FLASH PULMONARY EDEMA IN MULTIPLE SCLEROSIS

Background: Neurogenic pulmonary edema (NPE) occurs in the setting of an acute neurological insult and in the absence of a primary cardiopulmonary cause. No unifying theory on NPE pathogenesis exists. NPE triggered by a discrete neurological lesion is rare, but such cases offer valuable insight into NPE pathogenesis. Objective: To describe an unusual and instructive case of NPE in multiple sclerosis. Case Report: A young woman with multiple sclerosis presented to the Emergency Department in acute respiratory failure. She was cyanotic centrally, hypertensive, and tachycardic. The chest X-ray study suggested pulmonary edema. She required non-invasive mechanical ventilation for 12 h. Echocardiography revealed left ventricular hypokinesis. The asymmetrical pulmonary infiltrate raised the suspicion of pneumonia; she was given intravenous antibiotics. By 36 h, she had persistent dyspnea, paroxysmal tachycardia, nausea, and facial flushing; carcinoid syndrome was excluded. By 48 h, she had facial numbness and ataxia. Magnetic resonance imaging (MRI) revealed a demyelinating lesion at the rostromedial medulla. Her symptoms promptly resolved with intravenous steroids, as did the perilesional edema on follow-up MRI. Conclusion: Life-threatening pulmonary edema can complicate medullary demyelination. Lack of awareness of this diagnostic possibility and an asymmetrical pulmonary infiltrate culminated in diagnostic delay in this case. The case provides clinico-radiological evidence of the pathogenic link between medullary lesions and NPE. The pathogenesis is likely to rely on lesion involvement of the nucleus tractus solitarius or its immediate pathways. Non-uniform vasoconstriction of the pulmonary arterial bed might account for the other peculiarity of this case: the asymmetrical pulmonary infiltrate. Timely diagnosis of NPE is essential because the condition is best managed by nullifying the neurogenic trigger. (c) 2013 Elsevier Inc.