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Query: UMLS:C0012739 (disseminated intravascular coagulation)
 8,673 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Coagulation studies were performed in a patient who had been bitten by a snake of the species Bothrops neuwiedi. The patient presented with hemorrhagic necrosis at the envenomization site and considerable bleeding from venous puncture sites. He developed a severe defibrination syndrome with a clottable fibrinogen level of approximately 0.1 g/l. Fibrinogen was not measurable by clotting time assay. Fibrin degradation products were greatly elevated. Treatment with antivenom caused an anaphylactic reaction within ten minutes and serum sickness after three days. In vitro experiments revealed that B. neuwiedi venom directly activates Factors II and X, but does not activate Factor XIII. In vivo consumption of Factor XIII after B. neuwiedi envenomization is ascribed to the action of Factor IIa. At low venom concentrations clotting is initiated by activation of prothrombin by the venom either directly or via Factor X activation. Treatment with heparin might be beneficial in coagulopathy secondary to snake bite by reducing circulating active thrombin. The venom contains thrombin-like proteases which cause slow clotting of fibrinogen, and plasmin-like components causing further proteolysis of fibrinogen and fibrin. Antivenom has no effect on the proteolytic action of the snake venom. The in vivo effects of antivenom are presumably caused by acceleration of the elimination of venom components from the circulation. Intravenous administration of antivenom caused normalization of blood coagulation parameters within 48 h.
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PMID:Coagulopathy after snake bite by Bothrops neuwiedi: case report and results of in vitro experiments. 229 86

Fibrin glue (FG), made with highly concentrated human fibrinogen and clotting factors, was used to achieve parenchymal organ hemostasis in patients with disordered coagulation secondary to massive transfusion, chronic disease, and disseminated intravascular coagulation; it was effective in controlling liver hemorrhage in seven patients and in the performance of a splenorrhaphy in one other patient. The coagulation profile was grossly abnormal in all patients, and the mean +/- SD intraoperative blood loss was 5.1 +/- 4.2 L; patients received 14 +/- 10 U of blood perioperatively. The amount of FG required to achieve hemostasis varied directly with the extent of injury and intraoperative blood loss (r = .84), and all patients with a blood loss greater than 4 L required at least 25 mL of FG to stop bleeding. Two patients died postoperatively secondary to cardiac arrest and adult respiratory distress syndrome. Because FG does not depend on adequate platelet or clotting factor levels to be effective, it is especially useful in patients with parenchymal organ hemorrhage and disordered coagulation.
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PMID:Fibrin glue achieves hemostasis in patients with coagulation disorders. 246 52

Hemostatic plugs consist of platelet aggregates and fibrin mesh containing blood cells and plasma components. Hemostatic efficiency depends on the rate of formation of hemostatic plugs as well as the structural integrity and stability of the formed hemostatic plugs. Fibrin elements are major constituents contributing to the structural integrity and stability, but they are subject to fibrinolytic activity occurring spontaneously after fibrin formation. Fibrinolysis is usually suppressed by endogenous inhibitors. Increase of a profibrinolytic component or deficiency of an inhibitor would result in an accelerated fibrinolysis, causing a premature lysis of hemostatic plugs before restoration of injured vessels, leading to a hemorrhagic tendency. Such a state can be seen typically in patients with congenital deficiency of alpha 2-plasmin inhibitor or a hereditary increase of plasminogen activator, and it is also seen in acquired situations such as amyloidosis, liver cirrhosis, disseminated intravascular coagulation (particularly in patients with acute promyelocytic leukemia) and thrombolytic therapy. The hemorrhagic tendency can be well controlled by an administration of an antifibrinolytic agent: epsilon-aminocaproic acid or tranexamic acid. In contrast to an accelerated fibrinolysis causing a hemorrhagic tendency, retarded fibrinolysis may predispose an individual to a thrombotic tendency. Retarded fibrinolysis may be due to either an increase in plasminogen activator inhibitors or decrease of plasminogen activators. Quantitative or qualitative deficiency of plasminogen may also lead to a thrombotic tendency.
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PMID:Hemostasis associated with abnormalities of fibrinolysis. 265 Jul 72

