Endoscopic Sclerotherapy Of Esophageal Varices Research Articles

Prognosis of bleeding recurrence after endoscopic sclerotherapy of esophageal varices

To improve prediction of recurrent bleeding after endoscopic sclerotherapy of esophageal varices. A prospective, observational, case-control study was performed. Immediate and long-term results of endoscopic sclerotherapy of esophageal varices were studied in 91 patients for the period from 2002 to 2016. Multiple regression analysis with binary response model was applied to analyze the prediction models. Recurrent bleeding occurred in 80.5 (20; 182) days after sclerotherapy (range 0-2557 days). Spearman's correlation analysis revealed a significant relationship between bleeding recurrence and erythrocyte count (R= -0.32), Child-Pugh class of liver cirrhosis (R=0.49), Child-Pugh score (5-15) (R=0.54), content of amino acids, HPro/Pro ratio (R=0.71). Prognostic indicators were selected by stepwise inclusion of predictors. Thus, the final version of regression equation is as follows: Y=exp (-0.17+0.93×Child-Pugh score-106.42×HPro/Pro)/[1+exp(-0.17+0.93×Child-Pugh score-106.42×HPro/Pro)]. High risk of recurrent bleeding from esophageal varices within 1 year after endoscopic sclerotherapy is determined by Y-value >0.5. An accuracy of this model is 89.6%, Se 94.3%, Sp 79.2%, PPV 90.9%, NPV 86.4%, OR 63.3, LR + 4.53, LR - 0.07. Thus, the proposed method is highly informative, effective, available and can be widely used in clinical practice.

Schistosomal portal hypertension: Randomized trial comparing endoscopic therapy alone or preceded by esophagogastric devascularization and splenectomy

Background. Upper gastrointestinal bleeding is a major cause of morbidity and mortality in patients with portal hypertension secondary to schistosomiasis mansoni.Aim. To evaluate the efficacy of combined surgery and sclerotherapy versus endoscopic treatment alone in the prophylaxis of esophageal variceal rebleeding due to portal hypertension in schistosomiasis.Material and methods. During a two-years period consecutive patients with schistosomiasis and a recent bleeding history were evaluated for prospective randomization. Absolute exclusion criteria were alcoholism or other liver diseases, whereas platelet count < 50,000/mm3, INR > 1.5 or presence of gastric varices were relative exclusion criteria. By random allocation 25 (group A) have received endoscopic sclerotherapy for esophageal varices alone and 22 (group B) combined treatment: esophagogastric devascularization with splenectomy followed by sclerotherapy. Interim analysis at 24 months has shown significant statistical differences between the groups and the randomization was halted.Results. Mean age was 38.9 ± 15.4 years and 58.46% were male. Mean follow-up was 38.6 ± 20.1 months. Endoscopic comparison of the size of esophageal varices before and after treatment did not show significant differences among the two groups. Treatment efficacy was assessed by the rate of recurrent esophageal variceal bleeding, that was more common in group A- 9/25 patients (36.0%) vs. 2/22 (9.0%) in group B (p = 0.029). Other complications were odynophagia, dysphagia and esophageal ulcer in group A and ascites and portal vein thrombosis in the surgical group.Conclusion. In portal hypertension due to schistosomiasis, combined surgical and endoscopic treatment was more effective for the prevention of recurrent esophageal variceal bleeding.

Combined caesarean with splenectomy in pregnancy with portal hypertension: defining plausibility

24-year-old woman at 28 weeks gestation was referred from peripheral hospital with diagnosis of pregnancy with portal hypertension. She had received multiple transfusion for pancytopaenia in the past and had...

