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

The high in-hospital mortality of ARDS has not diminished over the past 10 years, despite improvements in supportive intensive care. Much of the mortality arises from infections, particularly sepsis and pneumonia, and from organ failure, especially kidney failure. The rapid advances in understanding the interlocking pathophysiologic mechanisms of ARDS have not yet been translated into therapeutic trials of new methods for diminishing the injury or for stimulating normal repair. In part, this is because it is difficult to predict which high-risk patients will develop ARDS and then intervene early in the injury process. Patients in whom the risk for ARDS is extremely high have a very high mortality even without ARDS, thereby making efficacy of an early or prophylactic therapy quite difficult to prove. In spite of severe pathologic abnormalities, including fibrosis, early in the course of ARDS, most survivors return to almost normal pulmonary function. The few cases that have been studied with serial biopsies demonstrate resolution of fibrosis. This amazing recovery poses many fascinating questions about how the lung repairs itself. Given the heterogeneous causes of ARDS and the large number of structural, cellular, and biochemical abnormalities described, one can postulate that any one of numerous factors is important in normal repair. Most promising of these are the degree of basement membrane damage, the control of type II cell proliferation and differentiation, the control of collagen synthesis, the anatomic localization of fibrosis, and the control of collagenase action. These interactions of epithelial and mesenchymal tissues probably recreate the process of lung development in the injured adult lung. At a clinical level, the role of oxygen toxicity remains a significant issue. Oxygen acting as an oxidant may be partially responsible for the small airways disease seen in approximately one quarter to one third of survivors. The mortality data stress the need for better ways of preventing and diagnosing lung infections. Better definition of the clinical factors that put survivors at risk for persistent loss of lung function is also needed, and could define a subgroup in which trials of agents designed to improve repair would be most worthwhile. More information about the long-term pathologic course, though difficult to obtain, would also be very important. Perhaps some registry of ARDS survivors would permit closer follow-up and make available more late autopsy pathology when these people die of other causes. The rapid time course of ARDS provides an ideal testing ground for agents designed to either decrease lung injury or stimulate repair.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Pulmonary sequelae and lung repair in survivors of the adult respiratory distress syndrome. 333 67

Ultrastructural studies of the cartilaginous articular surfaces of human and rabbit joints have shown that cartilage is the target substratum for adhesion by Staphylococcus aureus, leading to intra-articular sepsis. Transmission and scanning electron microscope studies demonstrated bacteria in intimate contact with acellular cartilage matrix surfaces, particularly with collagen fibres. Certain strains of Staphylococcus aureus used in these experiments reveal a high binding capacity to collagen that is derived from a cartilage matrix. These studies indicate that the pathogenesis of intra-articular sepsis is based on the ability of certain strains of staphylococci to bind preferentially to a cartilage matrix.
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PMID:Staphylococcal adhesion to collagen in intra-articular sepsis. 334 17

Concentric joint space narrowing of the hip is an expected radiographic finding in cases of inflammatory arthritis such as rheumatoid arthritis or sepsis. However, similar joint space narrowing is associated with chronic hemorrhagic conditions that produce hemosiderotic synovitis. Hemosiderotic synovitis results from chronic intra-articular bleeding such as occurs in pigmented villonodular synovitis, generalized bleeding diathesis, synovial hemangioma, and chronic trauma. Five hips in five patients with concentric joint space narrowing not associated with inflammatory arthritis or with hemophilia were reviewed clinically, radiographically, and pathologically. All patients had a hemosiderotic synovitis. The definitive diagnosis of pigmented villonodular synovitis was made pathologically in two cases that demonstrated nodular areas of giant cell proliferation, collagen production, and lipid-laden histiocytes on histologic samples.
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PMID:Concentric joint space narrowing of the hip associated with hemosiderotic synovitis (HS) including pigmented villonodular synovitis (PVNS). 335 35

