Portal vein thrombosis; risk factors, clinical presentation and treatment (original) (raw)
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When endoscopic therapy or pharmacotherapy fails to control variceal bleeding: what should be done?
Langenbeck's Archives of Surgery, 2003
Immediate control of bleeding by TIPS? Epidemiology Acute bleeding from portal hypertensive collaterals is generally due to rupture of esophageal varices. These are observed in 60% of patients with portal hypertension and entail a risk of bleeding of about 30% [1]. It is related to the size, the presence of red color signs on the surface of the varices, and the liver function, for example, Child-Pugh class. Large varices with red color signs have a 1-year bleeding risk of up to 76% [2]. Gastric varices are another source of bleeding found in only about 20% of patients with portal hypertension. These are classified as gastroesophageal varices (90%) or isolated gastric varices (10%) [3]. In a minority of about 10% of patients the gastric varices develop secondary to the eradication therapy of esophageal varices. Their risk of bleeding is also related to the size [small vs. large: relative risk (RR) 4.75], the presence of red spots (RR 2.06), and the Child-Pugh class (A vs. C: RR 2.88) [4]. Finally, bleeding can occur from ectopic varices which are located in the small intestine, the colon, or even in the greater omentum. The latter may cause intra-abdominal bleeding which may be triggered by large volume paracentesis [5, 6].
The Predictors of Re-Bleeding in Chronic Liver Disease Patients After Endoscopic Variceal
Journal of Ayub Medical College Abbottabad, 2022
Background: Variceal bleeding is a key and most fatal complication observed in chronic liver disease patients with portal hypertension and is a major contributor to the high morbidity and mortality seen in these patients. Exploring the predictors of rebleeding in chronic liver disease patients is of paramount importance to alter disease course and impact on morbidity and mortality. Methods: About 50 patients with chronic liver disease who previously had evidence of varices on upper GI endoscopy and had at least one episode of rebleeding after EVBL were included in this study. Patients were assessed for the possible contributors to rebleeding through complete history, clinical examination, coagulation profile and platelet count, ultrasound features (splenic size and portal pressure), and upper GI endoscopic findings (site and grade of varices, red sign). Sample selection was done using non-probability purposive sampling technique and sample size calculated using the standard WHO formula. Data was entered and analyzed using SPSS version 20. Results: In this study, mean age of the patients was 51.34±6.34 years with male predominance (64%). Rebleeding was significantly associated with grade of varices, presence of red sign on upper GI endoscopy, site of varices, splenic size and coagulopathy. Conclusion: Rebleeding in chronic liver disease patients following EVBL is predicted by grade, extent and site of varices, red sign on upper GI endoscopy, splenic size and coagulation disturbances.
Hepatology, 2016
In patients with chronic noncirrhotic, nontumoral portal vein thrombosis (PVT), the usually recommended strategy for endoscopic screening and management of varices is the same as in cirrhosis. However, the efficacy of this policy in patients with PVT is unknown. We assessed the course of gastroesophageal varices in a large cohort of patients with chronic PVT. Patients prospectively registered in two referral centers for vascular liver disorders were eligible for the study. Endpoints were development and growth of varices and the incidence and outcome of portal hypertension‐related bleeding. Included were 178 patients with chronic PVT. Median follow‐up was 49 (1‐598) months. Variceal bleeding was the initial manifestation in 27 (15%) patients. Initial endoscopy in the remaining 151 patients showed no varices in 52 (34%), small esophageal varices in 28 (19%), large esophageal varices (LEVs) in 60 (40%), and gastric varices without LEVs in 11 (7%). Ascites and splenomegaly were indepen...
