Neurogenic Pulmonary Edema Research Articles

Extracorporeal Life Support as a Treatment for Neurogenic Pulmonary Edema and Cardiac Failure Secondary to Intractable Intracranial Hypertension: A Case Report and Review of the Literature

Extracorporeal Life Support as a Treatment for Neurogenic Pulmonary Edema and Cardiac Failure Secondary to Intractable Intracranial Hypertension: A Case Report and Review of the Literature

The role of nitric oxide in the development of neurogenic pulmonary edema in spinal cord-injured rats: the effect of preventive interventions

Neurogenic pulmonary edema (NPE) is an acute life-threatening complication following an injury of the spinal cord or brain, which is associated with sympathetic hyperactivity. The role of nitric oxide (NO) in NPE development in rats subjected to balloon compression of the spinal cord has not yet been examined. We, therefore, pretreated Wistar rats with the NO synthase inhibitor N(G)-nitro-L-arginine methyl ester (L-NAME) either acutely (just before the injury) or chronically (for 4 wk prior to the injury). Acute (but not chronic) L-NAME administration enhanced NPE severity in rats anesthetized with 1.5% isoflurane, leading to the death of 83% of the animals within 10 min after injury. Pretreatment with either the ganglionic blocker pentolinium (to reduce blood pressure rise) or the muscarinic receptor blocker atropine (to lessen heart rate decrease) prevented or attenuated NPE development in these rats. We did not observe any therapeutic effects of atropine administered 2 min after spinal cord compression. Our data indicate that NPE development is dependent upon a marked decrease of heart rate under the conditions of high blood pressure elicited by the activation of the sympathetic nervous system. These hemodynamic alterations are especially pronounced in rats subjected to acute NO synthase inhibition. In conclusion, nitric oxide has a partial protective effect on NPE development because it attenuates sympathetic vasoconstriction and consequent baroreflex-induced bradycardia following spinal cord injury.

Sudden unexpected death in epilepsy: risk factors and potential pathomechanisms

Sudden unexpected death in epilepsy (SUDEP) is the most common cause of death directly related to epilepsy, and most frequently occurs in people with chronic epilepsy. The main risk factors for SUDEP are associated with poorly controlled seizures, suggesting that most cases of SUDEP are seizure-related events. Dysregulation in cardiac and respiratory physiology, dysfunction in systemic and cerebral circulation physiology, and seizure-induced hormonal and metabolic changes might all contribute to SUDEP. Cardiac factors include bradyarrhythmias and asystole, as well as tachyarrhythmias and alterations to cardiac repolarization. Altered electrolytes and blood pH, as well as the release of catecholamines, modulate cardiac excitability and might facilitate arrhythmias. Respiratory symptoms are not uncommon during seizures and comprise central apnea or bradypnea, and, less frequently, obstruction of the airways and neurogenic pulmonary edema. Alterations to autonomic function, such as a reduction in heart rate variability or disturbed baroreflex sensitivity, can impair the body's capacity to cope with challenging situations of elevated stress, such as seizures. Here, we summarize data on the incidence of and risk factors for SUDEP, and consider the pathophysiological aspects of chronic epilepsy that might lead to sudden death. We suggest that SUDEP is caused by the fatal coexistence of several predisposing and triggering factors.

Mechanisms of disease/hypothesis: Neurogenic left ventricular dysfunction and neurogenic pulmonary oedema

Acute onset of cardiovascular dysfunction may be the result of insults to the central nervous and autonomic system. Several cerebral regions (insular cortex, lateral, hypothalamus, and brain stem) have been identified as part of the "central autonomic network". The brain stem plays an integral role in controlling and mediating autonomic tone. Case reports. These two case reports demonstrate the intimate connectivity between the cardiovascular/pulmonary system and the central nervous system in a 13-year-old girl with occipital angiomatosis, but no history of heart disease who developed profound left ventricular dysfunction and pulmonary oedema following pontine haemorrhage, and in a 5-year-old girl who developed severe pulmonary oedema after suffering from status epilepticus. The two case reports suggest that cardiovascular dysfunction secondary to central nervous insults and neurogenic pulmonary oedema are not two separate clinical entities, but may very well encompass two different presentations of central autonomic disturbances.

