scholarly journals Risk Factors for Esophageal Collateral Veins in Cirrhosis with and without Previous Endoscopic Esophageal Variceal Therapy

2022 ◽  
Vol 2022 ◽  
pp. 1-13
Author(s):  
Qianqian Li ◽  
Xiaozhong Guo ◽  
Ji Feng ◽  
Xiangbo Xu ◽  
Saurabh Chawla ◽  
...  

Background. Portosystemic collateral vessels are a sign of portal hypertension in liver cirrhosis. Esophageal collateral veins (ECVs) are one major type of portosystemic collateral vessels, which increase the recurrence of esophageal varices and bleeding after variceal eradication. However, the risk factors for ECVs were still unclear. Methods. We retrospectively screened cirrhotic patients who had contrast-enhanced computed tomography (CT) images to evaluate ECVs and upper gastrointestinal endoscopic reports to evaluate gastroesophageal varices at our department. Univariate and multivariate logistic regression analyses were performed to explore the independent risk factors for ECVs. Odds ratios (ORs) were calculated. Subgroup analyses were performed in patients with and without previous endoscopic variceal therapy which primarily included endoscopic variceal ligation (EVL) and endoscopic injection sclerotherapy (EIS). Results. Overall, 243 patients were included, in whom the prevalence of ECVs was 53.9%. The independent risk factors for ECVs were hepatitis C virus infection (OR = 0.250, p  = 0.026), previous EVL (OR = 1.929, p  = 0.044), platelet (OR = 0.993, p  = 0.008), and esophageal varices needing treatment (EVNTs) (OR = 2.422, p  = 0.006). The prevalence of ECVs was 60.8% (73/120) in patients undergoing EVL, 50% (10/20) in those undergoing EIS, and 47.5% (48/101) in those without previous endoscopic variceal therapy. The independent risk factors for ECVs were the use of nonselective beta-blockers (OR = 0.294, p  = 0.042) and EVNTs (OR = 3.714, p  = 0.006) in subgroup analyses of patients with and without previous endoscopic variceal therapy, respectively. Conclusions. The presence of ECVs should be closely associated with the severity of portal hypertension in liver cirrhosis. Risk of ECVs might be increased by previous EVL.

2018 ◽  
Vol 1 (1) ◽  
pp. 14-16
Author(s):  
Soonthorn Chonprasertsuk

The noncirrhotic portal hypertension is an uncommon cause of bleeding esophagealvarices. This condition must be suspected in patients with preserved liver function. We reporta 25-year old man with SLE disease who presented with hematemesis. He had no historyor risk factors for an underlying liver condition. A huge splenomegaly was detectedby physical examination. The EGD found three large varices with red wale sign, whereas liverfunction tests were unremarkable. The noncirrhotic portal hypertension was diagnosedand confirmed by liver histopathology. Figure 1 แสดงผลการส่องกล้องทางเดินอาหารส่วนบนพบ F3 varices with red wale sign


2018 ◽  
Vol 2018 ◽  
pp. 1-7 ◽  
Author(s):  
Du Kong ◽  
Wei Wang ◽  
Gang Du ◽  
Binyao Shi ◽  
Zhengchen Jiang ◽  
...  

Background. Although liver retraction using n-butyl-2-cyanoacrylate (NBCA) glue has been applied to laparoscopic upper abdominal surgery in noncirrhotic patients, there is still no consensus on its safety and feasibility for cirrhotic patients. In this study, we aimed to investigate the safety and effectiveness of liver retraction using NBCA glue during laparoscopic splenectomy and azygoportal disconnection (LSD) for gastroesophageal varices and hypersplenism secondary to liver cirrhosis and portal hypertension. Methods. Thirty-nine gastroesophageal varices and hypersplenism secondary to liver cirrhosis and portal hypertension patients were included in our study. We performed LSD in the presence of NBCA glue (n = 22, NBCA group) and absence of NBCA glue (n = 17, n-NBCA group), respectively. The operation time, blood loss, postoperative hospitalization, and liver function were compared between the two groups. Results. There was no mortality during the operation. One patient in non-NBCA group received open surgery due to parenchyma hemorrhage. Postoperative pleural effusion occurred in 2 cases of the NBCA group and 1 of the non-NBCA group. One showed left subphrenic abscess in the non-NBCA group. No postoperative bleeding occurred after 9-30 months of follow-up. The time of operation in NBCA group was significantly shorter than those in n-NBCA group (198.86±17.86 versus 217.81±20.25min, P<0.01). Blood loss in NBCA group was significantly lower than non-NBCA group (159.09±56.98 versus 212.50±88.51 ml, P<0.05). The levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were increased on day 1 after LSD and decreased to normal level on day 7 after LSD in both groups. There was no significant difference in postoperative hospitalization and liver function between the two groups. Conclusion. Liver retraction using NBCA glue during LSD for gastroesophageal varices and hypersplenism secondary to liver cirrhosis and portal hypertension is safe, effective, and feasible.


