Neurological Perspectives of Neurogenic Pulmonary Edema

Abstract

Background: Neurogenic pulmonary edema (NPE) is characterized by acute respiratory distress triggered by acute, severe compromise of the central nervous system (CNS). This review aims at summarizing and discussing recent and previous findings about the type and frequency of CNS triggers of NPE, pathogenesis, diagnosis, treatment, and outcome of patients experiencing NPE. Key Messages: NPE is diagnosed in the presence of pink, frothy sputum, pulmonary edema, bilateral opacities on X-ray, PaO2:PiO2 <200 mm Hg, acute CNS compromise with increased intra-cranial pressure, rapid resolution within 48–72 h, and the absence of alternative causes of respiratory distress. The most common cerebral triggers of NPE include enterovirus-71-associated brainstem encephalitis, subarachnoid bleeding, intracerebral bleeding, traumatic brain injury, epilepsy, ischemic stroke, intracranial/spinal surgery, multiple sclerosis, electroconvulsive therapy, subdural/epidural hematoma, intoxication, hypoxia, and hydrocephalus. Simultaneous treatment of CNS and pulmonary compromise is required. Cerebral treatment involves infectiologists, neurologists, and neurosurgeons. Pulmonary treatment is mainly supportive, but if ineffective, extracorporeal membrane oxygenation or thermodilution are alternative options. Applying intensive care measures, the outcome of NPE has improved. Summary: CNS-disease triggering NPE is more variegated than anticipated. Delineation of NPE from other pulmonary or cardiac conditions mimicking NPE is crucial to take appropriate measures and improve the outcome of these patients.