Comparison of Percutaneous Transhepatic Variceal Embolization (PTVE) Followed by Partial Splenic Embolization versus PTVE Alone for the Treatment of Acute Esophagogastric Variceal Massive Hemorrhage

Duan, Xuhua; Zhang, Kai; Han, Xinwei; Ren, Jianzhuang; Xu, Miao; Huang, Guo‐Hao; Zhang, Mengfan

doi:10.1016/j.jvir.2014.08.019

Cited by 23 publications

(25 citation statements)

References 24 publications

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“…Duan et al [85] reported de novo PHG developed in 13 of 34 patients (38%) after percutaneous transhepatic variceal embolization for massive esophagogastric variceal hemorrhage. These phenomena are attributed to increased portal pressure and flow after eradication of esophageal varices because of redistribution of residual blood flow that had passed through the previously patent varices [5,41,45,81,[86][87][88][89][90] .…”

Section: Esophageal Variceal Eradicationmentioning

confidence: 99%

“…Table 5 [8, 9,11,14,34,41,55,62,67,71,83,85] lists wellestablished risk factors for PHG; Table 6 [11,41, 44,55,[75][76][77]83,85,[98][99][100][101][102][103][104][105][106][107] lists therapies that affect the severity of PHG or the risk of bleeding from PHG, and Table 7 [8, 14,28,30,35,42,84,[108][109][110] lists the factors that do not affect the risk of PGH.…”

Section: Additional Risk Factorsmentioning

confidence: 99%

“…Hashizume et al [116] reported that cirrhotic patients have dilated small gastric blood vessels, including arterioles, precapillaries, capillaries, submucosal veins, and subserosal veins, with decreased arteriovenous resistance and straightening of arterioles. Percutaneous transhepatic variceal embolization [85] This hyperdynamic circulation impairs gastric mucosal defense mechanisms, causes release of proinflammatory mediators, and inhibits growth factors which render gastric mucosa more susceptible to injury [67,117] and impair mucosal healing [113,114,118,119] . This vulnerable mucosa becomes predisposed to bleeding [117,120] .…”

Section: Pathogenesismentioning

confidence: 99%

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Portal hypertensive gastropathy: A systematic review of the pathophysiology, clinical presentation, natural history and therapy

Gjeorgjievski¹

2016

WJH

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AIM:To describe the pathophysiology, clinical presentation, natural history, and therapy of portal hypertensive gastropathy (PHG) based on a systematic literature review. METHODS:Computerized search of the literature was performed via PubMed using the following medical subject headings or keywords: "portal" and "gastropathy"; or "portal" and "hypertensive"; or "congestive" and "gastropathy"; or "congestive" and "gastroenteropathy". The following criteria were applied for study inclusion: Publication in peer-reviewed journals, and publication since 1980. Articles were independently evaluated by each author and selected for inclusion by consensus after discussion based on the following criteria: Well-designed, prospective trials; recent studies; large study populations; and study emphasis on PHG. RESULTS:PHG is diagnosed by characteristic endoscopic findings of small polygonal areas of variable erythema surrounded by a pale, reticular border in a mosaic pattern in the gastric fundus/body in a patient with cirrhotic or non-cirrhotic portal hypertension. Histologic findings include capillary and venule dilatation, congestion, and tortuosity, without vascular fibrin thrombi or inflammatory cells in gastric submucosa. PHG is differentiated from gastric antral vascular ectasia by a different endoscopic appearance. The etiology of PHG is inadequately understood. Portal hypertension is necessary but insufficient to develop PHG because many patients have portal hypertension without PHG. Portal hypertensive gastropathy: A systematic review of the pathophysiology, clinical presentation, natural history and therapy PHG increases in frequency with more severe portal hypertension, advanced liver disease, longer liver disease duration, presence of esophageal varices, and endoscopic variceal obliteration. PHG pathogenesis is related to a hyperdynamic circulation, induced by portal hypertension, characterized by increased intrahepatic resistance to flow, increased splanchnic flow, increased total gastric flow, and most likely decreased gastric mucosal flow. Gastric mucosa in PHG shows increased susceptibility to gastrotoxic chemicals and poor wound healing. Nitrous oxide, free radicals, tumor necrosis factor-alpha, and glucagon may contribute to PHG development. Acute and chronic gastrointestinal bleeding are the only clinical complications. Bleeding is typically mild-to-moderate. Endoscopic therapy is rarely useful because the bleeding is typically diffuse. Acute bleeding is primarily treated with octreotide, often with concomitant proton pump inhibitor therapy, or secondarily treated with vasopressin or terlipressin. Nonselective β-adrenergic receptor antagonists, particularly propranolol, are used to prevent bleeding after an acute episode or for chronic bleeding. Iron deficiency anemia from chronic bleeding may require iron replacement therapy. Transjugular-intrahepaticportosystemic-shunt and liver transplantation are highly successful ultimate therapies because they reduce the underlying portal hypertension. SYSTEMA...

