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

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

The availability of safe and effective preparations of human immune globulin that can be administered intravenously has revolutionized replacement therapy for patients suffering from hypogammaglobulinaemia. Of equal importance and greater interest, however, has been the recognition that super physiological doses of IgG can manipulate an abnormal immune system. Future prospects for the use of immunoglobulin preparations to supply specific antibodies includes the standardization of procedures, whereby patients with acute sepsis may receive antibiotics and immunoglobulin simultaneously. Already there is in vitro evidence that suggests that opsonized bacteria are more readily affected by aminoglycosides. It seems certain that gamma globulin will be used routinely in the management of patients with a number of immunomalignancies, such as chronic lymphatic leukaemia and multiple myeloma that feature hypogammaglobulinaemia, especially when chemotherapy is being administered. Control trials are underway to determine whether gamma globulin given intravenously to premature babies will satisfactorily correct their immuno-deficient state and improve their chances of survival. The immunomanipulative capacity of immunoglobulin is yet to be fully realized. Success in ideopathic thrombocytopenic purpura had led to a trial of gamma globulin in a number of autoimmune conditions. Success has been reported in myasthenia gravis, rheumatoid arthritis, diabetes, patients with circulating antibodies to factor VIII and Kawasaki's disease. The mechanism of action is unknown but almost certainly multifactorial. Two proven mechanisms that will be added to in the future, include blockade of the Fc receptors on cells of the reticulo-endothelial system and manipulation of immunoregulatory T cells by the presence of anti-idiotypic antibodies in the preparation.
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PMID:The clinical use of intravenous gammaglobulin. 244 Jul 43

Twenty consecutive patients with severe sepsis were randomized to fluid challenge with 5% albumin or 10% low MW hydroxyethyl starch (pentastarch) solutions. Fluid challenge was administered iv as 250 ml of test colloid every 15 min until the pulmonary artery wedge pressure (WP) was greater than or equal to 15 mm Hg or a maximum dose of 2000 ml was infused. Hemodynamic, respiratory, and coagulation profiles were measured before and after fluid infusion. The amount of colloid required to achieve a WP of 15 mm Hg was comparable between groups. Both colloid infusions resulted in similar increases in cardiac output, stroke output, and stroke work. The effect of fluid infusion with pentastarch on coagulation was not significantly different from albumin, although pentastarch was associated with a 45% decrease in factor VIII:c. We conclude that pentastarch is equivalent to albumin for fluid resuscitation of patients with severe sepsis.
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PMID:Effects of pentastarch and albumin infusion on cardiorespiratory function and coagulation in patients with severe sepsis and systemic hypoperfusion. 246 47

Fatal multiple organ failure after severe infection may be related to an early activation of protease cascade systems. This study aimed to relate changes in coagulation, fibrinolysis, and kallikrein to shock and outcome. Of 53 patients with severe infection, 30 did not develop shock, 12 survived septic shock, and 11 died from organ failure after septic shock. No patient had overt disseminated intravascular coagulation. We measured 17 components of the coagulation/fibrinolysis/kallikrein pathways on admission and on the next 2 days. High values for fibrinogen, factor VIII:C, von Willebrand factor antigen, and D-dimer were seen in all patients; factor XII, prekallikrein, factor VII, antithrombin, protein C, and fibronectin were low. The patients thus appeared to be hypercoagulable. These disturbances were more pronounced in septic shock survivors, who also had low plasminogen and antiplasmin, indicating ongoing fibrinolysis. Nonsurvivors of sepsis were distinguished mainly by high plasminogen activator inhibitor values; this suggests an impaired functional fibrinolysis in fatal sepsis, with possible therapeutic implications. Cryoprecipitate infusion increased the fibronectin concentration, but did not influence the other factors studied.
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PMID:Coagulation, fibrinolysis, and kallikrein systems in sepsis: relation to outcome. 250 62

