Neurogenic Pulmonary Edema Research Articles

Exercise-Induced Pulmonary Edema in a Triathlon.

Introduction. Family physicians have more opportunities to attend athletic competitions as medical staff at first-aid centers because of the increasing popularity of endurance sports. Case. A 38-year-old man who participated in a triathlon race experienced difficulty in breathing after swimming and was moved to a first-aid center. His initial oxygen saturation was 82% and a thoracic computed tomography scan showed bilateral ground glass opacity in the peripheral lungs. His diagnosis was noncardiogenic pulmonary edema associated with exercise or swimming: exercise-induced pulmonary edema (EIPE) or swimming-induced pulmonary edema (SIPE). Treatment with furosemide and corticosteroid relieved his symptoms of pulmonary edema. Discussion. Noncardiogenic pulmonary edema associated with endurance sports is not common, but knowledge about EIPE/SIPE or neurogenic pulmonary edema associated with hyponatremia, which is called Ayus-Arieff syndrome, is crucial. Knowledge and caution for possible risk factors, such as exposure to cold water or overhydration, are essential for both medical staff and endurance athletes. Conclusion. To determine the presence of pulmonary edema associated with strenuous exercise, oxygen saturation should be used as a screening tool at a first-aid center. To avoid risks for EIPE/SIPE, knowledge about these diseases is essential for medical staff and for athletes who perform extreme exercise.

Expression of scavenger receptor class B, member 2 of death cases infected with enterovirus 71

Objective To analyze the clinical data, pathological features, and explore the expression of scavenger receptor class B member 2(SCARB2) of the lung, brain and spinal cord in 9 cases infected with enterovirus71(EV71). Methods The lung, brain and spinal cord tissues and clinical data of 9 cases infected with EV71(EV71 group) were selected as research group, 7 cases who died of accidents were selected as control group.The pathological features were observed by way of hematoxylin and eosin(HE) staining, and the expression of SCARB2 was tested by immunohistochemistry, the integrated optical density(IOD) was detected by using picture analysis software. Results Nine cases had fever, vomiting, startle response, shake, fatigue and pulmonary edema in chest X ray; Congestion, extensive edema and inflammatory cells infiltration in alveolar walls were found in lungs of 9 cases.Transparent membrane was seen obviously in alveolar lumen in 1 case.The brain showed degeneration and necrosis of nerve cells and perivascular cuffing of lymphocytes.Brainstem in 7 cases, brain and spinal cord in 3 cases both revealed cribriform softened, satellitism and neuronophagia, glial nodule.Immunohistochemistry results showed that SCARB2 in EV71 group and the control group were both positive, as the lung tissue IOD values in EV71 group and control group were 4.15×105 and 0.05×105, there was significant difference between the 2 groups(t=108.00, P 0.05). Conclusions The patients mainly died of severe encephalitis, brainstem encephalitis and neurogenic pulmonary edema after EV71 infection.EV71 infection severity and neurotropism may be associated with the high expression of SCARB2. Key words: Enterovirus 71; Scavenger receptor class B member 2; Clinical and pathological features; Immunohistochemistry

Successful Lung Salvage by Ex Vivo Reconditioning of Neurogenic Pulmonary Edema: Case Report

Liberalization in donor selection criteria allowed centers to increase the number of lung transplants, yet less than 25 % of all donors had lungs utilized for transplantation in the United States in 2013. Less than 5% of all transplanted donors deviate 3 or more criteria from the ideal donor. Ex vivo lung perfusion (EVLP) provides the opportunity to increase the percentage of used donors by acting on modifiable selection criteria such as oxygenation, contusion and pulmonary infiltrates. We report the pre-transplant use of EVLP in the salvage of lungs from a donor that developed neurogenic pulmonary edema -PaO2 188 mmHg-. The recipient had a lung allocation score of 69.3. The post-operative course was excellent and was discharged home after 15 days. He is alive and doing well 780 days after transplant. In this report the pre-transplant use of EVLP led not only to transplanting lungs that otherwise would not have been used by many centers, but also to a very short and typical period of post-operative mechanical ventilation and hospital stay.

A pH-dependent molecular switch for virion uncoating.

A pH-dependent molecular switch for virion uncoating.

