			Home About us Contact

Acute Respiratory Distress Syndrome (acute + respiratory_distress_syndrome)

Distribution by Scientific Domains

Medical Sciences	96%
2 Other Domains	4%

Distribution within Medical Sciences

Anesthesia & Pain Management	15%
General & Introductory Veterinary Medicine	9%
Geriatric Medicine	3%
17 Other Subdomains	64%

Kinds of Acute Respiratory Distress Syndrome

severe acute respiratory distress syndrome

Selected Abstracts

Alcohol Abuse Enhances Pulmonary Edema in Acute Respiratory Distress Syndrome

ALCOHOLISM, Issue 10 2009
David M. Berkowitz
Background:, Pulmonary edema is a cardinal feature of the life-threatening condition known as acute respiratory distress syndrome (ARDS). Patients with chronic alcohol abuse are known to be at increased risk of developing and dying from ARDS. Based upon preclinical data, we hypothesized that a history of chronic alcohol abuse in ARDS patients is associated with greater quantities and slower resolution of pulmonary edema compared with ARDS patients without a history of alcohol abuse. Methods:, A PiCCOÔ transpulmonary thermodilution catheter was inserted into 35 patients within 72 hours of meeting American European Consensus Criteria definition of ARDS. Pulmonary edema was quantified as extravascular lung water (EVLW) and measured for up to 7 days in 13 patients with a history of chronic alcohol abuse and 22 patients without a history of chronic alcohol abuse. Results:, Mean EVLW was higher in patients with a history of chronic alcohol abuse (16.6 vs. 10.5 ml/kg, p < 0.0001). Patients with alcohol abuse had significantly greater EVLW over the duration of the study (RM-ANOVA p = 0.003). There was a trend towards slower resolution of EVLW in patients with a history of alcohol abuse (a decrease of 0.5 ml/kg vs. 2.4 ml/kg, p = 0.17) over the study period. A history of alcohol abuse conferred a greater than 3-fold increased risk of elevated EVLW [OR 3.16, (1.26 to 7.93)] using multivariate logistic regression analysis. Conclusions:, In patients who develop ARDS, alcohol abuse is associated with greater levels EVLW and a trend towards slower resolution of EVLW. Combined with mechanistic and preclinical evidence linking chronic alcohol consumption and ARDS, targeted therapies should be developed for these patients. [source]

Acute Respiratory Distress Syndrome in Plasmodium vivax Malaria in Traveler Returning From Venezuela

JOURNAL OF TRAVEL MEDICINE, Issue 2 2006
Nuccia Saleri MD
No abstract is available for this article. [source]

Suggested Strategies for Ventilatory Management of Veterinary Patients with Acute Respiratory Distress Syndrome

JOURNAL OF VETERINARY EMERGENCY AND CRITICAL CARE, Issue 3 2001
Erika R. Mueller DVM
Abstract Objective: To review the current recommendations and guidelines for mechanical ventilation in humans and in animals with acute respiratory distress syndrome. Human data synthesis: Acute respiratory distress syndrome (ARDS) in humans in defined as an acute onset of bilateral, diffuse infiltrates on thoracic radiographs that are not the result of heart disease and a significant oxygenation impairment. These patients require mechanical ventilation. Research has shown that further pulmonary damage can occur as a result of mechanical ventilation. Various alveolar recruitment maneuvers and a low tidal volume with increased positive end expiratory pressure (PEEP) have been associated with an increased survival. Veterinary dat synthesis: Two veterinary reports have characterized ARDS in dogs using human criteria. There are no prospective veterinary studies using recruitment that ventilator-induced lung injury (VILI) occurs in dogs, sheep, and rats. Conclusion: Recruitment maneuvers in conjunction with low tidal volumes and PEEP keep the alveoli open for gas exchange and decrease VILI. Prospective veterinary research in needed to determine if these maneuvers and recommendation can be applied to veterinary patients. [source]

The short-term effect of hyperoncotic albumin, given alone or with furosemide, on oxygenation in sepsis-induced Acute Respiratory Distress Syndrome

ANAESTHESIA, Issue 3 2007
M. Kuper
Summary Two prospective non-randomised interventional case series were conducted consecutively at a single university hospital mixed intensive care unit, in patients with severe sepsis and acute respiratory distress syndrome. The first series describes the administration of 200 ml of 20% human albumin solution over 120 s in 13 patients, examining the hypothesis that raising plasma albumin should improve oxygenation. The second series describes the effect of administering 30 mg of furosemide intravenously along with the albumin in 15 patients, exploring whether this would produce more sustained improvement in oxygenation than albumin only. Oxygenation and haemodynamic parameters were measured for 4 h, during the period of peak oncotic effect. Hyperoncotic albumin given alone or with furosemide produced only transient improvement in oxygenation and haemodynamics, which was statistically significant only in the patients given albumin alone. Although the plasma albumin remained significantly elevated at 4 h in both series, no sustained improvement in oxygenation was seen. [source]

