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

Upon the plasmin digestion of human fibrinogen, an early cleavage product, which has been designated as fragment A, was isolated, and to study the action of plasmin in the circulation, radioimmunoassay for fragment A was carried out. This assay used rabbit immune serum obtained by injection of fragment A mixed with complete Freund's adjuvant, and fragment A was labeled with 125I using the Chloramin-T method. In 20 normal healthy donors its serum level was 3.57 +/- 1.62 microgram/ml (mean +/- SD), and it was increased significantly in certain diseases, such as acute leukemias, cardiovascular disorders, malignancies, renal failure, systemic lupus erythematosus and sepsis.
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PMID:Radioimmunoassay of an early plasmin degradation product of human fibrinogen, "fragment A", and its clinical application. 14 16

Review of the coagulation laboratory records and medical records at Memorial Sloan-Kettering Cancer Center over a three year period (1971--1974) revealed 89 patients with disseminated intravascular coagulation (DIC). The diagnosis of DIC was made if laboratory studies showed evidence of quantitative and qualitative changes in fibrinogen and significant thrombocytopenia. The patients included 19 with leukemia (17 acute), 3 with multiple myeloma, 15 with lymphoma, 46 with metastatic solid tumors, (10 lung, 9 breast, 8 gastrointestinal, 12 genitourinary, 7 miscellaneous) 4 with vascular tumors, and 3 without tumor. Other conditions which might have precipitated or initiated DIC such as gram-negative sepsis, liver impairment, or mucin secreting tumors were present in the majority of patients. Bleeding occurred in 75% of the patients and was fatal in 36%. Thromboembolism occurred in 22.5%. Thirteen percent were asymptomatic. Serum lactic dehydrogenase was elevated in over 75% of the patients at the time of, or subsequent to the occurrence of DIC. Treatment with heparin was helpful in only three of twenty patients. Eighty percent of the patients died within one to over 30 days of the onset of DIC. Post mortem evidence of DIC was present in 18 of 43 autopsies. Results of this study indicate that DIC is a frequent complication of a wide variety of tumors and that its occurrence causes morbidity and mortality in a significant number of patients. Treatment with heparin is of little help unless remission is induced and the precipitating factor(s) are reversed.
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PMID:Disseminated intravascular coagulation: experience in a major cancer center. 17 94

In a retrospective study 40 children were selected out of 53 cases of septicaemia with thrombocytopenia. They were divided into two coincidentally equally large groups of patients with consumption coagulopathy on the one side and patients with isolated thrombocytopenia without consumption coagulopathy on the other side. Both groups were of comparable age and sex distribution. Two-thirds of the children were under three months. For the differential diagnosis of both groups the activated partial thromboplastin time, the thrombotest, the factor V plasma concentration, the serum concentration of fibrin (fibrinogen) degradation products as well as control coagulation studies can be considered to have the greatest diagnostic value. The results of the study permit the following conclusions: 1. Platelet deficiency in sepsis does not prove the presence of consumption coagulopathy. 2. Consumption coagulopathy and isolated thrombocytopenia differ statistically significantly according to the bacteria cultured from the blood, the circulatory state and the pH of the blood. 3. The finding of thrombocytopenia in a patient with shock, acidosis and gramnegative septicaemia justify the suspicion of consumption coagulopathy.
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PMID:[Consumption coagulopathy and isolated platelet deficiency in childhood septicaemia]. 23 38

The unexplained occurrence of thrombocytopenia in cases of Gramnegative sepsis in man led us, in the light of animal experiments indicating the blood platelet as the target cell for endotoxin, to examine the effect of Salmonella enteritidis lipopolysaccharide B on human platelets. Human platelets were separated from a coat of plasma proteins by Sepharose 2B filtration or by a combined procedure of albumin gradient and Sepharose 2B filtration. The action of endotoxin on human platelets resulted in membrane changes manifested by dose-dependent release of [3H]serotonin and adenine nucleotides. Cytoplasmic marker, lactic dehydrogenase, and lysosomal marker, beta glucuronidase, were retained indicating that the release reaction was selective. Release of [3H]serotonin was specific for endotoxin since other particulates, zymosan and erythrocyte stroma, were without effect. Endotoxin, added to gel-filtered human platelets, induced a significant evolution of platelet factor 3 procoagulant activity. Preincubation of endotoxin with a membrane-rich homogenate of human platelets inhibited its labilizing effect on human platelets thus suggesting an interaction between endotoxin and the platelet membrane itself. Other plausible factors in this interaction [fibrinogen, adenine nucleotides, thrombin, sialic acid residues, and IgG] were eliminated on the basis of a series of control experiments. From the negligible effect of aspirin and indomethacin, we may infer that the interaction of endotoxin with platelets does not depend on the platelet prostaglandin synthesis pathway. The direct interaction of endotoxin with the human platelet membrane comprises a new mechanism which may help to clarify the pathogenesis of vascular and haemostatic disorders accompanying bloodstream infections due to Gram-negative bacteria.
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PMID:Membrane changes in human platelets induced by lipopolysaccharide endotoxin. 32 97