We evaluated the concept that the vascular entrance of both bacterial and nonbacterial particulate material could lead to hepatic parenchymal cell injury, either due to postphagocytic Kupffer cell activity or the margination of activated leukocytes in the liver. Injection of denatured, collagen-coated particles as well as heat-killed bacteria were used as particulate challenges. Hepatic parenchymal cell injury in vivo during postoperative sepsis was evaluated by plasma aspartate aminotransferase (AST) and ornithine carbamyl transferase (OCT) enzyme levels over 3-72 h. AST and OCT levels elevated following either laparotomy plus cecal ligation (mild sepsis) or laparotomy plus cecal ligation with puncture (severe sepsis), with the peak level at 24 h. In addition, the direct intravenous injection of either nonbacterial foreign particles or heat-killed Pseudomonas aeruginosa into normal rats also produced a dose-dependent elevation of AST and OCT. The plasma level of either AST or OCT actually increased 350-400% after injection of the non-bacterial particles. A similar dose related elevation in enzymes followed the intravenous injection of heat-killed Pseudomonas. To differentiate the potential contribution of activated hepatic Kupffer cells versus activated marginated neutrophils to the in vivo hepatic injury, we determined the release of the hepatic specific enzyme OCT by cultured hepatic parenchymal cells when they were exposed to isolated Kupffer cells or isolated PMNs that were activated by exposure to dead bacteria. Bacteria alone when added to cultured hepatocytes did not induce significant OCT release. In contrast, activated PMNs but not Kupffer cells induced a significant (p less than 0.05) release of OCT from parenchymal cells into the culture media. Thus, in vivo transient hepatic parenchymal cell injury with post-operative sepsis may be mediated by the margination of activated PMNs in the liver.
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PMID:Hepatocyte injury during post-operative sepsis: activated neutrophils as potential mediators. 342 80

In rats a standardized left colonic resection was performed and colonic continuity restored by an end-to-end anastomosis in one layer. The rats were subjected to an LD50 septic challenge by intraperitoneal injection of live Escherichia coli pre- or postoperatively. Controls received saline in a corresponding manner. Groups of animals were sacrificed on the 3rd or 7th postoperative day. The breaking strengths of the anastomosis and of the skin wound were measured. The collagen content of the anastomotic segments was analyzed. There were no differences in anastomotic or skin wound strength between septic animals and controls. Collagen content was unaffected. Wound healing was not influenced by sepsis in this model.
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PMID:Influence of intraperitoneal Escherichia coli with septicemia on the healing of colonic anastomoses and skin wounds. An experimental study in the rat. 388 40

The repair processes of incised wounds depend, in part, on fibroplasia induced by soluble mediators from monocytic macrophages. Two topical antimicrobials were evaluated, each of which effectively controlled wound sepsis and yet each had widely different effects on fibroplasia and wound strength. Paired-incision dermal wounds on the flanks of guinea pigs were treated with a substance containing reactive chlorine (Alcide) or with a compound that is a mixture of two surfactants. One side of each guinea pig was treated with one of the antimicrobials (treated wounds); the opposite side was treated with isotonic saline solution (control wounds). At 7, 10, and 16 days after surgery, tensiometric measurements of C31G (a surfactant)-treated wounds were 99%, 139%, and 195% of control wound values, respectively. Alcide-treated wounds were 76%, 58%, and 88% of control wounds, respectively. Wounds treated with chlorhexidine had reduced strength at 7 days (73%) and at 10 days (78%), but by 14 days, they were similar to control wounds (94%). The main difference between the wounds was the amount of collagen formation. Alcide-treated wounds incorporated less than 50% of the amount of 14C-proline than did the wounds treated with C31G. However, Alcide-treated wounds epithelialized as rapidly as did control wounds, and had minimal scar formation. Microscopic evaluations indicated greatly reduced inflammatory infiltrates in Alcide-treated wounds, indicating that reduced wound strength may be associated with lack of fibroblast-stimulating activity by monocytes.
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PMID:Controlled wound repair in guinea pigs, using antimicrobials that alter fibroplasia. 394 14

Intravenous infusion of live. E. coli bacteria in cats did not induce microscopic damage to the gastric mucosa within 3 hours. However, if the cats before the induction of bacteremia were given 80 mM HCl and 0.6 ml gallbladder bile/kg b.w. microscopic mucosal damage developed regularly in the corpus-fundus area of the stomach. The gastric mucosal damage was not associated with significant decrease of total gastric blood flow as measured continuously electromagnetically or decreased gastric mucosal blood flow measured early and late during sepsis using radioactively labelled microspheres. Neither was the development of gastric mucosal damage associated with reduced gastric wall collagen concentration nor in RNA, DNA concentrations or RNA/DNA ratio in the gastric mucosa.
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PMID:Acute gastric mucosal ulceration in septic shock. An experimental study on pathogenic mechanisms. 608 89