Combination of Inhaled Nitric Oxide Therapy and Inverse Ratio Ventilation in Patients with Sepsis-Associated Acute Respiratory Distress Syndrome

ARTIFICIAL ORGANS, Issue 11 2000
Kazufumi Okamoto
Abstract: Inverse ratio ventilation (IRV) is a ventilatory technique that uses an inspiratory to expiratory ratio (I:E) greater than 1:1. We studied the effects of mechanical ventilation with an I:E of 1:3, 1:1, and 2:1 on arterial oxygenation in 10 patients with sepsis-associated acute respiratory distress syndrome (ARDS). At each I:E, patients received 0 and 4 ppm of inhaled nitric oxide (INO) in random order for 30 min. Respiratory and cardiovascular parameters were measured. Of the 10 patients studied, 7 responded to IRV and 3 did not. An increase in the I:E and the addition of INO significantly improved arterial oxygenation in the responders (p < 0.0001 and p < 0.006, respectively). The combination of an increase in the I:E and INO had an additive effect on arterial oxygenation. The combined use of IRV and INO is a more effective method of avoiding hypoxemia than either INO or IRV alone. [source]

Molecular mechanisms underlying inflammatory lung diseases in the elderly: Development of a novel therapeutic strategy for acute lung injury and pulmonary fibrosis,

GERIATRICS & GERONTOLOGY INTERNATIONAL, Issue 3 2005
Takahide Nagase
In the elderly, inflammatory lung diseases, including acute lung injury and pulmonary fibrosis, are significant in terms of both mortality and difficulty in management. Acute respiratory distress syndrome (ARDS) is an acute lung injury and the mortality rate for ARDS ranges from 40 to 70% despite intensive care. Idiopathic pulmonary fibrosis (IPF) is a progressive and fatal disorder of the lung parenchyma. No useful drugs are currently available to treat IPF. However, molecular mechanisms underlying these lung diseases are little understood and the development of a novel therapeutic strategy is urgently needed. Platelet-activating factor (PAF) and metabolites of arachidonic acid, i.e. eicosanoids, are lipid mediators that have various biological effects. A key enzyme for the production of these inflammatory mediators, including eicosanoids and PAF, is phospholipase A2. In particular, cytosolic PLA2 (cPLA2) is especially important. The purpose of this article is to report novel findings regarding the role of PAF and cPLA2 in lung inflammatory diseases, especially, acute lung injury and pulmonary fibrosis. To address this question, we used mutant mice, i.e. PAFR transgenic mice, PAFR gene-disrupted mice and cPLA2 gene-disrupted mice. We have shown that PAF and eicosanoids, downstream mediators of cPLA2, may be involved in the pathogenesis of ARDS and IPF, which are important diseases in the elderly. Although there exist extreme differences in clinical features between ARDS and IPF, both diseases are fatal disorders for which no useful drugs are currently available. On the basis of recent reports using mutant mice, cPLA2 might be a potential target to intervene in the development of pulmonary fibrosis and acute lung injury in the elderly. [source]

Suggested Strategies for Ventilatory Management of Veterinary Patients with Acute Respiratory Distress Syndrome

Acute respiratory distress syndrome by cytomegalovirus infection in an immunocompetent infant

PEDIATRIC PULMONOLOGY, Issue 8 2008
Jungi Choi MD
Abstract A 2-month-old female infant was admitted with progressive respiratory distress, fever, and diagnosed with acute respiratory distress syndrome (ARDS). The primary pulmonary pathogen was proven to be cytomegalovirus (CMV) from bronchoalveolar lavage fluid, urine, and blood specimens. Other immunologic findings were normal. CMV-induced ARDS has not been reported previously in immunocompetent infants. Pediatr Pulmonol. 2008; 43:824,827. © 2008 Wiley-Liss, Inc. [source]

Nonparametric Estimation in a Cure Model with Random Cure Times

BIOMETRICS, Issue 1 2001
Rebecca A. Betensky
Summary. Acute respiratory distress syndrome (ARDS) is a life-threatening acute condition that sometimes follows pneumonia or surgery. Patients who recover and leave the hospital are considered to have been cured at the time they leave the hospital. These data differ from typical data in which cure is a possibility: death times are not observed for patients who are cured and cure times are observed and vary among patients. Here we apply a competing risks model to these data and show it to be equivalent to a mixture model, the more common approach for cure data. Further, we derive an estimator for the variance of the cumulative incidence function from the competing risks model, and thus for the cure rate, based on elementary calculations. We compare our variance estimator to Gray's (1988, Annals of Statistics16, 1140,1154) estimator, which is based on counting process theory. We find our estimator to be slightly more accurate in small samples. We apply these results to data from an ARDS clinical trial. [source]