The diagnosis of defibrination syndrome in shock, sepsis and neonatal hypoxia is based, in addition to the clinical picture, upon a few parameters of the hemostatic system, which, in part as global tests, provide information about the course of coagulation. The parameters measured are partial thromboplastin time, thromboplastin time, plasma thrombin time, fibrinogen, thrombin-coagulase and reptilase times as well as platelet count. Normal values of these laboratory parameters were established for healthy newborns 1--5 days of age, and for healthy adults. It is suggested that especially partial thromboplastin time, the thrombin-coagulase and reptilase times, the latter influenced by fibrinolysis cleavage products, are representative for the tentative diagnosis of disseminated intravascular coagulation with fibrinolysis syndrome (DICFS). The platelet fall often lags 1--2 days behind the event. Moreover normal values for newborns, are markedly higher than those for older children or adults. In the presence of DICFS, a low-dose heparin therapy is immediately initiated. If completed defibrination is manifest, therapy is supplemented with urokinase and streptokinase, For DICFS with congenital sepsis, an exchange transfusion with heparinized fresh blood is the treatment of choice.
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PMID:[Diagnostic therapeutic problems of defibrination syndrome in shock, sepsis, and neonatal hypoxia (author's transl)]. 32 24

Analysis of the zymosan (Z)-induced human platelet response with washed platelets, fresh agammaglobulinemic plasma, and purified human IgG has identified a previously unrecognized role of IgG in this reaction, in addition to the previously reported requirements for C and fibrinogen. The rate-limiting step involves the assembly of C components on the Z particles and is independent of immunoglobulin. After the heat-labile components (supplied by agammaglobulinemic plasma) are Z bound, Z-specific IgG (apparently antibody) can bind to Z very rapidly, conferring on the previously inactive Z-complement-fibrinogen intermediate the capacity to induce platelet aggregation and serotonin release. The critical function of this Z-bound IgG appears to be in the interaction of the active Z complex with the platelet through Fc receptors, since soluble Fc fragments of each IgG subclass can totally block platelet activation. It is proposed that the human platelet requires a dual, or multi-site, stimulation to become activated during some forms of immunologic injury. These findings may provide some insight into clinical syndromes involving thrombocytopenia and intravascular coagulation during sepsis.
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PMID:Responses of human platelets to immunologic stimuli: independent roles for complement and IgG in zymosan activation. 62 28

