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Background: Impaired respiratory function remains underrecognized in patients with type 2 diabetes (T2D), despite common pulmonary impairment. Meanwhile, there is little data available on the respiratory effects of sodium glucose cotransporter 2 inhibitors (SGLT2i). Hence, we examined the association between SGLT2i use and the risk of adverse respiratory events in a real-world setting., Methods: We conducted a population-based, nationwide cohort study using an active-comparator new-user design and nationwide claims data of South Korea from January 2015 to December 2020. Among individuals aged 18 years or older, propensity score matching was done to match each new user of SGLT2is with dipeptidyl peptidase 4 inhibitors (DPP4is), with patients followed up according to an as-treated definition. The primary outcome was respiratory events, a composite endpoint of acute pulmonary edema, acute respiratory distress syndrome (ARDS), pneumonia, and respiratory failure. Secondary outcomes were the individual components of the primary outcome and in-hospital death. Cox models were used to estimate hazard ratios (HRs) and 95% CIs., Results: Of 205,534 patient pairs in the propensity score matched cohort, the mean age of the entire cohort was 53.8 years and 59% were men, with a median follow-up of 0.66 years; all baseline covariates achieved balance between the two groups. Incidence rates for overall respiratory events were 4.54 and 7.54 per 1000 person-years among SGLT2i and DPP4i users, respectively, corresponding to a rate difference of 3 less events per 1000 person-years (95% CI - 3.44 to - 2.55). HRs (95% CIs) were 0.60 (0.55 to 0.64) for the composite respiratory endpoint, 0.35 (0.23 to 0.55) for acute pulmonary edema, 0.44 (0.18 to 1.05) for ARDS, 0.61 (0.56 to 0.66) for pneumonia, 0.49 (0.31 to 0.76) for respiratory failure, and 0.46 (0.41 to 0.51) for in-hospital death. Similar trends were found across individual SGLT2is, subgroup analyses of age, sex, history of comorbidities, and a range of sensitivity analyses., Conclusions: These findings suggest a lower risk of adverse respiratory events associated with patients with T2D initiating SGLT2is versus DPP4is. This real-world evidence helps inform patients, clinicians, and guideline writers regarding the respiratory effects of SGLT2i in routine practice., (© 2023. The Author(s).)

Background: No direct approach assessing pulmonary vascular permeability exists in the current therapeutic strategy for patients with acute respiratory distress syndrome (ARDS). Transpulmonary thermodilution measures hemodynamic parameters such as pulmonary vascular permeability index and extravascular lung water, enabling clinicians to assess ARDS severity. The aim of this study is to explore a precise transpulmonary thermodilution-based criteria for quantifying the severity of lung injury using a clinically relevant septic-ARDS pig model., Methods: Thirteen female pigs (weight: 31 ± 2 kg) were intubated, mechanically ventilated under anesthesia, and either assigned to septic shock-induced ARDS or control group. To confirm the development of ARDS, we performed computed tomography (CT) imaging in randomly selected animals. The pulmonary vascular permeability index, extravascular lung water, and other hemodynamic parameters were consecutively measured during the development of septic lung injury. Lung status was categorized as normal (partial pressure of oxygen/fraction of inspired oxygen ≥ 400), or injured at different degrees: pre-ARDS (300-400), mild-to-moderate ARDS (100-300), or severe ARDS (< 100). We also measured serum inflammatory cytokines and high mobility group box 1 levels during the experiment to explore the relationship of the pulmonary vascular permeability index with these inflammatory markers., Results: Using CT image, we verified that animals subjected to ARDS presented an extent of consolidation in bilateral gravitationally dependent gradient that expands over time, with diffuse ground-glass opacification. Further, the post-mortem histopathological analysis for lung tissue identified the key features of diffuse alveolar damage in all animals subjected to ARDS. Both pulmonary vascular permeability index and extravascular lung water increased significantly, according to disease severity. Receiver operating characteristic analysis demonstrated that a cut-off value of 3.9 for the permeability index provided optimal sensitivity and specificity for predicting severe ARDS (area under the curve: 0.99, 95% confidence interval, 0.98-1.00; sensitivity = 100%, and specificity = 92.5%). The pulmonary vascular permeability index was superior in its diagnostic value than extravascular lung water. Furthermore, the pulmonary vascular permeability index was significantly associated with multiple parameters reflecting clinicopathological changes in animals with ARDS., Conclusion: The pulmonary vascular permeability index is an effective indicator to measure septic ARDS severity., (© 2022. The Author(s).)

Background: Acute lung injury (ALI) is the most serious complication of subarachnoid hemorrhage (SAH). We investigated role of autophagy and inflammatory signaling pathways in lung damage and therapeutic effects of dexmedetomidine (DEX)., Methods: Fifty male Wistar rats were randomly divided into five groups: sham, SAH, SAH+ DEX5, SAH+DEX25, and SAH+DEX50. SAH was induced using endovascular perforation technique. All rats received mechanical ventilation for 60 minutes. At 2 and 24 h of SAH induction, SAH+DEX groups were treated with 5, 25, and 50 µg/kg of DEX, respectively. Histological ALI score and pulmonary edema were assessed after 48 h. Lung expression of LC3B, ATG3, p62, TLR4, TLR9, and NFκB was assessed using western blotting and quantitative PCR. Blood levels of IL-6, IL-1β, IFN-γ, and TNFα were also assessed., Results: SAH induced ALI and pulmonary edema, which were attenuated in SAH+DEX5 (P < 0.001 for both) and SAH+DEX25 groups (P = 0.001 and P < 0.001 for ALI and edema, respectively). Lung expressions of LC3B and ATG3 were upregulated in SAH group, which was attenuated in SAH+DEX5 and SAH+DEX25 groups. Lung expressions of TLR4, TLR9, and NFκB were increased in SAH group, which was attenuated in SAH+DEX5 group. Blood IL-6 level was increased in SAH group and attenuated in SAH+DEX5 and SAH+DEX25 groups. Blood IFN-γ level was lower in SAH group than in sham group, and it was increased in SAH+DEX25 group., Conclusions: Low-dose DEX treatment after SAH may protect against ALI by disrupting pathological brain-lung crosstalk and alleviating autophagy flux and TLR-dependent inflammatory pathways.

Background: Residual congestion detected using handheld ultrasound may be associated with increased risk of readmission and death after hospitalization for acute decompensated heart failure (ADHF). However, effective application necessitates routine use by nonexperts delivering clinical care., Objectives: The objective of this study was to determine the ability of heart failure (HF) nurses to deliver a predischarge lung and inferior vena cava (IVC) assessment (LUICA) to predict 90-day outcomes., Methods: In this multisite, prospective, observational study, HF nurses scanned 240 patients with ADHF (median age: 77 years; 56% men) using a 9-zone LUICA protocol. Obtained images were reviewed by independent nurses who were blinded to clinical characteristics and outcomes. Based on a B-line cut-off of 10, patients were dichotomized as congested (n = 115) or not congested (n = 125)., Results: Congested patients were more likely to have previous cardiac operations, long-standing HF (>6 months), and renal impairment. At 90 days, HF readmission or mortality occurred in 42 congested patients (37%) compared with 18 noncongested patients (14%). Pulmonary congestion increased at 30-day (OR: 3.86; 95% CI: 1.65-8.99; P < 0.01) and 90-day (OR: 3.42; 95% CI: 1.82-6.4; P < 0.01) HF readmission or mortality risk and 90-day mortality (OR: 5.18; 95% CI: 1.44-18.69; P < 0.01). Pulmonary congestion increased the 90-day odds of HF readmission and/or death by 3.3- to 4.2-fold (P < 0.01), independent of demographics, HF characteristics, comorbidities, and event risk score. Over 90 days, days alive out of hospital were fewer (78.3 ± 21.4 days vs 85.5 ± 12.4 days; P < 0.01) in congested patients., Conclusions: LUICA can be a powerful tool for detection of predischarge residual congestion. HF nurses can obtain images and provide diagnostic reports that are predictive of ADHF outcomes., Competing Interests: Funding Support and Author Disclosures Supported in part by a “Keeping Australians out of Hospital” grant from the Medical Research Future Fund (1176629), Canberra, Australia, and a National Health and Medical Research Council (NHMRC) Partnership grant (1059738), Canberra, Australia. Dr Huynh is supported by an Early Career Fellowship, National Heart Foundation, Melbourne, Victoria, Australia. Dr Zisis is supported by a postgraduate research scholarship from The University of Melbourne and Baker Institute. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose., (Copyright © 2022 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.)