2020 ◽  
pp. 1-2
Author(s):  
Revathy Marimuthu Shanmugam ◽  
Vinay C ◽  
Sathya Gopalasamy ◽  
Chitra Shanmugam

BACKGROUND: Many noninvasive surrogate marker for Portal hypertension or for the presence or grade of esophageal varices were studied..Splenomegaly along with splenic congestion secondary to splenic hyperdynamic circulation is seen secondary to Portal hypertension in cirrhotic patients that can be quantified by elastography. AIM:The aim of this study was to investigate whether spleen stiffness, assessed by TE, useful tool for grading chronic liver diseases and to compare its performance in predicting the presence and size of esophageal varices in liver cirrhosis patients. METHODOLOGY:86 patients with cirrhosis and 80 controls underwent transient elastography of liver and spleen for the assessment of liver stiffness (LSM) and spleen stiffness (SSM) . Upper GI endoscopy done in all Cirrhotic patients. RESULTS: Spleen stiffness showed higher values in liver cirrhosis patients as compared with controls: 58.2 kpa vs14.8 kpa (P < 0.0001) and also found to be significantly higher in cirrhotic patients compared with varices and those without varices (69.01 vs 42.05 kpa, P < 0.0001). Liver stiffness was also found to be higher in cirrhotic patients with varices when compared to patients without varices (38.5vs 21.2 kpa). Using both liver and spleen stiffness measurement we can predicted the presence of esophageal varices correctly. CONCLUSION: Spleen stiffness can be assessed using transient elastography, higher value correlated well with liver cirrhosis and presence of esophageal varices although it couldn’t correlate with grade of Esophageal Varix. Combined assessment of spleen and liver stiffness had better prediction of presence of Esophageal Varix.


2010 ◽  
Vol 67 (2) ◽  
pp. 166-169 ◽  
Author(s):  
Jelena Djordjevic ◽  
Petar Svorcan ◽  
Dusica Vrinic ◽  
Branka Dapcevic

Backgroud/Aim. Splenomegaly is a frequent finding in patients with liver cirrhosis and portal hypertension and may cause hypersplenism. The occurrence of thrombocytopenia in those patients can be considered as an event with multiple etiologies. Two mechanisms may act alone or synergistically with splenic sequestration. One is central which involves either myelosuppression because of hepatitis viruses or the toxic effects of alcohol abuse on the bone marrow. The second one involves the presence of antibodies against platelets. It also depends upon the stage and etiology of liver disease. The aim of the study was to investigate a correlation between the platelet count and spleen size and the risk factors for thrombocytopenia in patients with liver cirrhosis. Methods. We studied 40 patients with decompensated liver cirrhosis who were hospitalized in the Department of Gastroenterohepatology. The liver function was graded according to Child Pugh score. Spleen size was defined ultrasonografically on the basis of craniocaudal length. Suspicion of portal hypertension was present when longitudinal spleen length was more than 11 cm. Thrombocytopenia was determined by platelet count under 150 000/mL. Results. We did not find any significant correlation between hepatic dysfunction and spleen size (p = 0.9), and between hepatic dysfunction and thrombocytopenia (p = 0.17). Our study did not find any significant correlation between spleen size and peripheral platelet count (p = 0.5), but we found a significant correlation between thrombocytopenia and etiology of cirrhosis - decreased platelet count was more common among patients with cirrhosis of alcoholic etiology than in other etiologies of cirrhosis (p = 0.001). Conclusion. According to our study, liver cirrhosis, portal hypertension and thrombocytopenia could be present even in the absence of enlarged spleen suggesting the involvement of other mechanisms of decreasing platelet account.


