Risk Factors For Variceal Bleeding Research Articles

Platelet Count/Spleen Thickness Ratio and the Risk of Variceal Bleeding in Cirrhosis With Esophagogastric Varices.

IntroductionThe platelet count/spleen thickness ratio (PC/ST ratio) is associated with the grade of esophagogastric varices (EGV) in cirrhotic patients, but little is known about its relationship with esophagogastric variceal bleeding (EGVB). The aim of this study was to investigate the association between the PC/ST ratio and the risk of EGVB within 1 year in cirrhotic patients.MethodsA total of 1,354 patients with cirrhosis who had EGV were enrolled in this cohort study. A logistic regression model was used to determine the association between the PC/ST ratio and the risk of EGVB within 1 year in patients with cirrhosis by adjusting the PC/ST ratio with all the important clinical variables and confounders.ResultsThe quartile values of the PC/ST ratio were 1.01, 1.36, and 1.98, respectively. The PC/ST ratio was an independent risk factor for variceal bleeding in cirrhotic patients with moderate or severe EGV. After adjusting for multiple variables, the relationship was still unchanged. The odds ratios of the first EGVB in these patients were 5.07-fold at non-adjustment and 3.28-fold after multivariate adjustment. The odds ratios of rebleeding in these patients from the lowest to the highest quartile were 2.34-fold at non-adjustment and 2.01-fold after multivariable adjustment. The PC/ST ratio ≤ 1.36 elevated the 1-year risk of first-time variceal bleeding or rebleeding in cirrhotic patients with moderate or severe EGV (All P < 0.05).ConclusionThe PC/ST ratio ≤ 1.36 is an independent risk factor for the onset of first bleeding or rebleeding in cirrhotic patients with moderate or severe EGV.

The Predictive Role of Variceal Band Ligation in the Development of Portal Vein Thrombosis in Cirrhotic Patients

Abstract Introduction. It is well known that portal vein thrombosis (PVT) can accelerate liver decompensation, reducing overall survival(1). In the literature, the topic whether PVT is a risk factor for variceal bleeding or it influences the effectiveness of variceal band ligation (VBL) remains of great interest The aim of this study was to assess if VBL is a potential risk factor for PVT development. An observational and retrospective study was conducted in a single tertiary center from 2010 to 2021 and included data from 285 patients with liver cirrhosis. Results. Of the 285 patients, gender distribution described 47.32% female (n =135) and 52.8% male (n =150) with a mean age of 55 years (range =23-79). The average MELD score was 12.5 (range 7-27). Of the total number of patients, 48.8% (n=139) had previous VBL: 20% (n=57) underwent primary prophylactic VBL and 34.7% (n=99) underwent secondary prophylaxis. Thus, 285 VBL procedures had been performed and the average number of VBL session was 2 (range 1-10) The mean time follow up was 92.55 months (range 22-230. During the follow up period PVT was diagnosed in 41.4% of patients (n =118) of which 67.77% (n =80) had at least one previous session of VBL: 33% of patients (n =39) had performed primary prophylaxis and 34.74% (n =41) secondary. A logistic regression was conducted to assess if VBL (primary and/or secondary prophylaxis) are risk factors for PVT development. The model was significant for primary prophylaxis (p =0.002, OR 3.28, CI 1.53-7.02) resulting that the risk of PVT is increasing around 3 times after primary prophylactic VBL. Conclusion. Our study showed a certain predisposition for cirrhotic patients to develop PVT after VBL performed as primary prophylaxis thus raising the question: does VBL impact the occurrence of PVT in cirrhotic patients? Furthermore, to our knowledge, this is the first study in the literature that focuses on this topic. More studies should be performed to evaluate and describe the relationship between VBL and the risk of PVT.

