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

A critically ill patient with disseminated intravascular coagulation (DIC) secondary to gram negative septicemia is reported. Low dose (5-10 mu/kg/h) heparin by intravenous infusion promptly inhibited intravascular coagulation, as reflected by laboratory studies. Fibrin monomer (FM) became undetectable, concentration of fibrin degradation products (FDP) fell, fibrinogen rose, and the activated partial thromboplastin time (PTT) shortened. Unintentional, temporary interruption of heparin resulted in transient return of abnormal laboratory values. The patient went on to make a complete recovery. Although the therapeutic contribution of heparin could not be proven in this patient, the laboratory data suggested that it was a valuable adjunct and in the dosage given unlikely to potentiate bleeding. The monitoring of heparin therapy in DIC by measurement of FDP, FM, and fibrinogen rather than clotting time is recommended.
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PMID:Case report: low-dose intravenous heparin in the treatment of disseminated intravascular coagulation. 91 96

Fibrin deposition in response to bacterial peritonitis appears to predispose to residual infection in the peritoneal cavity. Our previous studies have demonstrated that intraperitoneal fibrinolysis using human recombinant tissue plasminogen activator (t-PA) prevented abscess formation in a rat intra-abdominal sepsis model. To investigate the potential adverse side effects of its use in the peritoneal cavity, the effect of t-PA on colonic anastomotic wound healing and on systemic coagulation parameters was examined in the rat. T-PA did not adversely affect colonic healing five and ten days after anastomosis. In animals infected intraperitoneally at the time of the anastomosis, t-PA reversed the inhibition of healing induced by perianastomotic abscesses at five days. This effect was mediated by the ability of t-PA to prevent perianastomotic abscess formation. After intraperitoneal administration, t-PA had no effect on prothrombin and partial thromboplastin times in either uninfected or infected animals and there was no evidence of clinical bleeding related to its use. These studies suggest that intraperitoneal fibrinolysis using t-PA may provide a safe, effective form of adjuvant therapy in the management of fibrinopurulent peritonitis.
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PMID:Tissue plasminogen activator reverses the deleterious effect of infection on colonic wound healing. 210

Fibrin formation plays an important role in glomerular injury. We therefore examined the procoagulant signal produced by cultured rat mesangial cells. Actively growing mesangial cells produced procoagulant activity (PCA) that was present in intact cells (surface-associated), was inhibitable by cyclohexamide and which, by clotting assay, had the characteristics of tissue factor. This PCA decreased with incubation of cells in serum-deprived medium. Incubation with bacterial lipopolysaccharide (LPS) and tumor necrosis factor (TNF alpha) induced increased detectable tissue factor by mesangial cells within two hours which was maximal by four hours. We conclude that quiescent mesangial cells produce a small amount of tissue factor-like procoagulant activity, and that this PCA can be stimulated by incubation with TNF alpha, LPS or when cells are actively growing in high serum medium. Therefore mesangial cells have the capability of contributing to fibrin formation during inflammatory glomerular injury or sepsis.
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PMID:Tissue factor production by cultured rat mesangial cells. Stimulation by TNF alpha and lipopolysaccharide. 234 26

Silastic catheters were inserted by the percutaneous route, and tunneled subcutaneously, in 315 patients who needed venous access for total parenteral nutrition. The catheters were managed with a daily program that included heat sterilization of the metal hub with an electrical soldering iron. This study aimed to evaluate prospectively the incidence of catheter-related sepsis and thrombosis. There was one case of pneumothorax. All catheters were x-rayed post-insertion: eight catheters were malpositioned initially. The median catheter duration was 18 days with a range of 2-138 days. The total duration was 240 catheter-months. Twenty-seven catheters were removed due to mechanical problems. Nine were removed because of suspected sepsis; six patients had negative blood and catheter cultures, while three grew pathogens. The sepsis rate was thus 0.95%. There were no clinical signs of thrombosis. Pull-out venography was performed in 93 patients. Fibrin sleeves were seen in the majority of cases. Two patients had wall-adherent, non-occlusive thrombus masses (2%); they both had proximal catheter positions. We conclude that there is a low risk of catheter-related sepsis and thrombosis with this technique.
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PMID:Percutaneous, tunneled silicone elastomer central venous catheters for total parenteral nutrition: low sepsis and thrombosis rate. A prospective study of 315 catheters. 252 Feb 52

