title: Evidence for a hydrostatic mechanism in human neurogenic pulmonary edema.
abstract: OBJECTIVE
  To identify the relative contribution of hydrostatic and permeability mechanisms to the development of human neurogenic pulmonary edema.
  
  
  METHODS
  Retrospective review of patients with neurogenic pulmonary edema who had pulmonary edema fluid analysis.
  
  
  METHODS
  University hospital ICU.
  
  
  METHODS
  Twelve patients with neurogenic pulmonary edema in whom the associated neurologic condition was subarachnoid hemorrhage (n = 8, 67%), postcraniotomy (n = 2), and stroke (n = 2).
  
  
  METHODS
  Protein concentration was measured from pulmonary edema fluid and plasma samples obtained shortly after the onset of clinical pulmonary edema.
  
  
  RESULTS
  The mechanism of pulmonary edema was classified according to the initial alveolar edema fluid to plasma protein concentration ratio. A hydrostatic mechanism (ratio < or = 0.65) was observed in seven patients, none of whom had cardiac failure or intravascular volume overload. Five patients had evidence for increased permeability (ratio > 0.70). Patients with a hydrostatic mechanism had better initial oxygenation (mean +/- SD PaO2/FIO2 [fraction of inspired oxygen] = 233 +/- 132) compared with patients with increased permeability (PaO2/FIo2 = 80 +/- 42), and oxygenation improved more rapidly in the hydrostatic patients. Overall mortality (58%) was high, but it was related to unresolved neurologic deficits, not to respiratory failure.
  
  
  CONCLUSIONS
  Many of our patients had a hydrostatic mechanism for neurogenic pulmonary edema. This is a novel observation in humans since prior clinical case reports have emphasized increased permeability as the usual mechanism for neurogenic pulmonary edema. These findings are consistent with pulmonary venoconstriction or transient elevation in left-sided cardiovascular pressures as contributing causes to the development of human neurogenic pulmonary edema.
authors.affiliation: Department of Neurology, University of California, San Francisco 94143-0114, USA.
authors.forename: W S
authors.initials: WS
authors.lastname: Smith
authors.forename: M A
authors.initials: MA
authors.lastname: Matthay
mesh_terms: D000328:Adult; D000368:Aged; D001794:Blood Pressure; D001798:Blood Proteins / Q000032:analysis; D001810:Blood Volume; D002199:Capillary Permeability; D002303:Cardiac Output, Low / Q000503:physiopathology; D002423:Cause of Death; D002561:Cerebrovascular Disorders / Q000150:complications; D003399:Craniotomy / Q000009:adverse effects; D005122:Exudates and Transudates / Q000737:chemistry; D005260:Female; D006801:Humans; D006874:Hydrostatic Pressure; D008168:Lung / Q000098:blood supply; D008297:Male; D008875:Middle Aged; D010100:Oxygen / Q000097:blood; D010101:Oxygen Consumption; D011506:Proteins / Q000032:analysis; D011650:Pulmonary Alveoli / Q000378:metabolism / Q000503:physiopathology; D011654:Pulmonary Edema / Q000209:etiology* / Q000378:metabolism / Q000503:physiopathology; D012131:Respiratory Insufficiency / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology; D012189:Retrospective Studies; D013345:Subarachnoid Hemorrhage / Q000150:complications*; D014661:Vasoconstriction
chemical_list: D001798:Blood Proteins; D011506:Proteins; D010100:Oxygen