Risk of Bacteremia after Endoscopic Sclerotherapy of Esophageal Varices: A Systematic Review

Risk of Bacteremia after Endoscopic Sclerotherapy of Esophageal Varices: A Systematic Review

Pill-induced Intramural Hematoma of the Esophagus

Intramural hematoma of the esophagus is a rare cause of chest pain. Varying degrees of submucosal dissection and rupture of the esophagus can induce intramural hematoma of the esophagus. It is viewed as a complication of endoscopic sclerotherapy of esophageal varices, and is likely caused by an elevation in intraesophageal pressure due to factors such as blood coagulation abnormality, drugs, trauma or vomiting. We describe one case of pill-induced spontaneous intramural hematoma that was successfully managed by conservative treatment and discuss the case with a review of the literature. (Korean J Helicobacter Up Gastrointest Res 2013;13: 124-127)

Parturients Expect Safe and Clean Regional Anesthesia

Parturients Expect Safe and Clean Regional Anesthesia

Endoscopic Sclerotherapy of Esophageal Varices. M. V. Sivak Jr. 240 × 160 mm. Pp. 157 + ix. Illustrated. 1984. New York: Praeger Publishers. £34.50

Journal Article Endoscopic Sclerotherapy of Esophageal Varices. M. V. Sivak Jr. 240 × 160 mm. Pp. 157 + ix. Illustrated. 1984. New York: Praeger Publishers. £34.50 Get access Endoscopic Sclerotherapy of Esophageal Varices. MV Sivak Jr. 240 × 160 mm. Pp. 157 + ix. Illustrated. 1984. New York: Praeger Publishers. £34.50 J L Dawson J L Dawson Search for other works by this author on: Oxford Academic Google Scholar British Journal of Surgery, Volume 72, Issue 4, April 1985, Page 331, https://doi.org/10.1002/bjs.1800720450 Published: 08 December 2005

Devascularization following endoscopic sclerotherapy of oesophageal varices: Dangers and difficulties

Twenty-three patients underwent devascularization operations for acute variceal bleeding. All had received endoscopic sclerotherapy, either long-term or just before surgery. The oesophagus and peri-oesophageal tissues showed either oedematous or fibrotic reaction depending on the number and duration of sessions of sclerotherapy. These changes in the oesophagus and surrounding tissues were responsible for intraoperative oesophageal perforation and postoperative anastomotic leaks. To obviate these problems, stapling of the anterior and posterior walls of the stomach was tried and found to be safer than stapled transection of the oesophagus. During follow-up, varices reappeared in over 75 per cent of patients and were managed by further sclerotherapy. Patients who did not receive sclerotherapy had a higher incidence of rebleeding.

Intramural Duodenal Hematoma after Endoscopic Therapy for a Bleeding Duodenal Ulcer in a Patient with Liver Cirrhosis

We report a case of intestinal obstruction due to intramural hematoma of the duodenum following therapeutic endoscopy for a bleeding duodenal ulcer in a patient with liver cirrhosis. A 44-year-old man was admitted to our hospital with severe epigastralgia, nausea and tarry stool. Two years previously he had undergone endoscopic sclerotherapy for esophageal varices caused by alcoholic liver cirrhosis. Endoscopy revealed an open ulcer with a bleeding vessel in the duodenal bulb, and sclerotherapy was performed by clipping the vessel and injecting 20 ml of 0.2% epinephrine. His platelet count was 3.5x10(4)/mul. Twelve hours later, he again developed epigastralgia and hypotension. Emergency computed tomography and ultrasonography revealed an intramural hematoma, 15x18 cm in diameter, at the dorsal and lateral duodenum. Endoscopy and upper gastrointestinal series revealed severe stenosis of the duodenal lumen caused by intramural hematoma. He received parenteral feeding for 22 days and within 8 weeks the hematoma was gradually absorbed using conservative management. Intramural duodenal hematoma may be diagnosed as a complication of the endoscopic procedure in a patient with a bleeding tendency, such as liver cirrhosis.

Radiologic diagnosis of benign esophageal strictures: a pattern approach.