Fifty cirrhotic Japanese patients with oesophageal varices underwent sclerotherapy in a prospective randomized trial carried out to examine the effects of human thrombin given concomitantly with the sclerosant 5 per cent ethanolamine oleate. The two groups (25 patients each) were comparable with regard to size of the oesophageal varices, and the aetiology and severity of the liver disease. Twenty-five patients, 13 and 12 in the thrombin + and - groups, respectively, had at least one episode of variceal bleeding. The remaining 25 were given prophylactic injections. There was a significantly lower rate of occurrence of bleeding from injection sites when the injection needle was removed at the initial session of sclerotherapy in the thrombin + group, where human thrombin was injected (0.2-0.3 ml, 100-150 units per injection) just before removal of the injection needle. Endoscopy at 1 week after the initial session showed a significantly (P less than 0.05) higher rate of disappearance of red colour signs on varices in the thrombin + group (96 per cent) than in the thrombin - group (72 per cent). Fibrin degradation product E-fraction (FDP-E) values increased 1 h, 1 day and 6 days after the initial session of sclerotherapy in the two groups. The rate of increase in FDP-E values 1 h after sclerotherapy was significantly larger (P less than 0.001) in the thrombin + than in the thrombin - group. There was no clinical sign of disseminated intravascular coagulation. Administration of human thrombin plus a sclerosant seems to be useful and efficacious, especially for patients with huge oesophageal varices.
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PMID:Human thrombin plus 5 per cent ethanolamine oleate injected to sclerose oesophageal varices: a prospective randomized trial. 276 8

Two patients, a 58-year-old male and a 41-year-old female, who had poorly differentiated adenocarcinoma with signet ring cells of the stomach, developed progressive multiple organ failure following their surgical treatment, even though they did not have any direct surgical complications. Their abdominal explorations revealed primary gastric tumors with deep infiltration and metastases to the regional lymph nodes. Their clinical courses were characterized by acute renal failure and respiratory distress associated with disseminated intravascular coagulation. Histopathological examination at autopsy revealed diffuse cortical necrosis of the kidneys and marked congestion, edema, and hemorrhage with or without alveolar fibrosis of the lungs. Fibrin thrombi in the lesions of the kidneys and lungs strongly suggested the existence of disseminated intravascular coagulation. It is likely that the widely spreading cancer cells themselves produced the subclinical background for disseminated intravascular coagulation, which appeared to play an important role in the development of the multiple organ failure.
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PMID:Multiple organ failure without sepsis following surgical treatment of advanced gastric carcinoma. 285 82

A 56-year-old woman came to the hospital with fever and skin eruptions. A rise in myogenic enzyme and the presence of antileucocyte antibody were noticed, along with the gradual appearance of myalgia in both lower extremities, and muscle weakness. Steroid therapy was started under the diagnosis of polymyositis. The steroid was reduced because of mental disturbance but immediately the patient developed high fever. Various forms of treatment were carried out but there was no improvement, and the patient died. At autopsy there were scattered purpura on the skin, and the muscles were atrophic and yellowish-grey in color. Histopathologically, there was inflammatory cell infiltration and muscle fiber degeneration visible in many of the muscles, and the findings showed evidence of polymyositis. There were intranuclear inclusions in the lungs, ovaries, and adrenal glands, and this was diagnosed as generalized cytomegalic inclusion disease. Fibrin thrombi were found in the kidneys, lungs, and adrenal glands and this was pathologically diagnosed as disseminated intravascular coagulation. Endothelial cell damage caused by cytomegalovirus was assumed to be involved to a large extent in triggering the disseminated intravascular coagulation.
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PMID:Disseminated intravascular coagulation induced by generalized cytomegalic inclusion disease during steroid therapy for polymyositis. 299 60