Objectives: The aim of the study was to determine whether cardiogenic pleural effusion in cats is associated with a lower risk of arterial thromboembolism (ATE) compared with cats with cardiac disease without evidence of pleural effusion., Methods: A cross-sectional study was conducted on owned cats with natural occurring cardiac diseases. Cats included were classified in three groups: those with cardiac disease but no evidence of congestive heart failure (CHF); those with evidence of cardiogenic pulmonary oedema; and those with evidence of cardiogenic pleural effusion. Prevalence of ATE was calculated and the variables analysed for an association with this outcome were the presence and type of CHF, sex and neuter status, age, breed, type of cardiac diseases and left atrial (LA) dimension. A multivariable logistic regression model was used to fit the association between ATE and these variables., Results: A total of 366 cats with cardiac disease met the inclusion criteria: 179 were included in the group with cardiac disease but no evidence of CHF, 66 in the group with evidence of cardiogenic pulmonary oedema and 121 in the group with evidence of cardiogenic pleural effusion. Prevalence of ATE (58/366 [15.8%]) was significantly different among groups (with no evidence of CHF, 28/179 [15.6%]; with evidence of cardiogenic pulmonary oedema, 22/66 [33.3%]; with evidence of cardiogenic pleural effusion, 8/121 [6.6%]; P <0.001). Cats with ATE had a significantly higher LA to aortic root ratio (2.30 ± 0.46) than those without ATE (2.04 ± 0.46; P <0.001). Multivariable logistic regression analysis indicated that the group with evidence of cardiogenic pleural effusion was associated with a lower risk of developing ATE compared with groups with cardiac disease but no evidence of CHF and with evidence of cardiogenic pulmonary oedema ( P  = 0.005 and P <0.001, respectively)., Conclusions and Relevance: Presence of cardiogenic pleural effusion is associated with a lower risk of developing ATE, while LA enlargement is a risk factor for ATE.

Acute respiratory distress syndrome (ARDS), caused by noncardiogenic pulmonary edema (PE), contributes significantly to Coronavirus 2019 (COVID-19)-associated morbidity and mortality. We explored the effect of transmembrane osmotic pressure (OP) gradients in PE using a fluorescence resonance energy transfer-based Intermediate filament (IF) tension optical probe. Angiotensin-II- and bradykinin-induced increases in intracellular protein nanoparticle (PN)-OP were associated with inflammasome production and cytoskeletal depolymerization. Intracellular protein nanoparticle production also resulted in cytomembrane hyperpolarization and L-VGCC-induced calcium signals, which differed from diacylglycerol-induced calcium increment via TRPC6 activation. Both pathways involve voltage-dependent cation influx and OP upregulation via SUR1-TRPM4 channels. Meanwhile, intra/extracellular PN-induced OP gradients across membranes upregulated pulmonary endothelial and alveolar barrier permeability. Attenuation of intracellular PN, calcium signals, and cation influx by drug combinations effectively relieved intracellular OP and pulmonary endothelial nonselective permeability, and improved epithelial fluid absorption and PE. Thus, PN-OP is pivotal in pulmonary edema in ARDS and COVID-19, and transmembrane OP recovery could be used to treat pulmonary edema and develop new drug targets in pulmonary injury., (© 2022. The Author(s).)

Background: Systemic lupus erythematosus (SLE) is a chronic multisystem autoimmune inflammatory disease predominantly found in women of child-bearing age. Neurogenic pulmonary edema (NPE) is a recalcitrant complication that occurs after injury to the central nervous system and has an acute onset and rapid progression. Limbic encephalitis is an inflammatory encephalopathy caused by viruses, immune responses, or other factors involving the limbic system. NPE caused by SLE is rare., Case Presentation: Here, we report a case of a 21-year-old woman with SLE who experienced five episodes of generalized tonic-clonic seizure after headache and dyspnea. Anti-α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR) 2 antibody was tested positive in the serum and cerebrospinal fluid. Electrocardiography (EEG) indicated paroxysmal or sporadic medium amplitude theta activity. In addition, chest computed tomography (CT) showed multiple diffuse consolidations and ground-glass opacities. We finally considered a diagnosis of NPE and AMPAR limbic encephalitis. The patient's symptoms improved obviously after methylprednisolone pulse therapy and antiepileptic treatment., Conclusions: NPE can be a complication of neuropsychiatric lupus erythematosus (NPSLE). AMPAR2 antibodies may be produced in NPSLE patients, especially in those with high polyclonal IgG antibody titers. More basic and clinical studies are required to confirm these observations and elucidate the pathogenicity of encephalitis-related autoantibodies in SLE patients., (© 2022. The Author(s).)

Vizcarra-Vizcarra, Cristhian A. and Angélica L. Alcos-Mamani. High-altitude pulmonary edema in a chronic kidney disease patient-Is peritoneal dialysis a risk factor? High Alt Med Biol . 23:96-99, 2022.-High-altitude pulmonary edema is a cause of acute respiratory failure secondary to hypobaric hypoxia, which occurs after ascent above 2,500 m (8,202 feet), in susceptible people or without prior acclimatization. We present the case of a 20-year-old man with chronic kidney disease (CKD) on peritoneal dialysis (PD), living at sea (Mollendo, Peru) who presented with dyspnea and pulmonary congestion, after ascending to a high-altitude city (Juliaca, Peru at 3,827 m or 12,555 feet). The patient required diuretics, nifedipine, PD, tracheal intubation, and mechanical ventilation, but recovered and was discharged without complications. We think that CKD and PD could be risk factors for the development of high-altitude pulmonary edema, secondary to pulmonary hypertension and fluid overload, so this diagnosis should be considered in this group of patients when they ascend to high altitude.

Sporadic occurrences and outbreaks of hand, foot, and mouth disease (HFMD) caused by Coxsackievirus A2 (CVA2) have frequently reported worldwide recently, which pose a great challenge to public health. Epidemiological studies have suggested that the main cause of death in critical patients is pulmonary edema. However, the pathogenesis of this underlying comorbidity remains unclear. In this study, we utilized the 5-day-old BALB/c mouse model of lethal CVA2 infection to evaluate lung damage. We found that the permeability of lung microvascular was significantly increased after CVA2 infection. We also observed the direct infection and apoptosis of lung endothelial cells as well as the destruction of tight junctions between endothelial cells. CVA2 infection led to the degradation of tight junction proteins (e.g., ZO-1, claudin-5, and occludin). The gene transcription levels of von Willebrand factor (vWF), endothelin (ET), thrombomodulin (THBD), granular membrane protein 140 (GMP140), and intercellular cell adhesion molecule-1 (ICAM-1) related to endothelial dysfunction were all significantly increased. Additionally, CVA2 infection induced the increased expression of inflammatory cytokines (IL-6, IL-1β, and MCP-1) and the activation of p38 mitogen-activated protein kinase (MAPK). In conclusion, the disruption of the endothelial barrier contributes to acute lung injury induced by CVA2 infection; targeting p38-MAPK signaling may provide a therapeutic approach for pulmonary edema in critical infections of HFMD.