Overcoming surfactant inhibition with polymers

ACTA PAEDIATRICA, Issue 12 2000
PA Dargaville
Inhibition of the function of pulmonary surfactant in the alveolar space is an important element of the pathophysiology of many lung diseases, including meconium aspiration syndrome, pneumonia and acute respiratory distress syndrome. The known mechanisms by which surfactant dysfunction occurs are (a) competitive inhibition of phospholipid entry into the surface monolayer (e.g. by plasma proteins), and (b) infiltration and destabilization of the surface film by extraneous lipids (e.g. meconium-derived free fatty acids). Recent data suggest that addition of non-ionic polymers such as dextrano and polyethylene glycol to surfactant mixtures may significantly improve resistance to inhibition. Polymers have been found to neutralize the effects of several different inhibitors, and can produce near-complete restoration of surfactant function. The anti-inhibitory properties of polymers, and their possible role as an adjunct to surfactant therapy, deserve further exploration. [source]

Acute lung injury and acute respiratory distress syndrome: fashionable names for old conditions or new clinical entities in their own right?

EQUINE VETERINARY JOURNAL, Issue 5 2005
E. JOSE-CUNILLERAS
No abstract is available for this article. [source]

Are Aggressive Treatment Strategies Less Cost-Effective for Older Patients?

JOURNAL OF AMERICAN GERIATRICS SOCIETY, Issue 4 2001
Aggressive Care for Patients with Acute Respiratory Failure, The Case of Ventilator Support
OBJECTIVES: A common assumption is that life-sustaining treatments are much less cost-effective for older patients than for younger patients. We estimated the incremental cost-effectiveness of providing mechanical ventilation and intensive care for patients of various ages who had acute respiratory failure. DESIGN: Retrospective analysis of data on acute respiratory failure from Study to Understand Prognoses and Preferences for Outcomes and Risks of Treatments (SUPPORT). SETTING: Acute hospital. PARTICIPANTS: 1,005 with acute respiratory failure; 963 received ventilator support and 42 had ventilator support withheld. MEASUREMENTS: We studied 1,005 patients enrolled in a five-center study of seriously ill patients (SUPPORT) with acute respiratory failure (pneumonia or acute respiratory distress syndrome and an Acute Physiology Score ,10) requiring ventilator support. For cost-effectiveness analyses, we estimated life expectancy based on long-term follow-up of SUPPORT patients and estimated utilities (quality-of-life weights) using time-tradeoff questions. We used hospital fiscal data and Medicare data to estimate healthcare costs. We divided patients into three age groups (<65, 65,74, and ,75 years); for each age group, we performed separate analyses for patients with a ,50% probability of surviving at least 2 months (high-risk group) and those with a> 50% probability of surviving at least 2 months (low-risk group). RESULTS: Of the 963 patients who received ventilator support, 44% were female; 48% survived 6 months; and the median (25th, 75th percentile) age was 63 (46, 75) years. For the 42 patients for whom ventilator support was withheld, the median survival was 3 days. For low-risk patients (>50% estimated 2-month survival), the incremental cost (1998 dollars) per quality-adjusted life-year (QALY) saved by providing ventilator support and aggressive care increased across the three age groups ($32,000 for patients age <65, $44,000 for those age 65,74, and $46,000 for those age ,75). For high-risk patients, the incremental cost-effectiveness was much less favorable and was least favorable for younger patients ($130,000 for patients age <65, $100,000 for those age 65,74, and $96,000 for those age ,75). When we varied our assumptions from 50% to 200% of our baseline estimates in sensitivity analyses, results were most sensitive to the costs of the index hospitalization. CONCLUSIONS: For patients with relatively good short-term prognoses, we found that ventilator support and aggressive care were economically worthwhile, even for patients 75 years and older. For patients with poor short-term prognoses, ventilator support and aggressive care were much less cost-effective for adults of all ages. [source]

Visualization of alveolar recruitment in a porcine model of unilateral lung lavage using 3He-MRI

ACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 10 2009
A. RUDOLPH
Background: In the acute respiratory distress syndrome potentially recruitable lung volume is currently discussed. 3He-magnetic resonance imaging (3He-MRI) offers the possibility to visualize alveolar recruitment directly. Methods: With the approval of the state animal care committee, unilateral lung damage was induced in seven anesthetized pigs by saline lavage of the right lungs. The left lung served as an intraindividual control (healthy lung). Unilateral lung damage was confirmed by conventional proton MRI and spiral-CT scanning. The total aerated lung volume was determined both at a positive end-expiratory pressure (PEEP) of 0 and 10 mbar from three-dimensionally reconstructed 3He images, both for healthy and damaged lungs. The fractional increase of aerated volume in damaged and healthy lungs, followed by a PEEP increase from 0 to 10 mbar, was compared. Results: Aerated gas space was visualized with a high spatial resolution in the three-dimensionally reconstructed 3He-MR images, and aeration defects in the lavaged lung matched the regional distribution of atelectasis in proton MRI. After recruitment and PEEP increase, the aerated volume increased significantly both in healthy lungs from 415 ml [270,445] (median [min,max]) to 481 ml [347,523] and in lavaged lungs from 264 ml [71,424] to 424 ml [129,520]. The fractional increase in lavaged lungs was significantly larger than that in healthy lungs (healthy: 17% [11,38] vs. lavage: 42% [14,90] (P=0.031). Conclusion: The 3He-MRI signal might offer an experimental approach to discriminate atelectatic vs. poor aerated lung areas in a lung damage animal model. Our results confirm the presence of potential recruitable lung volume by either alveolar collapse or alveolar flooding, in accordance with previous reports by computed tomography. [source]

Modelling survival in acute severe illness: Cox versus accelerated failure time models

JOURNAL OF EVALUATION IN CLINICAL PRACTICE, Issue 1 2008
John L. Moran MBBS FRACP FJFICM MD
Abstract Background, The Cox model has been the mainstay of survival analysis in the critically ill and time-dependent covariates have infrequently been incorporated into survival analysis. Objectives, To model 28-day survival of patients with acute lung injury (ALI) and acute respiratory distress syndrome (ARDS), and compare the utility of Cox and accelerated failure time (AFT) models. Methods, Prospective cohort study of 168 adult patients enrolled at diagnosis of ALI in 21 adult ICUs in three Australian States with measurement of survival time, censored at 28 days. Model performance was assessed as goodness-of-fit [GOF, cross-products of quantiles of risk and time intervals (P , 0.1), Cox model] and explained variation (,R2', Cox and ATF). Results, Over a 2-month study period (October,November 1999), 168 patients with ALI were identified, with a mean (SD) age of 61.5 (18) years and 30% female. Peak mortality hazard occurred at days 7,8 after onset of ALI/ARDS. In the Cox model, increasing age and female gender, plus interaction, were associated with an increased mortality hazard. Time-varying effects were established for patient severity-of-illness score (decreasing hazard over time) and multiple-organ-dysfunction score (increasing hazard over time). The Cox model was well specified (GOF, P > 0.34) and R2 = 0.546, 95% CI: 0.390, 0.781. Both log-normal (R2 = 0.451, 95% CI: 0.321, 0.695) and log-logistic (R2 0.470, 95% CI: 0.346, 0.714) AFT models identified the same predictors as the Cox model, but did not demonstrate convincingly superior overall fit. Conclusions, Time dependence of predictors of survival in ALI/ARDS exists and must be appropriately modelled. The Cox model with time-varying covariates remains a flexible model in survival analysis of patients with acute severe illness. [source]

ECMO in ARDS: a long-term follow-up study regarding pulmonary morphology and function and health-related quality of life

ACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 4 2009
V. B. LINDÉN
Background: A high survival rate can be achieved in patients with severe acute respiratory distress syndrome (ARDS) using extracorporeal membrane oxygenation (ECMO). The technique and the costs are, however, debated and follow-up studies in survivors are few. The aim of this study was to evaluate long-term pulmonary health after ECMO and severe ARDS. Methods: Twenty-one long-term survivors of severe ARDS and ECMO were studied in a follow-up program including high-resolution computed tomography (HRCT) of the lungs, extensive pulmonary function tests, pulmonary scintigraphy and the pulmonary disease-specific St George's Respiratory Questionnaire (SGRQ). Results: The majority of patients had residual lung parenchymal changes on HRCT suggestive of fibrosis, but the extension of morphologic abnormalities was limited and without the typical anterior localization presumed to indicate ventilator-associated lung injury. Pulmonary function tests revealed good restitution with mean values in the lower normal range, while T½ for outwash of inhaled isotope was abnormal in all patients consistent with subclinical obstructivity. Most patients had reduced health-related quality of life (HRQoL), according to the SGRQ, but were stating less respiratory symptoms than conventionally treated ARDS patients in previous studies. The majority were integrated in normal work. Conclusion: The majority of ECMO-treated ARDS patients have good physical and social functioning. However, lung parenchymal changes on HRCT suggestive of fibrosis and minor pulmonary function abnormalities remain common and can be detected more than 1 year after ECMO. Furthermore, most patients experience a reduction in HRQoL due to the pulmonary sequelae. [source]

Organophosphate poisoning complicated by a tachyarrhythmia and acute respiratory distress syndrome in a child

