scholarly journals Esophageal Variceal Ligation Monotherapy versus Combined Ligation and Sclerotherapy for the Treatment of Esophageal Varices

2021 ◽  
Vol 2021 ◽  
pp. 1-5
Author(s):  
Jianbo Wang ◽  
Shenghui Chen ◽  
Yehia M. Naga ◽  
Junwei Liu ◽  
Mugen Dai ◽  
...  
Keyword(s):  
Chest Pain ◽  
Hospital Stay ◽  
Esophageal Varices ◽  
Length Of Hospital Stay ◽  
Injection Sclerotherapy ◽  
Endoscopic Variceal Ligation ◽  
Variceal Hemorrhage ◽  
Esophageal Variceal ◽  
Gastroesophageal Varices ◽  
Number Of Treatment

Currently, endoscopic variceal ligation (EVL) monotherapy is the standard therapy for managing esophageal variceal hemorrhage. Patients generally need several sessions of endoscopy to achieve optimal variceal ablation, and the varices can recur afterward. Endoscopic injection sclerotherapy (EIS) is an older technique, associated with certain complications. This study aimed to evaluate the clinical efficacy of EVL alone versus combined EVL and EIS in the treatment of esophageal varices. This retrospective study included 84 patients, of which 40 patients were treated with EVL monotherapy and 44 patients were treated with combined EVL + EIS. The main outcomes were rebleeding rates, recurrence at six months, number of treatment sessions, length of hospital stay, cost of hospitalization, and procedural complications. At six months, the rebleeding rate and recurrence were significantly lower in the EVL + EIS group compared to the EVL group (2.3% versus 15.0%; and 9.1% versus 27.5%, respectively). The number of treatment sessions, length of hospital stay, and cost of hospitalization were significantly lower in the EVL + EIS group compared to those in the EVL group (2.3 ± 0.6 versus 3.2 ± 0.8 times; 14.5 ± 3.4 versus 23.5 ± 5.9 days; and 23918.6 ± 4220.4 versus 26165.2 ± 4765.1 renminbi, respectively). Chest pain was significantly lower in the EVL + EIS group compared to that in the EVL group (15.9% versus 45.0%). There were no statistically significant differences in the presence of fever or esophageal stricture in both groups. In conclusion, combined EVL + EIS showed less rebleeding rates and recurrence at six months and less chest pain and was more cost effective compared to EVL alone in the treatment of gastroesophageal varices.

Portal Hypertension and Variceal Hemorrhage

2015 ◽  
Author(s):  
Amir Qamar
Keyword(s):  
Portal Hypertension ◽  
Natural History ◽  
Esophageal Varices ◽  
Variceal Hemorrhage ◽  
Portal Hypertensive Gastropathy ◽  
Gastric Antral Vascular Ectasia ◽  
Esophageal Variceal ◽  
Gastroesophageal Varices ◽  
Vascular Ectasia ◽  
History Of

Gastrointestinal bleeding in patients with cirrhosis can occur from a number of different causes, including portal hypertension, gastric antral vascular ectasia, and acute variceal hemorrhage. The management of these conditions involves a combined medical and endoscopic approach, with radiologic and surgical therapies restricted to refractory cases. This review covers the natural history of gastroesophageal varices, portal hypertensive gastropathy, and gastric antral vascular ectasia; diagnostic principles; primary and secondary prophylaxis relating to esophageal variceal hemorrhage; and treatment overviews for gastric variceal hemorrhage, portal hypertensive gastropathy, and gastric antral vascular ectasia. Figures show the pathophysiology of complications of cirrhosis, esophageal varices as seen during an upper endoscopic procedure, natural history of esophageal varices in patients with cirrhosis, portal hypertensive gastropathy, gastric antral vascular ectasia, and management principles for acute variceal hemorrhage, esophageal variceal ligation, and gastric varices. Tables list the prevalence of various etiologies of hemorrhage in patients with cirrhosis, current recommendations for follow-up screening and surveillance of varices, sensitivities and specificities of some noninvasive markers, and principles of initial management of acute variceal hemorrhage. This review contains 8 highly rendered figures, 4 tables, and 44 references.