Acute and critical care management of a pediatric patient with medullo-cerebellar impaling

The authors present a child with an accidental cervical medullo-cerebellar impaling by an aluminum rod. Careful planning for safe removal of the rod as well as vigilant attention to early cardiac instability and flash neurogenic pulmonary edema were paramount to her successful recovery. This patient illustrates that it is possible to survive impaling of the brainstem but it requires both innovation and collaboration by multiple specialists across different departments. The value of well coordinated and collaborative neuro surgical intensive care is demonstrated in this young girl’s nearly complete recovery from the accident.

Alteration of Neuropeptides in the Lung Tissue Correlates Brain Death-Induced Neurogenic Edema

Increased intracranial pressure induces neurogenic pulmonary edema (NPE), potentially explaining why only lungs from less than 20% of brain dead organ donors can be used for transplantation. This study investigated the underlying mechanisms of NPE, focusing on neuropeptides, which potently induce vasoconstriction, vasodilatation, and neurogenic inflammation. Brain death was induced in 10 pigs by increasing the intracranial pressure. Eight additional pigs served as controls. Neuropeptide Y (NPY), calcitonin gene-related peptide (CGRP), and substance P were analyzed in plasma, bronchoalveolar lavage (BAL) fluid, and homogenized lung tissue 6 hours after brain death. Pulmonary oxygen exchange was estimated using partial pressure of arterial oxygen (Pao2)/fraction of inspired oxygen (Fio2), and pulmonary edema by wet/dry weight ratio. Brain death induced a decrease in Pao(2)/Fio2 (p < 0.001) and increased the wet/dry weight of both apical (p = 0.01) and basal lobes (p = 0.03). NPY and CGRP concentrations were higher in the BAL fluid of brain-dead animals compared with controls (p = 0.02 and p = 0.02) and were positively correlated with the wet/dry weight ratio. NPY content in lung tissue was lower in brain-dead animals compared with controls (p = 0.04) and was negatively correlated with the wet/dry weight ratio. There were no differences in substance P concentrations between the groups. NPY was released from the lung tissue of brain-dead pigs, and its concentration was related to the extent of pulmonary edema. NPY may be one of several crucial mediators of neurogenic pulmonary edema, raising the possibility of treatment with NPY-antagonists to increase the number of available lung donors.

Acute Lung Injury in Patients with Severe Brain Injury: A Double Hit Model

The presence of pulmonary dysfunction after brain injury is well recognized. Acute lung injury (ALI) occurs in 20% of patients with isolated brain injury and is associated with a poor outcome. The "blast injury" theory, which proposes combined "hydrostatic" and "high permeability" mechanisms for the formation of neurogenic pulmonary edema, has been challenged recently by the observation that a systemic inflammatory response may play an integral role in the development of pulmonary dysfunction associated with brain injury. As a result of the primary cerebral injury, a systemic inflammatory reaction occurs, which induces an alteration in blood-brain barrier permeability and infiltration of activated neutrophils into the lung. This preclinical injury makes the lungs more susceptible to the mechanical stress of an injurious ventilatory strategy. Tight CO2 control is a therapeutic priority in patients with acute brain injury, but the use of high tidal volume ventilation may contribute to the development of ALI. Establishment of a therapeutic regimen that allows the combination of protective ventilation with the prevention of hypercapnia is, therefore, required. Moreover, in patients with brain injury, hypoxemia represents a secondary insult associated with a poor outcome. Optimal oxygenation may be achieved by using an adequate FiO2 and by application of positive end-expiratory pressure (PEEP). PEEP may, however, affect the cerebral circulation by hemodynamic and CO2-mediated mechanisms and the effects of PEEP on cerebral hemodynamics should be monitored in these patients and used to titrate its application.

Not All Swelling Is Edema in Eclampsia: A Rare and Life-threatening Potential Complication of Eclamptic Seizures