1987 ◽  
Author(s):  
V De Angelis ◽  
M Zambon ◽  
L Toffolo ◽  
C Donada ◽  
G L Molaro ◽  
...  

Coagulation abnormalities are among the number of potential risk factors toinitiate the bleeding episodes from gastrcr-esophageal varices in liver cirrhosis. The impairment of liver clearance of activated coagulation factors, the release of thromboplastin-like activity from the necrotic liver cells and the hemodynamic changes due to expanded bollaterals may all contribute to activate the coagulation cascade.However, little is known about the mechanisms leading to this activation. Activated Factor VII (FVIIa) is known totrigger both intrinsec and extrinsec coagulation pathway. Therefore, we measured FVIIa in a group of 33 cirrhotic patients in order to see if a difference between bleeders and non-bleeders patients would correlate with Factor VII activation. The patients were divided in two groups according to the presence or the absence of major bleeding from gastroesophageal varices; haemorragic episodes were confirmed by a gastroscopic examination performed during or immediately after bleeding episodes. Factor VII coagulant assay (VII:C - one stage clotting method) and Factor VII coupled amidolytic assay (VII:CHR) were performed and a factor VII activity ratio (VIIa) was calculated as VII:C/VII:CHR. The results (mean ± S.E.) are summarized in this table:No difference in Vila distribution was seen when the patients were divided on the base of liver impairment (according to Child’s criteria) .Our study shows that FVII activation is related to bleeding from esophageal varices but not to the degree of liver impairment and strongly suggests the existence of an hypercoagulable state in liver cirrhosis, probably related to major bleeding from gastroesophageal varices in cirrhotic patients.


2020 ◽  
Vol 3 (Supplement_1) ◽  
pp. 86-88
Author(s):  
J Ghaith ◽  
P James ◽  
F Wong

Abstract Background One of the complications of portal hypertension, with or without the presence of cirrhosis, is the development of varices along the length of the gastrointestinal tract. The commonest sites are along the esophagus or in the stomach. Ectopic varices in the small and large bowels can also be observed, but ectopic varices in the pharynx are extremely uncommon. Aims To present a case series and review the literature regarding pharyngeal varcies. Methods - Results Three elderly female patients presented for esophagogastric varices surveillance gastroscopy were diagnosed with pharyngeal varices. One patient has hepatitis C cirrhosis, while the other two non-cirrhotic patients have myeloproliferative neoplasm (MPN). None of the patients had thromboses of the portal vein or its tributaries. All three patient have concomitant esophageal varices, but only one required band ligation of her esophageal varices. All patients are asymptotic except for mild dysphagia. No patient has bled from their pharyngeal varices to date. Two patients have had prophylactic treatment of their portal hypertension with non-selective beta blocker (NSBB), while the third one has not received NSBB prophylaxis because of her age. Conclusions Pharyngeal varices are extremely rare. To date, there are three case reports in the literature, however, we have been able to identify three cases in our practice. The previous two cases reported possible left-sided portal hypertension with splenic vein thrombosis, leading to the development of collateral vessels including a gastrocaval shunt, which by some contiguous route connects to the brachiocephalic vein; and a third case was a complication of neck dissection surgery. In our case series, none of our patients had splenic vein thrombosis. However, none of them has had a careful CT angiogram to delineate the portal vein tributaries and the collateral vessels, which may further help to define their pathogenesis. It is unclear whether NSBB would be effective as primary prophylaxis against their bleeding, The plan is to continue to monitor these patients to learn about the natural history of these pharyngeal varices. Funding Agencies None


2019 ◽  
Vol 2 (2) ◽  
pp. 192-196
Author(s):  
Buddhi Sagar Lamichhane ◽  
Manoj Koirala ◽  
Bishwo Raj Baral

