Portal Hypertension and Variceal Hemorrhage

Toubia, Nagib; Sanyal, Arun J.

doi:10.1016/j.mcna.2007.12.003

Cited by 72 publications

(65 citation statements)

References 118 publications

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“…General measures for patients presenting with acute bleeding from PHG include volume resuscitation and cautious transfusion of packed erythrocytes, as necessary, to maintain the hemoglobin level at 8 g/dL [192,259,260] . Over-transfusion to a higher hemoglobin level could promote bleeding from PHG by raising portal pressure, as reported for bleeding from esophageal varices [261,262] . However, patients with cardiopulmonary disease or severe other comorbidities may require a hemoglobin level of 9-10 g/dL [263] .…”

Section: Summary Of Clinical Treatmentmentioning

confidence: 81%

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: Summary Of Clinical Treatmentmentioning

confidence: 81%

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

Gjeorgjievski¹

2016

WJH

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“…These collaterals decompress the portal circulation by shunting the blood to the heart via the systemic venous circulation and the major sites of these collaterals are the esophagus, rectum, umbilicus and retro peritoneum. 3,4,5 Gastro esophageal varices are present in approximately 50% of patients with cirrhosis with a lifetime incidence of 90%. Their presence also correlate with the severity of disease, being more common in Child Pugh Class C patients as compared to Child Pugh Class A patients (85% versus 40%) 6,7,8 ( Table 1).…”

Section: Introductionmentioning

confidence: 99%

Non-invasive parameters for the detection of variceal bleed in patients of liver cirrhosis, an experience of a tertiary care hospital in Pakistan

et al. 2014

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Objective: Cirrhotic patients commonly undergo screening endoscopy for the existence of esophageal varices. The use of this invasive procedure which is expensive, poorly tolerable and generally not acceptable for the patients is increasing due to increasing number of patients with chronic liver disease and their enriched survival. In this study, our aim is to identify clinical, biochemical, and ultrasonography parameters which might noninvasively predict the presence of esophageal varices and risk of bleeding in patients with liver cirrhosis. Material and Methods: Total 150 Patientsof chronic liver disease admitted in ward-5, JPMC (Sep 2011-Feb 2012 with a complaint of hematemesis or melena were included in the study. Platelet counts of 75,000 to 150,000/µL was defined as grade 1 thrombocytopenia, 50,000 to <75,000/µL as grade II, 25,000 to <50,000/µL as grade III and below 25,000/µL as grade IV. The normal range for the INR is 0.8-1.2. Portal vein size of 1.2 cm or above was taken as dilated. Spleen of >13 cm was considered as enlarged in our study. Results: Out of 72 patients of variceal bleed 69 (46%) were males and 81(54%) were females. Thrombocytopenia was present in 64 (88%) patients with mean platelet count of 85.86/µL (±69.79). Deranged coagulation profile was present in 56 (77%) cases with mean INR of 1.63 (±0.5). Portal vein diameter (PVD) of >1.2 cm was found in 46(63.8%) of patients with mean PVD of 1.22(±0.3023) and splenic size of >13 cm was reported in 54 (75%) cases with mean splenic diameter of 14.5 cm (±2.39). Conclusion: Thrombocytopenia, deranged coagulation profile, large splenic size, and dilated portal vein strongly predict the risk of variceal bleeding.

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“…The cause of GAVE is unknown, but Jabbari 1 had proposed that it could result from repetitive low-grade trauma caused by repeated prolapse of the loosely attached mucosa of the distal antrum into the duodenum during gastric peristalsis due to antral hypercontractility, primary or acquired, with consequent elongation and secondary reactive muscular hyperplasia and ectasia of the mucosal vessels. Thrombosed ectatic vessels are a distinctive feature and are seen only in GAVE 18,19 . Since GAVE is not acid related pharmacotherapy with histamine receptor antagonists and proton pump inhibitors is ineffective.…”

Section: Discussionmentioning

confidence: 99%

Watermelon stomach, hemorrhagic pericarditis, small cell carcinoma of the lung and synchronous squamous cell carcinoma of the tongue base

Murinello

Damásio

Figueiredo³

et al. 2010

Revista Portuguesa de Pneumologia (English Edition)

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ResumoBaseados num caso de gastropatia antral com ectasia vascular (estômago em melancia) associado a pericardite hemorrágica e a um carcinoma de pequenas células do pulmão com metástases ganglionares ao longo do mediastino e a um carcinoma pavimentocelular sín-crono da base da língua, os autores fazem uma revisão dos aspectos clínicos, endoscópicos e histopatológicos deste tipo de gastropatia, da sua associação a outras doenças e das possibilidades terapêuticas actuais por via endoscópica. Referem-se igualmente as causas mais frequentes de pericardite hemorrágica, salientando-se a AbstractBased on a case of gastric antral vascular ectasia (watermelon stomach) that was associated with hemorrhagic pericarditis, small cell lung carcinoma with mediastinal lymph node metastases and a synchronous squamous cell carcinoma of the base of the tongue, the authors made a review of the clinical, endoscopic and histopathological aspects of this type of gastropathy, and its association with other diseases, and of the results of its endoscopic therapy. The causes of hemorrhagic pericarditis are considered, emphasizing the necessity to know if the effusion has Estômago em melancia, pericardite hemorrágica, tumor de pequenas células do pulmão e carcinoma pavimentocelular síncrono da base da língua Watermelon stomach, hemorrhagic pericarditis, small cell carcinoma of the lung and synchronous squamous cell carcinoma of the tongue base

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Portal Hypertension and Variceal Hemorrhage

Cited by 72 publications

References 118 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

Non-invasive parameters for the detection of variceal bleed in patients of liver cirrhosis, an experience of a tertiary care hospital in Pakistan

Watermelon stomach, hemorrhagic pericarditis, small cell carcinoma of the lung and synchronous squamous cell carcinoma of the tongue base

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