The study is aimed at investigating the changes in expressions of heat shock protein 27 (HSP27), HSP70, and soluble glycoprotein (SGP) in heart failure (HF) rats complicated with pulmonary edema and exploring their potential correlations with cardiopulmonary functions. The rat model of HF was established, and the rats were divided into HF model group (model group, n = 15) and normal group ( n = 15). After successful modeling, MRI and ECG were applied to detect the cardiac function indexes of the rats. The myocardial function indexes were determined, the injury of myocardial tissues was observed via hematoxylin and eosin (HE) staining, and the content of myeloperoxidase (MPO), matrix metalloproteinase-9 (MMP-9), and tumor necrosis factor-alpha (TNF- α ) in the blood was measured. The partial pressure of oxygen (PaO 2 ) and oxygenation index (OI) were observed, and the airway resistance and lung compliance were examined. Moreover, quantitative polymerase chain reaction (qPCR) and Western blotting assay were performed to detect the gene and protein expression levels of HSP27, HSP70, and SGP130. The levels of serum creatine kinase (CK), creatine (Cr), and blood urea nitrogen (BUN) were increased markedly in model group ( p < 0.05). Model group had notably decreased fractional shortening (FS) and ejection fraction (EF) compared with normal group ( p < 0.05), while the opposite results of left ventricular end-diastolic diameter (LVEDD) and left ventricular end-systolic diameter (LVESD) were detected. In model group, the content of serum MPO, MMP-9, and TNF- α was raised remarkably ( p < 0.05), OI and PaO 2 were reduced notably ( p < 0.05), the airway resistance was increased ( p < 0.05), and the lung compliance was decreased ( p < 0.05). Obviously elevated gene and protein expression levels of HSP27, HSP70, and SGP130 were detected in model group ( p < 0.05). The expressions of HSP27, HSP70, and SGP130 are increased in HF rats complicated with pulmonary edema, seriously affecting the cardiopulmonary functions of the rats., Competing Interests: The authors declare that they have no competing interests., (Copyright © 2021 Yingcai Hong et al.)

The present study was to investigate the effect of mesenteric lymph duct drainage on lung inflammatory response, histological alteration, and endothelial cell apoptosis in septic rats. Animals were randomly assigned into four groups: control, sham surgery, sepsis, and sepsis plus mesenteric lymph drainage. We used the colon ascendens stent peritonitis (CASP) procedure to induce the septic model in rats, and mesenteric lymph drainage was performed with a polyethylene (PE) catheter inserted into mesenteric lymphatic. The animals were sacrificed at the end of CASP in 6 h. The mRNA expression levels of inflammatory mediators were measured by qPCR, and the histologic damage were evaluated by the pathological score method. It was found that mesenteric lymph drainage significantly reduced the expression of TNF- α , IL-1 β , and IL-6 mRNA in the lung. Pulmonary interstitial edema and infiltration of inflammatory cells were alleviated by mesenteric lymph drainage. Moreover, increased mRNA levels of TNF- α , IL-1 β , IL-6 mRNA, and apoptotic rate were observed in PMVECs treated with septic lymph. These results indicate that mesenteric lymph duct drainage significantly attenuated lung inflammatory injury by decreasing the expression of pivotal inflammatory mediators and inhibiting endothelial apoptosis to preserve the pulmonary barrier function in septic rats., Competing Interests: The authors declare that there are no conflicts of interest., (Copyright © 2020 Yongjun Liu et al.)

Neurogenic pulmonary edema (NPE) following acute stroke is an acute respiratory distress syndrome (ARDS) with clinical characteristics that include acute onset, apparent pulmonary interstitial fluid infiltration and rapid resolution. The pathological process of NPE centers on sympathetic stimulation and fulminant release of catecholamines, which cause contraction of resistance vessels. Elevated systemic resistance forces fluid into pulmonary circulation, while pulmonary circulation overload induces pulmonary capillary pressure that elevates, and in turn damages the alveolar capillary barrier. Damage to the alveolar capillary barrier leads to pulmonary ventilation disorder, blood perfusion disorder and oxygenation disorder. Eventually, NPE will cause post-stroke patients' prognosis to further deteriorate. At present, we lack specific biological diagnostic indicators and a meticulously unified diagnostic criterion, and this results in a situation in which many patients are not recognized quickly and/or diagnosed accurately. There are no drugs that are effective against NPE. Therefore, understanding how to diagnose NPE early by identifying the risk factors and how to apply appropriate treatment to avoid a deteriorating prognosis are important scientific goals. We will elaborate the progress of NPE after acute stroke in terms of its pathophysiological mechanisms, etiology, epidemiology, clinical diagnosis and early prediction, comprehensive treatment strategies, and novel drug development. We also propose our own thinking and prospects regarding NPE., (Copyright © 2020 The Author(s). Published by Elsevier Masson SAS.. All rights reserved.)

Background: Noninvasive ventilation (NIV) has been reported to be beneficial for patients with acute respiratory failure in intensive care unit (ICU); however, factors that influence the clinical outcome of NIV were unclarified. We aim to determine the factors that predict the failure of NIV in critically ill patients with acute respiratory failure (ARF). Setting . Adult mixed ICU in a medical university affiliated hospital. Patients and Methods . A retrospective clinical study using data from critical adult patients with initial NIV admitted to ICU in the period August 2016 to November 2017. Failure of NIV was regarded as patients needing invasive ventilation. Logistic regression was employed to determine the risk factor(s) for NIV, and a predictive model for NIV outcome was set up using risk factors., Results: Of 101 included patients, 50 were unsuccessful. Although more than 20 variables were associated with NIV failure, multivariate logistic regression demonstrated that only ideal body weight (IBW) (OR 1.110 (95%1.027-1.201), P =0.009), the maximal heart rate during NIV period (HR-MAX) (OR 1.024 (1.004-1.046), P =0.021), the minimal respiratory rate during NIV period (RR-MIN) (OR 1.198(1.051-1.365), P =0.007), and the highest body temperature during NIV period (T-MAX) (OR 1.838(1.038-3.252), P =0.037) were independent risk factors for NIV failure. We set up a predictive model based on these independent risk factors, whose area under the receiver operating characteristic curve (AUROC) was 0.783 (95% CI: 0.676-0.899, P < 0.001), and the sensitivity and specificity of model were 68.75% and 71.43%, respectively, with the optimal cut-off value of 0.4863., Conclusion: IBW, HR-MAX, RR-MIN, and T-MAX were associated with NIV failure in patients with ARF. A predictive model based on the risk factors could help to discriminate patients who are vulnerable to NIV failure., Competing Interests: The authors declare that they have no conflicts of interest., (Copyright © 2020 Qimin Chen et al.)

