scholarly journals Efficacy of long-acting somatostatin analogs in recurrent variceal bleeding in a patient with pre-hepatic portal vein thrombosis

2015 ◽  
Vol 72 (3) ◽  
pp. 283-286
Author(s):  
Tamara Alempijevic ◽  
Ana Balovic ◽  
Aleksandra Pavlovic-Markovic ◽  
Dino Tarabar ◽  
Miodrag Krstic ◽  
...  
Keyword(s):  
Portal Hypertension ◽  
Surgical Treatment ◽  
High Risk ◽  
General Condition ◽  
Variceal Bleeding ◽  
Somatostatin Analogue ◽  
Variceal Hemorrhage ◽  
Gastroesophageal Varices ◽  
Vein Thrombosis ◽  
Long Acting

Introduction. Bleeding from esophageal varices is a serious medical problem because of the risk of recurrent bleeding and high mortality rate (17-54%). Gastroesophageal varices develop in 50% of cirrhotic patients with portal hypertension, but can also develop in other pre- or post-hepatic causes of portal hypertension. Case report. We reported a 48-year-old female patient with portal hypertension caused by mesenterial vein thrombosis due to congenital thrombophilia. The patient was hospitalized several times because of recurrent gastroesophageal bleeding. Thrombosis of portal, lienal and mesenteric veins was diagnosed using multislice computed tomography (MSCT) angiography. Sclerotherapy and/or variceal ligation could not be used due to variceal size and distribution. Beta blockers were ineffective. Balloon tamponade and octreotide were used in each massive bleeding episode. Carvedilol therapy was introduced but rebleeding occured. Surgical treatment was considered a high risk procedure due to massive thrombosis of mesenterial veins, patient's general condition and high risk of postoperative thrombotic events. Thus, long-acting somatostatin analogue - Sandostatin? LAR was initiated at a dose of 30 mg im/month. The patient responded to the therapy well and variceal bleeding did not occur for the following 3 months. After 3 months another episode of gastric variceal hemorrhage occurred and surgical treatment was reconsidered. Total gastrectomy was performed in order to prevent repeated bleeding from large gastric varices and the patient recovered successfully, and after 1 year is symptom-free. Conclusion. Long-lasting somatostatin analogue was used for the first time in treatment of gastroesophageal variceal hemorrhage in the patient with prehepatic portal hyperten-sion. It was effective as temporary therapeutic option allowing the improvement of the patients general condition and adequate planning of elective surgical procedure. Futher reports are needed in order to compare efficacy in treatment of patients with variceal bleeding, where poor outcome is expected.

scholarly journals Management of variceal hemorrhage: current concepts

2014 ◽  
Vol 27 (2) ◽  
pp. 138-144 ◽  
Author(s):  
Fabricio Ferreira COELHO ◽  
Marcos Vinícius PERINI ◽  
Jaime Arthur Pirola KRUGER ◽  
Gilton Marques FONSECA ◽  
Raphael Leonardo Cunha de ARAÚJO ◽  
...  
Keyword(s):  
Portal Hypertension ◽  
Surgical Treatment ◽  
Variceal Bleeding ◽  
Endoscopic Therapy ◽  
Beta Blockers ◽  
Primary Prophylaxis ◽  
Underlying Disease ◽  
Secondary Prophylaxis ◽  
Variceal Hemorrhage ◽  
Cirrhotic Patients