It has been experimentally shown that endotoxin induces a marked increase in the levels of a fast-acting inhibitor of plasminogen activator (PAI). The plasma PAI activity and tissue-type plasminogen activator (t-PA) concentrations were measured in 61 patients with human septicaemia and results were compared with those observed in healthy controls. There was a markedly significant increase of PAI in plasma and platelet extracts of patients with septicaemia as compared to controls (p less than 0.0001). No correlation between PAI and endotoxin concentration was observed. Fibrin autography of plasma samples confirmed that activator inhibition was associated with the formation of an enzyme-inhibitor complex. t-PA activity was similar in patients and controls, whereas t-PA Ag showed a significant increase in patients (p less than 0.0001). A significant inverse correlation between t-PA activity and PAI was observed (p less than 0.05). PAI activity was higher in patients with positive blood cultures (p less than 0.0001) and gram-negative septicaemia (p less than 0.0001). There was also a significant increase of PAI levels in patients with disseminated intravascular coagulation (DIC) as compared with patients without DIC (p less than 0.001). We conclude that there is a marked increase of PAI in patients with sepsis. Increased PAI activity may contribute to the pathogenesis of DIC associated with septicaemia.
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PMID:Plasminogen activator inhibitor activity in bacterial infection. 314 82

A clinicopathological study was undertaken in 15 cases of massive hepatic necrosis after shock. The GOT and GPT level exceeded 1000 units in 10 cases. The 15 cases consisted of 3 diagnosed as fulminant hepatitis clinically and 12 diagnosed as disseminated intravascular coagulation (DIC) or multiple systemic organ failure (MOF) from the unremarkableness of liver dysfunction. It was noteworthy that sepsis and surgery were closely associated with these lesions. The weight of the liver at autopsy ranged from 800 to 2,700 g. Liver necrosis was macroscopically characterized by clear demarcation of the necrotic areas sharply separated from the surrounding liver parenchyma, showing the appearance of so-called "map-like necrosis". Microscopically, the lesions in these subjects showed mainly the pattern of centrilobular necrosis. As observed in the burn shock case (case 12), the shock which provoked in different phases of time seemed to have repeated its attack. These liver necroses were considered to result from severe systemic circulatory disturbance or intrahepatic circulatory disturbance. The possibility is indicated that the generalized or univisceral Shwartzman reaction, and repeated and combined severe shock participated in the pathogenesis. Fibrin thrombi aggrevate tissue perfusion and accelerate anoxia. Heparin therapy seemed effective in these cases if administered at an appropriate time.
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PMID:Fatal hepatic necrosis after shock. 371 91

Previous studies have suggested that plasma fibronectin is a component of the physiological antithrombotic mechanism and is related to resistance to cardiopulmonary failure during sepsis. The current study addresses the hypothesis that fibronectin deficiency results in increased sensitivity to thrombosis during sepsis, whereas increased fibronectin results in enhanced resistance. Rats were injected with purified fibronectin, antiserum to fibronectin, antiserum to albumin or vehicle prior to intraaortic infusion of saline, live Escherichia coli (10(7)--10(8)/100 gm) or E coli endotoxin (0.001--0.1 mg/100 gm). Infusion of the higher doses was associated with greater mortality in antifibronectin groups than the other groups. Mean arterial blood pressure fell transiently in all groups following injection of antifibronectin but not following the other pretreatment. Both endotoxin and bacterial infusion resulted in severe thrombocytopenia in antifibronectin-treated animals and to a lesser extent following antialbumin. Fibrinogen consumption was increased in all groups after antifibronectin treatment in bacteria infused animals after pretreatment with antialbumin or fibronectin. Fibrin degradation products were increased by bacterial infusion in animals treated with either antiserum. The current data support a relationship between plasma fibronectin and resistance to thrombosis. The relationship was not as clear-cut as that previously observed for nonseptic thrombotic states.
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PMID:Plasma fibronectin and resistance to thrombosis during sepsis. 675 30