Benign esophageal strictures are a leading cause of dysphagia. Therefore, radiologists have an important role in detecting esophageal strictures and determining their cause. The most common cause of strictures in the distal esophagus is gastroesophageal reflux disease. Reflux-induced ("peptic") strictures may be associated with sacculations, fixed transverse folds, or esophageal intramural pseudodiverticula. In addition, scleroderma, nasogastric intubation, Zollinger-Ellison syndrome, and alkaline reflux esophagitis may be associated with stricture formation in the distal esophagus. Upper and midesophageal strictures may be caused by Barrett esophagus, mediastinal irradiation, ingestion of drugs or caustic substances, congenital esophageal stenosis, skin diseases, or esophageal intramural pseudodiverticulosis. Other unusual causes of esophageal stricture formation include Crohn disease, Candida esophagitis, graft-versus-host disease, eosinophilic esophagitis, Behçet disease, endoscopic sclerotherapy for esophageal varices, and glutaraldehyde contamination at endoscopy. Esophageal strictures are best evaluated with biphasic esophagography that includes both single- and double-contrast spot images. When esophageal strictures are detected at barium examination, the underlying cause can often be determined with a pattern approach that takes into account the clinical history, the appearance and location of the strictures, and the presence of other associated radiographic findings.

Portal vein thrombosis after variceal endoscopic sclerotherapy in cirrhotic patients: role of genetic thrombophilia.

Portal vein thrombosis is a rare event in patients with liver cirrhosis in the absence of a related neoplasm. Endoscopic sclerotherapy of esophageal varices has been anecdotally associated with the development of portal vein thrombosis. We tested the hypothesis that genetic thrombophilia plays a role in the development of portal vein thrombosis in patients with liver cirrhosis undergoing endoscopic sclerotherapy. From June 1998 to December 1999, 61 consecutive patients underwent multiple sessions of endoscopic sclerotherapy for bleeding esophageal varices. Doppler ultrasound of the portal vein was performed before sclerotherapy and every 3 months thereafter. Antiphospholipid antibodies, factor V Leiden (FVL) mutation, prothrombin mutation G20210A (PTHRA20210) and mutation TT677 of methylenetetrahydrofolate reductase (MTHFR C677T) were evaluated in all patients. Portal vein thrombosis developed in 16 % of the patients (10 of 61) after a mean follow-up period of 16 months. A genetic cause for thrombosis was found in 70 % of patients with liver cirrhosis who developed portal vein occlusion, but only in 8 % of patients without this complication. Endoscopic sclerotherapy of esophageal varices may represent a trigger factor for portal vein thrombosis in cirrhotic patients with genetic thrombophilia.

10 P Endoscopic sclerotherapy of esophageal varices in children with portal vein Thrombosis twenty years of experience and long term follow up

10 P Endoscopic sclerotherapy of esophageal varices in children with portal vein Thrombosis twenty years of experience and long term follow up

Indications of Prophylactic Endoscopic Sclerotherapy for Esophageal Varices in Infants and Children

Indications of Prophylactic Endoscopic Sclerotherapy for Esophageal Varices in Infants and Children

Endoscopic sclerotherapy of esophageal varices in children: Ten years follow-up, after erdication

Endoscopic sclerotherapy of esophageal varices in children: Ten years follow-up, after erdication

Cirrhosis: a new, but expected cause of biliary sludge.

Biliary sludge is increasingly recognized as a natural stage in gallstone formation. Logically, cirrhosis, a well-documented cause of black pigment cholelithiasis, should be another condition predisposing to the development of sludge. The aim of this study was to assess the prevalence of biliary sludge in an unselected population and to test the hypothesis that cirrhosis could be one of the causes of sludge. We reviewed the clinical findings and ultrasonograms of 2138 patients, hospitalized or not, consecutively seen in our department between January 1993 and December 1994. Sonograms showing biliary sludge mixed with stones were excluded. Three hundred and eighty-eight of the 2138 were cirrhotic patients. The overall prevalence of biliary sludge was 4%. Sludge was found in 44 of 388 (11%) of the cirrhotic patients (alcoholism, n = 39; chronic viral B hepatitis, n = 3; hemochromatosis, n = 1; and cryptogenic, n = 1), compared with 42 of 1750 (2%) noncirrhotic patients (p < 0.000001). Thirteen cirrhotic patients received intravenous alimentation for 2 to 17 days, 8 were given somatostatin for variceal bleeding, and 7 have previously had 1 to 5 sessions of endoscopic sclerotherapy of esophageal varices with polidocanol. This study convincingly demonstrates that cirrhosis must be added to the growing list of conditions associated with biliary sludge.