Aims: Increases in extravascular lung water (EVLW) during exercise contribute to symptoms, morbidity, and mortality in patients with heart failure and preserved ejection fraction (HFpEF), but the mechanisms leading to pulmonary congestion during exercise are not well-understood., Methods and Results: Compensated, ambulatory patients with HFpEF (n = 61) underwent invasive haemodynamic exercise testing using high-fidelity micromanometers with simultaneous lung ultrasound, echocardiography, and expired gas analysis at rest and during submaximal exercise. The presence or absence of EVLW was determined by lung ultrasound to evaluate for sonographic B-line artefacts. An increase in EVLW during exercise was observed in 33 patients (HFpEFLW+, 54%), while 28 (46%) did not develop EVLW (HFpEFLW-). Resting left ventricular function was similar in the groups, but right ventricular (RV) dysfunction was two-fold more common in HFpEFLW+ (64 vs. 31%), with lower RV systolic velocity and RV fractional area change. As compared to HFpEFLW-, the HFpEFLW+ group displayed higher pulmonary capillary wedge pressure (PCWP), higher pulmonary artery (PA) pressures, worse RV-PA coupling, and higher right atrial (RA) pressures during exercise, with increased haemoconcentration indicating greater loss of water from the vascular space. The development of lung congestion during exercise was significantly associated with elevations in PCWP and RA pressure as well as impairments in RV-PA coupling (area under the curve values 0.76-0.84)., Conclusion: Over half of stable outpatients with HFpEF develop increases in interstitial lung water, even during submaximal exercise. The acute development of lung congestion is correlated with increases in pulmonary capillary hydrostatic pressure that favours fluid filtration, and systemic venous hypertension due to altered RV-PA coupling, which may interfere with fluid clearance., Clinical Trial Registration: NCT02885636., (Published on behalf of the European Society of Cardiology. All rights reserved. © The Author(s) 2019. For permissions, please email: journals.permissions@oup.com.)

Background: Numerous studies have shown that exposure to air pollution, especially particulate matter (PM) with a diameter <2.5 μm (PM2.5), was associated with various diseases. We tried to determine the impact of PM2.5 and other weather factors on acute lung edema in patients with Stage 5 nondialysis chronic kidney disease (CKD Stage 5-ND)., Methods: In total, 317 CKD Stage 5-ND (estimated glomerular filtration rate 6.79 ± 4.56 mL/min) patients residing in central Taiwan who developed acute lung edema and initiated long-term dialysis were included in this case-crossover study. Pearson's correlation test was used to examine the relationship of acute lung edema cases with PM2.5 levels and ambient temperature separately., Results: The average PM2.5 level within the 7-day period correlated with acute lung edema incidence in the fall [adjusted odds ratio (OR) 3.23, P = 0.047] and winter (adjusted OR 1.99, P < 0.001). In winter, even a 3-day exposure to PM2.5 was associated with increased risk (adjusted OR 1.55, P < 0.001). The average temperatures within 3 days in spring and summer were correlated positively with the risk (adjusted OR 2.77 P < 0.001 and adjusted OR 2.72, P < 0.001, respectively). In the fall and winter, temperatures were correlated negatively with the risk (adjusted OR 0.36, P < 0.001 and adjusted OR 0.54, P < 0.001, respectively)., Conclusions: A high PM2.5 level was associated with an increased risk of acute lung edema. High ambient temperature in hot seasons and low ambient temperature in cold seasons were also associated with increased risk. It is essential to educate these patients to avoid areas with severe air pollution and extreme ambient temperature., (© The Author(s) 2018. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved.)

Background: Acute mountain sickness (AMS) is a common disease that may have a pulmonary component, as suggested by interstitial pulmonary edema quantified by the B-line score (BLS) on ultrasound (US). This subclinical pulmonary edema has been shown to increase with ascent to high altitude and AMS severity, but has not been prospectively associated with AMS incidence in a large prospective study. Materials and Methods: This prospective observational study was part of a randomized controlled trial enrolling healthy adults over four weekends ascending White Mountain, California. Subjects were assessed by lung US and the Lake Louise Questionnaire at 4110 ft (1240 m), upon ascent to 12,500 ft (3810 m), and the next morning at 12,500 ft (3810 m). Results: Three hundred five USs in total were completed on 103 participants, with 73% total incidence of AMS. The mean (±standard deviation) BLS increased from baseline (1.15 ± 1.80) to high altitude (2.56 ± 2.86), a difference of 1.37 (±2.48) ( p  = 0.04). Overall BLS was found, on average, to be higher among those diagnosed with AMS than without (2.97 vs. 2.0, p  = 0.04, 95% confidence interval [CI] -∞ to -0.04). The change in BLS (ΔBLS) from low altitude baseline was significantly associated with AMS (0.88 vs. 1.72, r 2  = 0.023, 95% CI -∞ to -0.01, p  = 0.048). Conclusions: Interstitial subclinical pulmonary edema by lung US was found to have a small but significant association with AMS.

Background: The negative pressure pulmonary edema is rare clinical situation which caused mainly by upper airway obstruction. However except upper airway obstruction, there may be other pathophysiological disorders making patients more vulnerable to pulmonary edema. Based on these disorders, upper airway obstruction is the trigger to induce negative pressure pulmonary edema., Case Presentation: This case was a 5-year-old girl with tumor on saddle area, her hormones level were abnormal preoperatively, such as cortisol, adrenocorticotrophic hormone, free T4 and total T4. During the stage of induction, negative pressure pulmonary edema took place due to mild upper airway obstruction. And the instant chest Computer tomography proved diagnosis clue. After intensive care, most lung field of this girl recovered to normal within 48 h., Conclusion: The patient with abnormal hormone levels is vulnerable to pulmonary edema, mild upper airway obstruction triggered negative pressure pulmonary. Thus pre-operation hormones supplement is as important as keeping upper airway unobstructed.

Primary graft dysfunction (PGD) is a major limitation in short- and long-term lung transplant survival. Recent work has shown that mitochondrial damage-associated molecular patterns (mtDAMPs) can promote solid organ injury, but whether they contribute to PGD severity remains unclear. We quantitated circulating plasma mitochondrial DNA (mtDNA) in 62 patients, before lung transplantation and shortly after arrival to the intensive care unit. Although all recipients released mtDNA, high levels were associated with severe PGD development. In a mouse orthotopic lung transplant model of PGD, we detected airway cell-free damaged mitochondria and mtDNA in the peripheral circulation. Pharmacologic inhibition or genetic deletion of formylated peptide receptor 1 (FPR1), a chemotaxis sensor for N-formylated peptides released by damaged mitochondria, inhibited graft injury. An analysis of intragraft neutrophil-trafficking patterns reveals that FPR1 enhances neutrophil transepithelial migration and retention within airways but does not control extravasation. Using donor lungs that express a mitochondria-targeted reporter protein, we also show that FPR1-mediated neutrophil trafficking is coupled with the engulfment of damaged mitochondria, which in turn triggers reactive oxygen species (ROS)-induced pulmonary edema. Therefore, our data demonstrate an association between mtDAMP release and PGD development and suggest that neutrophil trafficking and effector responses to damaged mitochondria are drivers of graft damage., (© 2018 The American Society of Transplantation and the American Society of Transplant Surgeons.)

Rationale: Diffuse alveolar hemorrhage (DAH) is a rare life-threatening condition that accompanies general anesthesia. Negative-pressure pulmonary edema (NPPE) is a rare cause of DAH., Patient Concerns: A 25-year-old male patient developed hemoptysis following remifentanil administration by bolus injection with sugammadex at the emergence from general anesthesia., Diagnosis: Chest x-ray and computed tomography showed DAH., Interventions: Conservative care was provided with 4L of oxygen via nasal prong, 20 mg of Lasix and 2500 mg of tranexamic acid., Outcomes: The patient was discharged uneventfully., Lessons: Muscle rigidity by remifentanil and the dissociated reversal of neuromuscular blockade by sugammadex was suspected as the cause of NPPE-related DAH. Therefore, the possibility NPPE-related DAH should be considered when using a bolus of remifentanil and sugammadex during emergence from general anesthesia.

