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

We reported a case of 64 a year-old male patient of miliary tuberculosis associated with ARDS, DIC and pneumothorax, who had a history of gastric ulcer and pulmonary tuberculosis. On admission his chief complaints were fever, fatigue, palpitation, appetite loss and weight loss, and most noticeable abnormalities were bleeding from the gastric ulcer and miliary shadow on the chest x-ray film with hypoxemia. On the day after admission to the hospital he was diagnosed as ARDS as he showed severe hypoxemia due to extensive tuberculous infiltration in bilateral lung fields, and treatment with antituberculous drugs and steroids were started. On the third hospital day DIC appeared on laboratory data, Gabexate mesilate (FOY) for DIC and respirator for ARDS were introduced. Two weeks later pulmonary infiltration, PaO2 and general condition were somewhat improved. On the 15th day after admission pneumothorax occurred on the right side, and on the 20th day on the left. Tube drainage of both pleural cavities, and instillation of OK-432 and Fibrinogen HT into the right pleural cavity were done, but it showed no effect. Two months after admission pouring Fibrinogen HT and thrombin into the left B1+2 and right B1 with cannula washing pipe through the instrument channel of bronchoscope was carried out. A few days later air leakage stopped and collapsed lungs were completely expanded. This method is effective in the case of incurable pneumothorax with pulmonary hypofunction.
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PMID:[A case of miliary tuberculosis associated with ARDS, DIC and bilateral pneumothorax]. 259 62

Conformational and structural changes on conversion of fibrinogen to fibrin and its cross-linking by Factor XIIIa lead to the development of new antigenic determinants that permit differentiation between their plasminolytic cleavage products. A monoclonal antibody (DD-3B6/22) that is specific for cross-linked fibrin derivatives containing the D dimer configuration has been used in developing a latex agglutination procedure that can detect fibrin degradation products in either plasma or serum. Fibrinogen or its degradation products do not cross-react with this antibody. Results were calibrated with an enzyme immunoassay, which used a purified D dimer standard. Plasmas from 40 normal subjects, all having D dimer levels below 250 ng/mL measured by enzyme immunoassay, were all negative by latex assay. In contrast, positive latex agglutination titers were obtained with 87 of 88 patients with demonstrated deep venous thrombosis, pulmonary embolism, or disseminated intravascular coagulation. Compared to enzyme immunoassay, latex agglutination assay is less sensitive, but this latex procedure provides a rapid and less elaborate test for elevated levels of cross-linked fibrin degradation products in patients with thrombosis. Plasma assays for fibrin degradation products are preferable to those using serum.
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PMID:Rapid detection of cross-linked fibrin degradation products in plasma using monoclonal antibody-coated latex particles. 287 46

Disseminated intravascular coagulation (DIC) was produced by an infusion of a prothrombin activator (Echis carinatus venom; 30 minutes; 0.5 NIH thrombin equivalent U/kg) in mongrel dogs (Echis group, n = 7). Fibrinogen declined to below measurable levels (less than 25 mg/dl), and fibrin-fibrinogen degradation products appeared (53 +/- 8 micrograms/ml) at end venom infusion in the Echis group. These alterations were not seen when an irreversible thrombin inhibitor, D-phenylalanyl-L-prolyl-L-arginine-L-chloromethyl ketone (PPACK) (57 nmol/kg/min for 120 minutes), was given alone (PPACK group, n = 5) or in association with venom (Echis + PPACK group, n = 5). Factor II activity (1% +/- 1%) in the Echis and Echis + PPACK groups was significantly below the PPACK (55% +/- 9%) and the control (79% +/- 2%) levels at 120 minutes. In contrast, factor VIII coagulant (factor VIII:C) activity in the Echis group (1% +/- 1%) remained significantly below that in the Echis + PPACK (68% +/- 8%), PPACK (78% +/- 10%), and control (91% +/- 9%) groups at this interval. No change in factors X (91% +/- 7% to 81% +/- 7%, P not significant) and VII (64% +/- 10% to 48% +/- 11%, P not significant) activities were observed. Hemolysis was observed only in the Echis group, whereas thrombocytopenia and leukopenia were noted in both the Echis and the Echis + PPACK groups. These data show that large amounts of E. carinatus venom produce rapid DIC in vivo, because of the activation of prothrombin. In contrast, the decline in factor VIII:C activity appeared to be the result of the liberated thrombin. PPACK antagonized all of the venom-released thrombin without any major deleterious clotting abnormalities. This inhibitor appears to prevent thrombin-mediated DIC in vivo. In contrast, heparin was found to be an unreliable antagonist of the venom-released thrombin in vitro. PPACK also inhibited the marked hemolysis usually observed after venom. In addition, we found that the esterolytic (N-benzoyl-L-prolyl-L-phenylalanyl-L-arginine-p-nitroanilide HCL) activity of E. carinatus venom degrades fibrinogen in vitro.
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PMID:Disseminated intravascular coagulation following Echis carinatus venom in dogs: effects of a synthetic thrombin inhibitor. 308 70