Endoscopic sclerotherapy for esophageal varices in children with extrahepatic portal venous obstruction: a follow-up study.

Results of treatment with endoscopic sclerotherapy for esophageal varices in children extrahepatic portal venous obstruction are limited. A prospective study was undertaken of fifty children (mean age, 7.4 +/- 3.8 years; range, 4 months to 14 years) with esophageal variceal bleeding caused by extrahepatic portal venous obstruction (EHPVO) treated by repeated intravariceal endoscopic sclerotherapy (EST) at intervals of 2-3 weeks until eradication (no varices on endoscopy). Eradication of varices was achieved in 44 children (88%) with a mean of eight sessions per child. In six other cases, variceal grade decreased by 50% from the initial grades. Bleeding episodes at presentation were controlled in all of the children with first ET >. Over a mean follow-up period of 19 months (range, 12-36 months), a total of 15 episodes of rebleeding occurred in 13 children (26%) before the third session of EST and all were controlled with EST. Risk of rebleeding in children with eradicated varices (n = 44) significantly decreased from 0.2 episodes per month to nil after eradication. None of the children without eradicated varices had rebleeding. Thus, EST was successful in controlling rebleeding in all of the cases. Recurrence of varices was observed in five children (10%). None of our children either required surgery for EST failure or died. EST is a safe and effective nonsurgical mode of therapy in controlling esophageal variceal bleeding in children with EHPVO. Significant variceal bleeding did not occur during the relatively short follow-up in this series.

Portacaval shunt for portal hypertensive gastropathy.

Portal hypertensive gastropathy is a vascular disorder of the gastric mucosa distinguished by ectasia of the mucosal capillaries and submucosal veins without inflammation. During 1988 to 1993, 12 patients with biopsyproven cirrhosis (10 alcoholic, 2 posthepatitic) were evaluated and treated prospectively by portacaval shunt for active bleeding from severe portal hypertensive gastropathy. Eleven patients had been hospitalized for bleeding three to nine times previously, and one was bleeding uncontrollably for the first time. Requirement for blood transfusions ranged from 11 to 39 units cumulatively, of which 8 to 30 units were required specifically to replace blood lost from portal hypertensive gastropathy. Admission findings were ascites in 9 patients, jaundice in 8, severe muscle wasting in 10, hyperdynamic state in 9. Child's risk class was C in 7, B in 4, A in 1. Ten of the 12 patients had previously received repetitive endoscopic sclerotherapy for esophageal varices, which has been reported to precipitate portal hypertensive gastropathy. Eight patients had failed propranolol therapy for bleeding. Portacaval shunt was performed emergently in 11 patients and electively in 1, and permanently stopped bleeding in all by reducing the mean portal vein-inferior vena cava pressure gradient from 251 to 16 mm saline. There were no operative deaths, and two unrelated late deaths after 13 and 24 months. During 1 to 6.75 years of followup, all shunts remained patent by ultrasonography, the gastric mucosa reverted to normal On serial endoscopy, and there was no gastrointestinal bleeding. Recurrent portal-systemic encephalopathy developed in only 8% of patients. Quality of life was generally good. It is concluded that portacaval shunt provides definitive treatment of bleeding portal hypertensive gastropathy by eliminating the underlying cause, and makes possible prolonged survival with an acceptable quality of life.