INTRODUCTION: The treatment of portal hypertension is complex and the the best strategy depends on the underlying disease (cirrhosis vs. schistosomiasis), patient's clinical condition and time on it is performed (during an acute episode of variceal bleeding or electively, as pre-primary, primary or secondary prophylaxis). With the advent of new pharmacological options and technical development of endoscopy and interventional radiology treatment of portal hypertension has changed in recent decades. AIM: To review the strategies employed in elective and emergency treatment of variceal bleeding in cirrhotic and schistosomotic patients. METHODS: Survey of publications in PubMed, Embase, Lilacs, SciELO and Cochrane databases through June 2013, using the headings: portal hypertension, esophageal and gastric varices, variceal bleeding, liver cirrhosis, schistosomiasis mansoni, surgical treatment, pharmacological treatment, secondary prophylaxis, primary prophylaxis, pre-primary prophylaxis. CONCLUSION: Pre-primary prophylaxis doesn't have specific treatment strategies; the best recommendation is treatment of the underlying disease. Primary prophylaxis should be performed in cirrhotic patients with beta-blockers or endoscopic variceal ligation. There is controversy regarding the effectiveness of primary prophylaxis in patients with schistosomiasis; when indicated, it is done with beta-blockers or endoscopic therapy in high-risk varices. Treatment of acute variceal bleeding is systematized in the literature, combination of vasoconstrictor drugs and endoscopic therapy, provided significant decline in mortality over the last decades. TIPS and surgical treatment are options as rescue therapy. Secondary prophylaxis plays a fundamental role in the reduction of recurrent bleeding, the best option in cirrhotic patients is the combination of pharmacological therapy with beta-blockers and endoscopic band ligation. TIPS or surgical treatment, are options for controlling rebleeding on failure of secondary prophylaxis. Despite the increasing evidence of the effectiveness of pharmacological and endoscopic treatment in schistosomotic patients, surgical therapy still plays an important role in secondary prophylaxis.

scholarly journals Prevention and Management of Variceal Hemorrhage

2013 ◽  
Vol 2013 ◽  
pp. 1-6 ◽  
Author(s):  
Dong Hyun Kim ◽  
Jun Yong Park
Keyword(s):  
High Risk ◽  
Endoscopic Sclerotherapy ◽  
Variceal Hemorrhage ◽  
Gastroesophageal Varices ◽  
Mortality And Morbidity ◽  
First Line Therapy ◽  
Advanced Cirrhosis ◽  
Proven Efficacy ◽  
Advanced Liver Cirrhosis ◽  
Small Varices

Variceal hemorrhage is a common and devastating complication of portal hypertension and is a leading cause of death in patients with cirrhosis. The management of gastroesophageal varices has evolved over the last decade resulting in improved mortality and morbidity rates. Regarding the primary prevention of variceal hemorrhaging, nonselectiveβ-blockers should be the first-line therapy in all patients with medium to large varices and in patients with small varices associated with high-risk features such as red wale marks and/or advanced cirrhosis. EVL should be offered in cases of intolerance or side effects toβ-blockers, or for patients at high-risk for variceal bleeding who have medium or large varices with red wale marks or advanced liver cirrhosis. In acute bleeding, vasoactive agents should be initiated along with antibiotics followed by EVL or endoscopic sclerotherapy (if EVL is technically difficult) within the first 12 hours of presentation. Where available, terlipressin is the preferred agent because of its safety profile and it represents the only drug with a proven efficacy in improving survival. All patients surviving an episode of bleeding should undergo further prophylaxis to prevent rebleeding with EVL and nonselectiveβ-blockers.

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).

scholarly journals Rupture of esophageal varices due to portal hypertension

2010 ◽  
Vol 50 (5) ◽  
pp. 316
Author(s):  
Yusri Dianne Jurnalis ◽  
Yorva Sayoeti ◽  
Marlinda Marlinda
Keyword(s):  
Portal Hypertension ◽  
Esophageal Varices ◽  
Variceal Bleeding ◽  
Variceal Hemorrhage ◽  
Common Cause ◽  
Initial Episode ◽  
One Year ◽  
The One ◽  
Upper Gastrointestinal ◽  
Emergent Case

Variceal bleeding is the most common cause of serious upper gastrointestinal (UGI) bleeding in children. Most variceal bleeding is esophageal.1 Hemorrhages from esophageal varices due to portal hypertension are a major cause of morbidity and mortality. There is a 30% mortality rate following an initial episode of variceal hematemesis. Mortality increases to 70% with recurrent variceal hemorrhage. Moreover, the one year survival rate after variceal hemorrhage is often poor (32 to 80%).2-4 We report a case of esophageal varices rupture caused by portal hypertension, an emergent case in the Pediatric Gastrohepatology division.