Reinfusion of mediastinal blood after coronary bypass grafting reduces the need for homologous transfusion with its hazards. To determine the efficacy of autotransfusion using the cardiotomy reservoir used during operation as a postoperative collection system, we studied the characteristics of reservoir blood (minimum 500 ml, mean 810 ml) and compared the hematologic profiles of 21 patients before and after blood infusion. The mean hematocrit value of the shed blood was 25% +/- 7%, platelet count 60,000 +/- 39,000/microliter, fibrinogen 19 +/- 25 mg/dl, and factor VIII 11% +/- 7%. The fibrinopeptide A concentration was 400 ng/ml, and the B beta 15-42 peptide was 28 +/- 14 pmol/ml. These values indicate defibrination of the blood before collection (no clots were found in the reservoirs), and no significant differences were detected between the types of reservoirs used (Bentley, n = 10, Shiley, n = 11). Infusion of reservoir blood between 500 and 1860 ml did not significantly affect the factor VIII, fibrinopeptide A, or B beta 15-42 peptide levels. Fibrinogen levels increased from 254 to 395 mg/dl (p less than 0.001). Only six of 21 patients received bank blood before discharge. These findings indicate that extensive coagulation occurs within the mediastinum before the blood is collected, that mediastinal blood can be safely infused without inducing fibrinolysis or disseminated intravascular coagulation, and that use of the cardiotomy reservoir is a safe and inexpensive method of autotransfusion after coronary artery bypass grafting.
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PMID:Autotransfusion after cardiac operation. Assessment of hemostatic factors. 326 Mar 14

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

Reports in the literature on the difficulty of differential diagnosis between Disseminated Intravascular Coagulation (DIC) Pseudo-DIC and Primary Fibrinolysis (PF) in patients with liver disease, stimulated a study of various coagulation parameters (PT, PTT, Platelets, Fibrinogen, FDP) in 28 cirrhotic patients. The study confirmed reports in the literature on the high incidence of circulating FDP among liver disease patients. The vital role these play in maintaining alterations in haemostasis means that cirrhosis cases must be approached with extreme caution, avoiding any therapeutic or instrumental procedure liable to worsen the already disturbed coagulation pattern in such patients.
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PMID:[Evaluation of several parameters of coagulation in liver cirrhosis: disseminated intravascular coagulation or pseudo-disseminated intravascular coagulation?]. 336

This study was designed to clarify whether or not leukotoxin (9, 10-epoxy-12-octadecenoate), which is biosynthesized by neutrophils, might be involved in the genesis of coagulating abnormalities. Twelve dogs were divided into 2 groups. In the test group (n = 6), 100 mumol/kg of leukotoxin was injected intravenously, and in the control group (n = 6), 100 mumol/kg of linoleate was injected. In each group, a series of blood samples were collected and used for coagulation studies. After the end of the experimental period, a histological study was performed on organs removed from the dogs. In the leukotoxin group, fibrin and fibrinogen degradation products (FDP) was increased time-dependently. Fibrinogen was decreased, and prothrombin time and activated partial thromboplastin time were prolonged in parallel with the increase in FDP. A decrease in number of platelets was also observed. Intravascular coagulation was observed in sections of lung. These data were compatible with a diagnosis of disseminated intravascular coagulation (DIC). No significant changes in these parameters were observed in the linoleate group. Leukotoxin has been confirmed to show antifungal and antibacterial activity, and its production might be a defensive response to infection. Over-production of leukotoxin associated with severe infection might therefore account for infection-induced DIC.
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PMID:The role of leukotoxin (9,10-epoxy-12-octadecenoate) in the genesis of coagulation abnormalities. 339 95

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

Twenty-seven attacks of acute human pancreatitis of different severity were analysed concerning clinical outcome and activation of the coagulation and fibrinolytic systems. Consumptive coagulopathy was suggested by decreased platelet counts, decreased prothrombin values and consumption of fibrinogen during the first days in severe attacks. Factor X was slightly decreased the first 5 days in all attacks. Increased fibrinolysis was suggested by decreased plasminogen values in severe attacks. Fibrinogen degradation products were seen in 40% of the patients in blood and in 100% of the patients in the peritoneal fluid. The four main protease inhibitors of the two systems all showed protease-antiprotease complexation and lower functional than quantitative values. Plasma levels of antithrombin III and alpha 2-macroglobulin were low, while the levels of C1-inhibitor and alpha 2-antiplasmin were high. Functional levels of all the four protease inhibitors were almost zero in the peritoneal fluid in severe attacks. It is concluded that severe acute pancreatitis results in both consumptive coagulopathy and in increased fibrinolysis. A local antiprotease deficiency is seen in the peritoneal cavity and high levels of protease-antiprotease complexes are also seen in plasma. All these changes are closely correlated to the severity of the disease and may probably determine the clinical outcome of the acute attack.
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PMID:Consumptive coagulopathy, fibrinolysis and protease-antiprotease interactions during acute human pancreatitis. 351 16

The laboratory tests of 38 patients in pediatric age with Disseminated Intravascular Coagulation (DIC) were retrospectively evaluated. In all patients were performed PT, aPTT, platelets count, FDP dosage and biological assay of Fibrinogen. In most of them the activity of FII, FV, FVII, FX and FVIII was assaied. According to the diagnostic criteria of FSP greater than 8 micrograms/ml, Platelets less than 150 10(9)/1 and Fibrinogen less than 150 ml/dl, in 16 patients the diagnosis of DIC was possible since first examination, while in 9 patients it became possible within 2-4 days; in 13 patients we never could diagnose DIC, although it was reasonably present, since the criteria above mentioned were never simultaneously satisfied. Looking back in our experience, we confirm that the platelets count and the quantitation of plasmatic Fibrin Degradation Products (FDP) are the most useful tests for the diagnosis of full blown DIC, and that the biological assay of plasmatic fibrinogen helps to follow the disorder. A low level of FVIII:C seems to be a forecast of failure. None of the other test performed give any useful information for diagnosis when it is not possible with the above mentioned tests.
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PMID:[Diagnostic usefulness and predictive value of laboratory tests in disseminated vascular coagulation]. 369 26


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