A 24-yr-old, 65-kg, 152-cm primigravida woman with severe pre-eclampsia and a history of asthma was admitted at 38 weeks’ gestationfor magnesium administration and oxytocin induction of labor. Herlaboratory studies and physical examination were within normal limitsexcept for proteinuria, hypertension, and moderate generalized edemawithout obvious facial edema at admission. Because of her preeclamp-sia, an epidural catheter was easily inserted early before onset of activelabor or pain. Three hours later, the patient had a witnessed tonic–clonic eclamptic seizure, which subsided shortly after administrationof 4 mg intravenous lorazepam and assisted mask ventilation. Becauseof recurring fetal heart rate deceleration, an urgent cesarean deliverywas planned. However, the patient was combatively uncooperativedespite a bilateral T4 anesthetic level achieved epidurally while heroxygen saturation remained 100% and blood pressure was 140/85mmHg. The patient was noted to have a Mallampati class I airway withmoderate generalized edema and mild facial edema. Rapid sequencegeneral anesthesia induction was performed with successful atrau-matic intubation on the first attempt, followed by verification of bilat-eral symmetrical breath sounds. Maintenance of anesthetic consisted ofvolume-controlled mechanical ventilation, 50% oxygen, 50% nitrousoxide, 1–2% sevoflurane, midazolam, and opioid without the need foradditional neuromuscular blocker other than succinylcholine at induc-tion. Intraoperative blood pressure and heart rate were maintainedwithin 20% of preoperative values while oxygen saturation was main-tained at 99–100%, end-tidal carbon dioxide between 30–35 mmHg,and airway pressures less than 25 cm H

Mechanisms of disease: Neurogenic left ventricular dysfunction and neurogenic pulmonary edema

Background: Acute onset of cardiovascular dysfunction may be the result of insults to the central nervous and autonomic system. Several cerebral regions (insular cortex, lateral, hypothalamus, brain stem) have been identified as part of the “central autonomic network“. The brain stem plays an integral role in controlling and mediating autonomic tone.

Clinical application of early chest CT examination in patients with traumatic brain injury combined with chest injury

Objective To discuss the clinical effect of early chest CT examination in patients with traumatic brain injury combined with chest injury. Methods A total of 163 patients with traumatic brain injury combined with chest injury treated in two hospitals between 2000 and 2008 were involved in the study and divided into two groups according to different early examination methods, ie, Group A (ear-ly head CT and chest X-ray from January 2000 to October 2006) and Group B (early head and chest CT from October 2006 to December 2008) for a comparative study. Results The patients were at age of (49±20) years in Group A and at (48±18) years in Group B. Lung infection occurred in 25 patients (30%) in Group A and 10 (13%) in Group B. ARDS occurrod in nine patients (11%) in Group A and one (1%) in Group B. Neurogenic pulmonary edema occurred in eight patients (10%) in Group A and one (1%) in Group B. The coma lasted for average 41 days in Group A and 15 days in Group B. Con-dusion Early chest CT examination has great help for clear diagnosis of traumatic brain injury combined with chest injury and hence can reduce lung infection, ARDS and neurogenic pulmonary edema, shorten coma time and improve curative effect. Key words: Brain injuries ; Chest injuries ; Tomography, X-ray computed; Complications

Atropine may prevent the development of neurogenic pulmonary edema

Neurogenic pulmonary edema is an acute life-threatening complication of central nervous system injury. We introduce a hypothesis that early i.v. administration of high-dose atropine can prevent neurogenic pulmonary edema development on the basis of the prevention of baroreflex-induced bradycardia, which was recognized as a major factor in neurogenic pulmonary edema formation. To validate this hypothesis, a clinical trial in patients suffering from subarachnoid haemorrhage should be performed, with atropine administered i.v. immediately after the maintenance of the living functions, intubation and ability to monitor patient.

Evaluation of pulmonary GLUT1 and VEGF mRNA levels in relation to lung weight in medicolegal autopsy cases

The present study focuses attention upon the relationship among postmortem mRNA levels of pulmonary glucose transporter (GLUT1) and vascular endothelial growth factor (VEGF) to lung weight to investigate pulmonary pathophysiology in the death process. Autopsy cases ( n = 173, within 48 h postmortem) of blunt injury, including head injury (brain contusions and acute subdural hemotoma) and non-head injury, sharp instrument injury, mechanical asphyxiation, drowning, acute myocardial infarction/ischemia (AMI) and idiopathic cerebral hemorrhage (ICH) were examined. GLUT1 and VEGF mRNAs were quantified by TaqMan real-time RT-PCR for the upper lobes of the bilateral lungs. Combined lung weight was normalized against height for statistical analyses. GLUT1 mRNA showed a higher level for ICH. GLUT1 and VEGF mRNA levels were higher for brain contusions than for acute subdural hematoma, which showed a significantly lower VEGF mRNA level. Lung weight showed a larger value for saltwater drowning and ICH, and was larger for acute subdural hematoma than for brain contusions. GLUT1 mRNA level was correlated with lung weight in cases of ICH and brain contusions (survival time <24 h), and VEGF mRNA showed a similar tendency. Such findings were not detected for other groups. These findings indicate parallel increases in hypoxia-induced responses and lung weight in ICH and brain contusions, suggesting different pulmonary hemodynamics with milder alveolar damage compared with other groups, including AMI and acute subdural hematoma. Different mechanisms might be involved in non-cardiogenic or neurogenic pulmonary congestion and edema for ICH/brain contusions and subdural hematoma.

