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

An autopsy case of clostridial gas gangrene occurring in a 54-year-old man with colon adenocarcinoma, liver cirrhosis, and diabetes mellitus is reported. The patient died 4 days after the onset of symptoms with episodes of vomiting and abdominal pain. Gangrene of both hips and perineum, hemolysis, renal failure, and disseminated intravascular coagulation were the dominant clinical features. Clostridium septicum was isolated from the subcutaneous tissue fluid. Adenocarcinoma of the ascending colon with ulceration found at autopsy was supposed to be an entry of the organism. Histologically, lesions of subcutaneous tissue and muscles were characterized by the absence of inflammatory infiltrates in spite of extensive necrosis. A summary of 35 cases of gas gangrene hospitalized to the Osaka University Hospital for the past 16 years indicates that clostridial gas gangrene patients with underlying diseases such as malignant neoplasm, diabetes, liver cirrhosis or immunodeficiency have a relatively poor prognosis.
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PMID:A case of nontraumatic clostridial gas gangrene occurring in a patient with colon adenocarcinoma, liver cirrhosis, and diabetes mellitus. 373 9

A Denver peritoneovenous (PV) shunt was inserted in 54 consecutive patients for relief of malignant (24 patients) or cirrhotic (30) refractory ascites. The median age of both groups was 58 years, and the most frequent diagnoses were gastrointestinal (15) or ovarian (7) cancers and alcoholic cirrhosis (25). Median survival time was 1.7 and 3.5 months (range, 0.1-15.5 and 0.1-50.5), and the 1-month mortality 42% and 27%, respectively. Postoperative 24-h urinary output increased by 2-31, and the 1-week weight reduction was 8 and 11 kg, respectively, compared with before shunting. Complete shunt failure was encountered early in two patients, due to catheter malposition and clotting. Four more patients experienced transient failure, for an early dysfunction rate of 11%. A shunt-related operative mortality of 6% was caused by pulmonary oedema (two patients) and sepsis (one patient). Shunt malfunction intervened in almost half (6 of 14) of the cancer patients surviving 1 month but was relieved in all but 1. In 3 of 22 cirrhotic 1-month survivors, the Denver shunt had to be removed owing to clotting or sepsis (2 patients) or revised because of blockage. Seven patients with cirrhosis are alive a median of 18 months (range, 2-51) after PV shunt surgery. Side effects were detected in 22 patients (41%): thromboembolism (9 patients), sepsis (7), initially bleeding oesophageal varices (3), DIC syndrome (2), postoperative hepatic coma (2), ascitic leakage (2), and pulmonary oedema (2). Patients with gastrointestinal cancers or severe cardiac disease did not benefit from the procedure. A history of hepatic encephalopathy or a serum bilirubin level above about 100 mumol/l was a bad prognostic sign. We could confirm the reported considerable morbidity and mortality after PV shunting, but also its efficiency in certain cases. Careful patient selection and follow-up study, timing of operation, and adherence to technical details are mandatory to improve the results.
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PMID:Denver peritoneovenous shunting for malignant or cirrhotic ascites. A prospective consecutive series. 380 91

The blood level of endotoxin after operations in patients with digestive diseases, mainly liver cirrhosis and obstructive jaundice, and the complications most likely related to the presence of endotoxemia were investigated. Twenty-seven patients without either liver cirrhosis or obstructive jaundice showed a minimal elevation of the endotoxin level in blood, as shown by 6.1 +/- 3.9 (mean +/- S.E.) pg/ml at the first postoperative day and there was only one anastomotic leakage. On the other hand, 18 patients with liver cirrhosis showed a notable and persistent endotoxemia after surgery. The cirrhotic patients who especially underwent splenectomy and hepatectomy showed marked elevations of endotoxin level at the first postoperative day, with values of 151.0 +/- 46.1 pg/ml and 101.3 +/- 36.2 pg/ml, respectively, and one of these patients died of hepatic failure. Thirteen patients with obstructive jaundice developed endotoxemia evidenced by the value of 21.6 +/- 4.8 pg/ml at the first day after surgery. Among these patients, two had gastrointestinal bleeding and one developed disseminated intravascular coagulation (DIC). The markedly high and persistent levels of endotoxin in patients with liver cirrhosis or obstructive jaundice may be possibly related with the development of multiple organ failure (MOF).
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PMID:Endotoxemia after abdominal surgery. 382 74

