Neurogenic pulmonary edema (NPE) is an increase in pulmonary interstitial and alveolar fluid that is due to an acute central nervous system injury and usually develops rapidly after the injury . It is sometimes classified as a form of the acute respiratory distress syndrome (ARDS), but its pathophysiology and prognosis are different.
The clinical features, differential diagnosis, diagnosis, etiology, pathogenesis, and treatment of NPE are reviewed here. ARDS and noncardiogenic pulmonary edema due to other causes are discussed elsewhere. (See "Acute respiratory distress syndrome: Clinical features and diagnosis" and "Noncardiogenic pulmonary edema".)
NPE characteristically presents within minutes to hours of a severe central nervous system insult such as subarachnoid hemorrhage or traumatic brain injury. However, more rapid onset (immediate) and delayed onset (hours to days) have been described [2-4]. Resolution usually occurs within several days .
Dyspnea is the most common symptom, although mild hemoptysis is present in many patients. The physical examination generally reveals tachypnea, tachycardia, and basilar rales. Chest radiographs typically show a normal size heart with bilateral alveolar opacities, although unilateral opacities have also been described [6-8]. Hemodynamic measurements are usually normal by the time NPE is diagnosed, including the blood pressure, cardiac output, and pulmonary capillary wedge pressure.
There is a broad range of severities of NPE and mild cases may never be detected. While NPE can be fulminant and contribute to death, mortality is more commonly due to the neurologic insult that precipitated the onset of NPE.