Protective effect of an angiotensin-converting-enzyme inhibitor on neurogenic pulmonary edema in rabbits

Neurogenic pulmonary edema (NPE ) was indicative of poor prognosis in the epidemic of enterovirus 71 infections. The pathogenesis of NPE remains poorly understood. The objectives of this experimental study were to explore whether RAS is activated during NPE in rabbit models induced by fibrin and the effects of an angiotensin converting enzyme inhibitor (enalaprilat) on NPE. NPE models were induced by intracisternal injection of fibrinogen and thrombin. According to random number table method, 18 healthy adult New Zealand rabbits were assigned to three groups (with 6 in each) : normal control group (Con group), NPE group and enalaprilat treated (Ena) group. After establishment of NPE models, rabbits in Ena group were given intravenous enalaprilat 0.5 mg/kg. Expression of ACE,ACE2,AT1R mRNA of the lung tissue were evaluated by real-time polymerise chain reaction; and Ang II of the lung tissue was determined by enzyme linked immunosorbent assay ( ELISA ). Meanwhile, histopathological lung injury scores were evaluated. ACE mRNA expression level in NPE group ( 17.2 ± 3.3) appeared an increasing trend in contrast to Con group ( 12.6 ± 5.2 ) and Ena group ( 11.5 ± 2.4, both P > 0.05 ). Compared with Con group (81 ± 22 ), ACE2 mRNA expression levels of NPE group ( 52 ± 6 ) and Ena group ( 45 ± 13 ) both decreased ( both P < 0.05 ) . ACE mRNA/ACE2 mRNA expression levels of NPE group ( 0.33 ± 0.06 ) and Ena group ( 0.26 ± 0.04 ) were higher than those of Con group ( 0.16 ± 0.05, both P < 0.05 ), as well as the ratio of Ena group decreased compared with untreated NPE group ( 0.26 ± 0.04 vs. 0.33 ± 0.06, P < 0.05 ) . There were no statistically significant differences in expression of AT1 mRNA of the lung tissue among three groups, but Ena group ( 4.8 ± 1.1) in contrast to NPE group ( 6.7 ± 1.3) has no significant difference (P > 0.05). Lung AngII level of NPE group [(540 ± 147) pg/ml] was significantly higher than that of Con group [(253 ± 37 ) pg/ml] and Ena group [(309 ± 35 ) pg/ml, both P < 0.05 ]. Gross pathologic examination showed that pink foamy edema fluid appeared in the tracheal tubes in NPE group, but spontaneously appeared in neither Con group nor Ena group; and the level of pulmonary subpleural bleeding in Con group, 12 graded 0; in NPE group, 2 graded II, 10 graded III; in Ena group, 2 graded, 8 grade II, 2 grade III. The histopathologic lung injury scores in Ena group was decreased in contrast to NPE group (1.36 ± 0.26 vs.2.32 ± 0.49, P < 0.05) and mainly for the improvement of alveolar overdistension and interstitial edema. The present study showed that when NPE occurs, a high lung AngII concentration was associated with an imbalance between ACE mRNA to ACE2 mRNA expression level. Activated local RAS in lung tissue resulted in lung injury. Enalaprilat treatment may attenuate lung injury by interventing local RAS in lung tissue with decreased ratio of ACE mRNA to ACE2 mRNA and lung AngII concentration. The result will be significant for the angiotensin converting enzyme inhibitor used in the theatment of NPE.

Enterovirus 71 outbreak in Northern Sydney, 2013: case series and initial response.