Esophageal Variceal Hemorrhage Presenting as Sudden Death in Outpatients

2002 ◽  
Vol 126 (10) ◽  
pp. 1197-1200 ◽  
Author(s):  
M. Tsokos ◽  
E. E. Türk
Keyword(s):  
Sudden Death ◽  
Esophageal Varices ◽  
Venous Blood ◽  
Variceal Hemorrhage ◽  
Blood Alcohol ◽  
Time Of Death ◽  
Esophageal Variceal ◽  
Death Scene ◽  
Medicolegal Autopsy ◽  
Blood Alcohol Levels

Abstract Context.—Some autopsy studies have dealt with histologic features of esophageal varices after different therapeutic procedures. However, to the best of our knowledge, no reports have been published describing outpatient characteristics that are associated with fatal esophageal variceal hemorrhage in a medicolegal autopsy population. Objectives.—To (1) assess the incidence of sudden deaths from esophageal variceal hemorrhage in an unselected medicolegal autopsy population and (2) determine demographics of outpatients dying from esophageal variceal hemorrhage with special reference to blood alcohol concentrations at the time of death. Design.—We performed a retrospective study of all autopsy cases of sudden death from esophageal variceal hemorrhage from a total of 6038 medicolegal autopsies performed over a 5-year period (1997–2001). We analyzed individual cases to determine gender, age, location and histology of bleeding esophageal varices, pathogenic mechanism for esophageal varices, concomitant underlying diseases contributing to fatal outcome, body mass index, circumstances at the death scene, and blood alcohol levels at the time of death. We reviewed the results of toxicologic analyses of alcohol concentrations in samples of femoral venous blood and urine obtained at autopsy; concentrations had been determined by gas chromatography with mass spectroscopy and enzymatic assays. Results.—We identified 45 cases of fatal esophageal variceal hemorrhage that occurred out of hospital and presented as sudden death; the corresponding 5-year incidence in this autopsy population was 0.75%. All of the deceased were white; the male-female ratio was 1.6:1, and the mean age was 50.6 years. Ruptured esophageal varices were located in the lower third of the esophagus in 44 cases. Cirrhosis of the liver was present in all cases (alcoholic cirrhosis of the liver in 42 cases), and a hepatocellular carcinoma was present in 3 cases. Alcohol-induced pancreatic tissue alterations were frequently found. The results of toxicologic analysis were positive for alcohol in femoral venous blood and urine in 30 cases. Blood alcohol levels at the time of death were less than 100 mg/dL (21.7 mmol/L) in 15 cases, between 100 and 200 mg/dL (21.7 and 43.4 mmol/L) in 8 cases, and greater than 200 mg/dL (43.4 mmol/L) in the remaining 7 cases. Conclusions.—Apart from abnormalities in coagulation due to poor liver function in long-term alcohol users, acute alcohol intake may represent an important factor influencing mortality in individuals with esophageal variceal hemorrhage. Acute alcohol intake has transient effects on blood clotting time caused by ethanol and its main metabolites. In the present study, bloodstains at the death scene and unusual body positions of the deceased that aroused suspicion of a violent death were leading reasons for conducting a medicolegal autopsy. Apart from aspects of forensic pathology, the demographics of our study population are also noteworthy from the viewpoint of social medicine. The data we present stress the importance of fatal esophageal variceal hemorrhage as a relevant cause of sudden death occurring outside the hospital in socially isolated, alcohol-addicted individuals.

scholarly journals Medical Management of Variceal Bleeding in Patients with Cirrhosis

2004 ◽  
Vol 18 (2) ◽  
pp. 109-113 ◽  
Author(s):  
Juan G Abraldes ◽  
Alessandra Dell'Era ◽  
Jaime Bosch
Keyword(s):  
Variceal Bleeding ◽  
Endoscopic Therapy ◽  
Portal Pressure ◽  
Portosystemic Shunt ◽  
Factor Vii ◽  
Injection Sclerotherapy ◽  
Variceal Hemorrhage ◽  
Elastic Band ◽  
Recombinant Activated Factor Vii ◽  
Gastroesophageal Varices

