Chest
Volume 111, Issue 5, May 1997, Pages 1326-1333
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Clinical Investigations in Critical Care
Evidence for a Hydrostatic Mechanism in Human Neurogenic Pulmonary Edema

https://doi.org/10.1378/chest.111.5.1326Get rights and content

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.

Section snippets

MATERIALS AND METHODS

The hospital charts of all patients who developed potential neurogenic pulmonary edema (see below) and had pulmonary edema fluid analysis between October 1982 and May 1994 at Moffitt-Long Hospital at the University of California, San Francisco were reviewed retrospectively.

Patients were classified as having potential neurogenic pulmonary edema if marked pulmonary edema occurred in the setting of a sudden change in their neurologic condition. Sixteen patients were identified who satisfied these

Patient Diagnoses and Demographics

Sixteen patients over a 12-year period developed sudden onset of pulmonary edema following a change in neurologic condition; all had pulmonary edema fluid obtained for analysis. Patients with concomitant cardiac disease, gastric aspiration, or another potential cause (reexpansion pulmonary edema) were excluded (four patients, see “Materials and Methods” section) to focus on patients with no cause for pulmonary edema other than a sudden change in neurologic status. These 12 patients constitute

DISCUSSION

Neurogenic pulmonary edema is characterized by an increase in extravascular lung water in patients who have sustained a sudden change in neurologic condition.28,37 The mechanism by which neurogenic pulmonary edema occurs is not clear, and two divergent theories have been proposed to explain its development: increased lung capillary permeability or increased pulmonary vascular hydrostatic pressures.

Increased permeability as a mechanism for neurogenic pulmonary edema is supported by some animal

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