Background: One of the major causes of morbidity and mortality in Nepal is portal hypertension due to liver cirrhosis. In rural areas where a lot of cases of cirrhosis of liver are prevalent and endoscopic expertise and facilities are not available, predicting the presence of esophageal varices through non-invasive means may reduce a large number of unnecessary endoscopies. This study is to identify the relationship of platelet count /splenic bipolar diameter ratio with the presence of esophageal varices in portal hypertension. Materials and methods: Eighty patients were included in this study between Jestha 2072 to Baisakh 2073 with the diagnosis of portal hypertension admitted in Bir hospital, Kathmandu which is a tertiary hospital of government of Nepal, which were mostly due to liver cirrhosis. The patients fulfilling the inclusion criteria underwent lab investigations, ultra sonogram and UGI endoscopy. The data were assessed for descriptive studies and means were compared using t-test. The cut off value of platelet count to spleen diameter ratio of 1150 was used to predict the presence or absence of oesophageal varices. Statistical analysis was done using SPSS 20 software Results: Platelet count to splenic diameter ratio with a cut off value of 1150 has sensitivity of 89.7%, specificity of 83.3%, positive predictive value of 96.8% and negative predictive value of 58.8% (p= 0.002, CI=95%) with 89.5 % accuracy. Conclusion: Platelet count to splenic bipolar diameter ratio can be a good predictor of presence of esophageal varices in patients with portal hypertension in the resource poor settings.


2016 ◽  
Vol 94 (7) ◽  
pp. 503-509
Author(s):  
Dmitry V. Garbuzenko

The principles of primary prevention of bleeding from esophageal varices in patients with liver cirrhosis are discussed with reference to the stage ofportal hypertension. The information was collectedfrom the PubMed database, Google Scholar retrieval system, Cochrane reviews, and lists of references from relevant publications for 1980-2015 using the key words «bleeding from esophageal varices», «prophylaxis», «portal hypertension». Inclusion criteria were confined to primary prophylaxis of bleeding from esophageal varices in patients with liver cirrhosis. The analysis showed that the drugs of choice for primary prophylaxis of bleeding from esophageal varices in patients with liver cirrhosis are non-selective beta-adrenoblockers, but their application is indicated only in case of clinicallyl significant portal hypertension in patients with large and mediumsize esophageal varices. When the use of these drugs is contraindicated, endoscopic ligation of esophageal varices can be recommended.


2016 ◽  
Vol 34 (4_suppl) ◽  
pp. 352-352
Author(s):  
Hong-Gui Qin ◽  
Jian-Hong Zhong ◽  
Yan-Yan Wang ◽  
Shi-Dong Lu ◽  
Bang-De Xiang ◽  
...  

352 Background: Hepatectomy is widely used to treat patients with hepatocellular carcinoma (HCC), even those with intermediate and advanced disease. Despite its well-demonstrated clinical efficacy in many patients, postoperative mortality is an inevitable problem. This study aims to investigate the risk factors of mortality after hepatectomy. Methods: A consecutive sample of 1518 patients with HCC who underwent initial hepatectomy from January 1, 2004 to October 31, 2013 were retrospective analyzed. Multivariate analysis to identify independent risk factors of postoperative mortality was carried out using the Cox proportional hazards model. Parameters for multivariate analyses included age, gender, tumor size, tumor number, preoperative serum albumin, alanine aminotransferase, total bilirubin, α-fetoprotein, prothrombin time, tumor capsule, macrovascular invasion, portal hypertension, diabetes mellitus, ascites, major hepatectomy, surgical time, blood loss, blood transfusion, and clamping portal hepatis time. Results: A total of 18 (1.19%) and 45 (2.96%) patients died within 30 and 90 days after hepatectomy, respectively. Multivariate analysis revealed that tumor number ( ≥ 4), macrovascular invasion, and major hepatectomy were independent risk factors of 30 and 90 days mortality, while portal hypertension was also an independent risk factor of 90 days mortality. Conclusions: Among HCC patients with tumor number equal or more than four, macrovascular invasion, portal hypertension, or underwent major hepatectomy, intensive postoperative care management are in particular.


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