Four patients with hemophilia A have undergone liver transplantation in our institution, three successfully. The first was a 21-year-old man with chronic active hepatitis (CAH) in whom the effects of previous abdominal operations prevented the satisfactory technical insertion of the new liver. He died intraoperatively. The second patient was a 15-year-old boy with CAH who began to synthesize factor VIII coagulant activity (F VIII:C) within 18 hours of successful liver transplantation and has continued to do so for almost 2 years (F VIII:C range 0.89 to 3.20 U/mL). The first 2 months of his postoperative course were complicated by infections, but since that time he has done well and has returned to school. The third patient was a 48-year-old man with portal fibrosis and severe ascites. He synthesized F VIII:C (range 0.96 to 1.50 U/mL) within six hours after reestablishment of circulation through the new liver. His postoperative course was complicated by numerous infections, and he died with sepsis and an acquired immunodeficiency-like syndrome 4 months after transplantation. The fourth patient was a 47-year-old mild hemophiliac with CAH who produced adequate factor VIII:C levels following transplantation (range 0.79 to 2.80 U/mL). These patients demonstrate that liver transplantation in hemophiliacs with end-stage liver disease may be lifesaving and results in correction of the F VIII:C deficiency and associated hemorrhagic tendency.
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PMID:Liver transplantation in hemophilia A. 1947 Apr 40

The factor VIII coagulant activity (FVIII:C), factor VIII related antigen (FVIII:RAG), and factor VIII ristocetin cofactor activity (FVIII:RCF) was determined in the cord blood samples of 30 healthy term newborns. Sodium citrate anticoagulant, cold, and a proteolytic inhibitor were used in sample processing. All three factor VIII activities were elevated in infants compared to adults; additionally, FVIII:RAG was significantly higher in vaginally compared with caesarean section delivered infants. Crossed immunoelectrophoresis of the term infant plasma showed a consistently normal factor VIII mobility. An additional group of 22 sick premature and term infants had determinations of factor VIII antigen and crossed immunoelectrophoresis. The FVIII:RAG of sick infants was approximately twice that of the well term infants. Infants with severe lung disease, asphyxia, thrombosis and sepsis had normal electrophoretic mobility despite marked elevations in FVIII:RAG. Abnormal, symmetrical, more anodal migrations were seen only in a group of severely ill newborns with dissiminated intravascular coagulation (DIC) or signs of activated fibrinolysis. These results suggest that the elevated FVIII activities seen in well infants and most sick newborns are the result of increased release of a normal form of the FVIII molecule. Those elevations seen in sick newborns with DIC result from increased release and the production of an altered, faster moving FVIII molecule.
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PMID:Newborn factor VIII complex: elevated activities in term infants and alterations in electrophoretic mobility related to illness and activated coagulation. 678 64

An analysis was made of 41 cases of disseminated intravascular coagulation in dogs, with the objective of evaluating routine and nonroutine laboratory tests used in making the diagnosis. The dogs were grouped on the basis of underlying disease, which included neoplasia (39%), pancreatitis (30%), chronic active hepatitis (15%), heat stroke (12%), and sepsis (4%). Of the diagnostic tests evaluated, those for determination of activated partial thromboplastin time, antithrombin III activity, prothrombin time, and the platelet count were the most valuable. Of the clotting factors, factor V activity was decreased more frequently than the activity of factor VIII:C (factor VIII: procoagulant). The factor VIII:C activity was in conflict with prevailing dogma that reflects depression of this factor in disseminated intravascular coagulation. Factor VIII:C activity was decreased in only 29% of dogs studied. Activation of the fibrinolytic system was manifested by decreased plasminogen activity in 49% of the dogs studied. Sixty-one percent of the dogs had increased amounts of fibrin (ogen) degradation products.
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PMID:Disseminated intravascular coagulation: antithrombin, plasminogen, and coagulation abnormalities in 41 dogs. 726 67

