Database : MEDLINE
Search on : pulmonary and edema [Words]
References found : 28521 [refine]
Displaying: 1 .. 10   in format [Detailed]

page 1 of 2853 go to page                         

  1 / 28521 MEDLINE  
              next record last record
select
to print
Photocopy
Full text

[PMID]: 29522519
[Au] Autor:Wagener BM; Hu PJ; Oh JY; Evans CA; Richter JR; Honavar J; Brandon AP; Creighton J; Stephens SW; Morgan C; Dull RO; Marques MB; Kerby JD; Pittet JF; Patel RP
[Ad] Address:Department of Anesthesiology and Perioperative Medicine, University of Alabama at Birmingham, Birmingham, Alabama, United States of America.
[Ti] Title:Role of heme in lung bacterial infection after trauma hemorrhage and stored red blood cell transfusion: A preclinical experimental study.
[So] Source:PLoS Med;15(3):e1002522, 2018 Mar.
[Is] ISSN:1549-1676
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:BACKGROUND: Trauma is the leading cause of death and disability in patients aged 1-46 y. Severely injured patients experience considerable blood loss and hemorrhagic shock requiring treatment with massive transfusion of red blood cells (RBCs). Preclinical and retrospective human studies in trauma patients have suggested that poorer therapeutic efficacy, increased severity of organ injury, and increased bacterial infection are associated with transfusion of large volumes of stored RBCs, although the mechanisms are not fully understood. METHODS AND FINDINGS: We developed a murine model of trauma hemorrhage (TH) followed by resuscitation with plasma and leukoreduced RBCs (in a 1:1 ratio) that were banked for 0 (fresh) or 14 (stored) days. Two days later, lungs were infected with Pseudomonas aeruginosa K-strain (PAK). Resuscitation with stored RBCs significantly increased the severity of lung injury caused by P. aeruginosa, as demonstrated by higher mortality (median survival 35 h for fresh RBC group and 8 h for stored RBC group; p < 0.001), increased pulmonary edema (mean [95% CI] 106.4 µl [88.5-124.3] for fresh RBCs and 192.5 µl [140.9-244.0] for stored RBCs; p = 0.003), and higher bacterial numbers in the lung (mean [95% CI] 1.2 × 107 [-1.0 × 107 to 2.5 × 107] for fresh RBCs and 3.6 × 107 [2.5 × 107 to 4.7 × 107] for stored RBCs; p = 0.014). The mechanism underlying this increased infection susceptibility and severity was free-heme-dependent, as recombinant hemopexin or pharmacological inhibition or genetic deletion of toll-like receptor 4 (TLR4) during TH and resuscitation completely prevented P. aeruginosa-induced mortality after stored RBC transfusion (p < 0.001 for all groups relative to stored RBC group). Evidence from studies transfusing fresh and stored RBCs mixed with stored and fresh RBC supernatants, respectively, indicated that heme arising both during storage and from RBC hemolysis post-resuscitation plays a role in increased mortality after PAK (p < 0.001). Heme also increased endothelial permeability and inhibited macrophage-dependent phagocytosis in cultured cells. Stored RBCs also increased circulating high mobility group box 1 (HMGB1; mean [95% CI] 15.4 ng/ml [6.7-24.0] for fresh RBCs and 50.3 ng/ml [12.3-88.2] for stored RBCs), and anti-HMGB1 blocking antibody protected against PAK-induced mortality in vivo (p = 0.001) and restored macrophage-dependent phagocytosis of P. aeruginosa in vitro. Finally, we showed that TH patients, admitted to the University of Alabama at Birmingham ER between 1 January 2015 and 30 April 2016 (n = 50), received high micromolar-millimolar levels of heme proportional to the number of units transfused, sufficient to overwhelm endogenous hemopexin levels early after TH and resuscitation. Limitations of the study include lack of assessment of temporal changes in different products of hemolysis after resuscitation and the small sample size precluding testing of associations between heme levels and adverse outcomes in resuscitated TH patients. CONCLUSIONS: We provide evidence that large volume resuscitation with stored blood, compared to fresh blood, in mice increases mortality from subsequent pneumonia, which occurs via mechanisms sensitive to hemopexin and TLR4 and HMGB1 inhibition.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:In-Data-Review
[do] DOI:10.1371/journal.pmed.1002522

