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

OBJECTIVE

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.

DESIGN

Retrospective study of mechanically ventilated patients with re-expansion pulmonary edema.

SETTING

Two academic tertiary care hospitals.

PATIENTS

Seven patients with acute onset of re-expansion pulmonary edema after tube thoracostomy or thoracentesis.

INTERVENTIONS

Pulmonary edema fluid and plasma were collected at the time of onset of re-expansion edema.

MEASUREMENTS AND RESULTS

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.

CONCLUSIONS

This study provides the first direct evidence that hydrostatic forces may contribute to the development of re-expansion pulmonary edema.