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Query: UMLS:C0036690 (sepsis)
 59,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The incidence of gram-negative bacteremia is significantly increasing in recent years by the wide-spread use of cytotoxic and immunosuppressive drugs. Although, the effective antimicrobial drugs are being used in treatment, the mortality rate is still high. In this study, we searched for the histopathological changes occurring on lung tissue in E. coli sepsis, and their severity in different models. Microscopically, all the specimens were examined by the presence of interstitial and peribronchiolar inflammation, congestive atelectasis, and emphysema. The differences between the ratios of histopathological changes in treatment subgroups were not statistically significant. However, the ratio of interstitial and peribronchiolar inflammation and emphysema was significantly decreased in mice received cyclophosphamide, when compared with control group. Besides, the ratio of peribronchiolar inflammation was significantly increased in mice received steroid when compared with control group.
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PMID:[The histopathological effects of different treatments on lung tissue of mice pretreated with cyclophosphamide and steroids in experimental E. coli sepsis]. 179 59

Pulmonary effects, lung clearance, and tissue retention of blood-borne Pseudomonas aeruginosa were compared in dogs (n = 5) and pigs (n = 5) during continuous 6-hour intravenous infusion of 1.2(10(9)) bacteria/min/20 kg. Control pigs received an equal volume of sterile saline. In contrast to controls, experimental pigs developed pulmonary artery (PA) hypertension (mean, 30 +/- SE 3; baseline, 17 mm Hg) and pulmonary failure manifested by hypoxemia (mean PaO2, 49 +/- 4; baseline, 78 +/- 2 mm Hg; p less than 0.001), increased intrapulmonary shunting (40 to 50%), noncardiogenic pulmonary edema, and congestive atelectasis, a pattern of pulmonary failure very similar to sepsis-induced ARDS in humans. In dogs, PA pressures wee unchanged from baseline, no edema was detected, and comparable hyperventilation was associated with an increase in PaO2 from 77 +/- 4 (baseline) to 87 +/- 2 mm Hg (p less than 0.001). Tissue retention of viable blood-borne organisms in pigs was greatest in the lungs. In dogs, lung retention was minimal and greatest tissue retention occurred in the liver and spleen. We conclude that both lung clearance of blood-borne organisms and bacteremia-induced pulmonary failure are quite host dependent.
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PMID:Bacteremia: host-specific lung clearance and pulmonary failure. 678 63

It has been known for decades that shock and sepsis can cause a syndrome of acute respiratory failure with characteristics of non-cardiogenic pulmonary edema. Over the years, this syndrome has been given a number of names, including congestive atelectasis, traumatic wet lung, and shock lung. In 1967 the modern counterpart to this syndrome was described and subsequently called the "acute respiratory distress syndrome" (ARDS). This syndrome results from lung injury and inflammation. As with inflammation elsewhere, ARDS is accompanied by many cellular and molecular processes, some of them specific to the syndrome, others perpetuating the syndrome, and others inactivating the by-products of inflammation. Since no specific clinical sign or diagnostic test has yet been described that identifies ARDS, its diagnosis is based on a constellation of clinical, hemodynamic, and oxygenation criteria. Current ARDS treatment is mainly supportive, since these patients frequently have coexisting conditions. Although in 1994 a new standard ARDS definition was accepted, that definition failed to standardize the measurement of the oxygenation defect and does not recognize different severities of pulmonary dysfunction. Based on current evidence there is a need for a better definition and classification system that could help us to identify ARDS patients who would be most responsive to supportive therapies and those unlikely to benefit because of the severity of their disease process. This paper examines our current understanding of ARDS and discusses why the current definition may not be the most appropriate for research and clinical practice.
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PMID:What is the acute respiratory distress syndrome? 2294 59