Helicobacter pylori versus platelet-to-spleen ratio as a risk factor for variceal bleeding in patients with liver-cirrhosis-related portal hypertension

Background Acute upper gastrointestinal (GIT) bleeding is a common medical emergency clinically manifested by hematemesis and/or melena. This study aimed to elucidate the roles of Helicobacter pylori and the platelet-spleen ratio as risk factors for variceal bleeding in patients with portal hypertension secondary to liver cirrhosis.Methods The study was conducted on 200 patients with liver cirrhosis of various etiologies who were divided into two groups: group 1 included 100 patients with liver cirrhosis and portal hypertension with or without a history of upper GIT bleeding, and group 2 included 100 patients with liver cirrhosis without portal hypertension. Upper GIT endoscopy was performed, and biopsy samples were taken from the gastric antral mucosa for rapid urease testing. The platelet-spleen diameter ratio was calculated for all patients.Results In group 1, most patients who had a history of variceal bleeding were H. pylori-negative whereas most patients without a history of variceal bleeding were H. pylori-positive, implying that H. pylori may play a significant role as a protective factor against variceal bleeding. The calculated odds ratio for the rapid urease test was low (0.851), whereas the calculated odds ratio for the platelet-spleen diameter ratio was higher (9.766) than that for the rapid urease test. Thus, the rapid urease test plays a significantly higher role than the platelet-spleen ratio as a risk factor for bleeding (p-value = 0.001).Conclusions H. pylori has a more significant relationship with upper GIT bleeding than the platelet-spleen diameter ratio.

Bacteremia as a risk factor for variceal upper gastrointestinal tract bleeding in cirrhotic patients: a hospital-based study

BackgroundThe presence of bacteremia as a complication of variceal bleeding in patients with liver cirrhosis had been investigated by many studies. The aim of this study was to assess the bacteremia as a risk factor for variceal upper gastrointestinal tract bleeding in cirrhotic patients. A cross-sectional study was conducted on 99 patients with chronic liver disease divided into three groups: group I included 35 patients presented with first attack of variceal bleeding, group II included 35 patients presented with recurrent attacks of variceal bleeding, and group III included 29 patients with no history of previous variceal bleeding as a control group. Routine laboratory tests were done, upper GI endoscopy, blood culture, and measurement of procalcitonin level in blood.ResultsPatients with recurrent variceal bleeding had statistically (p < 0.05) the highest percentage of positive blood culture followed by patients with first variceal bleeding and the control (60% vs 45.7% vs 24.1%) respectively. In addition to procalcitonin results, patients with recurrent variceal bleeding had statistically the highest values of PCT followed by patients with first variceal bleeding and the control (1.92 vs 0.325 vs 0.22 ng/ml) respectively. Multivariate regression analysis showed that procalcitonin and hemoglobin only was the significant predictors for variceal bleeding. Hemoglobin at cutoff value of ≤ 9.6 and procalcitonin (ng/dl) at cutoff value of > 1.76 is the most specific in predicting bleeding 86.21%, 86.21% (CI 95%) respectively.ConclusionBacteremia and procalcitonin are risk factor for variceal bleeding in cirrhotic patients. Procalcitonin can be used as easily measurable and surrogate biomarker for bacteremia and variceal bleeding.

Variceal bleeding is aggravated by portal venous invasion of hepatocellular carcinoma: a matched nested case-control study

BackgroundWe hypothesized that portal vein tumor thrombosis (PVTT) in hepatocellular carcinoma (HCC) increases portal pressure and causes esophageal varices and variceal bleedings. We examined the incidence of high-risk varices and variceal bleeding and determined the indications for variceal screening and prophylaxis.MethodsThis study included 1709 asymptomatic patients without any prior history of variceal hemorrhage or endoscopic prophylaxis who underwent upper endoscopy within 30 days before or after initial anti-HCC treatment. Of these patients, 206 had PVTT, and after 1:2 individual matching, 161 of them were matched with 309 patients without PVTT. High-risk varices were defined as large/medium varices or small varices with red-color signs and variceal bleeding. Bleeding rates from the varices were compared between matched pairs. Risk factors for variceal bleeding in the entire set of patients with PVTT were also explored.ResultsIn the matched-pair analysis, the proportion of high-risk varices at screening (23.0% vs. 13.3%; P = 0.003) and the cumulative rate of variceal bleeding (4.5% vs. 0.4% at 1 year; P = 0.009) were significantly greater in the PVTT group. Prolonged prothrombin time, lower platelet count, presence of extrahepatic metastasis, and Vp4 PVTT were independent risk factors related to high-risk varices in the total set of 206 patients with PVTT (Adjusted odds ratios [95% CIs], 1.662 [1.151–2.401]; 0.985 [0.978–0.993]; 4.240 [1.783–10.084]; and 3.345 [1.457–7.680], respectively; Ps < 0.05). During a median follow-up of 43.2 months, 10 patients with PVTT experienced variceal bleeding episodes, 9 of whom (90%) had high-risk varices. Presence of high-risk varices and sorafenib use for HCC treatment were significant predictors of variceal bleeding in the complete set of patients with PVTT (Adjusted hazard ratios [95% CIs], 26.432 [3.230–216.289]; and 5.676 [1.273–25.300], respectively; Ps < 0.05).ConclusionsPVTT in HCC appears to increase the likelihood of high-risk varices and variceal bleeding. In HCC patients with PVTT, endoscopic prevention could be considered, at least in high-risk variceal carriers taking sorafenib.

