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Query: UMLS:C0036690 (sepsis)
 59,461 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

Every surgical procedure taxes the hemostatic defenses of the patient. If his hemostatic mechanism is sound, he is unlikely to have a bleeding problem during or after an operation, unless, of course, a suture or clip slips off. Two classes of patients do present bleeding problems to the surgeon. One group has a pre-existing bleeding tendency, the other acquires it during or after the operation. The recognition of patients with severe hemostatic disabilities, such as hemophilia, presents no problem since the patient is aware of the disease. The mild bleeder is less likely to be detected by screening tests than by adroit questioning. The major hemostatic defect that may develop during an operation, or shortly thereafter, is disseminated intravascular coagulation. This syndrome, always secondary, may accompany shock, mismatched blood transfusion, septicemia, or extensive malignancy. Its prevention or early recongnition is much easier than treatment after circulating platelets and some coagulation factors have been consumed and fibrinolysis is destroying fibrin and fibrinogen.
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PMID:Surgical hemostasis. 37 88

A highly virulent strain of Salmonella tyhimurium was given orally to produce disease experimentally in 21 normal colostrum-fed calves 3 to 9 weeks old. The challenge inoculum varied from 10(4) to 10(11) organisms. The disease was characterized by fever, depressed attitude, and decreased appetite. Many calves given larger challenge dose levels also had diarrheic feces containing mucus, fibrin, and blood. Fecal cultures were positive for salmonella. Septicemia occurred in some calves (9 of 15 calves cultured were positive). Eleven calves died and 10 calves survived challenge exposure. Survival was inversely related to the size of the challenge inoculum and directly related (although to a lesser degree) to age of the calf. White blood cell total and differential counts were variable. Both neutropenia and neutrophilia were observed. Plasma proteins decreased markedly in calves with diarrhea, probably indicating fecal protein loss. Fibrinogen increased during the acute stages of diarrhea.
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PMID:Bovine salmonellosis: experimental production and characterization of the disease in calves, using oral challenge with Salmonella typhimurium. 39 44

The morphologic and clinical findings in seven fatal cases of meningococcal septicemia are described and interpreted in light of recent experimental and clinical studies. We include evidence that suggests the disease has two distinct pathogenetic mechanisms. First, a shock-like terminal phase is associated with the development of widespread pulmonary microvascular thrombosis. These thrombi, composed largely of platelets and leukocytes, produce severe cor pulmonale that cannot be prevented with heparin sodium treatment. Meningococcal endotoxin also produces disseminated intravascular coagulation, which includes the rapid consumption of fibrinogen and the formation of fibrin thrombi in adrenal and renal glomerular capillaries, causing hemorrhagic infarction of the adrenal glands and renal cortical necrosis. This secondary phase of the disease can be modified with heparin therapy, but its control does not improve survival because the parenchymal lesions produced are not immediately life threatening.
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PMID:Fatal meningococcal septicemia. 57 4

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


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