  2 / 28521 MEDLINE  
              first record previous record next record last record
select
to print
Photocopy
Full text

[PMID]: 29366758
[Au] Autor:Yuhong L; Tana W; Zhengzhong B; Feng T; Qin G; Yingzhong Y; Wei G; Yaping W; Langelier C; Rondina MT; Ge RL
[Ad] Address:Research Center for High Altitude Medicine, Qinghai University, Xining 810001, China; Department of Respiratory Medicine, The Affiliated Hospital of Qinghai University, Xining 810001, China.
[Ti] Title:Transcriptomic profiling reveals gene expression kinetics in patients with hypoxia and high altitude pulmonary edema.
[So] Source:Gene;651:200-205, 2018 Apr 20.
[Is] ISSN:1879-0038
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:OBJECTIVE: High altitude pulmonary edema (HAPE) is a life threatening condition occurring in otherwise healthy individuals who rapidly ascend to high altitude. However, the molecular mechanisms of its pathophysiology are not well understood. The objective of this study is to evaluate differential gene expression in patients with HAPE during acute illness and subsequent recovery. METHODS: Twenty-one individuals who ascended to an altitude of 3780 m were studied, including 12 patients who developed HAPE and 9 matched controls without HAPE. Whole-blood samples were collected during acute illness and subsequent recovery for analysis of the expression of hypoxia-related genes, and physiologic and laboratory parameters, including mean pulmonary arterial pressure (mPAP), heart rate, blood pressure, and arterial oxygen saturation (SpO ), were also measured. RESULTS: Compared with control subjects, numerous hypoxia-related genes were up-regulated in patients with acute HAPE. Gene network analyses suggested that HIF-1α played a central role in acute HAPE by affecting a variety of hypoxia-related genes, including BNIP3L, VEGFA, ANGPTL4 and EGLN1. Transcriptomic profiling revealed the expression of most HAPE-induced genes was restored to a normal level during the recovery phase except some key hypoxia response factors, such asBNIP3L, EGR1, MMP9 and VEGF, which remained persistently elevated. CONCLUSIONS: Differential expression analysis of hypoxia-related genes revealed distinct molecular signatures of HAPE during acute and recovery phases. This study may help us to better understand HAPE pathogenesis and putative targets for further investigation and therapeutic intervention.
[Mh] MeSH terms primary: Altitude Sickness/genetics
Hypertension, Pulmonary/genetics
Pulmonary Edema/genetics
[Mh] MeSH terms secundary: Acute Lung Injury/etiology
Acute Lung Injury/genetics
Adult
Case-Control Studies
Cohort Studies
Gene Expression Profiling
Humans
Up-Regulation
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[Js] Journal subset:IM
[Da] Date of entry for processing:180126
[St] Status:MEDLINE

  3 / 28521 MEDLINE  
              first record previous record next record last record
select
to print
Photocopy
Full text

