scholarly journals Recent Advances in the Management of Acute Variceal Hemorrhage

2021 ◽  
Vol 10 (17) ◽  
pp. 3818
Author(s):  
Alberto Zanetto ◽  
Sarah Shalaby ◽  
Paolo Feltracco ◽  
Martina Gambato ◽  
Giacomo Germani ◽  
...  
Keyword(s):  
Portal Hypertension ◽  
Portal Pressure ◽  
Indirect Measurement ◽  
Secondary Prophylaxis ◽  
Variceal Hemorrhage ◽  
Esophageal Variceal ◽  
Gastroesophageal Varices ◽  
Recent Advances ◽  
Risk Patients ◽  
Clinically Significant

Gastrointestinal bleeding is one of the most relevant causes of death in patients with cirrhosis and clinically significant portal hypertension, with gastroesophageal varices being the most frequent source of hemorrhage. Despite survival has improved thanks to the standardization on medical treatment aiming to decrease portal hypertension and prevent infections, mortality remains significant. In this review, our goal is to discuss the most recent advances in the management of esophageal variceal hemorrhage in cirrhosis with specific attention to the treatment algorithms involving the use of indirect measurement of portal pressure (HVPG) and transjugular intrahepatic portosystemic shunt (TIPS), which aim to further reduce mortality in high-risk patients after acute variceal hemorrhage and in the setting of secondary prophylaxis.

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.

scholarly journals Brief Review of Portal Hypertension Related Complications

2021 ◽  
Author(s):  
Achyut Bikram Hamal
Keyword(s):  
Portal Hypertension ◽  
Pressure Gradient ◽  
Beta Blockers ◽  
Venous Pressure ◽  
Portal Pressure ◽  
Hepatopulmonary Syndrome ◽  
Portal Blood Flow ◽  
Variceal Hemorrhage ◽  
The Difference ◽  
Clinically Significant

The pathologic increase in the pressure gradient between portal vein and inferior venacava is called portal hypertension. Increased portal blood flow and increased resistance in the portal venous system cause portal hypertension. The structural components and the functional components contribute to the resistance. Hepatic venous pressure gradient (HVPG) reflects the degree of portal pressure in liver disease. HVPG is calculated as the difference between the wedged hepatic venous pressure (WHVP) and the free hepatic venous pressure (FHVP). Clinically significant portal hypertension (CSPH) is defined as HVPG ≥10. Different values of HVPG have been defined as threshold for different consequences of portal hypertension. Variceal hemorrhage, portal hypertensive gastropathy, ascites, colopathy, biliopathy and hepatopulmonary syndrome are main complications of portal hypertension. Besides nonselective beta blockers, other drugs like statins, antioxidants, antidiabetic, anti-inflammatory and antiapoptotic drugs have also been seen to be effective in reducing portal pressure.

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 Insulin resistance in patients with cirrhosis and portal hypertension

2012 ◽  
Vol 302 (12) ◽  
pp. G1458-G1465 ◽  
Author(s):  
Eva Erice ◽  
Elba Llop ◽  
Annalisa Berzigotti ◽  
Juan G. Abraldes ◽  
Ignacio Conget ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Portal Hypertension ◽  
Endothelial Dysfunction ◽  
Intracellular Signaling ◽  
Venous Pressure ◽  
Portal Pressure ◽  
Model Assessment ◽  
Hepatic Hemodynamics ◽  
Clinically Significant ◽  
The Relationship

Insulin resistance (IR) is involved in the pathogenesis of endothelial dysfunction and is also present in patients with cirrhosis. Intrahepatic endothelial dysfunction plays a major role, increasing hepatic vascular resistance and promoting portal hypertension (PH). In addition, β-adrenergic agonists and insulin share several intracellular signaling pathways. Thus IR may influence the response to β-blockers. This study aimed at evaluating the relationship between IR and hepatic hemodynamics in patients with cirrhosis and with the portal pressure response to acute β-blockade. Forty-nine patients with cirrhosis and PH were included. Hepatic and systemic hemodynamics were measured, and IR was estimated by using the updated homeostasis model assessment (HOMA)-2 index. Patients with HOMA-2 > 2.4 were considered IR. In patients with hepatic venous pressure gradient (HVPG) ≥ 10 mmHg) [clinically significant PH (CSPH)], hemodynamic measurements were performed again 20 min after intravenous propranolol. Mean HOMA-2 index was 3 ± 1.4. Fifty-seven percent of patients had IR. A weak correlation between HOMA-2 index and HVPG was observed. Eighty-six percent of patients had CSPH. HOMA-2 index was an independent predictor of CSPH. However, in patients with CSPH, the correlation between HOMA-2 index and HVPG was lost. HVPG, but not IR, predicted the presence of esophageal varices. Response to propranolol was not different between patients with or without IR. In nondiabetic patients with cirrhosis, HOMA-2 index is directly associated with the presence of CSPH and indirectly with varices, but does not allow either grading HVPG or predicting its response to propranolol.

