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Query: UMLS:C0243026 (sepsis)
 52,417 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 63-year-old healthy man developed acute meningitis. A Gram-stain of the cerebrospinal fluid showed Gram-negative rods, which grew slowly. They were identified by 16S ribosomal RNA sequence-analysis as Capnocytophaga canimorsus, an oral commensal found in various animal species including dogs. Upon further questioning, the patient mentioned a superficial dog bite. Using fluorescence-in situ-hybridisation with specific DNA probes, C. canimorsus cells were detected in a gingiva swab from his dog. The strains isolated from the patient and his dog were identical. The patient made a quick recovery following therapy with cefotaxime. Infections with C. canimorsus are associated with immune suppression (especially splenectomy or alcohol abuse), yet 40% of the patients have no predisposing conditions. Documented infections concern mainly sepsis or meningitis, with a mortality of approximately 30%. Due to its fastidious growth, C. canimorsus may be missed in standard culture methods. Therefore, in each case of unexplained sepsis or meningitis contact with animals should be enquired about.
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PMID:[Meningitis after a superficial dog bite]. 1191 19

Chronic alcohol abuse is of significant clinical and economic relevance. A major part of internal medical pathology is associated with chronic alcoholism. 50% of all accidents with subsequent traumatic injuries are related to alcohol intake. Patients who are chronic alcohol abusers have prolonged hospital stays and substantial increases in postoperative morbidity. A sophisticated diagnosis of alcoholism within standard clinical routine is often difficult, and in most cases the treatment of alcohol-related diseases and complications is protracted and requires increased energy expenditure by the treating physicians. In surgical patients, chronic alcohol abuse is associated with a 3- to 4-fold risk of infections, sepsis, cardiac and bleeding complications. Therefore, the patients themselves, along with the general practitioner and an in-hospital interdisciplinary team should cooperate in medical and operative treatment in order to attain better clinical outcome. Each patient history should include a detailed assessment of the quantity of daily alcohol intake. Alcoholic diagnostic regimens including questionnaires (i.e. CAGE, AUDIT) in combination with specific laboratory markers (CDT, GGT, MCV), if implemented, could prove valuable, especially in cases where major surgical procedures are considered. Strict abstinence by alcoholic patients with organ pathology in medical and elective surgical settings as well as the prophylactic treatment of pre-operative alcohol withdrawal appear to be useful strategies to reduce the risk of complications. Short-term interventions are associated with reduced alcohol intake and decreased incidence of re-trauma. Considering the clinical relevance of alcohol abuse, sufficient screening, interventions, and open approaches to address alcohol problems should be important components of the daily clinical routine in outpatient clinics, emergency rooms, in GPs' offices and in general hospitals.
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PMID:[The alcoholic patient in the daily routine]. 1460 33

Alcohol abuse increases the incidence of acute respiratory distress syndrome more than threefold in patients with septic shock. We have shown that chronic ethanol ingestion in a rat model impairs alveolar epithelial barrier function and enhances lung injury during sepsis. We speculated that transforming growth factor beta(1) (TGFbeta(1)), a pluripotent cytokine implicated in models of epithelial barrier disruption and lung injury, could mediate alveolar epithelial injury in the alcoholic lung. We report that chronic ethanol ingestion (6 weeks) in rats increased both TGFbeta(1) mRNA and protein tissue expression (p < 0.05), but alone did not induce the release of TGFbeta(1) into the alveolar space. However, during endotoxemia, ethanol-fed rats released fivefold more TGFbeta(1) protein (by ELISA, p < 0.05) into the alveolar space than control-fed rats. Furthermore, lung lavage fluid from endotoxemic, ethanol-fed rats had more biologically active TGFbeta(1) protein than control-fed rats (p < 0.05), as reflected by anti-TGFbeta(1) antibody-inhibitable induction of permeability in rat alveolar epithelial monolayers in vitro. We conclude that chronic ethanol ingestion increases lung expression of TGFbeta(1,) which, during endotoxemia, is released and activated in the alveolar space in which it can disrupt the normally tight epithelial barrier. We speculate that this mechanism could contribute to the increased risk of acute respiratory distress syndrome in alcoholic patients.
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PMID:Transforming growth factor beta1 expression and activation is increased in the alcoholic rat lung. 1510 63

The authors describe a fatal case of purpura fulminans with symmetrical peripheral gangrene and sepsis caused by Capnocytophaga canimorsus in a 45-year-old, previously healthy woman who was bitten by a dog at an animal shelter where she was employed. Absent in this patient were the usual risk factors, including immunosuppression, alcohol abuse, corticosteroid therapy, and splenectomy. The patient's presentation to the emergency room late in the course of the infection probably effected her death. C canimorsus should be strongly suspected in any case of septicemia following a dog bite. Prompt therapy may influence the potentially fatal course of systemic infection. Employees and/or volunteers who work in animal shelters should be cognizant of the potential risks of a dog or cat bite and follow recommended procedures when such an incident occurs.
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PMID:Capnocytophaga canimorsus sepsis with purpura fulminans and symmetrical gangrene following a dog bite in a shelter employee. 1520 55