[PMID]: 29519682
[Au] Autor:Biasato I; Zanatta R; Maniscalco L; Evangelista R; Iotti B; Iussich S
[Ad] Address:Department of Veterinary Sciences, University of Turin, Largo Paolo Braccini 2, 10095, Grugliasco (TO), Italy. Electronic address: ilaria.biasato@unito.it.
[Ti] Title:Left subclavian artery dissection associated with connective tissue abnormalities resembling Marfan-like syndrome in an English bulldog.
[So] Source:J Vet Cardiol;, 2018 Mar 05.
[Is] ISSN:1875-0834
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:The unexpected demise of a 12-year-old male neutered English bulldog solicited a gross examination, which revealed a blood-filled space occurring in the proximal left subclavian artery (LSA). It originated about 1 cm from the branching point of the vessel and progressively dilated for 3 cm distal to this origin. Histopathological investigation showed that the tunica media of the LSA was more than 50% split, with the blood-filled space dissecting through the arterial wall. In the tunica media of the LSA, severe multifocal fragmentation and/or loss of the elastic fibers was observed. The retained disorganized elastic fibers were separated and disoriented due to accumulations of acid mucopolysaccharide. Marked, diffuse medial, and adventitial fibrous tissue deposition was also identified. The cause of death was attributed to acute hemorrhagic and necrotizing pancreatitis with pulmonary edema, suggesting that LSA dissection was an incidental finding. Subclavian artery dissection is extremely rare in humans, where the involvement of the LSA in cases of aortic dissection both with or without Marfan syndrome has been reported. Aortic and pulmonary artery dissection in bovines and aortic aneurysm and dissection in dogs have been reported to be associated with Marfan and Marfan-like syndromes, respectively. Histopathological findings suggestive of underlying connective tissue abnormalities resembling Marfan-like syndrome (i.e., the appearance of the elastic tissue and the degenerative changes of the tunica media) were detected in the first case of LSA dissection in dogs and veterinary medicine, herein described.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:Publisher

  4 / 28521 MEDLINE  
              first record previous record next record last record
select
to print
Photocopy
Clinical Trials Registry
Full text

[PMID]: 29506579
[Au] Autor:Azoulay E; Lemiale V; Mokart D; Nseir S; Argaud L; Pène F; Kontar L; Bruneel F; Klouche K; Barbier F; Reignier J; Stoclin A; Louis G; Constantin JM; Mayaux J; Wallet F; Kouatchet A; Peigne V; Perez P; Girault C; Jaber S; Oziel J; Nyunga M; Terzi N; Bouadma L; Lebert C; Lautrette A; Bigé N; Raphalen JH; Papazian L; Rabbat A; Darmon M; Chevret S; Demoule A
[Ad] Address:Medical Intensive Care Unit, APHP, Hôpital Saint-Louis. ECSTRA Team, and Clinical Epidemiology, UMR 1153, (Center of Epidemiology and Biostatistics, Sorbonne Paris Cité, CRESS), INSERM, Paris Diderot Sorbonne University, Paris, France. elie.azoulay@aphp.fr.
[Ti] Title:High-flow nasal oxygen vs. standard oxygen therapy in immunocompromised patients with acute respiratory failure: study protocol for a randomized controlled trial.
[So] Source:Trials;19(1):157, 2018 Mar 05.
[Is] ISSN:1745-6215
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:BACKGROUND: Acute respiratory failure (ARF) is the leading reason for intensive care unit (ICU) admission in immunocompromised patients. High-flow nasal oxygen (HFNO) therapy is an alternative to standard oxygen. By providing warmed and humidified gas, HFNO allows the delivery of higher flow rates via nasal cannula devices, with FiO values of nearly 100%. Benefits include alleviation of dyspnea and discomfort, decreased respiratory distress and decreased mortality in unselected patients with acute hypoxemic respiratory failure. However, in preliminary reports, HFNO benefits are controversial in immunocompromised patients in whom it has never been properly evaluated. METHODS/DESIGN: This is a multicenter, open-label, randomized controlled superiority trial in 30 intensive care units, part of the Groupe de Recherche Respiratoire en Réanimation Onco-Hématologique (GRRR-OH). Inclusion criteria will be: (1) adults, (2) known immunosuppression, (3) ARF, (4) oxygen therapy ≥ 6 L/min, (5) written informed consent from patient or proxy. Exclusion criteria will be: (1) imminent death (moribund patient), (2) no informed consent, (3) hypercapnia (PaCO ≥ 50 mmHg), (4) isolated cardiogenic pulmonary edema, (5) pregnancy or breastfeeding, (6) anatomical factors precluding insertion of a nasal cannula, (7) no coverage by the French statutory healthcare insurance system, and (8) post-surgical setting from day 1 to day 6 (patients with ARF occurring after day 6 of surgery can be included). The primary outcome measure is day-28 mortality. Secondary outcomes are intubation rate, comfort, dyspnea, respiratory rate, oxygenation, ICU length of stay, and ICU-acquired infections. Based on an expected 30% mortality rate in the standard oxygen group, and 20% in the HFNO group, error rate set at 5%, and a statistical power at 90%, 389 patients are required in each treatment group (778 patients overall). Recruitment period is estimated at 30 months, with 28 days of additional follow-up for the last included patient. DISCUSSION: The HIGH study will be the largest multicenter, randomized controlled trial seeking to demonstrate that survival benefits from HFNO reported in unselected patients also apply to a large immunocompromised population. TRIAL REGISTRATION: ClinicalTrials.gov, ID: NCT02739451 . Registered on 15 April 2016.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[Cl] Clinical Trial:ClinicalTrial
[St] Status:In-Data-Review
[do] DOI:10.1186/s13063-018-2492-z