Bleeding from gastroesophageal varices is a frequent and often deadly complication of cirrhosis. The key factor in the natural history of esophageal varices is increased portal pressure, which in cirrhosis is due to the combination of increased hepatic vascular resistance and increased portal collateral blood flow. The maintenance and aggravation of this situation leads to the progressive dilation of the varices and thinning of the variceal wall, until the tension exerted by the variceal wall exceeds the elastic limit of the vessel, leading to variceal hemorrhage. Mortality from a variceal bleeding episode has decreased in the last two decades from 40% to 20% due to the implementation of effective treatments and improvement in the general medical care. Initial treatment should include adequate fluid resuscitation and transfusion to maintain the hematocrit at 25% to 30%, and prophylactic antibiotics (norfloxacin or amoxicillin-clavulanic acid). It is currently recommended that a vasoactive drug be started at the time of admission. Drug therapy may be started during transferal to hospital by medical or paramedical personnel and maintained for up to five days to prevent early rebleeding. Terlipressin, a vasopressin derivative, is the preferred agent because of its safety profile and proven efficacy in improving survival. Somatostatin is as effective as terlipressin, but may require higher than the usually recommended dosage. Octreotide is effective in conjunction with endoscopic therapy, but is the second choice because it has not been shown to reduce mortality. Vasopressin may be used where terlipressin is not available, but should be given in combination with transdermal nitroglycerin. Endoscopic elastic band ligation is the recommended endoscopic treatment, but injection sclerotherapy is still employed in many centres for active variceal bleeding. Failures of medical therapy (drugs plus endoscopic therapy) should undergo a second course of endoscopic therapy before proceeding to transjugular intrahepatic portosystemic shunt or, in rare occasions, to portosystemic shunt surgery. Administration of recombinant activated factor VII may decrease the number of treatment failures among patients with advanced liver failure (Child-Pugh class B and C).

Comparison of endoscopic variceal injection sclerotherapy and ligation for the treatment of esophageal variceal hemorrhage: A prospective randomized trial

Hepatology ◽  
1995 ◽  
Vol 21 (6) ◽  
pp. 1517-1522 ◽  
Author(s):  
Ming-Chih Hou ◽  
Han-Chieh Lin ◽  
Benjamin Ing-Tiau Kuo ◽  
Chen-Hsiang Chen ◽  
Fa-Yauh Lee ◽  
...  
Keyword(s):  
Randomized Trial ◽  
Prospective Randomized Trial ◽  
Injection Sclerotherapy ◽  
Variceal Hemorrhage ◽  
Esophageal Variceal

scholarly journals Duodenal Varices: A Rare Manifestation of Portal Hypertension

2019 ◽  
Vol 37 (3) ◽  
pp. 156-159
Author(s):  
Deepankar Kumar Basak ◽  
Richmond Ronald Gomes ◽  
Md Samsul Arfin
Keyword(s):  
Portal Hypertension ◽  
Short Review ◽  
Injection Sclerotherapy ◽  
Endoscopic Variceal Ligation ◽  
Endoscopic Injection ◽  
Esophageal Variceal ◽  
Esophageal Variceal Bleeding ◽  
Duodenal Varices ◽  
Vein Thrombosis ◽  
Ectopic Varices

We report a case of haematemesis & melaena due to ectopic varices located in the duodenum in a patient with NASH related CLD. Duodenal varices are a rare but potentially serious consequence of portal hypertension in the event of a bleeding. The etiology of duodenal varices can be classified into hepatic (e.g. cirrhosis) or extra hepatic (e.g. portal, splenic or superior mesenteric vein thrombosis). Endoscopic injection sclerotherapy (EIS) and endoscopic variceal ligation (EVL) are widely accepted as primary therapies for esophageal variceal bleeding whereas bleeding gastric fundal varices are usually treated with cyanoacrylate injection or shunt procedures. However there is no widely accepted treatment modality for duodenal varices. In the case presented, we used injection sclerotherapy with ethanolamine oleate, to obliterate varices and control bleeding. A short review on the etiology pathogenesis and management of ectopic varices is presented. J Bangladesh Coll Phys Surg 2019; 37(3): 156-159

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