Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0012739 (disseminated intravascular coagulation)
 8,673 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

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

Current management of hemorrhage in cirrhotic patients is disappointing, probably because it deals only with the portal hypertension, while the coagulation disorders are neglected. Some new suggestions can be made : 1) Hemorrhage originates in coagulation disorders. The mechanical lesion of the mucosa is only the opportunity for these disorders to become apparent. The lesion may be : infrequently, a ruptured esophageal varix or a gastroduodenal peptic ulcer ; a lesion of the cardia (hiatal hernia, reflux, esophagitis, minimal traumatic tears) ; a gastric anomaly (hemorrhagic gastritis, superficial ulcerations, petechiae) ; in some cases no mucosal lesion is apparent. 2) Any widespread liver disease results in lasting hypercoagulability which is responsible for : permanent lysis, consumption, DIC. The spleen is responsible for the functional alteration of the platelets. Splenectomy is followed by permanent recovery. 3) Changes involving the platelets are responsible for most hemorrhages. Thrombopenia and severe anomalies of platelet aggregation are common findings in liver cirrhosis. Further deterioration can be induced by acetylsalicylic acid, especially if it is absorbed after an immoderate ingestion of alcohol. Emergency treatment consists in platelet transfusions. 4) Stasis in the portal system may, however, result in permanent activation of coagulation. 5) Cirrhosis results in chronic hypercoagulability and severe platelet deterioration. Any stress involving coagulation mechanisms may therefore induce hemorrhage : infection, acetyl salicylic acid, respiratory distress, estrogens, massive transfusion. It is always dangerous to "feed" consumption or to restrain lysis. 6) Coagulation tests should be performed rapidly, in order to evaluate hypercoagulability, consumption, lysis, and evidence of DIC ; FDP can probably be responsible for inflammatory changes in the liver and spleen. 8) Coagulation disorders are permanent since the hepatic alterations are irreversible.
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PMID:[Hemorrhage in liver cirrhosis : new suggestions (author's transl)]. 627 81

In 24 cirrhotic patients at different stages of hepatic failure, factor VIII:C (F VIII:C), factor VIIIR:AG (F VIIIR:AG), factor VIII AG/C ratio (F VIII AG/C), and serum fibrin-fibrinogen degradation products (FDP) were investigated. In 11 of the 24 patients, several instances of gastrointestinal bleeding due to esophageal varices rupture were documented and 5 patients died of unarrestable bleeding. In our study, we evaluated whether the cause of bleeding was the development of intravascular coagulation or the severity of hepatic failure. A statistically significant difference between F VIII:C, F VIIIR:AG/C ratio, and serum FDP was found in bleeding in comparison with non-bleeding patients. An inverse correlation between the F VIII:C plasma level and serum FDP as well as a direct correlation between F VIII AG/C ratio and serum FDP in the group of bleeding patients were also found. These data seem to suggest a hypercoagulable state which was more significant in the 5 patients who died owing to bleeding. Furthermore, only 1 of these patients had severe hepatic failure. From this study it appears that, in cirrhotic patients, bleeding is related more to the appearance of disseminated intravascular coagulation, as a consequence of both hemodynamic and endothelial changes, than to the degree of hepatic failure itself.
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PMID:Bleeding in cirrhotic patients: a precipitating factor due to intravascular coagulation or to hepatic failure? 641 23

In order to establish whether injection sclerotherapy of oesophageal varices could bring about a worsening of the coagulation abnormalities of patients with cirrhosis, the platelet count and the coagulation profile were monitored prior to, then 30 min and 18 h after, the injection in 8 patients undergoing 18 sclerotherapy sessions. Under basal conditions the platelet count, prothrombin activity, normotest and antithrombin III were all reduced; fibrinogen was in the low, and partial thromboplastin time in the high, normal range. A significant shortening of PTT and a further reduction in the platelet count, in the normotest and in fibrinogen occurred after 30 min. On one occasion laboratory evidence of disseminated intravascular coagulation was observed. After 18 h most parameters approached basal values, but the normotest remained persistently reduced. Even though a transient activation of the coagulation process, with consumption of platelets and the liver-dependent clotting factors took place after sclerotherapy in most cases, leading in one to self-limiting disseminated intravascular coagulation, haemorrhagic complications did not occur in our patients. These results suggest that injection sclerotherapy did not lead to clinically significant deterioration of coagulation even in patients with abnormal coagulative function. The observed changes appeared to be self-limiting and confined to the laboratory level in all cases.
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PMID:Study on coagulation profile of patients with cirrhosis of the liver undergoing elective fibreoptic injection sclerotherapy of oesophageal varices. 646 1