Extensive gangrene of both lower extremities necessitating bilateral above-the-knee amputations complicated the adult respiratory distress syndrome (ARDS) caused by Escherichia coli pneumonia and septicemia in a 52-yr-old man. Concurrent with the evolution of tissue necrosis, peripheral blood leukocyte and platelet counts fell, and pulmonary vascular resistance increased. Adequacy of the cardiac output was confirmed by repeated thermodilution cardiac output measurements, and major vascular occlusion was excluded surgically. Fibrin degradation products and thrombocytopenia were present, but the other usual criteria for disseminated intravascular coagulation were absent. Small vessel thrombosis by fibrin and leukocytes was observed histologically in the amputated extremities. These findings suggest that gangrene was due to the "microembolism syndrome"--diffuse small vessel occlusion by fibrin thrombi complicating ARDS. This unusual complication of ARDS may occur without abnormalities suggestive of diffuse intravascular coagulation in routine laboratory tests of blood coagulation. It should be suspected and treated promptly to avoid severe disability in survivors.
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PMID:Ischemic necrosis of both lower extremities as a result of the microembolism syndrome complicating the adult respiratory distress syndrome caused by Escherichia coli pneumonia and septicemia. 675 35

Fibrin has classically been considered a defense mechanism of the peritoneal cavity. We have studied the role of purified fibrin in the pathogenesis of intraperitoneal infection. Implantation of 0.5% bovine fibrin clots containing 2 X 10(8) E. coli into the rat peritoneal cavity reduces the 24-hour mortality rate from 100% to 0% compared to bacteria in a similar volume of saline solution. However, the 10-day mortality rate with fibrin is 90%; 100% develop intraperitoneal abscesses. Animals receiving sterile clots lyse than over 1 to 2 weeks without abscess formation. As few as 10(2) E. coli per fibrin clot produce abscesses, but 10(7) or more are required to produce death; without fibrin less than 10(7) E. coli neither kill nor produce intraperitoneal infections. Both late death and abscess size with 2 X 10(8) E. coli are directly proportional to the fibrin clot size but not the concentration of fibrin in the clot. Operative debridement of the fibrin at 4 or 24 hours completely eliminates abscess formation in surviving animals. In vitro growth of E. coli is neither stimulated nor inhibited by fibrin or fibrinogen. Fibrin delays systemic sepsis, but the entrapped bacteria cannot be easily eliminated by normal intraperitoneal bactericidal mechanisms and abscess formation occurs. Thus radical peritoneal debridement or anticoagulation may reduce the septic complications of peritonitis.
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PMID:Fibrin in peritonitis. I. Beneficial and adverse effects of fibrin in experimental E. coli peritonitis. 699 21

Disseminated intravascular coagulation (DIC) is a common occurrence during clinical sepsis and can be induced in the experimental host by LPS. Fibrin deposition in the hepatic microcirculation has been observed within 30 min of i.v. injection of LPS. Because mononuclear phagocytes have been shown to produce a PCA after exposure to LPS, we have examined the ability of a homogeneous population of explanted hepatic macrophages to express PCA. Addition of as little as 10 ng/ml of LPS stimulated a 15- to 20-fold increase in PCA over control culture levels within 7 1/2 hr post-treatment. The PCA was found to be membrane-associated, with approximately 90 to 95% of the total PCA present in the cellular lysates, and more than 85% was inhibited by pretreatment of the cells with the diazonium salt of sulfanilic acid, an inhibitor of ecto-enzymes. In contrast to tissue thromboplastin produced by other M phi populations, the H-M phi PCA was found to be markedly sensitive both to heat inactivation at 56 degrees C and to inhibition by 1 mM DFP. Additionally, assays involving both a 1-stage coagulation test as well as an enzyme assay with a Factor Xa-specific substrate (using normal and deficient human plasmas) demonstrated that the H-M phi PCA appears to activate Factor X directly. Unlike tissue thromboplastin, the H-M phi PCA is non-dependent of Factor VII activation. These studies: 1) demonstrate the LPS induces a unique PCA in the H-M phi, and 2) support a role for the H-M phi in the initiation of DIC in endotoxemic shock.
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PMID:The induction of a unique procoagulant activity in rabbit hepatic macrophages by bacterial lipopolysaccharides. 702 10


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