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Section: Esophageal Variceal Eradicationmentioning

confidence: 99%

Section: Additional Risk Factorsmentioning

confidence: 99%

Section: Pathogenesismentioning

confidence: 99%

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Portal hypertensive gastropathy: A systematic review of the pathophysiology, clinical presentation, natural history and therapy

Gjeorgjievski¹

2016

WJH

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“…Of the 44 full-text citations considered, 6 met the criteria for inclusion. [8910111213] The PRISMA template[14] for study selection is shown in Figure 1. The most common reasons for excluding the studies were that they were either not RCT or cohort studies or they only investigated hemodynamics indexes.…”

Section: Resultsmentioning

confidence: 99%

“…[8910111213] However, the beneficial effects of PSE for GEVH have not been validated. Therefore, we designed this study to analyze whether combinational therapies are more effective than conventional therapies in reducing variceal recurrence, variceal hemorrhage, and occurrence of serious complications, as well as in promoting overall survival (OS) in GEVH patients using systematic review and meta-analyses.…”

mentioning

confidence: 99%

Partial splenic embolization has beneficial effects for the management of gastroesophageal variceal hemorrhage

Wang

Liu

Tong

et al. 2016

Saudi J Gastroenterol

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Background/Aims:Partial splenic embolization (PSE) is used in the management of gastroesophageal variceal hemorrhage (GEVH). However, it is uncertain whether it has beneficial effects for GEVH patients in preventing variceal recurrence and variceal hemorrhage, as well as promoting overall survival (OS), when it is combined with conventional therapies.Materials and Methods:The databases including PubMed, EMBASE, Web of Science, Google scholar, and Cochrane Central Register of Controlled Trials were searched up to 11th of November, 2015. Meta-analyses were performed by using Review Manager 5.3 software for analyzing the risk of bias, Newcastle-Ottawa Scale for assessing the bias of cohort studies, and GRADEprofiler software for assessing outcomes obtained from the meta-analyses.Results:A total of 1505 articles were reviewed, and 1 randomized controlled trial and 5 cohort studies with 244 participants were eligible for inclusion. The pooled hazard ratio (HR) of variceal recurrence is 0.50 (95% confidence interval (CI) 0.37, 0.68; P< 0.00001; I2 = 0%). The pooled HR of variceal hemorrhage is 0.24 (95% CI 0.15, 0.39; P< 0.00001; I2 = 0%). The pooled HR of OS is 0.50 (95% CI 0.33, 0.67; P< 0.00001; I2 = 0%). Meta-analyses demonstrated statistically significant superiority of combinational therapies over conventional therapies in preventing variceal recurrence and variceal hemorrhage and prolonging OS. The complications related to PSE were mild or moderate and nonfatal.Conclusions:The results indicate that PSE has beneficial effects for GEVH patients, however, future investigation with a larger number of subjects in clinical trials is warranted.

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Gastrointestinal Bleeding as a Result of Portal Hypertension

Marshall

2019

Multidisciplinary Approaches to Common Surgical Problems

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Comparison of Percutaneous Transhepatic Variceal Embolization (PTVE) Followed by Partial Splenic Embolization versus PTVE Alone for the Treatment of Acute Esophagogastric Variceal Massive Hemorrhage

Cited by 23 publications

References 24 publications

Portal hypertensive gastropathy: A systematic review of the pathophysiology, clinical presentation, natural history and therapy

Portal hypertensive gastropathy: A systematic review of the pathophysiology, clinical presentation, natural history and therapy

Partial splenic embolization has beneficial effects for the management of gastroesophageal variceal hemorrhage

Gastrointestinal Bleeding as a Result of Portal Hypertension

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