Enteroviruses are a common cause of childhood disease which may manifest in a variety of ways. Enterovirus 71 (EV71) is a subtype of enterovirus which can cause meningoencephalomyelitis resulting in neurological sequelae including lethargy, weakness, ataxia, sleep myoclonus, urinary retention and, in severe cases, cardiorespiratory collapse due to neurogenic pulmonary oedema. EV71 was responsible for outbreaks in South East Asia in 1997-1998, in Western Australia in 1999 and in Sydney in 2000-2001. In 2013, we are experiencing another EV71 outbreak in Sydney. This study describes the discovery of a new outbreak in Sydney's Northern Beaches, the clinical findings as well as the public health response. Thirty-seven children in total presented with presumed EV71 to the Northern Beaches Health Service from December 2012 to April 2013. Most children presented with a prodrome lasting 2-7 days prior to seeking medical attention. Sleep myoclonus was a common presenting sign occurring in 65%. Neurological signs were subtle in the majority of children and were at times missed by clinicians on a child's first presentation. Forty-six per cent of children who presented to Northern Beaches Health Service during this outbreak required a transfer to a tertiary paediatric centre for more intensive care. The public health investigation was important in establishing that the disease was widespread throughout the community and not as a result to exposure to a single child care setting. Identification of risk factors enabled more targeted communication to medical practitioners, child care centres and parents within the local community. EV71 is in Australia and all clinicians seeing children in primary, secondary and tertiary care centres need to be aware of the disease, the subtle nature of initial symptoms and the potentially devastating consequences.

Early Endovascular Treatment of Aneurysmal Subarachnoid Hemorrhage Complicated by Neurogenic Pulmonary Edema and Takotsubo-Like Cardiomyopathy

Aneurysmal subarachnoid hemorrhage (SAH) may be associated with acute cardiopulmonary complications, like neurogenic pulmonary edema (NPE) and Takotsubo-like cardiomyopathy (TCM). These dysfunctions seem to result from a neurogenically induced overstimulation of the sympathetic nervous system through the brain-heart connection and often complicate poor grade aneurysmal SAH. The optimal treatment modality and timing of intervention in this clinical setting have not been established yet. Early endovascular therapy seems to be the fitting treatment in this particular group of patients, in which surgical clipping is often contraindicated due to the added risk of craniotomy. Herein we describe the case of a woman admitted to the emergency department with aneurysmal SAH complicated by NPE-TCM, in which early endovascular coiling was successfully performed. Our case, characterized by a favorable outcome, further supports the evidence that early endovascular treatment should be preferred in this peculiar clinical scenario.

Padronização e avaliação histológica de um modelo experimental de lesão medular

A lesão medular é incapacitante, irreversível e de custo econômico e social elevado. Neste estudo, objetivou-se padronizar um modelo de lesão medular, que produza paraplegia, com o uso de cateter e avaliar histologicamente a efetividade da lesão para estudos com terapia celular. Foram realizadas as lesões medulares em ratos Wistar, utilizando-se o cateter Fogarty n.3 e compressão na região toracolombar (T8-T9) durante 5 minutos. Foram estudados três grupos: grupo A, animais controle sem lesão medular; grupo B, animais submetidos à lesão, utilizando-se 50µL de compressão; grupo C, animais submetidos à lesão, utilizando-se 80µL de compressão. Foi realizada avaliação motora pela aplicação da escala BBB, antes da compressão, após recuperação anestésica, 24 e 72 horas depois da compressão e sete dias após a compressão. Após o sétimo dia da lesão, os animais foram submetidos à eutanásia, foi feita a retirada da medula espinhal, fígado e rins e realizada a análise histológica com a coloração hematoxilina-eosina. A mortalidade variou entre os grupos, com 0% no grupo A, 38,5% no B e 48% no C. Nesses dois últimos grupos, a causa da morte foi edema pulmonar neurogênico, confirmado clínica e histologicamente. As medulas espinhais histologicamente apresentaram diferentes graus de edema, congestão vascular e hemorragia, enquanto que os fígados e os rins apresentaram diferentes graus de congestão vascular e necrose. Em relação à recuperação dos movimentos, no grupo A, verificou-se 100% de escore 21; no B, 25% de escore 21; 37,5% de escore 11; e 37,5% de escore 0; enquanto, no grupo C, verificou-se 100% de escore 0. Conclui-se que o procedimento realizado utilizando-se 80µL de solução salina para preencher o balão do cateter foi mais eficiente, apesar de maior mortalidade, pois apresentou maior porcentagem de animais com lesão completa (paraplegia).