  5 / 28521 MEDLINE  
              first record previous record next record last record
select
to print
Photocopy
Full text

[PMID]: 29506505
[Au] Autor:Sobhakumari A; Poppenga RH; Pesavento JB; Uzal FA
[Ad] Address:California Animal Health and Food Safety Laboratory System, Davis branch, School of Veterinary Medicine, University of California Davis, Davis, USA.
[Ti] Title:Pathology of carbon monoxide poisoning in two cats.
[So] Source:BMC Vet Res;14(1):67, 2018 Mar 05.
[Is] ISSN:1746-6148
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:BACKGROUND: Carbon monoxide (CO), a common cause of poisoning in human beings has also been implicated in the death of animals. Though there are multiple studies on CO poisoning and relevant lethal blood COHb concentrations in humans, there are no reliable reports of diagnostic lethal carboxyhemoglobin percentage of saturation (COHb%) in cats. Additionally, due to shared housing environments, exposures to companion animals can be a surrogate for lethal exposures in human beings and provide valuable information in concurrent forensic investigations. CASE PRESENTATION: Two adult Singapura brown ticked cats were submitted to the California Animal Health and Food Safety Laboratory (CAHFS) for necropsy and diagnostic work-up. These animals were found dead along with their two deceased owners. Similar lesions were observed in both cats. At necropsy, gross lesions consisted of multifocal, large, irregular, bright red spots on the skin of the abdomen and the inner surface of ear pinnae, bright red muscles and blood. The carcasses, and tissues fixed in formalin retained the bright red discoloration for up to two weeks. Microscopic lesions included diffuse pulmonary congestion and edema, and multifocal intense basophilia of cardiomyocytes mostly affecting whole fibers or occasionally a portion of the fiber. Based on the clinical history,gross and microscopic changes, cyanide or carbon monoxide poisoning was suspected. Blood samples analyzed for carbon monoxide showed 57 and 41% carboxyhemoglobin COHb%. Muscle samples were negative for cyanide. CONCLUSION: There are no established reference values for lethal COHb concentration in cats. The COHb % values detected in this case which fell within the lethal range reported for other species, along with the gross lesions and unique histological findings in the heart suggest a helpful criteria for diagnosis of CO intoxication associated death in cats. This case demonstrates that since pets share the same environment as human beings and often are a part of their activities, they can be useful adjuncts in potential forensic investigations to help solve human cases.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:In-Process
[do] DOI:10.1186/s12917-018-1385-4

  6 / 28521 MEDLINE  
              first record previous record next record last record
select
to print
Photocopy
Full text