Fibronectin (FN) is a glycoprotein (disulfite-bonded dimer of 200 to 220 Kd submits) found in a soluble form in blood (concentration 250--500 microg/ml), it can be removed from it by cryoprecipitation and affinity chromatography on gelatin or heparin-agarose. It is also found in an insoluble fibrillar form as a component of connective tissue matrix like collagen, proteoglycans... FN fundamentally forms molecular complexes with collagen, fibrinogen or fibrin, heparin, activated factor XIII, bacteria, cellular membranes..., these various proteins binding with now well known functional "domains" on subunits. Thus FN mediates adhesion of cells to cells as well to biomaterials or tissue, cell migration and chemotactic activity, tissue stromal organization... The transformed cultured cells in presence of oncogen virus loose ability to secrete FN which contribute to their invasive tendency. FN also interacts with hemostatic and fibrinolytic systems, as component of the subendothelium (secreted, like Willbrand factor, by endothelial cells) and of platelet alpha-granules released by stimulated platelets. FN could then provoke platelet spreading on the subendothelium surface after collagen-platelet adhesion, triggered by Willebrand factor, has happened. FN is a part of the fibrinous clot. It participates in anchorage of the clot to subendothelium and mediates its colonisation by fibroblasts, first step to wound reparation. Lastly FN probably has an important role in organism defence. It acts as a non-immunological opsonin, promoting phagocytosis by RES macrophages of bacteria, cellular or fibrin fragments, immune complexes... present in blood. Plasmatic FN concentration is strongly decreased in several ill patients following major trauma, extensive burns, shock, sepsis, with or not evidence of DIVC, of respiratory distress... SABA and various other authors have obtained good results after injections of FN (as cryoprecipitates or concentrated fractions). It is yet necessary to confirm therapeutic role of FN.
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PMID:[Plasma fibronectin]. 641

Circulating immune complexes were studied using 3.5% polyethyleneglycol precipitation in 312 children with various diseases whose ages ranged from 1 month to 14 years. One hundred and one patients (32.6%) were positive and the groups with the highest percentage were those with viral hepatitis (90%), sepsis (80.7%), collagen diseases (76.4%) and Schonlein-Henoch purpura (57.1%). We found immune complexes less frequently in idiopathic thrombocytopenic purpura than in published series of adult cases, possibly due to the fact that the diseases in children is due to a different pathogenetic mechanism. The composition of the immune complexes was tested by 1% agarose immunodiffusion against a panel of antisera. IgG and IgM were found most frequently, and IgA was very uncommon except in some cases of hepatitis. C4 was the most frequently found complement component, followed by C3. Important differences between the various diseases studied were noted. Our results are very similar to those previously published by other authors. Whereas serum autoantibodies and autoimmune diseases are less common in children than in adults, circulating immune complexes seem to have a similar frequency in children to that already reported for adults. It is difficult to assess the significance of circulating immune complexes. They might be (a) a mere "marker" of no pathogenic significance (b) a mechanism of tissue damage by intravascular deposition, or (c) they might interfere with the cell membrane receptors of macrophages, producing a defect in phagocytosis. However, we were unable to demonstrate an increased number of infections in these patients.
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PMID:[Incidence of circulating immune complexes in pediatric diseases. Comparative study with adults]. 645 Nov 57

A new inherited neuromuscular disease was identified in 4 patients (1 male, 3 females), offspring of consanguineous marriages, belonging to the same kindred. The proband was a 24-year-old female with history of ptosis and ophthalmoplegia since childhood and progressive intestinal pseudo-obstruction for the last 4 years of her life. A sural nerve biopsy showed axonal and demyelinating neuropathy. Muscle biopsies of pectoral and gastrocnemius revealed myopathic alterations with marked variation in muscle fiber size, atrophy of both fiber types and normal mitochondria. An upper gastrointestinal study showed barium in the stomach after 8 h and jejunal diverticula. Tests for absorption of fat, protein, carbohydrate, folic acid and vitamin B12 were normal. Serum levels of vitamin A and lipoproteins were also normal. The patient underwent partial gastrectomy and gastrojejunostomy. Postoperatively, she developed severe pancreatitis, sepsis, peritonitis and expired. Tissue samples from the proband and from her brother, revealed normal mucosa, but degeneration of smooth muscle of the stomach and small intestine. The myenteric plexus and vagus nerves were normal. The biochemical studies of contractile proteins (myosin, actin, tropomyosin) in the fresh and cultured smooth muscle cells of the proband obtained at the time of gastrectomy showed a 50-75% decrease in the synthesis of different contractile proteins. Turnover of contractile proteins and synthesis and turnover of collagen showed normal values. The reduction in synthesis of contractile proteins may account for the weak peristalsis and be a factor in the pathogenesis of the intestinal pseudo-obstruction.
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PMID:Inherited ophthalmoplegia with intestinal pseudo-obstruction. 668 98


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