Primary prevention of bleeding from esophageal varices in patients with liver cirrhosis: An update and review of the literature.

All patients with liver cirrhosis and portal hypertension should be stratified by risk groups to individualize different therapeutic strategies to increase the effectiveness of treatment. In this regard, the development of primary prophylaxis of variceal bleeding and its management according to the severity of portal hypertension may be promising. This paper is to describe the modern principles of primary prophylaxis of esophageal variceal bleeding in patients with liver cirrhosis. The PubMed and EMbase databases, Web of Science, Google Scholar, and the Cochrane Database of Systematic Reviews were used to search for relevant publications from 1999 to 2019. The results suggested that depending on the severity of portal hypertension, patients with cirrhosis should be divided into those who need preprimary prophylaxis, which aims to prevent the formation of esophageal varices, and those who require measures that aim to prevent esophageal variceal bleeding. In subclinical portal hypertension, therapy should be etiological and pathogenetic. Cirrhosis with clinically significant portal hypertension should receive nonselective β-blockers if they have small esophageal varices and risk factors for variceal bleeding. Nonselective β-blockers are the first-line drugs for the primary prevention of bleeding from medium to large-sized esophageal varices. Endoscopic band ligation is indicated for the patients who are intolerant to nonselective β-blockers or in the case of contraindications to pharmacological therapy. In summary, the stratification of cirrhotic patients by the severity of portal hypertension and an individual approach to the choice of treatment may increase the effectiveness of therapy as well as improve survival rate of these patients.

Acute-on-chronic liver failure: A predictor of poor prognosis in patients with variceal bleeding or a risk factor for variceal bleeding?

Acute-on-chronic liver failure: A predictor of poor prognosis in patients with variceal bleeding or a risk factor for variceal bleeding?

Clinical significance of isolated gastric varices in liver cirrhotic patients: A single-referral-centre retrospective cohort study.

IntroductionGastric varices (GVs) occur in 10–30% of liver cirrhotic patients, with a mortality rate of up to 45%. Rupture of isolated GVs (IGVs) is less prevalent but often results in more severe hemorrhage and a higher risk of mortality than rupture of esophageal varices (EVs). However, there is no clear consensus yet about the optimal management for incidentally discovered IGVs.ObjectiveTo determine the clinical significance of IGVs in liver cirrhotic patients.MethodsThis was a retrospective cohort endoscopy database study within a 2‐year period (2016–2017). All study subjects were liver cirrhotic patients with OVs or GVs. The exclusion criteria were noncirrhotic portal hypertension, presence of malignancy, absence of varices, and incomplete data. Statistical analysis was performed using IBM SPSS 23.ResultsA total of 153 patients were included in this study. IGVs were found in 13 (8.49%) patients, whereas OVs were found in 112 (73.20%) patients and gastro‐OVs were found in 28 (18.30%) patients. Child‐Pugh class C (CP C) score was the strongest independent risk factor for variceal bleeding in bivariate analysis (hazard ratio [HR]: 10.21, 95% confidence interval [CI]: 4.15–25.12, P = 0.001) and multivariate analysis (HR: 12.49, 95% CI: 4.95–31.54, P 0.001); however, the presence of IGVs was not an independent risk factor. CP C score was also the only significant risk factor associated with 1‐year mortality in liver cirrhotic patients on multivariate analysis (HR: 26.77, 95% CI: 6.01–119.34, P 0.001).ConclusionThe presence of IGVs has no clinical significance in the occurrence of 1‐year rebleeding and in patient survival.

