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

Deep venous thrombosis and its complication pulmonary embolism are responsible for more than 50,000 deaths annually in the US, 2/3 of which occur postoperatively. Nearly 75% of such deaths could be avoided by adequate prophylaxis. All forms of surgery entail some risk of deep venous thrombosis, ranging from 10% after endoscopic prostate resection to over 50% for total hip replacement. 1.6 of thromboses will embolize and 1/4 of pulmonary emboli are fatal. The goal of prevention is to decrease the incidence of fatal pulmonary emboli while limiting the risks related to prevention. A secondary goal is to reduce the frequency of postthrombotic syndrome, a late complication of deep venous thrombosis which frequently causes invalidism. A preoperative evaluation of risks of deep venous thrombosis and of the likelihood of bleeding problems should be followed by selection of appropriate preventive measures. The evaluation should be repeated postoperatively, taking into account such factors as the duration of the intervention, the diagnosis, and the predicted duration of bed rest. Evaluation of the risk of deep venous thrombosis requires knowledge of its etiopathogenesis. Deep venous thrombosis results from a multifactorial process involving venous stasis, lesion of the vascular wall, and anomalies of blood composition. All the clinical risk factors for deep venous thrombosis are related to 1 or more of these elements. Risk factors related to stasis include immobilization, postoperative or postpartum status, pregnancy, and Cockett's syndrome. Risk factors related to lesions of the vascular wall include hip surgery, trauma, age, sepsis, varices and obesity, and postthrombotic syndrome. Risk factors related to blood anomaly include postoperative status, pregnancy, oral contraceptive use, cancer, nephrotic syndrome, hypercoagulability, trauma, and heredity. The most common clinical risk factors for deep venous thrombosis are age, surgical intervention, trauma, burns, cancer, pregnancy and delivery, oral contraceptive use, varices, obesity, and postthrombotic syndrome. The relative risk of deep venous thrombosis among OC users is 4.0 overall and higher for those with type A blood. The pathogenic mechanisms are similar to those of pregnancy except that the fibrinolytic capacity is not change. The principal mechanism is perhaps the declining level of antithrombin III, observed with estrogens and some progestins. Among methods of prevention are different forms of compression, use of heparin alone or in combination with other drugs, and oral anticoagulants.
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PMID:[Epidemiology and etiopathogenesis of deep venous thrombosis of the lower limbs]. 224 Apr 6

The relationship between serum elastase and antithrombin III was determined in septic surgical patients as a possible mechanism for intravascular thrombosis and hypercoagulability during sepsis. Eighteen patients with surgical infections and elevated white blood cell counts had their blood assayed daily for white blood cell count, serum elastase, and antithrombin III, until the patient's white blood cell count returned to normal. Antithrombin III was significantly lower (0.87%) when elastase was above the normal range (greater than 14.2 micrograms/ml). Elastase was significantly higher (30.6 micrograms/ml), when antithrombin III was less than normal. These data indicate that elevated serum elastase is associated with a significant reduction in circulating antithrombin III. Stimuli that increase serum elastase, i.e. surgery, trauma, or sepsis may promote intravascular thrombosis by the inhibition of antithrombin III at the blood-endothelial cell interface.
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PMID:The inactivation of antithrombin III by serum elastase in patients with surgical infections. 224 Aug 57

Plasma fibronectin was measured with Laurell's immunoelectroassay in 44 patients with meningococcal sepsis. The average value (15.0 +/- 7.9 mg/dl) was lower than that in normal children (27.4 +/- 8.7 mg/dl) (p less than 0.001). Fibronectin in patients correlated positively with antithrombin III (AT-III) values (p less than 0.02), but not with protein C (0.05 less than p less than 0.1). The decrease of fibronectin had no prognostic value. The fibronectin levels were lower in patients with disseminated intravascular coagulation (DIC+), than in those without DIC (DIC-) (p less than 0.02), but were lower in both groups than in a normal control group. A negative correlation between fibronectin and protein C was only present in DIC- patients (r: -0.773 = p less than 0.01). Fibronectin varied independent of AT-III and protein C in DIC+ patients. The study was repeated in 11 patients 24 hours after admission when fibronectin had decreased in 7/11 cases (mean decrease: -2.7 +/- 8.7 mg/dl). This variation correlated in a negative way with AT-III (r: -0.659 = p less than 0.05). In meningococcal sepsis fibronectin decreases very early, even in DIC- patients and its relationship to AT-III and protein C is different, depending on the presence of DIC and on the stage of evolution of the disease.
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PMID:Fibronectin in meningococcal sepsis. Correlation with antithrombin III and protein C. 231 65

