IS case 443: Neurogenic pulmonary edema
Imaging Sciences URMC 2010
Publication Date: 2010-08-30
Pulmonary edema is broadly divided into cardiogenic and non-cardiogenic etiologies. Non-cardiogenic forms are further subdivided into pulmonary edema associated with diffuse alveolar damage (DAD) and pulmonary edema without DAD. Neurogenic pulmonary edema is a mixed edema containing elements of both patterns and can occur in up to 50% of patients suffering an intracranial insult such as trauma, hemorrhage or seizure.
Edema with diffuse alveolar damage usually results from a cytotoxic agent directly contacting lung parenchyma or a systemic inflammatory process, both of which cause vascular/alveolar damage and increased permeability. Patients may initially present with subtle interstitial edema that progresses to widespread bilateral opacification compatible with acute respiratory distress syndrome. This pattern fails to resolve in 1-3 days and can progress to fluid sequestration with areas of confluent fibrosis. Edema without DAD generally presents as a diffuse bilateral interstitial pattern, but usually resolves within 3 days and tends to be caused by increased hydrostatic pressure.
Neurogenic pulmonary edema generally demonstrates a mixed pattern and is therefore a diagnosis of exclusion. The edema is caused by increased hydrostatic pressure occurring mainly in the pulmonary venules and increased cellular permeability by an unknown mechanism. The edema is widespread, but generally is not caused by cytotoxic injury and therefore is more often classified as edema without DAD. Chest x-ray opacifications are diffuse bilaterally with a slight mid to upper lung zone predominance. Significant cardiac enlargement and large pleural effusions suggestive of cardiac etiologies tend not to be seen in pure neurogenic pulmonary edema, but can occur in cardiac patients with cranial insults. The pattern may vary in homogeneity and usually resolves in 1-2 days despite the diffuse pattern on radiographs.
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