JOURNAL OF PAEDIATRICS AND CHILD HEALTH, Issue 5 2002
L Nel
Abstract: A 9-year-old child presented with documented organophosphate insecticide poisoning. His course was initially complicated by a tachyarrhythmia with QT-interval prolongation that responded promptly to intravenous magnesium. However, following partial recovery, he developed progressive acute respiratory distress syndrome characterized by irreversible fibrosis and obliteration of the lung parenchyma. [source]

Acute and Chronic Alcohol Exposure Impair the Phagocytosis of Apoptotic Cells and Enhance the Pulmonary Inflammatory Response

ALCOHOLISM, Issue 10 2010
Darren M. Boé
Background:, Alcohol abuse increases the risk for acute respiratory distress syndrome (ARDS). Efferocytosis, the clearance of apoptotic cells, is important in the resolution of inflammation and is regulated by RhoA and rho kinase (ROCK) activation. The effects of alcohol on pulmonary Rho pathway activation and efferocytosis have not been determined. We hypothesize that acute and chronic alcohol exposure impair pulmonary efferocytosis, leading to heightened inflammation during ARDS. Methods:, For in vivo experiments, C57BL/6 mice received either a single intraperitoneal injection of alcohol or chronic ethanol-in-water for 8 weeks prior to intratracheal instillation of apoptotic cells or lipopolysaccharide (LPS). Bronchoalveolar lavage (BAL) was performed for cells counts, calculation of the phagocytic index (PI), and Rho activity measurements. For in vitro studies, primary alveolar macrophages were cultured in alcohol (25,100 mM) and then co-cultured with apoptotic cells. RhoA activity was determined following alcohol exposure, and the PI was determined before and after treatment with the ROCK inhibitor, Y27632. Results:, Acute alcohol exposure was associated with impaired efferocytosis. Following LPS exposure, acute alcohol exposure was also associated with increased BAL neutrophils. Chronic alcohol exposure alone did not alter efferocytosis. However, following exposure to LPS, chronic alcohol exposure was associated with both impaired efferocytosis and increased BAL neutrophils. In vitro alcohol exposure caused a dose-dependent decrease in efferocytosis. Despite the fact that RhoA activity was decreased by alcohol exposure and RhoA inhibition did not alter the effects of alcohol on efferocytosis, treatment with the Rho kinase inhibitor, Y27632, reversed the effects of alcohol on efferocytosis. Conclusions:, Acute alcohol exposure impairs pulmonary efferocytosis, whereas exposure to chronic alcohol is only associated with impaired efferocytosis following LPS-induced lung injury. Both forms of alcohol exposure are associated with increased alveolar neutrophil numbers in response to LPS. The acute effects of alcohol on efferocytosis appear to be mediated, at least in part, by RhoA-independent activation of ROCK. Further studies are needed to dissect the differences between the effects of acute and chronic alcohol exposure on efferocytosis and to determine the effects of alcohol on alternative activators of ROCK. [source]

Involvement of thromboxane A2 (TXA2) in the early stages of oleic acid-induced lung injury and the preventive effect of ozagrel, a TXA2 synthase inhibitor, in guinea-pigs

JOURNAL OF PHARMACY AND PHARMACOLOGY: AN INTERNATI ONAL JOURNAL OF PHARMACEUTICAL SCIENCE, Issue 4 2004
Yoichi Ishitsuka
ABSTRACT An intravenous injection of oleic acid into animals can produce a lung injury with hypoxaemia and pulmonary vascular hyper-permeability. Although oleic acid lung injury is used as a model of acute respiratory distress syndrome (ARDS), the precise mechanisms of the lung injury are still unclear. We have investigated whether thromboxane A2 (TXA2) participated in the lung injury and have evaluated the efficacy of ozagrel, a TXA2 synthase inhibitor, on the lung injury in guinea-pigs. Oleic acid injection increased the plasma level of TXB2, a stable metabolite of TXA2, and the time-course of plasma TXB2 was similar to that of the decreased partial oxygen pressure of arterial blood (Pao2) induced with oleic acid. Ozagrel administered intravenously 30 min before oleic acid injection prevented the decrease in Pao2 and pulmonary vascular hyper-permeability. It also prevented increases in lactate dehydrogenase activity, a measure of lung cell injury, TXB2 and its weight ratio to 6-keto prostaglandin F1 , in bronchoalveolar lavage fluid. Although ozagrel administered simultaneously with oleic acid ameliorated the decrease in Pao2, post treatment showed little effect. We suggest that TXA2 participated in the oleic acid lung injury, as an "early phase" mediator, and rapidly-acting TXA2 synthase inhibitors were effective in the prevention of acute lung injury. [source]

Alcohol Abuse Enhances Pulmonary Edema in Acute Respiratory Distress Syndrome

N -Acetylcysteine Improves Group B Streptococcus Clearance in a Rat Model of Chronic Ethanol Ingestion