Neonatal group B streptococcal (GBS) sepsis and pneumonia cause lung endothelial cell injury. GBS invasion of the lung endothelium may be a mechanism for injury and the release of vasoactive eicosanoids. Pulmonary artery endothelial cells (PAEC) and lung microvascular endothelial cells (LMvEC) were isolated from neonatal piglets and were characterized as endothelial on the basis of morphology, uptake of acyl low-density lipoprotein, factor VIII staining, and formation of tube-like structures on Matrigel. PAEC and LMvEC monolayers were infected with COH-1 (parent GBS strain), isogenic mutants of COH-1 devoid of capsular sialic acid or all capsular polysaccharide, or a noninvasive Escherichia coli strain, DH5 alpha. Intracellular GBS were assayed by plate counting of colony-forming units resistant to incubation with extracellular antibiotics. All GBS strains invaded LMvEC significantly more than PAEC, showing that the site of lung endothelial cell origin influences invasion. DH5 alpha was not invasive in either cell type. Both isogenic mutants invaded PAEC and LMvEC more than COH-1 did, showing that GBS capsular polysaccharide attenuates invasion. Live GBS caused both LMvEC and PAEC injury as assessed by lactate dehydrogenase release; heat-killed GBS and DH5 alpha caused no significant injury. Supernatants from PAEC and LMvEC were assayed by radioimmunoassay for prostaglandin E2 (PGE2), the stable metabolite of prostacyclin (6-keto-PGF1 alpha), and the thromboxane metabolite thromoxane B2. At 4 h, live COH-1 caused no significant increases in eicosanoids from both PAEC and LMvEC. At 16 h, live COH-1, but not heat-killed COH-1, caused a significant increase in 6-keto-PGF1 alpha greater than PGE2 from LMvEC, but not PAEC. We conclude that live GBS injure and invade the lung microvascular endothelium and induce release of prostacyclin and PGE2. We postulate that GBS invasion and injury of the lung microvasculature contribute to the pathogenesis of GBS disease.
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PMID:Group B streptococci (GBS) injure lung endothelium in vitro: GBS invasion and GBS-induced eicosanoid production is greater with microvascular than with pulmonary artery cells. 780 66

Adult respiratory distress syndrome (ARDS) can develop as a complication of various disorders, including sepsis, but it has not been possible to identify which of the patients at risk will develop this serious disorder. We have investigated the ability of six markers, measured sequentially in blood, to predict development of ARDS in 26 patients with sepsis. At the initial diagnosis of sepsis (6-24 h before the development of ARDS), serum manganese superoxide dismutase concentration and catalase activity were higher in the 6 patients who subsequently developed ARDS than in 20 patients who did not develop ARDS. These changes in antioxidant enzymes predicted the development of ARDS in septic patients with the same sensitivity, specificity, and efficiency as simultaneous assessments of serum lactate dehydrogenase activity and factor VIII concentration. By contrast, serum glutathione peroxidase activity and alpha 1Pi-elastase complex concentration did not differ at the initial diagnosis of sepsis between patients who did and did not subsequently develop ARDS, and were not as effective in predicting the development of ARDS. Measurement of manganese superoxide dismutase and catalase, in addition to the other markers, should facilitate identification of patients at highest risk of ARDS and allow prospective treatment.
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PMID:Serum antioxidants as predictors of adult respiratory distress syndrome in patients with sepsis. 809 98

The existence of a confluently covering endothelium that is free of any thrombotic appositions can be proved 30 days after clinical implantation of an in vitro endothelialized expanded polytetrafluoroethylene graft. The recipient of the mesosystemic H-graft was a 69-year-old man who had a thrombosed portal vein following pancreatitis. Autologous endothelial cells were obtained from the external jugular vein under local anesthesia, applying the in situ cannulation technique. After low-density plating, first-passage mass cultures of 1.22 x 10(6) endothelial cells were obtained 14 days after vein excision. After precoating was accomplished with fibrinolytically inhibited fibrin glue, a 10 mm expanded polytetrafluoroethylene graft was confluently lined with the autologous endothelial cells at a seeding density of 1.2 x 10(5) cells/cm2. After a maturation period of an additional 9 days and the microbiologic exclusion of a possible infection, an 11 cm graft segment was implanted between the superior mesenteric vein and the inferior vena cava. In spite of a patent shunt the patient had a repeat bleeding episode, needed parenteral nutrition, and died of sepsis on day 30. Immediately after the graft had been taken out, specimens were processed by scanning electron microscopy and light microscopy for the immunohistochemical proof of the endothelial nature of the surface-covering cell layer. The entire graft surface displayed a confluent cell lining that was free of any thrombotic appositions. A strongly positive stain result for both factor VIII-related antigen and the fixation-resistant CD34 molecule identified these cells as endothelial. No alpha-actin-positive cells could be detected. The underlying protein matrix was well preserved and unaltered in thickness and appearance, compared with preimplantation samples. None of the specimens showed any evidence of infection. This human demonstration of an intact endothelium on a patent venous prosthesis further establishes in vitro lining as a method that actually creates a persistent and functioning endothelium on a synthetic graft surface.
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PMID:In vitro endothelialization of a mesosystemic shunt: a clinical case report. 812 70


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