title: Postobstructive pulmonary edema: a case for hydrostatic mechanisms.
abstract: BACKGROUND
  Postobstructive pulmonary edema is a well-recognized complication of upper airway obstruction. The mechanisms of edema formation are unclear and may be due to increased hydrostatic forces generated by high negative inspiratory pressure or by increased permeability of the alveolar capillary membrane. Measurement of the edema fluid/plasma protein ratio and the rate of net alveolar fluid clearance are two well-validated methods for classifying the underlying mechanism of edema formation. The goal of the current study was to investigate the mechanisms of pulmonary edema formation in patients with postobstructive pulmonary edema by serial sampling of undiluted pulmonary edema fluid.
  
  
  METHODS
  A retrospective review of 341 patients who had pulmonary edema fluid collected prospectively after the acute onset of pulmonary edema. All patients had serial samples of edema fluid and plasma collected over the first 8 h after intubation.
  
  
  RESULTS
  Ten of the 341 patients with acute pulmonary edema were identified as having postobstructive pulmonary edema. The mean (+/- SD) edema fluid/plasma protein ratio in these patients was 0.54 +/- 0.15. The mean rate of alveolar fluid clearance over 8 h was 14.0 +/- 17.4% per hour. Nine of the 10 patients survived the hospitalization.
  
  
  CONCLUSIONS
  Measurement of the edema fluid/plasma protein ratio and the presence of net alveolar fluid clearance in 10 patients with postobstructive pulmonary edema supports a hydrostatic mechanism for edema fluid formation. The predominantly fast rates of alveolar fluid clearance may explain the rapid resolution of clinical postobstructive pulmonary edema that is typically described.
authors.affiliation: Division of Allergy, Pulmonary and Critical Care Medicine, Vanderbilt University, T1218 MCN, 1161 Twenty-First Ave S, Nashville, TN 37232-2650, USA. richard.fremont@vanderbilt.edu
authors.forename: Richard D
authors.initials: RD
authors.lastname: Fremont
authors.forename: Richard H
authors.initials: RH
authors.lastname: Kallet
authors.forename: Michael A
authors.initials: MA
authors.lastname: Matthay
authors.forename: Lorraine B
authors.initials: LB
authors.lastname: Ware
mesh_terms: D000293:Adolescent; D000328:Adult; D000402:Airway Obstruction / Q000150:complications*; D001798:Blood Proteins / Q000378:metabolism; D002199:Capillary Permeability / Q000502:physiology; D045604:Extracellular Fluid / Q000378:metabolism; D005260:Female; D006801:Humans; D006874:Hydrostatic Pressure; D001239:Inhalation / Q000502:physiology; D008297:Male; D008875:Middle Aged; D011650:Pulmonary Alveoli / Q000098:blood supply / Q000473:pathology / Q000503:physiopathology*; D011654:Pulmonary Edema / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology*; D015656:Respiratory Mechanics / Q000502:physiology*; D020545:Respiratory Mucosa / Q000098:blood supply / Q000473:pathology / Q000503:physiopathology; D012189:Retrospective Studies
chemical_list: D001798:Blood Proteins