[PMID]: 29431734
[Au] Autor:Hook JL; Islam MN; Parker D; Prince AS; Bhattacharya S; Bhattacharya J
[Ad] Address:Lung Biology Laboratory, Division of Pulmonary, Allergy, and Critical Care Medicine, Department of Medicine.
[Ti] Title:Disruption of staphylococcal aggregation protects against lethal lung injury.
[So] Source:J Clin Invest;128(3):1074-1086, 2018 Mar 01.
[Is] ISSN:1558-8238
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Infection by Staphylococcus aureus strain USA300 causes tissue injury, multiorgan failure, and high mortality. However, the mechanisms by which the bacteria adhere to, then stabilize on, mucosal surfaces before causing injury remain unclear. We addressed these issues through the first real-time determinations of USA300-alveolar interactions in live lungs. We found that within minutes, inhaled USA300 established stable, self-associated microaggregates in niches at curved, but not at flat, regions of the alveolar wall. The microaggregates released α-hemolysin toxin, causing localized alveolar injury, as indicated by epithelial dye loss, mitochondrial depolarization, and cytosolic Ca2+ increase. Spread of cytosolic Ca2+ through intercellular gap junctions to adjoining, uninfected alveoli caused pulmonary edema. Systemic pretreatment with vancomycin, a USA300-cidal antibiotic, failed to protect mice infected with inhaled WT USA300. However, vancomycin pretreatment markedly abrogated mortality in mice infected with mutant USA300 that lacked the aggregation-promoting factor PhnD. We interpret USA300-induced mortality as having resulted from rapid bacterial aggregation in alveolar niches. These findings indicate, for the first time to our knowledge, that alveolar microanatomy is critical in promoting the aggregation and, hence, in causing USA300-induced alveolar injury. We propose that in addition to antibiotics, strategies for bacterial disaggregation may constitute novel therapy against USA300-induced lung injury.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:In-Data-Review

  7 / 28521 MEDLINE  
              first record previous record next record last record
select
to print
Photocopy
Full text

[PMID]: 29206727
[Au] Autor:Kotlyar S; Olupot-Olupot P; Nteziyaremye J; Akech SO; Uyoga S; Muhindo R; Moore CL; Maitland K
[Ad] Address:Department of Emergency Medicine, Yale School of Medicine, New Haven, CT.
[Ti] Title:Assessment of Myocardial Function and Injury by Echocardiography and Cardiac Biomarkers in African Children With Severe Plasmodium falciparum Malaria.
[So] Source:Pediatr Crit Care Med;19(3):179-185, 2018 Mar.
[Is] ISSN:1529-7535
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:OBJECTIVES: Perturbed hemodynamic function complicates severe malaria. The Fluid Expansion as Supportive Therapy trial demonstrated that fluid resuscitation, involving children with severe malaria, was associated with increased mortality, primarily due to cardiovascular collapse, suggesting that myocardial dysfunction may have a role. The aim of this study was to characterize cardiac function in children with severe malaria. DESIGN: A prospective observational study with clinical, laboratory, and echocardiographic data collected at presentation (T0) and 24 hours (T1) in children with severe malaria. Cardiac index and ejection fraction were calculated at T0 and T1. Cardiac troponin I and brain natriuretic peptide were measured at T0. We compared clinical and echocardiographic variables in children with and without severe malarial anemia (hemoglobin < 5 mg/dL) at T0 and T1. SETTING: Mbale Regional Referral Hospital. PATIENTS: Children 3 months to 12 years old with severe falciparum malaria. INTERVENTIONS: Usual care. MEASUREMENTS AND MAIN RESULTS: We enrolled 104 children, median age 23.3 months, including 61 children with severe malarial anemia. Cardiac troponin I levels were elevated (> 0.1 ng/mL) in n equals to 50, (48%), and median brain natriuretic peptide was within normal range (69.1 pg/mL; interquartile range, 48.4-90.8). At T0, median Cardiac index was significantly higher in the severe malarial anemia versus nonsevere malarial anemia group (6.89 vs 5.28 L/min/m) (p = 0.001), which normalized in both groups at T1 (5.60 vs 5.13 L/min/m) (p = 0.452). Cardiac index negatively correlated with hemoglobin, r equals to -0.380 (p < 0.001). Four patients (3.8%) had evidence of depressed cardiac systolic function (ejection fraction < 45%). Overall, six children died, none developed pulmonary edema, biventricular failure, or required diuretic treatment. CONCLUSIONS: Elevation of cardiac index, due to increased stroke volume, in severe malaria is a physiologic response to circulatory compromise and correlates with anemia. Following whole blood transfusion and antimalarial therapy, cardiac index in severe malarial anemia returns to normal. The majority (> 96%) of children with severe malaria have preserved myocardial systolic function. Although there is evidence for myocardial injury (elevated cardiac troponin I), this does not correlate with cardiac dysfunction.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1712
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:In-Data-Review
[do] DOI:10.1097/PCC.0000000000001411