Pathology of enterovirus 71 infection: an autopsy study of 5 cases

To study the clinicopathologic features of fatal enterovirus 71 (EV71) infection. Autopsy was performed in 5 neonates died of EV71 infection. Tissue samples from major organs were collected, formalin-fixed and examined under light microscopy. Immunohistochemical study was carried out in selected examples. Four of the 5 cases showed predominant changes in central nervous system, with encephalitis and encephalomyelitis identified mainly in brainstem and upper cervical spinal cord. Histologic findings included neuronal degeneration and necrosis, neuronophagia, perivascular cuffing and diffuse or nodular hyperplasia of macrophages/microglia. Cerebral edema, brain herniation and aseptic meningitis were also noted. The lungs showed mainly pulmonary congestion, neurogenic pulmonary edema and focal hemorrhage. There were minimal changes in the intestinal epithelium. The intestinal lymphoid tissue however was hyperplastic and associated with apoptosis of follicular center cells. The remaining case had cerebral edema and mild meningitis. The lung alveolar septa were thickened with lymphocytic infiltrates. Some alveolar cells were hyperplastic and associated with diffuse hyaline membrane formation. No specific abnormalities were identified in gastrointestinal tract. In all the 5 cases studied, there was enlargement of lung hilar and mesenteric lymph nodes, coupled with apoptosis of follicular center cells. In general, no significant pathologic changes were demonstrated in heart, liver and kidneys. In fatal EV71 infection, the major pathologic changes lie in the central nervous system. The pulmonary lesions are mainly secondary in nature. The usual cause of death is cerebral edema complicated by brain herniation and pulmonary edema. It is also noteworthy that some cases show only lung damages, without classic neurologic changes.

Quand un entérovirus émerge

Most of enterovirus infections are benign and the rate of mortality is low in countries with temperate climates. But since the late 1990s, Enterovirus 71 (EV-71) has become much more aggressive in Asian countries, with the outcome of a neurogenic pulmonary oedema syndrome and it is responsible for huge epidemics. The virological diagnosis rely upon viral isolation and identification by seroneutralisation, and upon the detection of specific IgM by ELISA and viral RNA by RT-PCR. There is no specific treatment to fight this virus, but innovative strategies, especially based on interfering RNA, are under investigation.

Autonomic dysreflexia and associated acute neurogenic pulmonary edema in a patient with spinal cord injury: a case report and review of the literature

A case report of a patient with spinal cord injury with autonomic dysreflexia and associated acute neurogenic pulmonary edema. To further describe autonomic dysreflexia as a potential cause of acute neurogenic pulmonary edema; specifically in a population with spinal cord injury. James A Haley Veterans Hospital, Tampa, FL, USA. A patient with a prior history of C5 AIS (ASIA impairment scale) B spinal cord injury was admitted for bowel preparation before a screening colonoscopy. During the 2-day bowel preparation, the patient developed severe autonomic dysreflexia. Due to persistent hypertension and acute onset respiratory failure, he required transfer to the intensive care setting. Following a complicated course, the patient expired without a definitive cause of death. Autopsy findings showed gross and microscopic evidence of pulmonary edema. To date, the association between autonomic dysreflexia and acute neurogenic pulmonary edema is not described in the spinal cord or rehabilitation literature. The purpose of this case report is to further describe the overlooked and/or under reported incidence of acute neurogenic pulmonary edema associated with episodes of dysreflexia in a population with spinal cord injury.