Hepatology, 2009
P reventing hemorrhage from esophageal varices has been attempted in many different ways over the years. 1 Historically, this was first approached by means of prophylactic portacaval surgical shunts. These procedures were very useful in preventing hemorrhage, but, as demonstrated in the first randomized controlled trials (RCTs) in the field of hepatology, shunting was associated with unacceptable rates of disabling encephalopathy and decreased survival. These results proscribed the further use of prophylactic shunt surgery (when thousands of prophylactic shunts had already been performed all over the world). The same restriction on prophylactic surgical shunts has been extended to the use of transjugular intrahepatic portosystemic shunts when this new type of portosystemic shunt became clinically available. The second type of therapy to prevent first variceal hemorrhage was endoscopic injection sclerotherapy (EIS). However, even though initial reports from singlecenter studies were enthusiastic, larger cooperative trials tempered this enthusiasm, and given uncertain results from meta-analyses and a high rate of complications, it became clear that EIS was not the answer either. From a pathophysiological point of view, it is clear that a therapeutic strategy which ameliorates portal hypertension-the primary factor leading to the formation, dilatation, and rupture of esophageal varices-should be more effective than a local therapy aimed at varices themselves. Even if varices are effectively "eradicated", recurrence is likely if portal pressure is not reduced. 4 Because of this, the advent of nonselective beta-blockers (NSBBs), mainly propranolol and nadolol, in the pharmacological treatment of portal hypertension appeared to solve the issue. In carefully conducted RCTs, these drugs were shown to be highly effective in decreasing the risk of variceal bleeding by about 50% 5,6 and in decreasing the risk of bleeding from portal hypertensive gastropathy. The beneficial effect of NSBBs has been linked to their ability to decrease the portal pressure gradient, assessed clinically through measurement of the hepatic vein pressure gradient (HVPG). 8 Many studies have shown that prevention of variceal hemorrhage (first or recurrent) is maximal when HVPG is reduced to values Յ12 mm Hg or by at least 20% from baseline values (the so-called "HVPG responders"). 9,10 Importantly, HVPG responders have a lower probability of developing other complications of portal hypertension that are frequently associated with varices, such as ascites, encephalopathy, and spontaneous bacterial peritonitis. 10-12 As such, and unlike local therapies, therapies that correct portal hypertension can change the natural history of cirrhosis and improve survival. The main inconvenience of NSBBs is that approximately 15% of patients may have absolute or relative contraindications to therapy and that another 15% require dose reduction or discontinuation due to its common side-effects (e.g., fatigue, weakness, shortness of breath) that resolve upon discontinuation but precludes patients from using these drugs. For years, prevention of variceal bleeding became the domain of NSBBs, the only innovation being the addition of low doses of mild vasodilators, such as isosorbide mononitrate to enhance portal pressure reduction, and the investigation of other drugs and drug combinations such as carvedilol, 14-16 the combination of propranolol and prazosin, 17 and more recently the use of statins, 18 which had a greater portal pressure-reducing effect than NSBBs. Also, efforts were directed at obviating repeat HVPG measurements and at better defining a "good response" in order to reduce the "grey zone" of patients that are HVPG nonresponders but who do not bleed during follow-up. The panorama changed when endoscopic band ligation of varices (EBL) emerged as a new local therapy that, compared to EIS, was safer and probably more effective. This prompted the performance of prospective studies to assess its efficacy in preventing first variceal hemorrhage. Initial studies comparing EBL versus no treatment deserve no comment. Such studies were unjustified (and are Abbreviations: EBL, endoscopic band ligation; EIS, endoscopic injection sclerotherapy; HVPG, hepatic vein pressure gradient; NSBB, nonselective beta-blocker; RCT, randomized controlled trial.