Background: During the past three decades conflicting evidences have been published on the use of non-invasive ventilation (NIV) in patients with acute cardiogenic pulmonary edema (ACPE). The aim of this study is to describe the management of acute respiratory failure (ARF) due to ACPE in twelve Italian emergency departments (EDs). We evaluated prevalence, characteristics and outcomes of ACPE patients treated with oxygen therapy, continuous positive airway pressure (CPAP) or Bi-level positive airway pressure (BiPAP) on admission to the EDs., Methods: In this multicenter, prospective, observational study, consecutive adult patients with ACPE were enrolled in 12 EDs in Italy from May 2009 to December 2013. Three study groups were identified according to the initial respiratory treatment: patients receiving oxygen therapy, those treated with CPAP and those treated with BiPAP. Treatment failure was evaluated as study outcome., Results: We enrolled 1293 patients with acute cardiogenic pulmonary edema. 273 (21%) began with oxygen, 788 (61%) with CPAP and 232 (18%) with BiPAP. One out of four patient who began with oxygen was subsequently switched to NIV and initial treatment with oxygen therapy had an odds ratio for treatment failure of 3.65 (95% CI: 2.55-5.23, p < 0.001)., Conclusions: NIV seems to be the first choice for treatment of ARF due to ACPE, showing high clinical effectiveness and representing a rescue option for patients not improving with conventional oxygen therapy.

Objective: Renal transplantation is a risk factor for premalignant and malignant changes of the endometrium. Thus, prompt and aggressive treatment of postoperative complications remains a major issue. We report the case of an asymptomatic postmenopausal woman with a history of renal transplantation who underwent surgery for uterine serous carcinoma (USC)., Case Report: An asymptomatic 59-year-old woman who had undergone renal transplantation presented with elevated serum CA-125 levels. Cancer screening revealed uterine serous carcinoma, for which she underwent total hysterectomy and bilateral salpingo-oophorectomy. Unfortunately, the postoperative course was complicated by cardiogenic shock and decompensated heart failure. The complexities of the cardiac problems and renal transplantation required a multidisciplinary approach involving different specialists. She was successfully discharged 48 days after the surgery., Conclusion: Gynecologic cancer screening in asymptomatic postmenopausal women after renal transplantation is warranted. If postoperative complications occur in this population, a multidisciplinary approach is recommended., (Copyright © 2018. Published by Elsevier B.V.)

Neurogenic pulmonary oedema (NPO) is a rare clinical syndrome of pulmonary oedema occurring secondary to an insult of the central nervous system (CNS). The exact aetiology of this disorder is unknown. NPO can be fatal and poor awareness and identification of this entity, particularly in terms of misdiagnosis as primary pulmonary or cardiac disease, can result in suboptimal management and outcomes. We describe the presentation and management of a 68-year-old woman with an acute left lateral medullary stroke complicated by pulmonary oedema. The likely aetiology is discussed, and important learning points are highlighted., Competing Interests: Competing interests: None declared., (© BMJ Publishing Group Limited 2018. No commercial re-use. See rights and permissions. Published by BMJ.)

Background: Curcumin (CUR) is a Chinese medicine monomer with antioxidant and anti-inflammatory properties. The aim of this study was to investigate the effects and mechanisms of CUR treatment on ventilator-induced lung injury (VILI) in rats., Methods: Total 50 SD rats were divided into five groups: sham, VILI, VILI+CUR-50 (CUR 50?mg/kg pretreated intraperitoneal), VILI+CUR-200 (CUR 200?mg/kg pretreated intraperitoneal) and VILI?+?DXM (5?mg/kg pretreated intraperitoneal). The morphology and ultrastructure were observed by microscope and transmission electron microscope. The wet to dry ratio, protein concentration in bronchoalveolar lavage fluid (BALF), evans blue dye (EBD) content, nuclear factor kappa B (NF-?B) activity, myeloperoxidase (MPO), malondialdehyde (MDA), xanthine oxidase (XO) and total antioxidative capacity (TAOC) levels were measured., Results: Histological studies revealed that inflammatory cells infiltration and alveolar edema were significantly severe in VILI as compared to other groups. CUR-200 and DXM treatment reversed lung injury significantly. The wet to dry ratio, protein concentration in BALF, EBD content, MPO activity, tumor necrosis factor (TNF)-? level and NF-?B activity were significantly increased in VILI group as compared to other groups. CUR-200 and DXM treatment significantly suppressed permeability and inflammation induced by ventilation. Furthermore, the significantly higher MDA content in VILI could be markedly decreased by CUR-200 and DXM treatment while the levels of XO and TAOC were markedly recovered only by CUR (200?mg/kg) treatment after VILI., Conclusion: CUR could inhibit the inflammatory response and oxidative stress during VILI, which is partly through NF-?B pathway., (Copyright © 2017 Elsevier Masson SAS. All rights reserved.)

Rationale: In the original 1974 in vivo study of ventilator-induced lung injury, Webb and Tierney reported that high Vt with zero positive end-expiratory pressure caused overwhelming lung injury, subsequently shown by others to be due to lung shear stress., Objectives: To reproduce the lung injury and edema examined in the Webb and Tierney study and to investigate the underlying mechanism thereof., Methods: Sprague-Dawley rats weighing approximately 400 g received mechanical ventilation for 60 minutes according to the protocol of Webb and Tierney (airway pressures of 14/0, 30/0, 45/10, 45/0 cm H 2 O). Additional series of experiments (20 min in duration to ensure all animals survived) were studied to assess permeability (n = 4 per group), echocardiography (n = 4 per group), and right and left ventricular pressure (n = 5 and n = 4 per group, respectively)., Measurements and Main Results: The original Webb and Tierney results were replicated in terms of lung/body weight ratio (45/0 > 45/10 ≈ 30/0 ≈ 14/0; P < 0.05) and histology. In 45/0, pulmonary edema was overt and rapid, with survival less than 30 minutes. In 45/0 (but not 45/10), there was an increase in microvascular permeability, cyclical abolition of preload, and progressive dilation of the right ventricle. Although left ventricular end-diastolic pressure decreased in 45/10, it increased in 45/0., Conclusions: In a classic model of ventilator-induced lung injury, high peak pressure (and zero positive end-expiratory pressure) causes respiratory swings (obliteration during inspiration) in right ventricular filling and pulmonary perfusion, ultimately resulting in right ventricular failure and dilation. Pulmonary edema was due to increased permeability, which was augmented by a modest (approximately 40%) increase in hydrostatic pressure. The lung injury and acute cor pulmonale is likely due to pulmonary microvascular injury, the mechanism of which is uncertain, but which may be due to cyclic interruption and exaggeration of pulmonary blood flow.

Objective: To investigate the risk factors for neurogenic pulmonary edema (NPE) in patients with severe hand, foot, and mouth disease (HFMD) and to provide evidence for the prevention and treatment of NPE., Methods: Several databases were searched (from inception to 2017) to identify case-control studies on risk factors for NPE among patients with severe HFMD. Data were analyzed via meta-analysis. The combined odds ratio (OR) and 95% confidence interval (CI) were calculated using fixed-effects and random-effects models, and a sensitivity analysis and evaluation of publication bias was also performed., Results: A total of 14 studies involving 557 cases (severe HFMD with NPE) and 1450 controls (severe HFMD) were included. Results for the categorical variables were as follows: hyperglycemia (OR 10.25, 95% CI 4.82-21.76), tachycardia (OR 6.21, 95% CI 3.02-12.75), hypertension (OR 3.79, 95% CI 2.90-4.95), respiratory rhythm abnormality (OR 7.86, 95% CI 2.46-25.12), drowsiness (OR 8.11, 95% CI 4.26-15.44), vomiting (OR 8.96, 95% CI 3.83-20.96), limb tremors (OR 8.96, 95% CI 3.83-20.96), atypical rash (OR 4.27, 95% CI 2.83-6.45). No significant publication bias was found for the different factors., Conclusions: Drowsiness ranks first among risk factors for NPE in children with severe HFMD, followed by vomiting, tachycardia, hypertension, breathing rhythm changes, limb tremors, atypical rash, and hyperglycemia., (Copyright © 2017 The Author(s). Published by Elsevier Ltd.. All rights reserved.)