Because chronic alcohol abuse alters immune defenses and increases infection in adults, we tested the hypothesis that maternal alcohol use during pregnancy would increase the risk of sepsis in very low birth weight (VLBW) premature newborns. We performed a case-controlled analysis of VLBW newborns born at Grady Memorial Hospital (Atlanta, GA). Alcohol exposure, as the predictive variable, was assessed by maternal self-report. The outcome variables were early-onset and multiple late-onset sepsis. Univariate analysis with Fisher exact test and multivariate analysis with the use of binary logistic regression were performed. Early-onset sepsis was 15-fold higher in the alcohol-exposed group (n=20) compared with findings for the matched control group (n=168) [alcohol-exposed group, 10%, vs. control group, 0.6%: odds ratio (OR) 6.8 (95% confidence interval [CI], 2.7-17.1), P < or = .05]. Early-onset sepsis in the alcohol+cocaine-exposed group (n=64) did not differ from findings for the control group. The prevalence of multiple late-onset sepsis did not differ among the exposure groups. Logistic regression analysis, controlling for chorioamnionitis and premature prolonged rupture of membranes, demonstrated an independent, increased risk of early-onset sepsis with alcohol exposure [OR 16 (95% CI, 1.2-210), P < or = .05]. We conclude that alcohol exposure significantly increased the risk of early-onset sepsis in this group of VLBW newborns. The effects of maternal alcohol abuse during pregnancy on the risk of infection in the VLBW newborn require further analysis.
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PMID:Is maternal alcohol use a risk factor for early-onset sepsis in premature newborns? 1552 11

The purpose of this paper is to review clinical studies on hypophosphatemia in pediatric intensive care unit patients with a view to verifying prevalence and risk factors associated with this disorder. We searched the computerized bibliographic databases Medline, Embase, Cochrane Library, and LILACS to identify eligible studies. Search terms included critically ill, pediatric intensive care, trauma, sepsis, infectious diseases, malnutrition, inflammatory response, surgery, starvation, respiratory failure, diuretic, steroid, antiacid therapy, mechanical ventilation. The search period covered those clinical trials published from January 1990 to January 2004. Studies concerning endocrinological disorders, genetic syndromes, rickets, renal diseases, anorexia nervosa, alcohol abuse, and prematurity were not included in this review. Out of 27 studies retrieved, only 8 involved pediatric patients, and most of these were case reports. One clinical trial and one retrospective study were identified. The prevalence of hypophosphatemia exceeded 50%. The commonly associated factors in most patients with hypophosphatemia were refeeding syndrome, malnutrition, sepsis, trauma, and diuretic and steroid therapy. Given the high prevalence, clinical manifestations, and multiple risk factors, the early identification of this disorder in critically ill children is crucial for adequate replacement therapy and also to avoid complications.
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PMID:Hypophosphatemia in critically ill children. 1554 5

Although pulmonary function is not altered, a history of alcohol abuse is an independent outcome variable in the development of acute respiratory distress syndrome. In the absence of cirrhosis, alcohol abuse decreased glutathione, the key antioxidant lining the alveolar space, by 80% and is associated with alveolar barrier leak. Neither the glutathione pool nor barrier leak was corrected by abstinence for 1 week. This aberrant glutathione homeostasis may contribute to enhanced alveolar permeability, thereby increasing susceptibility to the development of acute respiratory distress syndrome. In a rat model, chronic ingestion of ethanol decreased pulmonary glutathione concentration, increased alveolar barrier permeability, and increased the risk of acute lung injury. In alveolar type II cells, chronic ingestion of ethanol altered cellular functions such as decreased surfactant processing, decreased barrier integrity, and increased sensitivity to cytotoxin-induced apoptosis in vitro and in vivo. In alveolar macrophages, chronic ingestion of ethanol decreased phagocytosis of microorganisms and decreased cell viability, events that would increase the risk of pneumonia. A central role for glutathione availability was demonstrated by the normalization of cellular function and viability of type II cells and macrophages as well as decreased sensitivity to endotoxemia-induced acute lung injury when glutathione precursors were added to the ethanol diet. These results support the suggestion that chronic ingestion of ethanol increased the risk of acute lung injury not through ethanol per se but through the chronic oxidative stress that resulted from ethanol-induced glutathione depletion. Because chronic oxidative stress alters cellular functions and viability, the lung becomes more susceptible when a second hit such as sepsis occurs.
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PMID:Chronic ethanol ingestion and the risk of acute lung injury: a role for glutathione availability? 1559 87

