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Neurogenic pulmonary edema

INTRODUCTION

Neurogenic pulmonary edema (NPE) is an increase in pulmonary interstitial and alveolar fluid due to, and usually developing rapidly after, acute central nervous system injury [1]. This entity is frequently classified as a form of the acute respiratory distress syndrome (ARDS), although its pathophysiology and prognosis are significantly different.

The clinical features, pathogenesis, and treatment of NPE will be reviewed here. General aspects of ARDS and noncardiogenic pulmonary edema of other causes are discussed elsewhere. (See "Acute respiratory distress syndrome: Definition; epidemiology; diagnosis; and etiology" and "Noncardiogenic pulmonary edema".)

CLINICAL PRESENTATION

NPE characteristically presents within minutes to hours of a severe central nervous system insult. A more rapid onset of NPE was described in a 1969 autopsy series of 21 soldiers who died of massive head injuries [2]. Pulmonary edema was present in all of 21 patients, even in those with essentially instantaneous death. In contrast, the clinical features of NPE may evolve over hours or days in some patients with brain injuries [3,4]. Resolution of NPE usually occurs within several days [5].

Dyspnea is the most common associated symptom, and mild hemoptysis is also present in many patients. The physical examination generally reveals tachypnea, tachycardia, and basilar rales that are consistent with pulmonary edema. Chest radiographs typically show a normal size heart with evidence of bilateral alveolar filling, but may also mimic congestive heart failure with cephalization of blood flow [6,7]. Hemodynamic measurements, including blood pressure, cardiac output, and pulmonary capillary wedge pressure, usually are normal by the time NPE is diagnosed.

These findings may be confused with aspiration pneumonitis. Reliable differentiation of these two syndromes is difficult because they both commonly occur in settings of altered consciousness, such as postictal states. NPE tends to develop more rapidly than aspiration pneumonia, and the presence of fever and more focal infiltrates favors aspiration. A key retrospective distinction is that NPE will typically resolve within hours to several days (without antibiotics), while aspiration pneumonitis may take one to two weeks to resolve. Other causes of pulmonary edema such as congestive heart failure and acute respiratory distress syndrome must also be excluded. (See "Evaluation of the patient with suspected heart failure" and "Acute respiratory distress syndrome: Definition; epidemiology; diagnosis; and etiology".)
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