Hepatology, 2002
Endoscopic therapy, involving either injection sclerosis or band ligation, is considered the intervention of first choice for acute variceal bleeding (AVB). Pharmacologic agents have also been shown to be highly effective in the control of the bleeding episode. The purpose of this meta-analysis was to assess whether vasoactive drugs may improve the efficacy of endoscopic therapy (injection sclerosis or band ligation) in the control of AVB and thus increase survival rates. Computer databases and scientific meeting abstracts from 1994 to 2001 were used to search for randomized trials that compared the combined use of endoscopic and drug therapy with endoscopic therapy alone in the control of AVB. Eight trials involving 939 patients fulfilled the selection criteria and the following evaluated by standard meta-analysis methods: initial hemostasis, 5-day hemostasis, 5-day mortality, and adverse events. Combined treatment improved initial control of bleeding (relative risk [RR], 1.12; 95% confidence interval (CI), 1.02-1.23), and 5-day hemostasis (RR, 1.28; 95% CI, 1.18-1.39), with numbers of patients needed to treat (NNT) of 8 and 5, respectively. The difference in favor of combined treatment remained significant when trials that used drugs other than octreotide or that included a low proportion of alcoholic patients (<40%) or high-risk cirrhotic patients (<35%) were excluded. Mortality was not significantly decreased by combined therapy (RR, 0.73; 95% CI, 0.45-1.18). Severe adverse events were similar in both groups. In conclusion, in patients with AVB, pharmacologic agents improve the efficacy of endoscopic therapy to achieve initial control of bleeding and 5-day hemostasis, yet fail to affect mortality. (HEPATOLOGY 2002;35:609-615.)
Management of Variceal Bleeding in Patients with Noncirrhotic Portal Vein Thrombosis
Annals of Surgery, 1988
Since 1971, 70 patients have been seen at Emory University Hospital with gastroesophageal varices secondary to extrahepatic portal vein thrombosis (PVT). Thirty-seven of these patients had had prior major operative therapy. In only three patients (8%) was shunt surgery successful, and there was a high incidence of rebleeding, other morbidity, and mortality. Of especial note are the serious consequences of simple splenectomy; splenomegaly and thrombycytopenia should rarely, if ever, be used as indication for splenectomy in portal hypertension. In 1977, the use of selective distal splenorenal shunt (DSRS) was begun at Emory in this population and a selective shunt has been possible in 24 of 29 patients (83%) who had had no prior operative therapy. Results have been excellent with a greater than 90% patency rate, long-term portal perfusion in all, no encephalopathy, and late rebleeding in one patient. Quantitative studies at 3-6 years show stability of liver function, significant decrease in spleen size, and rise in platelet count. However, long-term follow-up (>15 years) is required in PVT patients before definitive assessment can be obtained. A specific problem of the PVT patient is late shunt stenosis which requires close observation; dilatation of the shunt was performed in six of the 24 patients with a patent shunt. Poor results with non-shunt operative procedures in PVT were again documented. The proper role of endoscopic variceal sclerotherapy is not yet clear, but appears to be an excellent addition to the therapeutic options. In conclusion, for patients with a patent splenic vein, initial therapy should be a selective shunt; for patients without a patent splenic venous system, endoscopic sclerotherapy is the procedure of choice. E n XTRAHEPATIC PORTAL VEIN THROMBOSIS (PVT) in the noncirrhotic is a relatively uncommon cause of portal hypertension in this country. Effective management of bleeding varices in PVT
Role of endoscopy for primary prophylaxis of variceal bleeding
Techniques in Gastrointestinal Endoscopy, 2005
Varices are seen in one-third of unselected patients with cirrhosis and of these approximately one-third will bleed within 2 years from the time of diagnosis. The mortality with each bleeding episode ranges from 20% to 40% depending on the severity of liver disease. Although cost-effective, universal prophylaxis without endoscopic confirmation of large varices or varices with red signs is not recommended because of the treatment associated side effects. All cirrhotic patients should be screened and staged in a consistent and reproducible manner. Those with small varices or no varices should be re-screened every 1 to 2 years, respectively, thereafter. All high-risk (large esophageal or gastric varices, and those with red signs) patients should be treated with adequate doses (target heart rate of 60 per minute or less) of nonselective -blockers. Endoscopic sclerotherapy has no role for primary prophylaxis. Endoscopic band ligation is as effective as -blockers, but it should be reserved for those who are noncompliant or intolerant of -blockers.