Investigation on Factors Associated with Severe Hand, Foot and Mouth Disease

Abstract Objective To analyze the clinical and laboratory features of patients with mild and severe HFMD to identify early predictive or diagnostic markers for severe cases. Methods Samples of feces, nasopharyngeal-swab specimens, peripheral blood, serum and cerebral spinal fluid were collected. Postmortem pathological examination was conducted on 2 dead patients with complication due to neurogenic pulmonary edema. Reverse transcription-polymerase chain-reaction (RT-PCR), culture and isolation of enterovirus 71 (EV71) were performed to detect EV71 infection. Both univariate and multivariate logistic analysis were used to identify factors associated with severe cases. Results EV71 was mainly responsible for HFMD. In this study, 5 isolated EV71 strains belonged to C4 gene subtype. Compared with mild patients, EV71-RNA detection rate was higher and CoxA16 detection rate was lower among severe patients (P &lt; 0.01). Inflammatory cell infiltration in the lung, cardiac and liver tissues were mild by postmortem pathological examination. It was found that body temperature, vomitting, limb tremor, neutrophil, blood glucose and EV71 infection were significantly related to the severe cases by univariate logistic analysis. However, after multivariate logistic regression analysis, only vomiting (OR 16.1, CI 2.3-110.5, P &lt; 0.01) and limb tremor (OR 117.6, CI 13.8-1004.5, P &lt; 0.01) were significantly and independently correlated with the severe cases. Conclusions EV71 was mainly responsible for HFMD, particularly for severe cases. Vomiting and limb tremor were predictive markers for severe cases.

Timing Is Everything in Protecting the Heart and Lungs in a “Sympathetic Storm”

Timing Is Everything in Protecting the Heart and Lungs in a “Sympathetic Storm”

Enterovirus Type 71-Related Brainstem Encephalitis: A Case Report and Literature Review

Enterovirus type 71 ( EV71) infections are mainly found in infants. The severe cases are characterised by nervous system damage, acute circulatory and respiratory failures. So far, there has been no report of EV71 infection involving central nervous system in teenagers or young adults. We first reported a case of 15-year-old Han Chinese male who was infected by EV71, developed neurogenic pulmonary oedema rapidly, and had the risk factors including hyperglycaemia, significant leukocytosis and acute flaccid paralysis. The nucleic acids for EV71 were positive by Reverse transcriptase polymerase chain reaction (RT-PCR). The patient didn't belong to high risk population. Maculopapular rashes and blisters were also not found in hand, foot and mouth. These might be responsible for the failure to make an early diagnosis. (Hong Kong j.emerg.med. 2014;21:176-180)

Cell and tissue tropism of enterovirus 71 and other enteroviruses infections

Enterovirus 71 (EV71) is a member of Picornaviridae that causes mild and self-limiting hand, foot, and mouth disease (HFMD). However, EV71 infections can progress to polio-like paralysis, neurogenic pulmonary edema, and fatal encephalitis in infants and young children. Large EV71 outbreaks have been reported in Taiwan, China, Japan, Malaysia, Singapore, and Australia. This virus is considered a critical emerging public health threat. EV71 is an important crucial neurotropic enterovirus for which there is currently no effective antiviral drug or vaccine. The mechanism by which EV71 causes severe central nervous system complications remains unclear. The interaction between the virus and the host is vital for viral replication, virulence, and pathogenicity. SCARB2 or PSGL-1 receptor binding is the first step in the development of viral infections, and viral factors (e.g., 5′ UTR, VP1, 3C, 3D, 3′ UTR), host factors and environments (e.g., ITAFs, type I IFN) are also involved in viral infections. The tissue tropism and pathogenesis of viruses are determined by a combination of several factors. This review article provides a summary of host and virus factors affecting cell and tissue tropism and the pathogenesis of enteroviruses.

Role of P2X Purinoceptor 7 in Neurogenic Pulmonary Edema after Subarachnoid Hemorrhage in Rats