  8 / 28521 MEDLINE  
              first record previous record next record last record
select
to print
Photocopy
Full text

[PMID]: 29514336
[Au] Autor:Lichtenberger JP; Kim AM; Fisher D; Tatum PS; Neubauer B; Peterson PG; Carter BW
[Ad] Address:Department of Radiology and Radiological Sciences, Uniformed Services University of the Health Sciences, 4301 Jones Bridge Road, Bethesda, MD 20814.
[Ti] Title:Imaging of Combat-Related Thoracic Trauma - Review of Penetrating Trauma.
[So] Source:Mil Med;183(3-4):e81-e88, 2018 Mar 01.
[Is] ISSN:1930-613X
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Introduction: Combat-related thoracic trauma is a significant contributor to morbidity and mortality of the casualties from Operation Enduring Freedom (OEF) and Operation Iraqi Freedom (OIF). Penetrating, blunt, and blast injuries were the most common mechanisms of trauma. Imaging plays a key role in the management of combat-related thoracic trauma casualties. This review discusses the imaging manifestations of thoracic injuries from penetrating trauma, emphasizing epidemiology and diagnostic clues seen during OEF and OIF. Materials and Methods: The assessment of radiologic findings in patients who suffer from combat-related thoracic trauma is the basis of this review article. The imaging modalities for this study include multi-detector computed tomography and chest radiography. Results: High-velocity penetrating projectile injuries appear as hemorrhage and re-expansion pulmonary edema from the temporary cavity and a linear, blood-filled track from the permanent cavity. In cases where the projectile passes totally through the body, entrance wounds at the skin surface and tracks through the subcutaneous tissues may be the only indications of penetrating trauma. When assessing vascular injury, special attention should be paid to the right hilum in contrast-enhanced multi-detector computed tomography, as contrast is concentrated in the superior vena cava and superior cavoatrial junction may obscure small fragments. Additionally, CT angiography may show vessel disruption or extravasation of contrast distal to normal vessel location in addition to intraluminal filling defects and pseudo-aneurysms. Tension pneumopericardium may rarely complicate penetrating or blunt chest trauma. On imaging, distension of the pericardial sack by pneumopericardium and compression of the heart support the diagnosis of tension. On multi-detector computed tomography in the acute trauma setting, fluid in the pleural space should be considered hemothorax, particularly when Hounsfield units are above 35. Acutely, extravasated blood will have similar attenuation to the thoracic vasculature, whereas clotted blood will have higher values of 50-90 Hounsfield units. Conclusion: Combat-related thoracic trauma continues to be a significant contributor to the morbidity and mortality of those injured during OEF and OIF. This review of the imaging manifestations of penetrating thoracic injury during OEF and OIF focuses on key diagnostic findings for clinicians caring for combat casualties. The distinct injury pattern and atypical imaging manifestations of penetrating trauma are important to recognize early due to the acuity of this patient population and the influence of accurate diagnosis on clinical management.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180307
[Lr] Last revision date:180307
[St] Status:In-Data-Review
[do] DOI:10.1093/milmed/usx034

  9 / 28521 MEDLINE  
              first record previous record next record last record
select
to print
Photocopy
Full text