We studied the clinical course of 35 patients with refractory ascites who underwent 51 peritoneovenous shunts. Nine of them had hepatorenal syndrome (HRS). Operative complications included shunt malfunction, shunt infection, ascitic leak, fluid overload, and disseminated intravascular coagulation. Two of the patients without HRS died postoperatively. The survival rate in this group was 67% at one year and 43% at two years. Ascites was completely controlled in 83% of the survivors at two months and 50% at two years. Neither survival nor shunt patency were predictable. The shunt reversed HRS in three patients, but failed to do so in the other six. Late complications included shunt malfunction and infection. During the first two years of follow-up, five patients bled from esophageal varices. Liver failure was the sole cause of late death. Peritoneovenous shunt should be reserved for patients with truly refractory ascites, for whom it provides excellent palliation.
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PMID:Peritoneovenous shunt for refractory ascites: operative complications and long-term results. 707 82

Esophageal varices were injected with 5% sodium morrhuate and a solution containing thrombin, concentrated dextrose, and cephalothin sodium using the flexible gastroscope with balloon cuff modification. Hematologic and coagulating parameters were checked before and after the procedure to look for evidence of disseminated intravascular coagulation. No effect was noted on hematocrit, hemoglobin, platelet count, haptoglobin, prothrombin time, partial thromboplastin time, fibrinogen, fibrin split products, factor V, or factor VIII. Injection sclerotherapy with currently available solutions appears to have no effect on the systemic coagulation system.
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PMID:Absence of disseminated intravascular coagulation with endoscopic sclerosis of esophageal varices. 708 44

The coagulation parameters of fourteen patients with advanced liver cirrhosis (3 in Child class B and 11 in class C) were prospectively determined quarterly for one year in order to evaluate the possible relationship between high D-dimer levels and incidence of disseminated intravascular coagulation (DIC) and of gastrointestinal bleeding. The values of D-dimer, fibrin(ogen) degradation products, platelets, fibrinogen, prothrombin activity and antithrombin III were fairly stable in almost all patients and no patient developed an overt DIC; one patient had a significant increase in D-dimer three months after the first control. During the one year follow-up, four patients died, one by the occurrence of hepatocellular carcinoma and three by digestive bleeding. Overall, four patients had upper digestive tract bleeding, three from esophageal varices and one from hemorrhagic gastritis. Hemorrhage was more frequent in patients with high D-dimer levels (3/7, 43%) than in patients with normal D-dimer levels (1/7, 14%). In conclusion, the detection of high D-dimer levels in patients with advanced cirrhosis is not predictive for the occurrence of a overt DIC but seems to be related with an increased risk of gastrointestinal bleeding.
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PMID:High D-dimer levels: a possible index of risk of overt disseminated intravascular coagulation and/or digestive bleeding in advanced liver cirrhosis? 801 48

Fibrinogen (Fg), plasminogen (Plg), alpha 2-antiplasmin (alpha 2-AP), plasminogen activator (PA), tissue plasminogen activator (tPA), plasminogen activator inhibitor (PAI), D-dimer (DD) and fibrin(ogen) degradation products (FDP) were studied in 60 subjects: 40 patients with endemic hepatosplenomegaly (20 during acute haematemesis from ruptured oesophageal varices, 20 with endemic hepatosplenomegaly assigned to the same grade of oesophageal varices but with no history of haematemesis) and 20 normal controls. All parameters were markedly altered in the disease groups. Reduced levels of Fg, Plg, alpha 2-AP and PAI were associated with increasing levels of PA, t-PA, DD and FDP. Alterations were most marked in the group complicated by acute bleeding. It was concluded that these patients have an enhanced fibrinolytic state. This was probably aggravated in the haematemesis group by an acute haemostatic imbalance that superimposed the low grade chronic DIC reported in cases of hepatosplenic schistosomiasis.
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PMID:Fibrinolytic parameters during acute haematemesis in endemic hepatosplenomegaly. 814 81

Results concerning 14 cirrhotic patients who underwent LeVeen peritoneo-venous shunt for refractory or complicated ascites are discussed. The most relevant early complications regard coagulation disorders (35.7%) with a 14.3% postoperative mortality. The functional result appears largely satisfactory, also in terms of long-term efficiency. Utility of a wide evacuation of ascitic fluid during the operation is underlined. Ascites drainage at operation doesn't compromise shunt function or renal resumption, furthermore it may prevent some life-threatening complications like DIC, esophageal varices rupture and congestive heart failure.
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PMID:[Early complications and long-term results of the LeVeen peritoneo-venous shunt in the treatment of refractory ascites]. 907 16


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