IntroductionNeurogenic pulmonary edema (NPE) is an acute and serious complication after subarachnoid hemorrhage (SAH) with high mortality. The present study aimed to test the therapeutic potential of brilliant blue G (BBG), a selective P2X purinoceptor 7 (P2X7R) antagonist, on NPE in a rat SAH model.MethodsSAH was induced by endovascular perforation. 86 Sprague-Dawley rats were randomly divided into sham, vehicle-, or BBG-treatment groups. Mortality, body weight, SAH grading, neurological deficits, NPE clinical symptoms, and pulmonary index were measured at 24 hours following SAH. Western blot, gelatin zymography, lung histopathology, and immunofluorescence staining were performed in the left lung lobe to explore the underlying mechanisms at 24 hours post-surgery.ResultsThe incidence of clinical symptoms was correlated with pulmonary index. P2X7R and the marker of alveolar type I epithelial cells (the mucin-type glycoprotein T1-α) immunoreactivities were generally co-localized. BBG administration decreased mature interleukin-1β, myeloperoxidase, and matrix metallopeptidase-9 activation, but increased tight junction proteins, such as ZO-1 and occludin, which ameliorated pulmonary edema via anti-inflammation and improved neurological deficits.ConclusionP2X7R inhibition prevented NPE after SAH by attenuating inflammation. Thus, BBG is a potential therapeutic application for NPE after SAH and warrants further research.

Medical image of the week: neurogenic pulmonary edema

Medical image of the week: neurogenic pulmonary edema

Role of &amp;#945;- and &amp;#946;-adrenergic Mechanisms in the Pathogenesis of Pulmonary Injuries Characterized by Edema, Inflammation and Fibrosis

Adrenergic mechanisms are involved in the formation of several types of pulmonary edema (PE) such as neurogenic pulmonary edema (NPE) or PE in patients with pheochromocytoma, but also in the development of pulmonary fibrosis and pulmonary hypertension. In severe cases of PE such as in the adult respiratory distress syndrome (ARDS), PE is typically accompanied by inflammation and followed by pulmonary vascular hypertrophy and pulmonary fibrosis. Norepinephrine and other adrenoceptor agonists are known to provoke activation of proinflammatory cytokines such as interleukin (IL)-1 and IL-6. These cytokines are involved both in the pathogenesis of PE and of pulmonary fibrosis. We therefore assume that adrenergic mechanisms may have an important role in the pathogenesis of pulmonary injuries characterized by edema, inflammation and fibrosis. The contribution of adrenoceptor stimulation, particularly the distinct role of α- and β-adrenergic mechanisms, to the development of PE and pulmonary fibrosis is reviewed in this paper.

Inhaled nitric oxide for the brain dead donor with neurogenic pulmonary edema during anesthesia for organ donation: a case report.

Neurogenic pulmonary edema (NPE) in brain dead organ donors occurring after an acute central nervous system insult threatens organ preservation of potential organ donors and the outcome of organ donation. Hence the active and immediate management of NPE is critical. In this case, a 50-year-old male was admitted to the intensive care unit (ICU) for organ donation. He was hypoxic due to NPE induced by spontaneous intracerebral hemorrhage and intraventricular hemorrhage. Protective ventilatory management, intermittent recruitment maneuvers, and supportive treatment were maintained in the ICU and the operating room (OR). Despite this management, the hypoxemia worsened after the OR admission. So inhaled nitric oxide (NO) therapy was performed during the operation, and the hypoxic phenomena showed remarkable improvement. The organ retrieval was successfully completed. Therefore, NO inhalation can be helpful in the improvement of hypoxemia caused by NPE in brain dead organ donors during anesthesia for the organ donation.

The harmful effects of subarachnoid hemorrhage on extracerebral organs.

Subarachnoid hemorrhage (SAH) is a devastating neurological disorder. Patients with aneurysmal SAH develop secondary complications that are important causes of morbidity and mortality. Aside from secondary neurological injuries, SAH has been associated with nonneurologic medical complications, such as neurocardiogenic injury, neurogenic pulmonary edema, hyperglycemia, and electrolyte imbalance, of which cardiac and pulmonary complications are most common. The related mechanisms include activation of the sympathetic nervous system, release of catecholamines and other hormones, and inflammatory responses. Extracerebral complications are directly related to the severity of SAH-induced brain injury and indicate the clinical outcome in patients. This review provides an overview of the extracerebral complications after SAH. We also aim to describe the manifestations, underlying mechanisms, and the effects of those extracerebral complications on outcome following SAH.