Alcohol abuse markedly increases the risk of sepsis-mediated acute lung injury. In a rat model, ethanol ingestion alone (in the absence of any other stress) causes pulmonary glutathione depletion, increased expression of transforming growth factor-beta1 (TGF-beta1), and alveolar epithelial barrier dysfunction, even though the lung appears grossly normal. However, during endotoxemia, ethanol-fed rats release more activated TGF-beta1 into the alveolar space where it can exacerbate epithelial barrier dysfunction and lung edema. Ethanol ingestion activates the renin-angiotensin system, and angiotensin II is capable of inducing oxidative stress and TGF-beta1 expression. We determined that lisinopril, an angiotensin-converting enzyme inhibitor that decreases angiotensin II formation, limited lung glutathione depletion, and treatment with either lisinopril or losartan, a selective angiotensin II type 1 receptor blocker, normalized TGF-beta1 expression. The glutathione precursor procysteine also prevented TGF-beta1 expression, suggesting that TGF-beta1 may be induced indirectly by angiotensin II-mediated oxidative stress and glutathione depletion. Importantly, lisinopril treatment normalized barrier function in alveolar epithelial cell monolayers from ethanol-fed rats, and treatment with either lisinopril or losartan normalized alveolar epithelial barrier function in ethanol-fed rats in vivo, as reflected by lung liquid clearance of an intratracheal saline challenge, even during endotoxemia. In parallel, lisinopril treatment limited TGF-beta1 protein release into the alveolar space during endotoxemia. Together, these results suggest that angiotensin II mediates oxidative stress and the consequent TGF-beta1 expression and alveolar epithelial barrier dysfunction that characterize the alcoholic lung.
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PMID:Angiotensin II mediates glutathione depletion, transforming growth factor-beta1 expression, and epithelial barrier dysfunction in the alcoholic rat lung. 1590 76

Alcohol is the most commonly used and abused drug in the United States. The deleterious health effects of alcohol can be attributed both to its acute intoxicating effects, which result in temporary impairment of judgment and motor skills, and to its more chronic and toxic effects on the liver, pancreas, heart, and brain, all of which may result in irreversible organ damage. Although recognized for more than a century as a major risk factor for pneumonia, alcohol abuse was until recently perceived to have no significant effects on lung structure and/or function. However, within the past decade, epidemiologic studies have revealed that alcohol abuse independently increases the risk of acute respiratory distress syndrome (ARDS) two- to fourfold in patients with sepsis or trauma and may play a role in ARDS pathogenesis in as many as half of all patients with the syndrome. Although alcohol abuse alone does not cause acute lung injury, it renders the lung susceptible to dysfunction in response to the inflammatory stresses of sepsis, trauma, and other clinical conditions recognized to cause ARDS. Recent investigations in both animal models of chronic ethanol ingestion and in human subjects with a history of alcohol abuse have explored this previously unrecognized connection between alcohol and acute lung injury and have uncovered multiple derangements, which we now characterize as the "alcoholic lung." This review summarizes the epidemiologic association between alcohol abuse and acute lung injury and the recent experimental findings that are unraveling the underlying pathophysiology.
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PMID:Alcohol abuse and acute lung injury: epidemiology and pathophysiology of a recently recognized association. 1604 57

Epidemiological evidence gathered only in the past decade reveals that alcohol abuse independently increases the risk of developing the acute respiratory distress syndrome by as much as three- to fourfold. Experimental models and clinical studies are beginning to elucidate the mechanisms underlying this previously unrecognized association and are revealing for the first time that chronic alcohol abuse causes discrete changes, particularly within the alveolar epithelium, that render the lung susceptible to acute edematous injury in response to sepsis, trauma, and other inflammatory insults. Recent studies in relevant animal models as well as in human subjects are identifying common mechanisms by which alcohol abuse targets both the alveolar epithelium and the alveolar macrophage, such that the risks for acute lung injury and pulmonary infections are inextricably linked. Specifically, chronic alcohol ingestion decreases the levels of the antioxidant glutathione within the alveolar space by as much as 80-90%, and, as a consequence, impairs alveolar epithelial surfactant production and barrier integrity, decreases alveolar macrophage function, and renders the lung susceptible to oxidant-mediated injury. These changes are often subclinical and may not manifest as detectable lung impairment until challenged by an acute insult such as sepsis or trauma. However, even otherwise healthy alcoholics have evidence of severe oxidant stress in the alveolar space that correlates with alveolar epithelial and macrophage dysfunction. This review focuses on the epidemiology and the pathophysiology of alcohol-induced lung dysfunction and discusses potential new treatments suggested by recent experimental findings.
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PMID:The alcoholic lung: epidemiology, pathophysiology, and potential therapies. 1722 Mar 70


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