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.

Pulmonary Edema and Stunned Myocardium in Subarachnoid Hemorrhage

“…Neurogenic pulmonary edema is diagnosed by the presence of pink-frothy sputum, PaO 2 :PiO 2 <200 mmHg, pulmonary edema, bilateral opacities on X-ray, the absence of alternative causes of respiratory illness, and rapid resolution within 48 to 72 hours. The most common causes of neurogenic pulmonary edema include subarachnoid bleeding, enterovirus-71-associated brain-stem encephalitis, traumatic brain injury, epilepsy, intracranial injury, multiple sclerosis, subarachnoid bleeding, electroconvulsive therapy, intracranial/spinal surgery, intoxication, and hypoxia [16].…”

Seizure followed by lung edema: An intriguing link between the brain and the lung

“…Such stress increases catecholamine release and/or the levels of inflammatory mediators and then causes NPE through increased permeability of the lung capillary vessels. 1 Meningioma is a rare cause of NPE, and only one case report has been published previously. 1,2 When observing pulmonary edema in patients without a causative lung and heart disorder, the possibility of NPE should be considered.…”

Non-gas exchange lung functions in experimental alcohol addiction and its combination with traumatic brain injury

“…Сочетание этаноловой интоксикации и ЧМТ усиливало степень гидратации лёгочной ткани, выявленной при длительном приёме этанола, что не исключает вовлечение центральных дизрегуляционных влияний, способствующих усилению отёка лёгких. По мнению J. Finsterer (2019) развитие нейрогенного отёка лёгких при повреждении мозга является закономерным явлением [16]. В частности, было обнаружено повышение общей жидкости лёгких при сосудистом поражении головного мозга [17].…”