scholarly journals A174 RARE BUT DEADLY: AN APPROACH TO MANAGEMENT OF DUODENAL VARICEAL HEMORRHAGE

2020 ◽  
Vol 3 (Supplement_1) ◽  
pp. 39-41
Author(s):  
M Dahiya ◽  
M Tomaszewski ◽  
G Ou ◽  
A Ramji
Keyword(s):  
Interventional Radiology ◽  
Case Report ◽  
Portal Hypertension ◽  
Literature Review ◽  
Gastrointestinal Bleeding ◽  
Variceal Bleeding ◽  
Variceal Hemorrhage ◽  
Cyanoacrylate Glue ◽  
Duodenal Varices ◽  
Ectopic Varices

Abstract Background Common etiologies of upper gastrointestinal bleeding (UGIB) in cirrhotic patients with portal hypertension include gastroesophageal varices (GOV), portal hypertensive gastropathy (PHG) and gastric antral vascular ectasia (GAVE). Less commonly, patients with portal hypertension develop varices in ectopic sites, including the rectum, biliary tree and duodenum. Ectopic varices are rare, contributing to 1–5% of all variceal bleeding, of which 17% is from duodenal varices. Aims To describe the management of duodenal variceal hemorrhage. Methods A case report and literature review was performed. Results Case report: We present a case of recurrent UGIB in a 59-year-old male with decompensated cirrhosis due to non-alcoholic steatohepatitis (CP-C; Meld 14). Initial endoscopy was negative for GOV, peptic ulcer, PHG, and GAVE, but an erosion over a mucosal bulge in the third segment of the duodenum was identified, raising possibility of vascular malformation versus ectopic varix. There was active bleeding after water provocation, so clips were deployed for hemostasis. CT imaging showed mesenteric venous collaterals abutting the duodenum, again raising possibility of duodenal varix, which was ultimately confirmed by endoscopic ultrasound (EUS). Patient had recurrent overt bleeding despite beta-blockage for prophylaxis, endoscopic clipping on four separate occasions, attempted angioembolization by interventional radiology, and cyanoacrylate glue. Transjugular intrahepatic porto-systemic shunt (TIPS) was not possible due to portal vein occlusion, so he underwent EUS-guided cyanoacrylate glue a second time. Literature review: Ectopic varices are rare, contributing to 1–5% of all variceal bleeding, of which 17% is from duodenal varices. Duodenal variceal hemorrhage can lead to hemorrhagic shock, and is potentially life threatening, with quoted mortality rates of 40%. Unfortunately, duodenal varices can be difficult to identify. Diagnosis is often delayed due to a combination of lower awareness and endoscopic challenges given the unusual serosal and submucosal location. Evidence-based guidelines for the management of ectopic varices are limited. For this reason, our current management strategies rely heavily on local expertise. Splanchnic vasoconstrictor medication, endoscopic ligation, EUS guided gluing, interventional radiology guided embolization, TIPS, balloon retrograde transvenous obliteration and surgical shunts are potential therapeutic options to manage the acutely bleeding varix. Following a variceal bleed, liver transplantation should be considered in eligible patients with no other contraindications. Conclusions Duodenal varices are a rare, potentially fatal, and underrecognized cause of gastrointestinal bleeding in patients with portal hypertension. Definitive therapy currently relies upon local expertise in the absence of clear guideline-based therapy. Funding Agencies None

scholarly journals Case Report of Gastrointestinal Bleeding in an Adult with Chronic Visceral Acid Sphingomyelinase Deficiency

2019 ◽  
Vol 2019 ◽  
pp. 1-5
Author(s):  
David Cassiman ◽  
Louis Libbrecht ◽  
Wouter Meersseman ◽  
Alexander Wilmer
Keyword(s):  
Portal Hypertension ◽  
Gastrointestinal Bleeding ◽  
Variceal Bleeding ◽  
Significant Risk ◽  
Acid Sphingomyelinase ◽  
Intestinal Bleeding ◽  
Intestinal Loop ◽  
Gastroesophageal Varices ◽  
Sphingomyelinase Deficiency ◽  
Venous Collaterals