1111 Clinical Significance of Isolated Gastric Varices in Liver Cirrhosis Patients: Re-Visited the Unsolved Problem

INTRODUCTION: Gastric varices (GV) presents in 10-30% of liver cirrhosis patients with mortality rate up to 45%. Isolated gastric varices rupture is less frequent than esophageal varices (EV) rupture, but the hemorrhage is often more severe, more difficult to control, and have higher risk of recurrent bleeding and mortality. However, there are still debatable and no clear consensus yet about optimal management especially for incidentally discovered IGV. METHODS: This was a cohort retrospective endoscopy database study at Dr. Cipto Mangunkusumo National General Hospital from 2016 until 2017. All liver cirrhosis (LC) patients’ database who underwent upper GI endoscopy were included. Patients without the presence of varices, patients with malignancy or uncomplete database were excluded. Patients’ characteristic including MELD score, and Child Pugh score were collected for data analysis. Data analysis was performed using IBM SPSS version 23 for Windows. RESULTS: Of 328 patients, there were 153 patients that can be included in this study with the mean age 51 years old. The most prevalent etiology of liver disease is hepatitis B virus. Child Pugh (CP) A was found in 74 (48.36%) patients, CP B was found in 53 (34.64%) patients, and CP C was found in 26 (16.99%) patients. Isolated GV (IGV) was found in 13 (8.49%) patients, meanwhile esophageal varices (EV) found in 112 (73.20%) patients, and both (Gastroesophageal Varices/GOV) in 28 (18.30%) patients. CP C, GV and EV were found to be independent risk factors for variceal bleeding. CP C is still the strongest independent risk factor for variceal bleeding occurrence in bivariate (HR: 10.21, 95% CI:4.15-25.12 P .001) as well as in multivariate analysis (HR: 12.49, 95% CI: 4.95-31.54 0 0.001), whereas the presence of GOV is an independent risk factor associated with bleeding incidence in bivariate analysis (HR: 2.51, 95% CI: 1.26-4.99 P .009) as well as in multivariate analysis (HR: 2.95, 95% CI: 1.40-6.19 P .004) but not IGV. However, CP C score is still the only significant risk factor associated with survival liver cirrhosis patients based on multivariate analysis (HR: 26.77 95% CI: 6.01-119.34 P .001). CONCLUSION: The concern of high potential of bleeding occurrence in the presence of IGV sometimes give a clinical dilemma regarding the potential risk and side effect of endoscopic therapy for IGV. Our study results showed that the presence of IGV is not the strongest risk factor for bleeding occurrence as well as patient's survival.

The incidence and predictors of post transarterial chemoembolization variceal bleeding in hepatocellular carcinoma patients

Transarterial chemoembolization (TACE) is the standard of care for intermediate stage hepatocellular carcinoma (HCC) patients. Variceal bleeding is a life-threatening complication and may alter the initial treatment plan. This study was aimed to elucidate the risk factors for variceal bleeding in HCC patients receiving TACE treatment. From 2005 to 2016, a total of 1233 treatment-naive HCC patients receiving first time TACE treatment in Chang Gung Memorial Hospital, Linkou medical center were recruited. Pre-TACE status including baseline characteristics, prior history of ascites, and parameters for liver function evaluation were analyzed. All the variables were compared between patients with and without variceal bleeding. Among the 1233 patients, the median age was 63.7 (range 25.8-91.5) years old, and 73.5% were male. Variceal bleeding events were documented in 19 patients (1.5%) within 3 months post TACE treatment. Patients with younger age, cirrhosis, pre-treatment ascites and advanced fibrosis status (higher MELD score, CTP score, ALBI grade, FIB-4 and APRI score) were more likely to encounter post-treatment variceal bleeding. Multivariate Cox regression analysis revealed existence of ascites (adjusted HR: 4.859 (1.947-12.124), p=0.001), and higher FIB-4 score (adjusted HR: 4.481 (1.796-11.179), p=0.001) were the independent predictive factors for variceal bleeding. Patients with post-TACE variceal bleeding are more likely to encounter tumor progression (42.1% vs. 20.3%, p=0.039) and mortality owing to GI bleeding (15.8% vs. 3%, p=0.032). The incidence of post-TACE variceal bleeding was 1.5%. Patients with post-TACE variceal bleeding have poorer TACE treatment response. The pre-treatment ascites and FIB-4 score are the independent predictors for post-TACE variceal bleeding.

Left-sided Portal Hypertension After Pancreaticoduodenectomy With Resection of the Portal Vein/Superior Mesenteric Vein Confluence in Patients With Pancreatic Cancer: A Project Study by the Japanese Society of Hepato-Biliary-Pancreatic Surgery.