ALCOHOLISM, Issue 7 2009
Sonja M. Tang
Background:, Sepsis is the most common risk factor associated with acute respiratory distress syndrome (ARDS) and results in a 40,60% mortality rate due to respiratory failure. Furthermore, recent epidemiological studies have demonstrated that a history of alcohol abuse increases the risk of ARDS by 3.6-fold. More recently, group B streptococcus (GBS) infections in nonpregnant adults have been increasing, particularly in alcoholics where there is an increased risk of lobular invasion and mortality. We have shown in an established rat model that chronic ethanol ingestion impaired macrophage internalization of inactivated infectious particles in vitro and enhanced bidirectional protein flux across the alveolar epithelial-endothelial barriers, both of which were attenuated when glutathione precursors were added to the diet. We hypothesized that chronic ethanol ingestion would increase the risk of infection even though GBS is less pathogenic but that dietary N -acetylcysteine (NAC), a glutathione precursor, would improve in vivo clearance of infectious particles and reduce systemic infection. Methods:, After 6 weeks of ethanol feeding, rats were given GBS intratracheally and sacrificed 24 hours later. GBS colony-forming units were counted in the lung, liver, spleen, and bronchoalveolar lavage fluid. Acute lung injury in response to GBS was also assessed. Results:, Chronic ethanol exposure decreased GBS clearance from the lung indicating an active lung infection. In addition, increased colonies formed within the liver and spleen indicated that ethanol increased the risk of systemic infection. Ethanol also exacerbated the acute lung injury induced by GBS. NAC supplementation normalized GBS clearance by the lung, prevented the appearance of GBS systemically, and attenuated acute lung injury. Conclusions:, These data suggested that chronic alcohol ingestion increased the susceptibility of the lung to bacterial infections from GBS as well as systemic infections. Furthermore, dietary NAC improved in vivo clearance of GBS particles, attenuated acute lung injury, and disseminated infection. [source]

Increased Fibronectin Expression in Lung in the Setting of Chronic Alcohol Abuse

ALCOHOLISM, Issue 4 2007
Ellen L. Burnham
Rationale: The incidence and severity of the acute respiratory distress syndrome (ARDS) is increased in individuals who abuse alcohol. One possible mechanism by which alcohol increases susceptibility to acute lung injury is through alterations in alveolar macrophage function and induction of tissue remodeling activity. Our objective was to determine whether alcohol abuse, independent of other comorbidities, alters fibronectin and metalloproteinase gene expression in alveolar macrophages and in epithelial lining fluid (ELF) of the lung. Methods: Otherwise healthy subjects with alcohol abuse (n=21) and smoking-matched controls (n=17) underwent bronchoalveolar lavage. Alveolar macrophage fibronectin and matrix metalloproteinase (MMP) mRNA expression were measured via reverse transcription-polymerase chain reaction. The supernatant from cultured alveolar macrophages and lung ELF were tested for their ability to induce fibronectin and MMP-9 gene transcription in cell-based assays. Results: Alveolar macrophages from subjects with alcohol abuse demonstrated increased fibronectin mRNA expression (p<0.001), and their ELF also elicited more fibronectin gene transcription in lung fibroblasts compared with controls (p<0.001). In contrast, alveolar macrophages from subjects with alcohol abuse had decreased MMP-9 and MMP-2 mRNA expression (p<0.03 and p<0.005, respectively). Similarly, the supernatant (p<0.001) and ELF (p<0.01) from these subjects induced less MMP-9 gene transcription in THP-1 cells. Discussion: Alcohol abuse is associated with increased fibronectin mRNA expression in alveolar macrophages and increased fibronectin-inducing activity in the ELF. This appears to be a specific effect as other tissue remodeling genes, such as MMPs, were not equally affected. These findings suggest activation of tissue remodeling that may contribute to the increased susceptibility for the ARDS observed in alcoholism. [source]

Effects of Chronic Alcohol Abuse on Alveolar Epithelial Barrier Function and Glutathione Homeostasis

ALCOHOLISM, Issue 7 2003
Ellen L. Burnham
Background: An association between the development and severity of the acute respiratory distress syndrome has been described in individuals who abuse alcohol chronically, possibly through a mechanism involving the deficiency of pulmonary glutathione. In a rodent model of chronic alcohol abuse, this antioxidant contributes to the maintenance of alveolar-capillary membrane integrity. We postulated that humans who chronically abuse alcohol will have similar alterations in alveolar-capillary barrier function. Methods: Bronchoalveolar lavage was performed in 18 healthy chronic alcoholics and 18 control subjects; total protein and glutathione concentrations were measured within the epithelial lining fluid. To examine possible protracted effects of alcohol abuse, a subset of 11 chronic alcoholic subjects underwent a second bronchoalveolar lavage after a week of abstinence. Results: Chronic alcoholic subjects had significantly elevated protein concentrations compared with controls (8.64 ,g protein/ng immunoglobulin A vs. 5.91 ,g protein/ng immunoglobulin A, p= 0.01). After a week of abstinence, no significant increase in either the glutathione levels or normalization of the protein concentrations in the epithelial lining fluid was demonstrable. Conclusions: Increased protein levels in the epithelial lining fluid of individuals who abuse alcohol chronically may signify abnormal alveolar epithelial barrier function that does not appear to readily reverse after a period of abstinence. [source]

