The Cause of Coagulopathy After Peritoneovenous Shunt for Malignant Ascites

Gleysteen, J.J.; Hussey, Clara V.; Heckman, Margaret G.

doi:10.1001/archsurg.1990.01410160060013

Cited by 11 publications

(2 citation statements)

References 14 publications

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“…The incidence of coagulopathy (prolongation of the prothrombin time or activated partial thromboplastin time) after peritoneovenous shunting in patients with malignant ascites is 0% to 10%. 7 1"12 By comparison, the incidence of coagulopathy in patients with alcoholic cirrhosis ranges between 40% and 91%4 12-14 and a higher proportion of these patients develop clinical problems.' 113 Our results confirm that alcoholic ascites contains plasminogen activating activity.…”

Section: Discussionmentioning

confidence: 99%

Fibrinolytic activity of ascites caused by alcoholic cirrhosis and peritoneal malignancy.

Scott‐Coombes

Whawell

Vipond

et al. 1993

Gut

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Coagulopathy is a well recognised complication of peritoneovenous shunting for ascites. The relative contributions of primary fibrinolysis and disseminated intravascular coagulation remain controversial. Plasminogen activating activity was significantly lower in malignant ascites (n=10, median <0.02 (range <0-02-1-26) IU/ml) than in alcoholic ascites (n=10, 1-07 (0.30-1-49) IU/ml) (p<0.05). Fibrinolytic activity was determined by a balance between tissue plasminogen activator and plasminogen activator inhibitor-i. There was no significant difference between the two groups in the concentration of tissue plasminogen activator (34 (12-64) ng/ml in malignant ascites v 29 (12-43) ng/ml in alcoholic ascites), but the concentration of plasminogen activator inhibitor-i was significantly higher in malignant ascites (736 (213-1651) ng/ml) than in alcohol ascites (29 (12-43) ng/ml) (p<0-05). Malignant ascites contained significantly higher concentrations of urokinase (0 7 (<0 1-1.3) ng/ml v 02 (<0.1-0.6) ng/ml in alcoholic ascites) and plasminogen activator inhibitor-2 (33 (<6-140) ng/ml v 9 (<6-28) ng/ml alcoholic ascites). The plasminogen activating activity of alcohol ascites may lead to primary fibrinolysis after peritoneovenous shunting. The considerably lower activity found in malignant ascites may explain why coagulopathy after shunting is less pronounced in this group of patients. (Gut 1993; 34: 1120- The peritoneovenous shunt is an established method of palliation for intractable benign and malignant ascites. Coagulopathy is a well recognised complication after the insertion of these shunts. The manifestations range from subclinical derangements of coagulation tests to life threatening haemorrhage. Controversy exists as to the relative contributions ofprimary fibrinolysis and disseminated intravascular coagulation to this coagulopathy.The increased concentrations of fibrin degradation products and concommitant reductions in the concentrations of plasminogen and fibrinogen in ascites compared with plasma, has provided indirect evidence that ascitic fluid posseses fibrinolytic properties." This has been confirmed by direct measurement of ascitic plasminogen activating activity56 and has led to speculation that an infusion of plasminogen activators could stimulate a coagulopathy mediated by primary fibrinolysis. 27 8 Increased concentrations of cross linked fibrin and fibrinogen degradation products and decreased platelet counts found in the plasma after peritoneovenous shunting has led others to suggest that the coagulopathy is secondary to disseminated intravascular coagulation induced either by fibrin degradation products4 or thromboplastin-like substances,3'6 and that ascitic plasminogen activators would be neutralised on entry into the systemic circulation.6 At present, the only agreement is that increased plasma concentrations of fibrinogen degradation products after insertion of a peritoneovenous shunt are an indication of shunt patency.The aim of this study was to measure the overall plasminogen act...

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Section: Discussionmentioning

confidence: 99%

Fibrinolytic activity of ascites caused by alcoholic cirrhosis and peritoneal malignancy.

Scott‐Coombes

Whawell

Vipond

et al. 1993

Gut

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“…12,18 Studies have suggested that the Denver shunt placement alters the coagulation systems by introducing fibrin rich procoagulants, found in reinfused ascites fluid, into the central circulation. [20][21][22][23][24] As such, DIC has been found to occur in up to 35% of Denver shunt patients. DIC is a systemic thrombohemorrhagic disorder associated with specific clinical situations and laboratory evidence of procoagulant activation, fibrinolytic activation, inhibitor consumption, and biochemical evidence of organ damage or failure.…”

Section: Dic 2 Variceal Hemorrhages and 3 Shunt Malfunction Or Occmentioning

confidence: 99%

Refractory Ascites: Treatment and Complications Utilizing Peritoneovenous (Denver) Shunt

Shadkam-Farrokhi

Lee

2017

Dig Dis Interv

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Intractable ascites has long been an antagonizing problem for patients and medical providers. It is debilitating and frequently cannot be prevented by standard medical therapy. Ascites is primarily managed with salt restrictions, diuretics, and repeated paracentesis for symptomatic relief. However, 10% of patients become refractory to this first line of treatment. Several surgical methods such as the insertion of peritoneovenous shunts and transjugular intrahepatic portosystemic shunts have become popularized treatment modalities for the control of refractory ascites. Nevertheless, controversy resides over what is the best treatment method for the improvement in patients' quality of life and survival rate. We herein explore the different medical and surgical methods available for the control of refractory ascites with a focus on the advantages and complications associated with the usage of Denver peritoneovenous shunts.

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Treatment Strategy on Chylolymphatic/Lymphatic Reflux

Papendieck

Amore

2017

Congenital Vascular Malformations

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The Cause of Coagulopathy After Peritoneovenous Shunt for Malignant Ascites

Cited by 11 publications

References 14 publications

Fibrinolytic activity of ascites caused by alcoholic cirrhosis and peritoneal malignancy.

Fibrinolytic activity of ascites caused by alcoholic cirrhosis and peritoneal malignancy.

Refractory Ascites: Treatment and Complications Utilizing Peritoneovenous (Denver) Shunt

Treatment Strategy on Chylolymphatic/Lymphatic Reflux

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