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.

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.

Diagnosis and management of variceal bleeding in the critically ill

2016 ◽  
Author(s):  
Deanna Blisard ◽  
Ali Al-Khafaji
Keyword(s):  
Venous Pressure ◽  
Portal Pressure ◽  
Primary Prophylaxis ◽  
Secondary Prophylaxis ◽  
Pharmacological Therapy ◽  
Variceal Haemorrhage ◽  
Gastroesophageal Varices ◽  
Endoscopic Intervention ◽  
Definitive Therapy ◽  
Haemorrhage Control

Cirrhosis is the most common cause of portal hypertension, which subsequently leads to development of gastroesophageal varices (GEV). Generally, presence of GEV correlates with the severity of cirrhosis and variceal haemorrhage can develop when hepatic venous pressure gradient exceeds 10–12 mmHg. The gold standard for diagnosis and often treatment of GEV is oesophagogastroduodenoscopy (OGD). Management of GEV is divided into primary prophylaxis, acute haemorrhage control, and secondary prophylaxis. Primary prophylaxis includes surveillance OGD and endoscopic intervention based on the size of the varices. Management of acute variceal haemorrhage includes resuscitation and endoscopic interventions. Basic resuscitative measures to maintain haemodynamic stability, vasoconstricting agents to decrease portal pressure, and the use of prophylactic antibiotics. Endoscopic intervention includes any of variceal band ligation, variceal sclerotherapy, and variceal obturation. Radiological or surgical portosystemic shunting markedly reduces portal pressure and are clinically effective therapy for patients who fail endoscopic or pharmacological therapy. Balloon tamponade is effective in temporarily controlling oesophageal variceal haemorrhage in over 80% of patients. Its use should be restricted to patients with uncontrollable bleeding, where more definitive therapy is planned within 24 hours. Secondary prophylaxis includes endoscopy plus pharmacological therapy of non-selective β‎−blockers.

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 Microbiota transplants from feces or gut content attenuated portal hypertension and portosystemic collaterals in cirrhotic rats

2021 ◽  
Author(s):  
Hui-Chun Huang ◽  
Ming-Hung Tsai ◽  
Ching-Chih Chang ◽  
Chon Kit Pun ◽  
Yi-Hsiang Huang ◽  
...  
Keyword(s):  
Liver Cirrhosis ◽  
Portal Hypertension ◽  
Liver Injury ◽  
Portal Pressure ◽  
Vascular Density ◽  
Variceal Hemorrhage ◽  
Distribution Method ◽  
Portosystemic Shunts ◽  
Duct Ligation ◽  
Portosystemic Collaterals

Liver cirrhosis and portal hypertension is the end of chronic liver injury with hepatic, splanchnic and portosystemic collateral systems dysregulation. Liver injury is accompanied by gut dysbiosis whereas dysbiosis induces liver fibrosis, splanchnic angiogenesis and dysregulated vascular tones vice versa, making portal hypertension aggravated. It has been proved that intestinal microbiota transplantation alleviates dysbiosis. Nevertheless, the influences of microbiota transplantation on cirrhosis related portal hypertension are not so clear. Liver cirrhosis with portal hypertension was induced by bile duct ligation in rats. Sham rats were surgical controls. Rats randomly received vehicle, fecal or gut (terminal ileum) material transplantation. The results showed that microbiota transplantation from feces or gut material significantly reduced portal pressure in cirrhotic rats (P = .010, .044). Hepatic resistance, vascular contractility, fibrosis and relevant protein expressions were not significantly different among cirrhotic rats. However, microbiota transplantation ameliorated splanchnic hyperdynamic flow and vasodilatation. Mesenteric angiogenesis, defined by whole mesenteric window vascular density, decreased in both transplantation groups and phosphorylated eNOS was downregulated. Portosystemic shunts determined by splenorenal shunt flow decreased in both transplantation groups (P = .037, .032). Shunting severity assessed by microsphere distribution method showed consistent results. Compared to sham rats, cirrhotic rats lacked Lachnospiraceae. Both microbiota transplants increased Bifidobacterium. In conclusion, microbiota transplantation in cirrhotic rats reduced portal pressure, alleviated splanchnic hyperdynamic circulation and portosystemic shunts. The main beneficial effects may be focused on portosystemic collaterals-related events, such as hepatic encephalopathy and gastroesophageal variceal hemorrhage. Further clinical investigations are mandatory.

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