Local injection of absolute ethanol was proven effective for hemostasis of gastrointestinal bleeding in our fundamental (Asaki et al. 1983a) and clinical (Asaki et al. 1983b) studies. The purpose of the present paper is to report the results obtained in 258 hemorrhagic foci in 152 unselected cases treated with this method at 6 major hospitals in the Tohoku area in Japan. Sixty (39%) of these 152 cases had shock symptoms due to hemorrhage. Gastric and duodenal ulcers were responsible for the hemorrhage in about 90% of the cases in which our method was applied to hemostasis. Eighty-nine (59%) of the 152 cases had some form of complications such as malignant tumors or liver cirrhosis. Hemorrhage due to postoperative stress ulcer after major surgeries including renal implantation or laryngectomy for resection of cancer was seen in 20 cases (13%). The condition of hemorrhage immediately before the treatment with our technique was classified as spouting hemorrhage for 8 foci (3%), pulsating hemorrhage for 22 foci (9%), adhesion of clot for 179 foci (69%), and hemorrhage from veins and capillaries for 49 foci (19%). In all of these cases temporary hemostasis was obtained. Rebleeding occurred in 17 cases (7%) including 5 cases in which hemostasis was successfully obtained by the repeated use of our method. In 4 of the 17 cases, in which repeated endoscopy was infeasible, emergency surgery was performed. In the remaining 8 lesions in 8 cases, new bleeding or rebleeding occurred more than 1 week after the initial hemostasis had been obtained. Six of these 8 cases died from rebleeding due to DIC syndrome. With our method complete hemostasis was obtained in 144 of 152 cases (95%) including 11 cases (7%) which underwent elective surgical operation.
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PMID:Multiinstitutional evaluation of local injection of absolute ethanol as the new hemostatic method for upper G-I tract bleeding. 388 49

Subnormal concentrations of alpha 2 Antiplasmin (alpha 2 AP) in liver cirrhosis may be due to an impaired hepatic synthesis and/or to a fibrinolysis activation in disseminated intravascular coagulation (DIC). In order to clarify this problem, in 26 cirrhotic patients (15 compensated and 11 decompensated) alpha 2 AP plasma activity and plasma Fibrinopeptide A (FPA) were measured. Serum albumin, p-Cholinesterase (p-CHE), Fibrinogen and Fibrinogen Degradation Products (FDP) were also carried out. Our data show that alpha 2 AP and FPA were equally abnormal in compensated and decompensated cirrhosis. The significant negative correlation obtained between alpha 2 AP and FPA as well as the lack of correlation between alpha 2 AP and albumin, alpha 2 AP and p-CHE in both groups suggests that, in our patients, alpha 2 AP decrease may be due to a fibrinolysis activation induced by a DIC which appears chronic since Fibrinogen and FDP were normal. These findings are in agreement with the results obtained in the four subgroups a posteriori selected on the basis of FPA levels: alpha 2 AP in subgroups with high FPA was significantly different from controls while it did not differ in subgroups with normal FPA.
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PMID:alpha 2 Antiplasmin and disseminated intravascular coagulation in liver cirrhosis. 397 73

Topically applied thrombin was known to be effective in hemostasis of local bleeding, but complications of shock, anaphylaxis or disseminated intravascular coagulation (DIC) have been reported recently in rare cases. In this experiment, the possibility of DIC was examined by intraperitoneal injection of topical thrombin (Parke-Davis) to rabbits with liver cirrhosis or acute liver damages induced by CCl4. No significant changes in the coagulation parameters were found in the groups of liver cirrhosis or the untreated control, but the injection of thrombin induced decreases of platelet count and fibrinogen and prolongation of prothrombin time and partial thromboplastin time in the groups of acute liver damages, 24 or 48 hr after CCl4 injection. When the "junk" prepared from the topical thrombin was injected to the 48 hr-damage group, no change was noted in these parameters. It was concluded that DIC could be induced by the intraperitoneal injection of topical thrombin only in cases of acute liver damages, where the increased permeability of peritoneum was postulated. However, such an immediate or marked change in coagulation was not found in our experiment as encountered in the clinical cases, which suggested the involvement of the anaphylactic reaction to the topical application of thrombin in the development of DIC in these clinical cases.
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PMID:[Effect of intraperitoneal injection of topical thrombin on the coagulation and fibrinolysis of rabbits with experimental liver damages]. 398 69

The biologic activity of Factor XIII was measured in four groups of patients: 20 with liver cirrhosis, ten with acute DIC, 30 with acute leukemia with DIC, and 20 with acute leukemia without DIC. In all groups, the plasma Factor XIII transamidating activity was reduced, but this deficiency was more evident in patients with DIC alone or with leukemia and DIC. The immunologic determination of the a and b subunits of Factor XIII was also performed. Both subunits were below the normal range in the groups of patients studied, except for subunit b, which was normal in patients with leukemia without coagulopathy. Acute DIC patients showed an equally reduced level of both subunits, whereas in patients with leukemia, even in the presence of a complicating coagulopathy, a lesser decrease of subunit b than subunit a was found. Both subunits were equally reduced in patients with cirrhosis, suggesting an impaired synthesis of these proteins. In conclusion, our findings do not support the use of Factor XIII subunit measurements in distinguishing between thrombin- or protease-mediated consumption coagulopathy, and they seem to suggest that the deficiency pattern of the subunits is not accounted for by a simple pathogenetic mechanism.
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PMID:A contribution to the pathology of acquired plasma factor XIII deficiency. 407 Oct 61

