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Evidence for a Hydrostatic Mechanism in Human Neurogenic Pulmonary Edema

Wade S. Smith; Michael A. Matthay
Author and Funding Information

Affiliations: From the Department of Neurology, University of California, San Francisco,  From the Department of Medicine, and Cardiovascular Research Institute, University of California, San Francisco

Affiliations: From the Department of Neurology, University of California, San Francisco,  From the Department of Medicine, and Cardiovascular Research Institute, University of California, San Francisco


1997 by the American College of Chest Physicians


Chest. 1997;111(5):1326-1333. doi:10.1378/chest.111.5.1326
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Abstract

Study objectives: To identify the relative contribution of hydrostatic and permeability mechanisms to the development of human neurogenic pulmonary edema.

Design: Retrospective review of patients with neurogenic pulmonary edema who had pulmonary edema fluid analysis.

Setting: University hospital ICU.

Patients: 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).

Measurements: 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 ≤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.

Conclusion: 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.


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