[PMID]: 29294094
[Au] Autor:Plantinga LC; King LM; Masud T; Shafi T; Burkart JM; Lea JP; Jaar BG
[Ad] Address:Department of Medicine, Emory University, Atlanta, GA, USA.
[Ti] Title:Burden and correlates of readmissions related to pulmonary edema in US hemodialysis patients: a cohort study.
[So] Source:Nephrol Dial Transplant;, 2017 Dec 25.
[Is] ISSN:1460-2385
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Background: Pulmonary edema is prevalent and may be a common cause of hospital readmissions in hemodialysis patients. We aimed to estimate the national burden of, and identify correlates of, readmissions related to pulmonary edema among hemodialysis patients. Methods: In this retrospective cohort study using national registry data, we identified prevalent US hemodialysis patients (n = 215 251) with index admissions while under Medicare primary coverage in 2011-13. We defined readmissions as admissions occurring within 30 days of the index discharge and pulmonary edema-related readmissions as readmissions with discharge diagnoses of fluid overload, heart failure or pulmonary edema. Multivariable logistic regression models were used to determine odds ratios (ORs) for pulmonary edema-related readmissions by patient and index admission characteristics. Results: About one-quarter (23%) of index hospital admissions were followed by a readmission, with nearly half (44%) of the readmissions being associated with pulmonary edema. The strongest independent correlate of pulmonary edema-related readmission was a pulmonary edema-related index admission [OR = 2.32; 95% confidence interval (CI) 2.22-2.41]. With the exception of dialysis vintage <1 year (OR = 1.18; 95% CI 1.14-1.22), chronic obstructive pulmonary disease (OR = 1.34; 95% CI 1.29-1.38), dialysis non-compliance (OR = 1.53; 95% CI 1.41-1.64) and congestive heart failure (OR = 1.85; 95% CI 1.77-1.93), patient characteristics were not generally associated with higher risk of pulmonary edema-related readmission. Conclusions: Readmissions related to pulmonary edema are common in hemodialysis patients. Interventions aimed at preventing such readmissions could have a substantial impact on readmissions overall, particularly targeted at incident hemodialysis patients with a prior history of heart failure and patients initially admitted for pulmonary edema.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1801
[Cu] Class update date: 180308
[Lr] Last revision date:180308
[St] Status:Publisher
[do] DOI:10.1093/ndt/gfx335

  10 / 28521 MEDLINE  
              first record previous record
select
to print
Photocopy
Full text

[PMID]: 29219267
[Au] Autor:Zhao YF; Zhao BQ; Ma KJ; Zhang J; Chen FY
[Ad] Address:Suzhou Municipal Public Security Bureau, Suzhou 234000, China.
[Ti] Title:[Forensic Analysis for 54 Cases of Suxamethonium Chloride Poisoning].
[So] Source:Fa Yi Xue Za Zhi;33(4):374-375, 2017 Aug.
[Is] ISSN:1004-5619
[Cp] Country of publication:China
[La] Language:chi
[Ab] Abstract:OBJECTIVES: To observe and analyze the performance of forensic science in the cases of suxa- methonium chloride poisoning, and to improve the identification of suxamethonium chloride poisoning. METHODS: Fifty-four cases of suxamethonium chloride poisoning were collected. The rules of determination of suxamethonium chloride poisoning were observed by the retrospective analysis of pathological and toxicological changes as well as case features. RESULTS: The pathological features of suxamethonium chloride poisoning were similar to the general changes of sudden death, which mainly included acute pulmonary congestion and edema, and partly showed myocardial disarray and fracture. Suxamethonium chloride could be detected in the heart blood of all cases and in skin tissue of part cases. CONCLUSIONS: Suxa-methonium chloride poisoning has the characteristics with fast death and covert means, which are difficult to rescue and easily miss inspection. For the cases of sudden death or suspicious death, determination of suxamethonium chloride should be taken as a routine detection index to prevent missing inspection.
[Pt] Publication type:ENGLISH ABSTRACT; JOURNAL ARTICLE
[Em] Entry month:1712
[Cu] Class update date: 180308
[Lr] Last revision date:180308
[St] Status:In-Process
[do] DOI:10.3969/j.issn.1004-5619.2017.04.008


page 1 of 2853 go to page                         
   


Refine the search
  Database : MEDLINE Advanced form   

    Search in field  
1  
2
3
 
           



Search engine: iAH v2.6 powered by WWWISIS

BIREME/PAHO/WHO - Latin American and Caribbean Center on Health Sciences Information