We describe a 36-year-old patient who was admitted to the emergency ward for acute dyspnea due to a spontaneous pneumothorax. He was successfully drained but shortly after presented a severe hypoxemia due to pulmonary oedema secondary to pulmonary re-expansion. The physiopathology behind this complication is still unknown. We will try to describe this complication and its predictive factors.

Transfusion-related acute lung injury (TRALI) is defined as a new episode of acute lung injury (ALI) occurring during transfusion or within 6 hours of transfusion completion. A 66-year-old man suffering from acute myeloid leukemia developed acute respiratory distress syndrome after platelet transfusion. TRALI was diagnosed clinically, but an autopsy showed leukemic cells in diffuse pulmonary edema. Anti-human neutrophil antigen (HNA)-3a antibodies were detected in the donor serum, and the HNA-3 genotype of the patient was identified as a/a. This case was considered to represent pulmonary involvement of acute myeloid leukemia, rather than TRALI. A revision of the definition of TRALI accounting for hematological malignancies should therefore be considered.

Chronic alcohol exposure is a clinically important risk factor for the development of acute respiratory distress syndrome, the most severe form of acute lung injury (ALI). However, the mechanisms by which alcohol sensitizes the lung to development of this disease are poorly understood. We determined the role of the antifibrinolytic protein plasminogen activator inhibitor-1 (PAI-1) in alcohol enhancement of experimental endotoxin-induced ALI. Wild-type, PAI-1 -/- , and integrin β 3 -/- mice were fed ethanol-containing Lieber-DeCarli liquid or a control diet for 6 weeks, followed by systemic LPS challenge. LPS administration triggered coagulation cascade activation as evidenced by increased plasma thrombin-antithrombin levels and pulmonary fibrin deposition. Ethanol-exposed animals showed enhanced PAI-1 expression and pulmonary fibrin deposition with coincident exaggeration of pulmonary inflammatory edematous injury. PAI-1 deficiency markedly reduced pulmonary fibrin deposition and greatly reduced inflammation and injury without impacting upstream coagulation. Interestingly, pulmonary platelet accumulation was effectively abolished by PAI-1 deficiency in ethanol/LPS-challenged mice. Moreover, mice lacking integrin α IIB β 3 , the primary platelet receptor for fibrinogen, displayed a dramatic reduction in early inflammatory changes after ethanol/LPS challenge. These results indicate that the mechanism whereby alcohol exaggerates LPS-induced lung injury requires PAI-1-mediated pulmonary fibrin accumulation, and suggest a novel mechanism whereby alcohol contributes to inflammatory ALI by enhancing fibrinogen-platelet engagement.

A 28-year-old pregnant woman presented at 28 weeks of gestation. She was diagnosed to have a left atrial myxoma 2 years earlier, but was lost to follow-up. During this pregnancy, the transthoracic echocardiography showed a 9 cm mass in the left atrium obstructing mitral valve inflow, interfering with mitral valve closure, causing severe mitral regurgitation and severe pulmonary hypertension. However, there were no clinical signs of pulmonary and systemic congestion or obstruction. Based on the clinical symptoms of the patient, the echocardiographic findings and the term of her pregnancy, the patient decided to schedule for a vaginal delivery with surgical correction after delivery. She gave birth at 32 weeks of gestation. During labour, pulmonary oedema developed but was detected early and it responded to therapy. Two weeks after delivery, a right anterior thoracotomy was performed to facilitate the removal of the left atrial myxoma and repair of the mitral valve., Competing Interests: Competing interests: None declared., (© BMJ Publishing Group Ltd (unless otherwise stated in the text of the article) 2017. All rights reserved. No commercial use is permitted unless otherwise expressly granted.)

The development of multiple organ failure in patients with hemorrhagic shock is significantly influenced by patient age. Adenosine monophosphate-activated protein kinase (AMPK) is a crucial regulator of energy homeostasis, which coordinates metabolic repair during cellular stress. We investigated whether AMPK-regulated signaling pathways are age-dependent in hemorrhage-induced lung injury and whether AMPK activation by 5-amino-4-imidazole carboxamide riboside (AICAR) affords lung protective effects. Male C57/BL6 young mice (3-5 mo), mature adult mice (9-12 mo), and young AMPKα1 knockout mice (3-5 mo) were subjected to hemorrhagic shock by blood withdrawing, followed by resuscitation with shed blood and lactated Ringer's solution. Plasma proinflammatory cytokines were similarly elevated in C57/BL6 young and mature adult mice after hemorrhagic shock. However, mature adult mice exhibited more severe lung edema and neutrophil infiltration, and higher mitochondrial damage in alveolar epithelial type II cells, than did young mice. No change in autophagy was observed. At molecular analysis, the phosphorylation of the catalytic subunit AMPKα1 was associated with nuclear translocation of peroxisome proliferator-activated receptor γ co-activator-α in young, but not mature, adult mice. Treatment with AICAR ameliorated the disruption of lung architecture in mice of both ages; however, effects in mature adult mice were different than young mice and also involved inhibition of nuclear factor-κB. In young AMPKα1 knockout mice, AICAR failed to improve hypotension and lung neutrophil infiltration. Our data demonstrate that during hemorrhagic shock, AMPK-dependent metabolic repair mechanisms are important for mitigating lung injury. However, these mechanisms are less competent with age.

Aim: Neurogenic pulmonary edema (NPE) is the most serious complication of subarachnoid hemorrhage (SAH). As vagal nerves have vital roles in lung functions, vagal ischemia may have a causative role in the pathogenesis of NPE. We examined whether there was a relationship between vagal complex ischemia and lung immune complexes occupying the lymph node infarct in SAH., Material and Methods: Thirty-two rabbits were divided into three groups: Control (n=5), SHAM (n=5) and SAH group (n=22). SAH was created by autologous blood injection into the cisterna magna and followed-up for 3 weeks. Vasospasm index (VSI) was defined as the ratio of the lung lymph node arteries (LLNA) wall section (wall ring) surface to the lumen surface. Degenerated axon numbers of vagal nerves, neuron densities of the nodose ganglion (NG) and VSIs of LLNA were compared for all groups., Results: The mean degenerated vagal nerve axon density, neuron density of NG, and VSI of LLNA were 26±8/mm < sup > 2 < /sup > , 30±5/mm < sup > 3 < /sup > , and 0.777±0.048 in the control group; 1300±100/mm2, 720±90/mm < sup > 3 < /sup > , and 1.148±0.090 in the animals with slight vasospasm (n=12); and 7300±530/mm < sup > 2 < /sup > , 5610±810/mm3, and 1.500±0.120 in the animals with severe vasospasm (n=10), respectively., Conclusion: Degenerated vagal axon and NG neuron density may be a causative factor in the development of LLNA vasospasm induced lymph node infarct in SAH. Lung lymph node infarct may be an important factor in the prognosis of NPE.

Epidemiological studies indicate that cigarette smoking (CS) increases the risk and severity of acute lung injury (ALI)/acute respiratory distress syndrome (ARDS). The mechanism is not understood, at least in part because of lack of animal models that reproduce the key features of the CS priming process. In this study, using two strains of mice, we characterized a double-hit mouse model of ALI induced by CS priming of injury caused by lipopolysaccharide (LPS). C57BL/6 and AKR mice were preexposed to CS briefly (3 h) or subacutely (3 wk) before intratracheal instillation of LPS and ALI was assessed 18 h after LPS administration by measuring lung static compliance, lung edema, vascular permeability, inflammation, and alveolar apoptosis. We found that as little as 3 h of exposure to CS enhanced LPS-induced ALI in both strains of mice. Similar exacerbating effects were observed after 3 wk of preexposure to CS. However, there was a strain difference in susceptibility to CS priming for ALI, with a greater effect in AKR mice. The key features we observed suggest that 3 wk of CS preexposure of AKR mice is a reproducible, clinically relevant animal model that is useful for studying mechanisms and treatment of CS priming for a second-hit-induced ALI. Our data also support the concept that increased susceptibility to ALI/ARDS is an important adverse health consequence of CS exposure that needs to be taken into consideration when treating critically ill individuals.