Effect of Chronic Ethanol Ingestion on Alveolar Type II Cell: Glutathione and Inflammatory Mediator-Induced Apoptosis

ALCOHOLISM, Issue 7 2001
Lou Ann S. Brown
Background : In septic patients, chronic alcohol abuse increases the incidence of the acute respiratory distress syndrome, a syndrome that requires alveolar type II cell proliferation and differentiation for repair of the damaged alveolar epithelium. We previously showed in a rat model that chronic ethanol ingestion decreased the antioxidant glutathione (GSH) in type II cells and exacerbated endotoxin-mediated acute lung injury. We hypothesized that this GSH depletion by ethanol, particularly mitochondrial GSH, predisposed type II cells to inflammatory mediator-induced apoptosis. Methods: Adult male rats were fed the Lieber-DeCarli diet for 2, 6, or 16 weeks. Alveolar type II cells were then isolated and treated with hydrogen peroxide or TNF-,. The effect on glutathione (cytosolic and mitochondrial), apoptotic events, and necrosis were determined. In other studies, rats were fed ethanol for 6 weeks and were treated with endotoxin and apoptosis of type II cells determined by the TUNEL method. Results: Chronic ethanol ingestion alone resulted in a progressive decrease in mitochondrial GSH and a progressive increase in the basal apoptosis and necrosis rate (p, 0.05). Furthermore, there was a progressive increase in the sensitivity of the cells to H2O2 or TNF-, induced cytochrome c release, caspase 3 activation, apoptosis, and necrosis (p, 0.05). Finally, there was a 2-fold increase in apoptotic type II cells in vivo when chronic ethanol ingestion was superimposed on endotoxemia. Conclusions: These results suggested that chronic ethanol ingestion resulted in a progressive depletion of mitochondrial GSH and sensitization of type II cells to inflammatory mediator-induced apoptosis and necrosis. These effects may be particularly relevant during acute stress when proliferation and differentiation of these cells are critical to repair of the damaged alveolar epithelium and may have important ramifications for the treatment of acute respiratory distress syndrome in patients with a history of alcohol abuse. [source]

Severe blunt trauma in dogs: 235 cases (1997,2003)

JOURNAL OF VETERINARY EMERGENCY AND CRITICAL CARE, Issue 6 2009
Stephen A. Simpson DVM
Abstract Objective , To evaluate population characteristics, injuries, emergency diagnostic testing, and outcome of dogs with blunt trauma requiring intensive care in an urban hospital. Design , Retrospective study 1997,2003. Setting , All data obtained from the University of Pennsylvania , Matthew J. Ryan Veterinary Hospital. Animals , Dogs admitted to the intensive care unit for treatment following blunt trauma. Interventions , None. Measurements and Main results , Of the 235 dogs that met inclusion criteria, 206 (88%) survived and 29 (12%) did not survive. Blunt vehicular trauma accounted for 91.1% of cases. Mild hyperglycemia and hyperlactatemia was common in both survivors and nonsurvivors. The chest was the most common region traumatized and the prevalence of polytrauma was 72.3%. Initial weight, vital signs, PCV, total plasma protein, BUN, glucose, lactate, acid-base status, and electrolytes did not differ between survivors and nonsurvivors. Nonsurvivors were significantly more likely to have had head trauma (P=0.008), cranium fractures (P<0.001), recumbency at admission (P<0.001), development of hematochezia (P<0.001), clinical suspicion of acute respiratory distress syndrome (P<0.001), disseminated intravascular coagulation (P<0.001), multiorgan dysfunction syndrome (P<0.001), development of pneumonia (P<0.001), positive-pressure ventilation (P<0.001), vasopressor use (P<0.001), and cardiopulmonary arrest (P<0.001). Conclusions , Outcome of severe blunt trauma in dogs treated with intensive care is very good. Despite the high survival rate, several features associated with poor outcome were identified. Neither admission lactate nor glucose was able to predict outcome. [source]

Suggested Strategies for Ventilatory Management of Veterinary Patients with Acute Respiratory Distress Syndrome

Role of Lung Surfactant in Respiratory Disease: Current Knowledge in Large Animal Medicine

