pulmonary edema by measuring net alveolar epithelial fluid transport in a subset of patients. Retrospective study of mechanically ventilated patients with re-expansion pulmonary edema. Two academic tertiary care hospitals. Seven patients with acute onset of re-expansion pulmonary edema after tube thoracostomy or thoracentesis. Pulmonary edema fluid and plasma were collected at the time of onset of re-expansion edema. Contrary to our hypothesis, the mean initial edema fluid to plasma protein ratio was 0.58+/-0.21, supporting a hydrostatic mechanism of edema formation. Four of the patients had an initial edema fluid to plasma protein ratio of less than 0.65, consistent with pure hydrostatic pulmonary edema, while the others had a slight increase in permeability (edema fluid to plasma ratios of 0.67, 0.71 and 0.77), perhaps due to capillary stress failure from hydrostatic stress. Alveolar fluid clearance (mean 9.8+/-8.0%/h) was intact in the subset of three patients in whom it was measured. This study provides the first direct evidence that hydrostatic forces may contribute to the development of re-expansion pulmonary edema.