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

Four solutions of bovine polymerized hemoglobin (BPHS) and rabbit plasma were used to replace one-third of the blood volume in five groups of rabbits. The first three solutions were "impure" because of the presence of stromal phosphatidyl-ethanolamine and phosphatidyl-serine in BPHS-1, environmental endotoxins in BPHS-2, and a large amount of higher molecular weight hemoglobin-glutaraldehyde polymers in BPHS-3. These solutions caused a 33 per cent mortality rate and significant morbidity which was characterized by hemodynamic instability, respiratory and renal insufficiency, elevation of hepatic enzyme levels, thrombocytopenia, leukopenia, disseminated intravascular coagulation (DIC) and activation of the alternate pathway of complement. Histopathologic changes found in the heart, lungs, liver, spleen and kidney were characterized by a combination of ischemic and inflammatory lesions. Fibrin thrombi were visible by immunofluorescence in the microcirculation. In contrast, the fourth solution (BPHS-4) was free of the aforementioned impurities; caused no deaths and minimal morbidity, which was limited to elevated levels of serum glutamic pyruvic transaminase and reduction of creatinine clearance; no DIC or complement activation, and mild histopathologic changes which were exclusively ischemic in nature. The results of this study indicated that the toxicity of polymerized hemoglobin solutions is due principally to the presence of impurities. Pure hemoglobin does exhibit mild toxicity when compared with a control solution which is most likely due to a vasoconstrictor effect of oxyhemoglobin.
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PMID:Toxicity of polymerized hemoglobin solutions. 334 50

Disseminated intravascular coagulation (DIC) and Primary Fibrinolysis (PF) are frequently reported in the literature as occurring in a wide variety of tumours whether subjected to chemotherapy or not and triggering a thrombohemorrhagic mechanism that is often fatal. It was therefore decided to assess the extent of the Fibrinogen-Fibrin Degradation Products (FDP) in a group of cancer patients in order to identify the primary, asymptomatic clinical expressions of these syndromes with a view to ascertaining the possibility of preventing more severe forms. The data confirm the presence of circulating FDP in a small percentage of the patients (26.9%) especially those with solid tumours metastasising to the liver. The involvement of that organ is therefore considered decisive for the onset of DIC and PF.
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PMID:[Determination of fibrinogen-fibrin degradation factors in neoplasms]. 335 45

Massive coagulopathy and bleeding continues to play a major role in the operative mortality and perioperative multi-system failure of patients requiring elective thoracoabdominal aneurysm repair. It was the purpose of this study to determine the coagulation defect that occurs with supraceliac aortic clamping and the effects of increasing aortic cross-clamp time (AXCT) on the coagulation system and its recovery. Through a standard thoracoabdominal incision, 16 mongrel dogs had their aortas cross-clamped simultaneously just above the diaphragm and at the aortic bifurcation. Animals were divided into four groups of four animals each; sham operation, 30 minute AXCT, 60 minute AXCT, and 90 minute AXCT. Central venous blood was sampled prior to aortic cross clamping (AXC), during AXC and 1 hour, 2 hours, 5 hours, 7 hours, 12 hours, and 24 hours after the clamp was removed. All samples were assayed for platelets, fibrinogen, fibrin split products, prothrombin time (PT) and partial thromboplastin time (PTT). Platelets and fibrinogen decreased as PT and PTT increased with increasing AXCT consistent with disseminated intravascular coagulation (DIC) (P less than .001). Fibrin split products were positive in the 90 minute AXCT group only. The drop in platelets was greater for increasing AXCT and continued to fall in the 30, 60 and 90 minute AXCT groups at 24 hours (p less than .001). Fibrinogen dropped to the lowest levels between two and twelve hours after AXC and returned to normal at twenty-four hours in the 60 and 90 minute AXCT groups (p less than .05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Disseminated intravascular coagulation as a result of supraceliac clamping: implications for thoracoabdominal aneurysm repair. 350 97


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