- © 2007 Canadian Medical Association
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![Figure](https://www.cmaj.ca/content/cmaj/177/3/249.1/F1.medium.gif)
Chest radiograph of a 57-year-old woman who presented with progressive dyspnea and profuse pink frothy sputum that began 6 hours after the onset of left hemiplegia.
The patient presented with progressive dyspnea that began after a right middle cerebral artery infarction. She had no history of loss of consciousness or obvious aspiration. A chest radiograph obtained on admission showed diffuse homogenous infiltrates compatible with a nonspecific diagnosis of pulmonary edema. An electrocardiogram and an echocardiogram appeared normal, and cardiac enzyme levels were within the normal range. A CT scan performed 3 days after admission showed an extensive middle cerebral artery infarct (Appendix 1, available online at www.cmaj.ca/cgi/content/full/177/3/249/DC1).
The diagnosis of neurogenic pulmonary edema is based on the occurrence of the edema after a neurologic insult and on the exclusion of other plausible causes.1 Although a number of central nervous system injuries are associated with neurogenic pulmonary edema, the most common is subarachnoid hemorrhage, which accounts for more than two-thirds of reported cases. The incidence of neurogenic pulmonary edema is 23% following subarachnoid hemorrhage, 20% following severe head injury and about 33% among patients with status epilepticus. More rare causes include multiple sclerosis, brain tumour, encephalitis, cervical spine injury and ischemic stroke.1,2 The exact pathophysiology of neurogenic pulmonary edema is unclear, but it probably involves an adrenergic response to the cerebral insult, which leads to increased pulmonary hydrostatic pressure and increased lung capillary permeability related to the inflammatory response.1,2
Neurogenic pulmonary edema characteristically presents within minutes to hours after a neurologic insult and usually resolves within 72 hours. Treatment ranges from supportive to endotracheal intubation with mechanical ventilation. The use of dobutamine, osmotic or loop diuretics and α-adrenergic blockers has been described. The condition is likely underdiagnosed; thus, the full distribution of outcomes is unclear. Without rapid diagnosis and appropriate management, the mortality is high. Physicians should consider neurogenic pulmonary edema when caring for patients with acute respiratory distress following a neurologic insult. In our case, the neurogenic pulmonary edema resolved 2 days after the patient was admitted to hospital, and she was discharged to a nursing home 2 weeks later.
Footnotes
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This article has been peer reviewed.
Competing interests: None declared.