Current guidelines for the management of patients with acute coronary syndromes (ACSs) focus on the electrocardiogram to divide patients into ST-elevation acute myocardial infarction (STEMI) or non-ST-elevation acute myocardial infarction (NSTEMI)/unstable angina (UA). Patients with STEMI in the earliest time will receive reperfusion therapy to destruct occlusive thrombus. An ST segment elevation is the 'sine qua non' for diagnosing acute total coronary occlusion causing transmural myocardial infarction. Left circumflex coronary artery (LCx) occlusion is often categorized as NSTEMI because of the absence of significant ST-elevation on the 12 lead standard electrocardiogram. An ST segment elevation is presented in fewer than 50% of patients with LCx total occlusion, such that the reperfusion therapy is delayed. We reported a 77 years old woman whom being diagnosed with NSTEMI because a 12 lead electrocardiogram showed ST segment depression in lead V2-V5. On coronary angiography, we found a total occlusion in the LCx artery as the culprit lession.

Background: We hypothesized that treatment with quercetin could result in improved hemodynamics, lung inflammatory parameters and mortality in a rat model of hemorrhagic shock., Methods: Rats were anesthetized (80 mg/kg ketamine plus 8 mg/kg xylazine i.p.). The protocol included laparotomy for 15 min (trauma), hemorrhagic shock (blood withdrawal to reduce the mean arterial pressure to 35 mmHg) for 75 min and resuscitation by re-infusion of all the shed blood plus lactate Ringer for 90 min. Intravenous quercetin (50 mg/kg) or vehicle were administered during resuscitation., Results: There was a trend for increased survival 84.6% (11/13) in the treated group vs. the shock group 68.4% (13/19, p > 0.05 Kaplan-Meier). Quercetin fully prevented the development of lung edema. The activity of aSMase was increased in the shock group compared to the sham group and the quercetin prevented this effect. However, other inflammatory markers such as myeloperoxidase activity, interleukin-6 in plasma or bronchoalveolar fluid were similar in the sham and shock groups. We found no bacterial DNA in plasma in these animals., Conclusions: Quercetin partially prevented the changes in blood pressure and lung injury in shock associated to hemorrhage and reperfusion.

Emphysema commonly accompanies various complications such as pneumonia. Sometimes, these comorbidities look so strange on images, because destroyed airspaces could change the usual disease progression. So, we demonstrated various cases of common comorbidities with unusual radiographic findings in emphysema patients. Awareness of various findings of emphysema with commonly coexistent diseases may aid in the proper diagnosis and management of emphysema patients., (Copyright © 2016 Canadian Association of Radiologists. Published by Elsevier Inc. All rights reserved.)

A 62-year-old African-American man admitted to the emergency room with chest pain and exertional dyspnoea. He was found to be in rapid atrial fibrillation with pulmonary oedema. A transoesophageal echocardiogram performed prior to cardioversion showed a depressed left ventricular function (ejection fraction 30%) and an extracardiac heterogeneous echodensity compressing the right atrium and the superior vena cava. CT of the chest confirmed an anterior mediastinal mass measuring 13.5×6.6×10.1 cm, exerting a mass effect on the right atrium with mediastinal and right hilar adenopathy. CT-guided biopsy of the mediastinal mass revealed thymic carcinoma (squamous cell subtype). The metastatic workup was negative. The mass was deemed surgically unresectable due to its proximity to the heart. Chemotherapy was initiated with carboplatin/paclitaxel every 3 weeks with plans for intensity modulated radiotherapy after one to two cycles of chemotherapy. The patient recently had a repeat CT scan of the chest showing regression of the tumour., (2016 BMJ Publishing Group Ltd.)

Background: Severe acidosis can cause noninvasive ventilation (NIV) failure in chronic obstructive pulmonary disease (COPD) patients with acute hypercapnic respiratory failure (AHRF). NIV is therefore contraindicated outside of intensive care units (ICUs) in these patients. Less is known about NIV failure in patients with acute cardiogenic pulmonary edema (ACPE) and obesity hypoventilation syndrome (OHS). Therefore, the objective of the present study was to compare NIV failure rates between patients with severe and non-severe acidosis admitted to a respiratory intermediate care unit (RICU) with AHRF resulting from ACPE, COPD or OHS., Methods: We prospectively included acidotic patients admitted to seven RICUs, where they were provided NIV as an initial ventilatory support measure. The clinical characteristics, pH evolutions, hospitalization or RICU stay durations and NIV failure rates were compared between patients with a pH ≥ 7.25 and a pH < 7.25. Logistic regression analysis was performed to determine the independent risk factors contributing to NIV failure., Results: We included 969 patients (240 with ACPE, 540 with COPD and 189 with OHS). The baseline rates of severe acidosis were similar among the groups (45 % in the ACPE group, 41 % in the COPD group, and 38 % in the OHS group). Most of the patients with severe acidosis had increased disease severity compared with those with non-severe acidosis: the APACHE II scores were 21 ± 7.2 and 19 ± 5.8 for the ACPE patients (p < 0.05), 20 ± 5.7 and 19 ± 5.1 for the COPD patients (p < 0.01) and 18 ± 5.9 and 17 ± 4.7 for the OHS patients, respectively (NS). The patients with severe acidosis also exhibited worse arterial blood gas parameters: the PaCO2 levels were 87 ± 22 and 70 ± 15 in the ACPE patients (p < 0.001), 87 ± 21 and 76 ± 14 in the COPD patients, and 83 ± 17 and 74 ± 14 in the OHS patients (NS)., respectively Further, the patients with severe acidosis required a longer duration to achieve pH normalization than those with non-severe acidosis (patients with a normalized pH after the first hour: ACPE, 8 % vs. 43 %, p < 0.001; COPD, 11 % vs. 43 %, p < 0.001; and OHS, 13 % vs. 51 %, p < 0.001), and they had longer RICU stays, particularly those in the COPD group (ACPE, 4 ± 3.1 vs. 3.6 ± 2.5, NS; COPD, 5.1 ± 3 vs. 3.6 ± 2.1, p < 0.001; and OHS, 4.3 ± 2.6 vs. 3.7 ± 3.2, NS). The NIV failure rates were similar between the patients with severe and non-severe acidosis in the three disease groups (ACPE, 16 % vs. 12 %; COPD, 7 % vs. 7 %; and OHS, 11 % vs. 4 %). No common predictive factor for NIV failure was identified among the groups., Conclusions: ACPE, COPD and OHS patients with AHRF and severe acidosis (pH ≤ 7.25) who are admitted to an RICU can be successfully treated with NIV in these units. These results may be used to determine precise RICU admission criteria.

A 44-year-old man, with a history of arterial hypertension, was referred with increasing shortness of breath due to a large pericardial effusion and imminent tamponade. Emergency ultrasound-guided pericardiocentesis resulted in the rapid withdrawal of 2760 cc of serous fluid. 3 hours later, the patient developed acute pulmonary oedema, which was successfully treated. Hypertrophic obstructive cardiomyopathy was later diagnosed and malignancy was excluded as a cause of the effusion. Clinicians performing pericardiocentesis need to be aware of pericardial decompression syndrome (PDS), a rare but serious complication. Although the underlying mechanisms causing PDS are not fully understood, patients with high left ventricular (LV) filling pressures are at particular risk. In other words: diastolic dysfunction of the LV is a risk factor for the occurrence of PDS., (2016 BMJ Publishing Group Ltd.)