Benign esophageal strictures in children and adolescents: etiology, clinical profile, and results of endoscopic dilation

Background: The problem of dysphagia in children and adolescents differs from that in adults, and therefore requires special consideration. Methods: Forty-one consecutive children and adolescents 16 years of age or younger (mean, 7.2 years), with benign esophageal strictures were evaluated in a prospective manner over a 7-year period. The most frequent causes of esophageal strictures were caustic ingestion and complications of endoscopic sclerotherapy of esophageal varices. Dilation was done on a weekly basis using bougies and was considered adequate if the esophageal lumen could be dilated to 15 mm diameter (11 mm in children less than 5 years old) with complete relief of dysphagia. Results: Of the 30 patients who could be adequately followed after initial dilation, 16 had corrosive strictures and 14 had strictures due to other causes. Patients with corrosive strictures required a significantly higher number of sessions for adequate initial dilation (7.8 ± 2.5 sessions vs 1.86 ± 0.48 sessions; p < 0.01). Patients with corrosive strictures had a higher number of mean symptomatic recurrences per patient month as compared to the noncorrosive stricture group (0.15 ± 0.01 vs 0.087 ± 0.03, p < 0.01). Six esophageal perforations occurred during a total of 327 dilation sessions (1.8%); there was one fatality. Conclusions: From our experience, we conclude that benign esophageal strictures in young patients can be treated effectively and with acceptable safety by means of endoscopic dilation. (Gastrointest Endosc 1996;43:474-7.)

The effect of endoscopic sclerotherapy of esophageal varices on the development of gastric varices.

The effect of sclerotherapy of esophageal varices on the development of gastric varices is a controversial question. The aim of the present study was to evaluate prospectively the presence and development of gastric varices as a consequence of esophageal variceal sclerotherapy. We prospectively studied 227 patients, all of whom had liver cirrhosis at the time of the first bleeding episode due to esophageal varices. All patients were treated with emergency endoscopic sclerotherapy, and further courses of sclerotherapy to eradicate the varices were given at seven-day intervals for three sessions, and then every fifteen days until eradication was complete. At the time of inclusion in the study, patients were divided in two groups: group A, with initial gastric varices, and group B, without any gastric varices initially. Group A included 138 patients (60.8%), in 99 of whom (71.7%) disappearance of the gastric varices was observed. In 63 cases (63.6%) the varices were eliminated during the sclerotherapy treatment, before the eradication of esophageal varices; in 36 cases (36.4%), the gastric varices disappeared after the eradication of the esophageal varices. Group B included 89 patients (32.9%); in 78 of them (87.6%), no appearance of gastric varices was observed, while in 11 (12.4%), gastric varices appeared. From these data, it can be concluded that sclerotherapy of esophageal varices cannot be a determinant factor either for the appearance of gastric varices or for their subsequent risk of bleeding.

食道静脈りゅうに対する内視鏡的硬化栓塞療法剤の検討 イオメプロールを配合したオレイン酸モノエタノールアミン注射液について

Monoethanolamine oleate injection containing 50% Iopamiron 370 (50% IP370-EO) has been previously prepared for endoscopic sclerotherapy of esophageal varices on X-ray TV monitor. However, the dischargeable pressure of this sclerosing agent was slightly insufficient during clinical use. We therefore prepared monoethanolamine oleate injection containing 50% Iomeron 350 (50% IM350-EO) or 75% Iomeron 350 (75%IM350-EO), and measured the physical characteristics such as viscosity and osmotic pressure of this agent. The time required to discharge a given volume of each agent through a syringe, a tube and a puncture needle under the pressure of 2kg/2.6cm2 was measured. The ability to visualize this process was observed in patients with esophageal varices by X-ray.The viscosity, which was inversely related to the injectability into varices, of 50% IM 350-EO was lower than that of 50% IP370-EO. The viscosity of 75% IM350-EO was also lower than that of 75% IP370-EO. The osmotic pressure ratio of 50% IM350-EO and 75% IM350-EO were lower than those of 50% IP370-EO and 75% IP370-EO, respectively. The time required to discharge 50% IM350-EO was the shortest. Good fluoroscopic visualization was obtained in all preparations. Better contrast was obtained in the cardiac zone with 75% IM350-EO than with 75% IP370-EO.These results suggest that 50% IM350-EO and 75% IM350-EO are more useful agents for endoscopic sclerotherapy of esophageal varices.