Understanding enterovirus 71 infection and neuropathogenesis: perspective from human and animal model studies

Enterovirus 71 (EV71) (family Picornaviridae, genus Human Enterovirus A) causes the relatively mild hand, foot and mouth disease in children. However, rare complications including meningitis, acute transverse myelitis, flaccid paralysis and encephalomyelitis may occur. Recently, many EV71 outbreaks with significant mortality in the Asia-Pacific region and beyond have posed serious public health concerns worldwide. Fatal encephalomyelitis is mainly the result of severe inflammation and neuronal damage in the brainstem, spinal cord and other parts of the brain. Medullary involvement is believed to result in neurogenic pulmonary oedema and sudden collapse typically found in fatal cases. A recent study has demonstrated viral replication in tonsillar crypt epithelium, suggesting that tonsil may be a portal for viral entry into the body. Presumably this is followed by viral replication in other sites (e.g. skin) and/or viraemia, leading to neuroinvasion possibly by a retrograde peripheral motor nerve route. There is also increasing evidence that the SCARB2 receptor may be an important receptor for human EV71 infection. A possible hypothesis for viral transmission into the body leading to CNS infection will be discussed. The value of human material and animal models to study viral infections in general and EV71 infection in particular is emphasized.

New vaccine against enterovirus 71 effective

Journal of Paediatrics and Child HealthVolume 50, Issue 1 p. 83-84 Heads UpFree Access New vaccine against enterovirus 71 effective First published: 07 January 2014 https://doi.org/10.1111/jpc.12479_4AboutSectionsPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat Enterovirus 71 (EV71) commonly causes hand-foot-and-mouth disease, but infection can be complicated occasionally by devastating brain-stem encephalitis presenting with myoclonic jerks in sleep, tachypnoea and collapse due to neurogenic pulmonary oedema. Other complications include acute flaccid paralysis resembling poliomyelitis. Outbreaks of EV71 infection have affected children across Asia and, more recently, Australia. In 2010, there were 1.8 million cases in China and 908 deaths. A Chinese randomised controlled trial1 in over 10 000 children aged 6–35 months found that two IM doses of an inactivated EV71 vaccine was 90% effective (95% CI 67.1–96.9) against hand-foot-and-mouth disease and 80.4% effective (95% CI 58.2–90.8) against EV71-asociated disease 2–14 months later. There were no serious adverse events. Use of the vaccine will depend on evidence of protection against severe disease and of cost-effectiveness. Reference 1 Zhu F-C et al. Lancet 2013; 381: 2024– 2032. CrossrefCASPubMedWeb of Science®Google Scholar Reviewer: David Isaacs, david.isaacs@health.nsw.gov.au Volume50, Issue1January 2014Pages 83-84 ReferencesRelatedInformation

Association between serum lactate levels and early neurogenic pulmonary edema after nontraumatic subarachnoid hemorrhage.

Few studies have described the risk factors associated with the development of neurological pulmonary edema (NPE) after subarachnoid hemorrhage (SAH). We have hypothesized that acute-phase increases in serum lactate levels are associated with the early development of NPE following SAH. The aim of this study was to clarify the association between lactic acidosis and NPE in patients with nontraumatic SAH. We retrospectively evaluated 140 patients with nontraumatic SAH who were directly transported to the Nippon Medical School Hospital emergency room by the emergency medical services. We compared patients in whom NPE developed (NPE group) and those in whom it did not (non-NPE group). The median (quartiles 1-3) arrival time at the hospital was 32 minutes (28-38 minutes) after the emergency call was received. Although the characteristics of the NPE and non-NPE groups, including mean arterial pressure (121.3 [109.0-144.5] and 124.6 [108.7-142.6] mm Hg, respectively; P=0.96), were similar, the median pH and the bicarbonate ion (HCO3(-)) concentrations were significantly lower in the NPE group than in the non-NPE group (pH, 7.33 [7.28-7.37] vs. 7.39 [7.35-7.43]); P=0.002; HCO3(-), 20.8 [18.6-22.6] vs. 22.8 [20.9-24.7] mmol/L; P=0.01). The lactate concentration was significantly higher in the NPE group (54.0 [40.3-61.0] mg/dL) than in the non-NPE group (28.0 [17.0-37.5] mg/dL; P<0.001). Multivariable regression analysis indicated that younger age and higher glucose and lactate levels were significantly associated with the early onset of NPE in patients with SAH. The present findings indicate that an increased serum lactate level, occurring within 1 hour of the ictus, is an independent factor associated with the early onset of NPE. Multicenter prospective studies are required to confirm our results.