Mesenteric venous thrombosis is a clinical entity, which is rarely recognized on admission. The patients are admitted with vague abdominal complaints and, eventually, abdominal sepsis might occur requiring laparotomy. Nowadays, underlying hypercoagulable states such as antithrombin-III, protein-C and protein-S deficiencies are recognized more frequently as a distinct cause of mesenteric venous thrombosis. In this paper, a case of mesenteric venous thrombosis due to protein-C deficiency is presented. The patients generally have a history of thromboembolism of the deep veins of the legs at young age. The combination of vague abdominal complaints and a history of thrombosis of the deep veins of the legs should arouse the suspicion of mesenteric venous thrombosis. In these cases, contrast-enhanced computerized tomography is a non-invasive diagnostic means which may provide the diagnosis. If infarction of the gut is present, resection is mandatory and a second-look operation should be performed. After surgery, heparinization is essential. This must be followed by administration of oral anticoagulants for an indefinite period in case of an underlying antithrombin III, protein-C or protein-S deficiency.
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PMID:Mesenteric venous thrombosis caused by deficiency of physiologic anti-coagulants: report of a case. 232 Feb 74

In order to assess precisely the fibrinolytic state in disseminated intravascular coagulation (DIC), plasma levels of fibrinogenolysis products (FgDP), fibrinolysis products (FbDP) and fibrinogenolysis plus fibrinolysis products (TDP) were measured with newly developed enzyme-linked immunosorbent assays based on monoclonal antibodies in 72 patients with DIC at presentation. Not only FbDP and TDP but also FgDP were markedly elevated in patients with DIC. When analyzed according to the underlying disease categories, the relative proportion of FgDP to TDP was high in patients with acute promyelocytic leukemia and vascular diseases, and it was the lowest in patients with sepsis. Correlation analysis revealed that plasma levels of FgDP correlated negatively with alpha 2-antiplasmin and positively with plasmin-alpha 2-antiplasmin complex (PAP) and a ratio of PAP to thrombin-antithrombin III complex (TAT). These findings indicate that besides fibrinolysis, fibrinogenolysis is markedly accelerated in the majority of the patients with DIC.
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PMID:Fibrinolysis and fibrinogenolysis in disseminated intravascular coagulation. 240 38

To discover the role of lysosomal enzyme release from polymorphonuclear (PMN) leukocytes during septicemia, plasma levels of PMN elastase were measured with a newly developed enzyme-linked immunosorbent assay for detection of the PMN elastase-alpha 1-proteinase inhibitor complex (E-alpha 1PI). Plasma samples from 41 patients were assayed continuously before and after major abdominal surgery. The patients were divided into a group without infection (group A) and two septicemia groups (survivors in group B and nonsurvivors in group C). The E-alpha 1PI levels of the 11 patients in group A without any signs of pre- or postoperative infection were in the normal range (a normal value of 86.5 +/- 25.5 ng/ml has been reported in 153 healthy subjects), except for a small increase to 208.8 +/- 25.6 ng/ml 12 hours after surgery. When septicemia was confirmed clinically in patients in groups B and C, the E-alpha 1PI levels rose on average to six times the norm in group B (649.9 +/- 116.3 ng/ml) and to more than 10 times the norm in group C (985.0 +/- 154.6 ng/ml). Peak values greater than 2,200 ng/ml could be measured in both groups. In patients in group B, the E-alpha 1PI levels returned to normal during recovery, while in those in group C they remained significantly elevated (560.5 +/- 174.7 ng/ml) until death. Correlations were demonstrated between the amount of elastase released into the circulation and the decrease in the activities of antithrombin III, coagulation factor XIII, and alpha 2-macroglobulin, as well as the increased C-reactive protein in plasma. We conclude that release of elastase and other lysosomal factors from PMN cells plays a major role in the pathobiochemical alterations during septicemia. In addition, significantly elevated E-alpha 1PI levels in the postoperative course seem to be a suitable indicator for onset and persistance of sepsis as well as of the severity of this disorder in patients after major surgery.
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PMID:Released granulocytic elastase: an indicator of pathobiochemical alterations in septicemia after abdominal surgery. 241 55

The level and functional activity of the major protease inhibitors in plasma and faecal extracts were analysed in 26 consecutive patients admitted during their first attack of acute severe colitis. The patients were retrospectively divided into two groups: one with total colitis and another with distal colitis. The patients with total colitis had a significantly lower alpha 2-macroglobulin level in plasma than normal individuals and patients with distal disease, whereas no difference in the levels of alpha 1-protease inhibitor, antichymotrypsin, antithrombin III, and alpha 2-antiplasmin was noted between the two groups. The protease-inhibiting capacity was saturated, and free proteolytic activity was present in the faecal extracts. In the extracts complex formation was demonstrated between leukocyte proteases and the antiproteases alpha 1-protease inhibitor and alpha 2-macroglobulin. It is concluded that the low plasma level of alpha 2-macroglobulin in patients with severe total colitis is mainly due to a consumption caused by complex formation with proteases, as earlier demonstrated in patients with acute pancreatitis and sepsis.
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PMID:Protease inhibitors in plasma and faecal extracts from patients with active inflammatory bowel disease. 242 96