Introduction. Acid sphingomyelinase deficiency (ASMD, also known as Niemann-Pick Type A and Type B disease) is a rare, inherited metabolic disorder. Liver-related issues, including cirrhosis and variceal haemorrhage, are a leading cause of early mortality in individuals with chronic forms of ASMD. Due to the rarity of this lysosomal storage disorder, there can be a lack of awareness that adults with chronic ASMD disease are at significant risk of cirrhosis, portal hypertension, and variceal bleeding. This case highlights an unusual presentation of recurrent variceal bleeding in an adult with cirrhosis and portal hypertension due to chronic visceral ASMD. Case Presentation. A patient with severe splenomegaly was diagnosed with ASMD at age of 25. At age 64 they had multiple hospital admissions for hematochezia (originally diagnosed as ischemic colitis) accompanied by hypotension (blood pressure 91/45 mmHg), anemia (hemoglobin 8.5g/dL, ref 12-16; INR 1.4, ref ≤1.2), and mild renal insufficiency (creatinine 1.33mg/dL, ref 0.51-0.95). Colonoscopy did not reveal a source of bleeding. Computerized tomography scanning imaging showed diffuse venous collaterals and ascites. Arteriographies during subsequent episodes of bleeding were negative for active arterial intestinal bleeding. Recurrent gastrointestinal bleeding was found to originate from a varicose vein cluster connected to the right iliac vein and the superior mesenteric vein, located in the submucosa of a small intestinal loop. Multiple varices were secondary to portal hypertension in the context of cirrhosis. The patient died from recurrent variceal bleeding that exacerbated liver failure worsened by pneumonia and hypovolemic and septic shock. Conclusions. The variceal bleeding in this patient was atypical in that it originated from venous collaterals bleeding into the small intestine rather than the more typical gastroesophageal varices observed in ASMD. With long standing liver dysfunction and gradual development of portal hypertension, intestinal varices rather than occult intestinal bleeding due to ischemia should be considered in ASMD patients presenting with either hematochezia or hematemesis.

Case Series Regarding Parastomal Variceal Bleeding: Presentation and Management

2018 ◽  
Vol 17 (5) ◽  
pp. 0-10
Author(s):  
John Romano ◽  
Charles V. Welden ◽  
Jordan Orr ◽  
Brendan McGuire ◽  
Mohamed Shoreibah
Keyword(s):  
Portal Hypertension ◽  
High Risk ◽  
Literature Review ◽  
Variceal Bleeding ◽  
Coil Embolization ◽  
Case Series ◽  
Treatment Modalities ◽  
Post Procedure ◽  
Lost To Follow Up

Parastomal variceal bleeding (PVB) is a serious complication occurring in up to 27% of patients with an ostomy and concurrent cirrhosis and portal hypertension. The management of PVB is difficult and there are no clear guidelines on this matter. TIPS, sclerotherapy, and /or coil embolization are all therapies that have been shown to successful manage PVB. We present a case series with five different patients who had a PVB at our institution. The aim of this case series is to report our experience on the management of this infrequently reported but serious condition. We also conducted a systemic literature review focusing on the treatment modalities of 163 patients with parastomal variceal bleeds. In our series, patient 1 had embolization and sclerotherapy without control of bleed and expired on the day of intervention due to hemorrhagic shock. Patient 2 had TIPS in conjunction with embolization and sclerotherapy and had no instance of rebleed 441 days after therapy. Patient 3 did not undergo any intervention due to high risk for morbidity and mortality, the bleed self-resolved and there was no further rebleed, this same patient died of sepsis 73 days later. Patient 4 had embolization and sclerotherapy and had no instance of rebleed 290 days after therapy. Patient 5 had TIPS procedure and was discharged five days post procedure without rebleed, patient has since been lost to follow-up.

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.

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