Neural histamine in the tuberomammillary nucleus regulates the onset of neurogenic pulmonary edema in rabbits

Objective To explore the effect of neural histamine in the tuberomammillary nucleus(TM) on neurogenic pulmonary edema (NPE) onset in rabbits and the function of the rostral ventrolateral medulla(RVLM) in the neural histamine modulation of NPE. Methods NPE was produced by the intracisternal injections of fibrinogen and thrombin. The contents of histamine in the TM and RVLM in rabbits were measured with high performance liquid chromatography(HPLC). Rabbits were placed on a stereotaxic frame and microinjection cannulae were inserted into the TM and RVLM using brain atlas coordinates. Animals were pretreated with R-α-methylhistamine(MeHA) in the TM and chlorphenamine Mmaleate/cimetidine in the RVLM prior to establishing the NPE model. Changes in the lung water ratio and mean arterial pressure(MAP) were recorded, and paraffin sections of lung tissue were observed by light microscope. Results We found that the contents of histamine(HA) in the TM and RVLM increased significantly with the onset of NPE. Pretreatment with MeHA in the TM and chlorphenamine Mmaleate in the RVLM significantly decreased MAP, and the lung water ratio and histological characteristics of the NPE in the rabbit model. Pretreatment with cimetidine in the RVLM had no effect on NPE. Conculsion The results suggest that neural histamine in the TM is involved in the onset of NPE, and this effect of neural histamine is mediated by H 1 receptor in the RVLM.

Rapid but not slow spinal cord compression elicits neurogenic pulmonary edema in the rat

The development of neurogenic pulmonary edema (NPE) can be elicited by an immediate epidural balloon compression of the thoracic spinal cord. To evaluate whether a slower balloon inflation could prevent NPE development, we examined the extent of NPE in animals lesioned with a rapid (5 microl - 5 microl - 5 microl) or slow rate (3 microl - 2 microl - 2 microl - 2 microl - 2 microl - 2 microl - 2 microl) of balloon inflation. These groups were compared with the NPE model (immediate inflation to 15 microl) and with healthy controls. Slow balloon inflation prevented NPE development, whereas the pulmonary index and histology revealed a massive pulmonary edema in the group with a rapid rate of balloon inflation. Pulmonary edema was preceded by a considerable decrease in heart rate during the inflation procedure. Moreover, rapid inflation of balloon in spinal channel to either 5 microl or 10 microl did not cause NPE. Thus, a slow rate of balloon inflation in the thoracic epidural space prevents the development of neurogenic pulmonary edema, most likely due to the better adaptation of the organism to acute circulatory changes (rapid elevation of systemic blood pressure accompanied by profound heart rate reduction) during the longer balloon inflation period. It should be noted that spinal cord transection at the same level did not cause neurogenic pulmonary edema.

Identification of a enterovirus 71 receptor; SCARB2

Enterovirus 71 (EV71) and coxsackievirus A16 (CVA16), belonging to family Picornaviridae, genus Enterovirus, species A, are causative agents of hand-foot-mouth disease (HFMD). Infections involving EV71, but not CVA16, can progress to severe neurological disease, including aseptic meningitis, encephalitis, acute flaccid paralysis and neurogenic pulmonary edema. EV71 is thus considered to be a neuropathogenic virus and EV71 outbreak has become a major public health concern. Human RD cells are highly susceptible to EV71, while mouse L929 cell are not. We established mouse cell lines that acquired EV71-susceptibility by transfecting human genomic DNA. We succeeded in identifying a human gene, scavenger receptor B2 (SCARB2), integrated in one of the transformant cells by microarray analysis and showed that SCARB2 can serve as a EV71 receptor. I will summarize this result, background and the methodology of the study.

Alteration of cardiopulmonary function after subarachnoid hemorrhage

Volume management is crucial in intensive care; however, in some patients it is very hard to achieve optimal water balance. The subarachnoid hemorrhage (SAH) patient is a representative example [1-3]. Cardiopulmonary complications are common after SAH: neurogenic pulmonary edema, cardiac failure, and so on. In this study we will present the time course of catecholamines and natriuretic polypeptides and fluid redistribution on pulse contour analysis calibrated by transpulmonary thermodilution PiCCO-plus monitoring after SAH.

Treatment Regimen in Patients With Neurogenic Pulmonary Edema After Subarachnoid Hemorrhage

Treatment Regimen in Patients With Neurogenic Pulmonary Edema After Subarachnoid Hemorrhage