Vitronectin, also known as serum-spreading factor or S-protein, mediates cell adhesion and inhibits formation of the membrane-lytic complex of complement and the rapid inactivation of thrombin by antithrombin III in the presence of heparin. Vitronectin is normally present in plasma at a concentration of approximately 300 micrograms/mL. The investigators quantified plasma vitronectin with an enzyme-linked immunosorbent assay and visualized reduced and nonreduced vitronectin by immunoblotting after separation of plasma or serum by sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE). The concentration of plasma vitronectin was markedly reduced in some patients with disseminated intravascular coagulation, especially in those with liver failure; it was near normal in patients with metastatic cancer and acute leukemia. Patients with vitronectin levels less than 40% normal invariably had low fibrinogen and antithrombin III and a prolonged prothrombin time. In both normal and patient plasmas there was heterogeneity in the ratio of the 75,000- and 65,000-mol wt polypeptides of reduced vitronectin: 18% had mostly the 75,000-mol wt polypeptide, 59% had roughly equal amounts of the two polypeptides, and 22% had mostly the 65,000-mol wt polypeptide. This polymorphism is inherited and appears to be due to two alleles that are present with approximately equal frequency. The blotting patterns of vitronectin in reduced and nonreduced plasmas were largely unaltered in plasma of patients with defibrination syndrome, fibrinolysis, liver failure, sepsis, metastatic cancer, and acute leukemia. There was no evidence of fragmentation of vitronectin or formation of the disulfide-bonded complex of vitronectin and thrombin-antithrombin III that is found when blood is clotted. Thus these results corroborate in vitro observations that the liver is the major source of plasma vitronectin, suggest that vitronectin may become depleted during disseminated intravascular coagulation, and define a genetic polymorphism of vitronectin.
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PMID:Plasma vitronectin polymorphism in normal subjects and patients with disseminated intravascular coagulation. 245 67

We have shown previously that fluid phase platelet-activating factor (PAF) can enhance or "prime" polymorphonuclear (PMN) responses to subsequent stimulation with agonists such as formyl-methionine-leucine-phenylalanine (FMLP). Since thrombin induces PAF production in endothelial cells, we tested whether this thrombin-provoked endothelial PAF primes responses of marginated PMNs. Monolayers of human umbilical vein endothelial cells were exposed to either thrombin (0.5-5.0 units/ml) or buffer for up to 5 min and then PMNs were layered on top of the endothelial cells. After a further 5 min incubation, the PMNs were stimulated with a suboptimal concentration of FMLP (10(-7) M), and their superoxide production, elastase release, adhesion to endothelium, and capacity to cause endothelial cell lysis and detachment were assessed. Thrombin pretreatment significantly enhanced each of these FMLP-stimulated neutrophil responses. The extent of this enhancement correlated with both the dose and duration of thrombin treatment of endothelial cells and also the duration of PMN incubation with thrombin-exposed endothelium. Evidence that the augmentation was due to endothelial-derived PAF was obtained as follows: (1) thrombin induced [3H]acetate incorporation into endothelial PAF (assayed in lipid extracts); (2) antithrombin III conjointly inhibited this [3H]acetate uptake and prevented the priming effect of thrombin-treated endothelium on PMN responses; and (3) the PAF receptor antagonist BN52021, when preincubated with PMNs, also effectively blocked the enhancement of PMN responses. We conclude that thrombin stimulation of endothelial cells initiates a sequence of events culminating in the production of PAF--a membrane phospholipid capable of priming marginated PMNs. We suggest that this coagulation-fostered endothelial/PMN interaction may underlie a paracrine response that may potentiate PMN-mediated endothelial injury during sepsis and other thrombin-generating disorders.
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PMID:Thrombin-treated endothelium primes neutrophil functions: inhibition by platelet-activating factor receptor antagonists. 254 22

Hemorrhagic and thrombotic complications are common in sick preterm infants and may reflect inadequate regulation of coagulation. All neonates have low levels of the pivotal regulator antithrombin III (ATIII) compared with adults. Plasma levels of ATIII are very low in preterm infants and are further diminished in infants with respiratory distress, necrotizing enterocolitis, sepsis, or disseminated intravascular coagulation. Babies with lower levels of ATIII in the cord blood have been shown to have a worse outcome than neonates with levels appropriate for gestational age, including higher mortality and increased incidence of intracranial hemorrhages and catheter-related thromboses. The origin of severe ATIII deficiency is unknown. Therapies with plasma replacement or anticoagulation have decreased the incidence and severity of hemorrhagic and thrombotic complications in high-risk infants in several clinical trials. These data lay the groundwork and rationale for potential use of ATIII replacement in deficient preterm infants.
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PMID:Neonatal antithrombin III deficiency. 267 71


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