From the analysis of 182 consecutive surgical patients who underwent hepatectomy and/or were associated with liver cirrhosis during 1963-1982, acute respiratory failure was proved to be so much often in those patients. The case rate of this complication tends to increase according to resected size of liver tissue and severity of liver cirrhosis. Those cases showed clinical signs of pulmonary interstitial edema and were often associated with coagulopathy and endotoxemia. In order to clarify the pathophysiological mechanism of the acute respiratory failure based on liver dysfunction, a canine experimental model in which blood inflow into the liver was completely blocked was newly devised, and respiratory state in this model was analysed. The following results were obtained. The increase of EVLW (extravascular lung water) measured by modified double indicator dilution method was linear to the increase of PWP (pulmonary wedge pressure) in both liver failure group and control group. But the coefficient of the regression line was three times larger in the former group than in the latter. It suggests that permeability of pulmonary capillary was highly increased in liver failure group. All dogs with liver failure showed typical symptomes of lung edema at maximal PWP. Disseminated intravascular coagulation, consumption of neutrophils, decrease of CH50 and serum opsonin were thought to be mediators of the increase of lung vascular permeability. Steroid and PGI2 blocked the increase of the lung vascular permeability completely but not the increase of lung vascular resistance in this experimental model.
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PMID:[Acute respiratory failure based on liver dysfunction in canine liver ischemia model]. 407 3

The metabolism of human fibrinogen labeled with radioactive iodine was studied in 50 patients with documented cirrhosis of the liver and in 35 healthy control subjects. Results in cirrhotic subjects were the following: plasma volume 47 +/- 10 ml/kg; plasma fibrinogen concentration 250 +/- 102 mg/100 ml; total plasma fibrinogen pool 118 +/- 59 mg/kg, representing 0.73 +/- 0.10 of the total body pool; fibrinogen half-life 2.99 +/- 0.59 days; fractional catabolic rate 0.34 +/- 0.09 of the plasma pool per day; absolute catabolic rate 39 +/- 20 mg/kg per day; fractional transcapillary efflux rate 0.82 +/- 0.30 of the plasma pool per day. Results in the control subjects were the following: plasma volume 42 +/- 7 ml/kg; plasma fibrinogen concentration 284 +/- 71 mg/100 ml; total plasma fibrinogen pool 119 +/- 40 mg/kg, representing 0.72 +/- 0.07 of the total body pool; fibrinogen half-life 4.14 +/- 0.56 days; fractional catabolic rate 0.24 +/- 0.04 of the plasma pool per day; absolute catabolic rate 28 +/- 9 mg/kg per day; fractional transcapillary efflux rate 0.60 +/- 0.26 of the plasma pool per day.A significant difference between cirrhotics and controls was observed for plasma volume, fibrinogen half-life, fractional and total catabolic rates, and transcapillary efflux rate. During heparinization of 10 cirrhotic patients the fibrinogen half-life was prolonged from 3.15 +/- 0.69 to 4.59 +/- 0.79 days. This was associated with a rise in plasma fibrinogen in six out of eight patients. Heparinization did not influence the fibrinogen half-life in five control subjects. Inhibition of the fibrinolytic system in 17 patients resulted in prolongation of the plasma radioactivity half-life of more than 1 day in only three patients, an incidence comparable with that in five control subjects. These results strongly support the concept of accelerated fibrinogen consumption by a process of disseminated intravascular coagulation in cirrhosis of the liver.
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PMID:Metabolism of fibrinogen in cirrhosis of the liver. 516 79

A nephelometric method is described for determination of plasminogen and two types of plasmin inhibitors in human plasma having different affinity toward plasmin. This method is based on the kinetic analysis of effects of whole plasma and plasmin inhibitor fraction obtained from plasma on the activity of exogenously added plasminogen which was determined by measuring the decrease of light scattering of fibrin suspension. With this method we have determined the activity of plasminogen and two types of inhibitors in the plasma of normal subjects and patients with high fibrinogen degradation product values. They include patients with various malignant tumors with DIC, chronic renal failure, sepsis, vascular diseases, and liver cirrhosis with hepatoma.
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PMID:Nephelometric determination of plasminogen and plasmin inhibitors in human plasma using fibrin suspension as a substrate. 622 10


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