This chapter has provided a review of available literature regarding alterations of hemostasis associated with CPB. The primary pathology of altered hemostasis during CPB appears to be two-fold: (1) a functional platelet defect of unclear etiology, which occurs in virtually all patients, and (2) a primary hyperfibino(geno)lytic defect which occurs in the majority of patients undergoing cardiopulmonary bypass. Significant thrombocytopenia does not appear to be a consistent problem, and is probably a function of perfusion technics; this may, however, be an important source of hemorrhage in some instances. Although hyperheparinemia, heparin rebound, and protamine excess have occasionally been incriminated as sources of hemorrhage during CPB, no well documented cases appear in the literature. Likewise, although DIC gained popularity in early reports of CPB hemorrahge, it appears that this syndrome rarely, if ever, arises as a consequence of CPB alone; it can be seen, however, in CPB patients who are provided a triggerin situation for DIC, such as shock, sepsis, or hemolytic transfusion reaction. It is likely that many reported alterations of hemostasis during CPB which were concluded to represent DIC actually were due to hyperfibino(geno)lysis. The key to prevention of CPB hemorrhage rests simply in obtaining an adequate preoperative workup. Of extreme importance is an adequate history with respect to bleeding tendencies in both patient and family; of equal importance is a careful history regarding antiplatelet drugs. A careful physical examination, searching for clues of a real or potential bleeding diathesis, also can often prevent catastrophic cases of CPB hemorrhage. Lastly, an adequate presurgical laboratory screen must be performed; in addition to the usual prothrombin time, partial thromboplastin time, and platelet count, a thrombin time and standardized template bleeding time must be added. The addition of these two simple modalities will insure against significant defects in fibrinogen, the fibrinolytic system, vascular function, and platelet function. When CPB hemorrhage occurs, simple laboratory screening will usually allow for a quick hemostasis evaluation. The parameters recommended in this review will distinguish between surgical and nonsurgical bleeding and should, therefore, allow for a quick decision regarding necessity for reexploration and the adequacy of hemostasis if reexploration is needed. In addition, this screen will distinguish between difficulties with heparin, protamine, and the fibrinolytic system. The vast majority of nonsurgical hemorrhages during CPB is due to a functional platlet defect, primary hyperfibrino(geno)lysis, or a combination of these. The quick administration of platelet concentrates, while awaiting laboratory evaluation, will control or significantly blunt most instances of CPB hemorrhage. If platelets fail to control bleeding, and reasonable laboratory evidence of primary hyperfibrino(geno)lysis is present, antifibrinolytics should then be used...
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PMID:Alterations of hemostasis associated with cardiopulmonary bypass: pathophysiology, prevention, diagnosis, and management. 79 78

Diagnosis of disseminated intravascular coagulation (DIC) was made in 64 cases (16.2%) among a total of 395 autopsy cases. There were 31 men and 33 women. Their ages ranged from 31 to 91 years (mean 76.3). Underlying diseases were mainly malignancy and sepsis. Fresh cardiac lesions were found in 40 cases (62.5%). Coronary thrombosis was found in 13 cases (20.3%) and myocardial necrosis in 24 cases (37.5%), with acute myocardial infarction in 9 and focal necrosis in 15. Nonbacterial thrombotic endocarditis was found in 17 cases (26.6%), mural thrombi in 11 (17.2%), and bleeding of the heart in 11 (17.2%). Platelet count, fibrinogen and euglobulin lysis time were not correlated with myocardial necrosis nor coronary thrombosis. Increase of fibrin degradation products correlated with the presence of coronary thrombosis with or without myocardial necrosis. DIC was found with a high incidence in the aged, and many of them were complicated with fresh cardiac lesions. Development of acute myocardial infarction depends on the small thrombi in the severe stenosis of the main coronary arteries or on the multiple microthrombi in the peripheral coronary branches.
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PMID:A clinicopathological study on cardiac lesions in 64 cases of disseminated intravascular coagulation. 84 48

The DIC syndrome is the most common cause of an abnormal hemorrhage tendency during pregnancy and the puerperium and reflects systemic activation of the coagulation cascade by circulating thromboplastic material, with secondary activation of the fibrinolytic system. Its presence in a pregnant patient almost invariably is evidence of an underlying obstetric disorder such as abruptio placentae, eclampsia, retention of a dead fetus, amniotic fluid embolism, placental retention or bacterial sepsis. Diagnosis of the DIC syndrome rests on the demonstration of reduced levels of fibrinogen and platelets, prolongation of the thrombin, prothrombin and partial thromboplastin times, and the presence of fibrin/fibrinogen degradation products (FDP) in the serum. Therapy consists of prompt removal of the source of procoagulant material, replacement of depleted clotting factors and, in some cases, anti-coagulation with heparin.
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PMID:Disseminated intravascular coagulation in pregnancy. 91 82

Serial measurements of coagulation activity, platelet counts, and platelet aggregation were done in patients with full-thickness burns involving 25% or more of body surface area to detect specific changes that might correlate with the onset of septicemia. Mean and maximal values for prothrombin time, partial thromboplastin time, thrombin time, activities of factor V and factor VIII, and concentrations of fibrinogen and fibrinogen-related antigens observed in the presence of bacterial septicemia did not differ significantly from those observed in the absence of septicemia. Mean platelet counts were significantly less with sepsis, but values in individual subjects were not indicative of the presence of septicemia. By contrast, platelet aggregation in response to adenosine diphosphate, epinephrine, and collagen always became severely abnormal with the onset of septicemia but not in the absence of sepsis.
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PMID:Platelet aggregation as a sign of septicemia in thermal injury. A prospective study. 94 30


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