Background: Tricyclic antidepressants (TCA) are becoming one of the most frequently used substances in self poisoning. Significant morbidity and mortality associated with TCA overdose are often related to and refractory hypotension. We report the first case of survival after severe amitriptyline poisoning, leading to prolonged cardiac arrest and ventricular tachycardia (VT), resuscitated with 3 h of uninterrupted cardiac massage and Direct current (DC) shocks., Case Presentation: A 25 year old girl presented with severe amitriptyline poisoning causing pulseless VT and prolonged cardiac arrest. After 3 h of uninterrupted external cardiac massage, together with nine DC shocks and intra venous bicarbonate injections the rhythm reverted to a nodal tachycardia, initial 2D echocardiogram showed left ventricular dysfunction, which recovered to normal after 2 weeks and the patient had a complete recovery subsequently., Conclusion: Our case highlights the importance of continued resuscitation in patients presenting with TCA poisoning and resistant arrhythmia, especially in young and otherwise healthy patients.

Introduction: Shortage of intensive care beds has led to more frequent use of noninvasive ventilation (NIV) outside respiratory units, and data on NIV efficacy and safety on general wards is lacking., Objective: The aim was to identify potential predictors for NIV failure., Methods: This was a retrospective analysis of patients treated with NIV at the Institute for Pulmonary Diseases of Vojvodina from 2009 to 2013. Demographics, blood gases, chest radiographs, setting, and outcomes were analyzed to identify predictors of NIV failure., Results: A total of 138 patients (65% men, mean age 66 ± 11 years) were treated with NIV. Indications for NIV were acute exacerbation of chronic obstructive pulmonary disease (85%) and cardiogenic pulmonary edema (7%), as well as respiratory insufficiency related to obesity and central hypoventilation (5%) and neuromuscular disease (3%). Rate of NIV failure was 34.8%. In 86 patients NIV was applied in the High Dependency Unit (HDU), while 52 received NIV on the general ward. Baseline characteristics in terms of gender, arterial blood gases, and the extent of consolidation on chest radiographs were similar. Patients treated in HDU were younger (64.4 ± 1.2 vs. 69.4 ± 1.5 years, p < 0.001). NIV on the general ward compared to HDU had higher rates of NIV failure (28/52 vs. 20/86, p < 0.001). Presence of consolidation involving two or more quadrants on chest radiograph (55% vs. 29%, p < 0.001) was associated with NIV failure. When adjusted for age and the extent of consolidation on chest radiograph, NIV failure was still less likely in patients treated in HDU (OR 0.23, 95% Cl 0.10-0.50)., Conclusion: Patients with consolidation on chest X-ray and patients treated with NIV outside of dedicated respiratory units are at a higher risk for NIV failure.

Background: Acute respiratory failure is a frequent cause of emergency medical missions. Continuous positive airway pressure (CPAP) therapy could be particularly beneficial, avoiding risks associated with intubation and invasive ventilation. Hardly any data exist from Germany on this matter., Patients and Methods: CPAP therapy with the Boussignac system as additional measure was introduced in cases of acute cardiogenic pulmonary edema (ACPE) or decompensated chronic obstructive pulmonary disease (COPD) in a physician-supported emergency medical services system (EMS)., Results: A total of 57 patients, 35 with ACPE and 22 with COPD, received CPAP. Oxygen saturation improved from 81.6% to 94.8%, and respiration rate from 26.9/min to 18.9/min (p<0.001). Seven patients (12.2%) needed secondary intubation [COPD: one patient; ACPE: six patients, including three with acute coronary syndrome (ACS)]., Conclusion: In physician-supported EMS, CPAP using the Boussignac system is an effective additional measure for ACPE or COPD. For causal ACS, the risk of therapy failure increases., (Copyright © 2016 International Institute of Anticancer Research (Dr. John G. Delinassios), All rights reserved.)

Background: Noninvasive ventilation (NIV) is used in critically ill patients with acute respiratory failure (ARF) to avoid endotracheal intubation. However, the impact of NIV use on ARF patient's outcomes is still unclear. Our objectives were to evaluate the rate of NIV failure in hypoxemic patients with an arterial carbon dioxide partial pressure (PaCO2) < 45 mmHg or ≥ 45 mmHg at ICU admission, the predictors of NIV failure, ICU and hospital length of stay and 28-day mortality., Methods: Prospective single center cohort study. All consecutive patients admitted to a mixed ICU during a three-month period who received NIV, except for palliative care purposes, were included in this study. Demographic data, APACHE II score, cause of ARF, number of patients that received NIV, incidence of NIV failure, length of ICU, hospital stay and mortality rate were compared between NIV failure and success groups., Results: Eighty-five from 462 patients (18.4 %) received NIV and 26/85 (30.6 %) required invasive mechanical ventilation. NIV failure patients were comparatively younger (67 ± 21 vs. 77 ± 14 years; p = 0.031), had lower arterial bicarbonate (p = 0.005), lower PaCO2 levels (p = 0.032), higher arterial lactate levels (p = 0.046) and APACHE II score (p = 0.034) compared to NIV success patients. NIV failure occurred in 25.0 % of patients with PaCO2 ≥ 45 mmHg and in 33.3 % of patients with PaCO2 < 45 mmHg (p = 0.435). NIV failure was associated with an increased risk of in-hospital death (OR 4.64, 95 % CI 1.52 to 14.18; p = 0.007) and length [median (IQR)] of ICU [12 days (8-31) vs. 2 days (1-4); p < 0.001] and hospital [30 (19-42) vs. 15 (9-33) days; p = 0.010] stay. Predictors of NIV failure included age (OR 0.96, 95 % CI 0.93 to 0.99; p = 0.007) and APACHE II score (OR 1.13, 95 % CI 1.02 to 1.25; p = 0.018)., Conclusion: NIV failure was associated with an increased risk of in-hospital death, ICU and hospital stay and was not affected by baseline PaCO2 levels. Patients that failed were comparatively younger and had higher APACHE II score, suggesting the need for a careful selection of patients that might benefit from NIV. A well-designed study on the impact of a short monitored NIV trial on outcomes is needed.

Haemoptysis is a serious symptom with various aetiologies. Our aim was to define the aetiologies, outcomes and associations with lung cancer in the entire population of a high-income country.This retrospective multicentre study was based on the French nationwide hospital medical information database collected over 5 years (2008-2012). We analysed haemoptysis incidence, aetiologies, geographical and seasonal distribution and mortality. We studied recurrence, association with lung cancer and mortality in a 3-year follow-up analysis.Each year, ~15 000 adult patients (mean age 62 years, male/female ratio 2/1) were admitted for haemoptysis or had haemoptysis as a complication of their hospital stay, representing 0.2% of all hospitalised patients. Haemoptysis was cryptogenic in 50% of cases. The main aetiologies were respiratory infections (22%), lung cancer (17.4%), bronchiectasis (6.8%), pulmonary oedema (4.2%), anticoagulants (3.5%), tuberculosis (2.7%), pulmonary embolism (2.6%) and aspergillosis (1.1%). Among incident cases, the 3-year recurrence rate was 16.3%. Of the initial cryptogenic haemoptysis patients, 4% were diagnosed with lung cancer within 3 years. Mortality rates during the first stay and at 1 and 3 years were 9.2%, 21.6% and 27%, respectively.This is the first epidemiological study analysing haemoptysis and its outcomes in an entire population. Haemoptysis is a life-threatening symptom unveiling potentially life-threatening underlying conditions., (Copyright ©ERS 2015.)