JOURNAL OF VETERINARY INTERNAL MEDICINE, Issue 2 2009
U. Christmann
Lung surfactant is produced by type II alveolar cells as a mixture of phospholipids, surfactant proteins, and neutral lipids. Surfactant lowers alveolar surface tension and is crucial for the prevention of alveolar collapse. In addition, surfactant contributes to smaller airway patency and improves mucociliary clearance. Surfactant-specific proteins are part of the innate immune defense mechanisms of the lung. Lung surfactant alterations have been described in a number of respiratory diseases. Surfactant deficiency (quantitative deficit of surfactant) in premature animals causes neonatal respiratory distress syndrome. Surfactant dysfunction (qualitative changes in surfactant) has been implicated in the pathophysiology of acute respiratory distress syndrome and asthma. Analysis of surfactant from amniotic fluid allows assessment of fetal lung maturity (FLM) in the human fetus and exogenous surfactant replacement therapy is part of the standard care in premature human infants. In contrast to human medicine, use and success of FLM testing or surfactant replacement therapy remain limited in veterinary medicine. Lung surfactant has been studied in large animal models of human disease. However, only a few reports exist on lung surfactant alterations in naturally occurring respiratory disease in large animals. This article gives a general review on the role of lung surfactant in respiratory disease followed by an overview of our current knowledge on surfactant in large animal veterinary medicine. [source]

Development of clinical guidelines for prone positioning in critically ill adults

NURSING IN CRITICAL CARE, Issue 2 2004
Article first published online: 25 FEB 200, Catherine Rowe
Summary , Literature reveals evidence that prone positioning can improve the oxygenation of critically ill patients suffering from acute lung injury or acute respiratory distress syndrome , Multicentre evidence, however, does not support the claim that it improves patients' outcome , The implementation of multiprofessional guidelines by which to direct the manoeuvre will facilitate the safe and effective management of patients in the prone position. They will thus heighten multiprofessional awareness of the technique and promote its proactive use at such time so as to achieve maximum clinical benefit [source]

Acute respiratory distress syndrome by cytomegalovirus infection in an immunocompetent infant

Outcome of pulmonary function in Lemierre's disease-associated acute respiratory distress syndrome,

PEDIATRIC PULMONOLOGY, Issue 4 2007
Jill M. Cholette MD
Abstract Pulmonary function in acute respiratory distress syndrome (ARDS) survivors typically returns to normal with the exception of a persistent reduction in carbon monoxide diffusion capacity (DLco). Septic thrombophlebitis of the internal jugular vein, (Lemierre's syndrome or postanginal sepsis) is a well-described, albeit uncommon cause of ARDS in which metastatic pulmonary thromboemboli precipitate respiratory failure requiring ventilatory support. We describe convalescent pulmonary function in two survivors of Lemierre's disease-associated ARDS, suggesting that the subset of Lemierre's syndrome induced ARDS survivors have an excellent long-term pulmonary prognosis. Pediatr Pulmonol. 2007; 42:389,392. © 2007 Wiley-Liss, Inc. [source]

Circulating levels of KL-6 in acute respiratory distress syndrome sepsis or traumatic brain injury in critically ill children

PEDIATRIC PULMONOLOGY, Issue 8 2006
George Briassoulis MD
Abstract KL-6 is a high molecular weight glycoprotein that is expressed on the apical borders of normal secretary alveolar epithelial cells. The aim of our study was to elucidate the potential role of circulating levels of KL-6, related to C-reacting protein (CRP), disease severity (PRISM, TISS), length of stay (LOS) or mechanical ventilation (LOMV), and outcome, in children with acute respiratory distress syndrome (ARDS), sepsis, or traumatic brain injury (TBI). KL-6 concentrations were monitored using solid phase sandwich enzyme-linked immunosorbent assay in plasma of nine patients with ARDS and compared to nine patients with TBI, nine with sepsis, and nine ventilated patients with cancer of matched illness severity on days 1, 3, 5, 7, and 10. Initial respiratory/ventilatory parameters (oxygenation index, plateau pressures) were recorded for ARDS patients. Patients with ARDS had higher early plasma levels of KL-6 (956,±,400 U/ml), as compared to patients with TBI (169,±,9 U/ml), sepsis (282,±,81 U/ml), and ventilated controls (255,±,40 U/ml). Significant correlations were demonstrated between plasma KL-6 concentration and oxygenation index, PaO2: FiO2 ratio, LOS and LOMV, but not with CRP or PRISM. Only in patients with ARDS, plasma KL-6 levels were higher in non-survivors than survivors (P,<,0.03). Plasma KL-6 levels have possible prognostic significance and may provide a useful marker for ARDS in critically ill children. Pediatr Pulmonol. 2006; 41: 790,795. © 2006 Wiley-Liss, Inc. [source]