Neurogenic Pulmonary Edema

Otero, Hansel J.; Pollock, Avrum N.

doi:10.1097/pec.0000000000000309

Cited by 4 publications

(3 citation statements)

References 14 publications

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“…Other symptoms commonly reported include headache, nausea and vomiting, but these are probably related to the central neurologic insult. Typical pulmonary oedema findings on thoracic radiography include bilateral diffuse alveolar infiltrates (Otero & Pollock, 2014). The results of the ultrasonic cardiogram, trans‐oesophageal Doppler and central venous pressure are typically within normal limits.…”

Section: Clinical Featuresmentioning

confidence: 99%

Role of autonomic system imbalance in neurogenic pulmonary oedema

Yang

Liu

Inoue

2022

Eur J of Neuroscience

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Neurogenic pulmonary oedema (NPE) is a life‐threatening complication that develops rapidly and dramatically after an injury to the central nervous system (CNS). The autonomic system imbalance produced by severe brain damage may play an important role in the development of NPE. Activation of the sympathetic nervous system and inhibition of the vagus nerve system are essential prerequisites for autonomic system imbalance. The more severe the damage, the more pronounced the phenomenon. Sympathetic hyperactivity is associated with increased release of catecholamines from peripheral sympathetic nerve endings, which can cause dramatic changes in haemodynamics and cause pulmonary oedema. On the other hand, the abnormal inflammatory response caused by vagus nerve inhibition may also play an important role in the pathogenesis of NPE. The perspective of autonomic system imbalance seems to perfectly integrate the existing pathogenesis of NPE and can explain the entire development progression of NPE.

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Section: Clinical Featuresmentioning

confidence: 99%

Role of autonomic system imbalance in neurogenic pulmonary oedema

Yang

Liu

Inoue

2022

Eur J of Neuroscience

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“…However, acute lung injury (ALI) induced by brain injury, which is also known as traumatic brain injury-induced acute lung injury (TBI-ALI) or neurogenic pulmonary oedema (NPE), is another salient cause of patient death 6, 7 . Although it has been reported that the incidence of TBI-ALI might reach 50% or more 8 , this disease has not received sufficient attention in clinical practice because it is relatively unpredictable, has a lack of specific, aetiological diagnostic markers and has similar clinical manifestations to severe pulmonary infection. Thus the diagnosis of TBI-ALI is mainly dependent on exclusion, and it is often overlooked or misdiagnosed 9, 10 .…”

Section: Introductionmentioning

confidence: 99%

Dramatic increases in blood glutamate concentrations are closely related to traumatic brain injury-induced acute lung injury

Bai

Zhu

Ning

et al. 2017

Sci Rep

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Traumatic brain injury-induced acute lung injury (TBI-ALI) is a serious complication after brain injury for which predictive factors are lacking. In this study, we found significantly elevated blood glutamate concentrations in patients with TBI or multiple peripheral trauma (MPT), and patients with more severe injuries showed higher blood glutamate concentrations and longer durations of elevated levels. Although the increase in amplitude was similar between the two groups, the duration was longer in the patients with TBI. There were no significant differences in blood glutamate concentrations in the patients with MPT with regard to ALI status, but the blood glutamate levels were significantly higher in the patients with TBI-ALI than in those without ALI. Moreover, compared to patients without ALI, patients with TBI showed a clearly enhanced inflammatory response that was closely correlated with the blood glutamate levels. The blood glutamate concentration was also found to be a risk factor (adjusted odds ratio, 2.229; 95% CI, 1.082–2.634) and was a better predictor of TBI-ALI than the Glasgow Coma Scale (GCS) score. These results indicated that dramatically increased blood glutamate concentrations were closely related to the occurrence of TBI-ALI and could be used as a predictive marker for “at-risk” patients.

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“…Severe pulmonary injuries occurred not only in stroke condition, but also induced in brain injuries, such as severe traumatic brain injury (TBI) or subarachnoid hemorrhage (SAH) [ 8 – 11 ]. As pulmonary dysfunction, such as pulmonary edema (NPE) [ 6 , 12 ], pneumonia [ 7 ], acute lung injury and the acute respiratory distress syndrome (ALI/ARDS) [ 9 ], is severe and often result in the increase of mortality, or lead to the poor neurological outcome and longer intensive care unit (ICU) and longer length of hospital stay after stroke [ 8 , 9 , 13 ]. Therefore, it is very important to find the effective method for the treatment of lung injury, and investigate the molecular mechanism for find the intervention strategy.…”

Section: Introductionmentioning

confidence: 99%

Transplantation of bone marrow-derived mesenchymal stem cells (BMSCs) improves brain ischemia-induced pulmonary injury in rats associated to TNF-α expression

Wang

et al. 2016

Behav Brain Funct

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BackgroundBone marrow mesenchymal stem cell (BMSCs)-based therapy seems to be a promising treatment for acute lung injury, but the therapeutic effects of BMSCs transplantation on acute lung injury induced by brain ischemia and the mechanisms have not been totally elucidated. This study explores the effects of transplantation of BMSCs on acute lung injury induced by focal cerebral ischemia and investigates the underlying mechanism.MethodsAcute lung injury model was induced by middle cerebral artery occlusion (MCAO). BMSCs (with concentration of 1 × 106/ml) were transplanted into host through tail vein 1 day after MCAO. Then, the survival, proliferation and migration of BMSCs in lung were observed at 4 days after transplantation, and histology observation and lung function were assessed for 7 days. Meanwhile, in situ hybridization (ISH), qRT-PCR and western blotting were employed to detect the expression of TNF-α in lung.ResultsNeurobehavioral deficits and acute lung injury could be seen in brain ischemia rats. Implanted BMSCs could survive in the lung, and relieve pulmonary edema, improve lung function, as well as down regulate TNF-α expression.ConclusionsThe grafted BMSCs can survive and migrate widespread in lung and ameliorate lung injury induced by focal cerebral ischemia in the MCAO rat models. The underlying molecular mechanism, at least partially, is related to the suppression of TNF-α.

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Neurogenic Pulmonary Edema

Cited by 4 publications

References 14 publications

Role of autonomic system imbalance in neurogenic pulmonary oedema

Role of autonomic system imbalance in neurogenic pulmonary oedema

Dramatic increases in blood glutamate concentrations are closely related to traumatic brain injury-induced acute lung injury

Transplantation of bone marrow-derived mesenchymal stem cells (BMSCs) improves brain ischemia-induced pulmonary injury in rats associated to TNF-α expression

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