The aim of this study was to evaluate how often left-sided portal hypertension (LPH) develops and how LPH affects the long-term outcomes of patients with pancreatic cancer treated with pancreaticoduodenectomy (PD) and resection of the portal vein (PV)/superior mesenteric vein (SMV) confluence. Little is known about LPH after PD with resection of the PV/SMV confluence. Overall, 536 patients who underwent PD with PV/SMV resection were enrolled. Among them, we mainly compared the SVp group [n=285; the splenic vein (SV) was preserved] and the SVr group (n = 227; the SV was divided and not reconstructed). The incidence of variceal formation in the SVr group increased until 3 years after PD compared with that in the SVp group (38.7% vs 8.3%, P < 0.001). Variceal bleeding occurred in the SVr group (n = 9: 4.0%) but not in the SVp group (P < 0.001). In the multivariate analysis, the risk factors for variceal formation were liver disease, N factor, conventional PD, middle colic artery resection, and SV division. The only risk factor for variceal bleeding was SV division. The platelet count ratio at 6 months after PD was significantly lower in the SVr group than in the SVp group (0.97 vs 0.82, P < 0.001), and the spleen-volume ratios at 6 and 12 months were significantly higher in the SVr group than in the SVp group (1.38 vs 1.00 and 1.54 vs 1.09; P < 0.001 and P < 0.001, respectively). PD with SV division causes variceal formation, bleeding, and thrombocytopenia.

Primary Prophylaxis for Variceal Bleeding and the Improved Survival of Patients with Newly Diagnosed Hepatocellular Carcinoma.

We evaluated the impact of primary variceal bleeding prophylaxis on long-term outcomes of patients newly diagnosed with hepatocellular carcinoma (HCC). A retrospective cohort of 898 patients newly diagnosed with HCC without a history of variceal bleeding [age 57.4±10.4, males 718 (80.0%)] were analyzed for new onset variceal bleeding during follow-up. Variceal bleeding occurred in 72 patients (8.0%) during follow-up. The presence of portal vein thrombosis [hazard ratio (HR) 3.90; 95% confidence interval (CI) 2.09-7.30; p<0.001] and the presence of the red color sign or ≥grade 2 varices at index endoscopy (HR 7.64; 95% CI 4.56-12.80; p<0.001) were independent risk factors for variceal bleeding. The occurrence of variceal bleeding was an independent risk factor for mortality (HR 1.39; 95% CI 1.06-1.82; p=0.015). The cumulative incidence rate of variceal bleeding at 1year was 2.1, 15.3, and 34.2% for those non-indicated for primary prophylaxis (n=760), indicated for primary prophylaxis and received prophylaxis (n=98), and indicated for primary prophylaxis but did not received prophylaxis (n=40) (p<0.001). Primary prophylaxis for variceal bleeding for indicated patients was associated with a reduced risk of mortality in all patients (HR 0.54; 95% CI 0.33-0.88; p=0.014) and in propensity-matched patients (HR, 0.54; 95% CI 0.31-0.95; p=0.033). Variceal bleeding was independent risk factor for survival of newly diagnosed HCC patients. Screening and providing primary prophylaxis for indicated patients should be considered for patients with HCC.

Esophageal variceal pressure is a major predictor of variceal bleeding in cirrhotic patients

Objective To prospectively study the main risk factors of variceal bleeding in cirrhotic patients. Methods Fifty-seven patients with liver cirrhosis and esophageal varices who had never experienced variceal bleeding were followed up for 12 months. The patients underwent measurements of esophageal variceal pressure by non-invasive endoscopic balloon technique. The endpoint of the study was the presence of a variceal hemorrhage. The relationship between variceal hemorrhage and endoscopic findings including varices, variceal pressure, Child-Pugh status, ascites, and etiology of cirrhosis was studied. Results Thirty-four patients (59.6% ) developed a variceal hemorrhage. In univariate analysis, the level of variceal pressure (P= 0. 001), the size of varices (P=0. 006), and the endoscopic red color sign on the variceal wall (P=0. 012) predicted higher risks of variceal hemorrhage. The multiple logistic regression revealed that variceal pressure was a major predictor of the risk for a first variceal bleeding (OR=2. 817, P=0. 003). The area under the receiver operating characteristic (ROC) of variceal pressure for predicting variceal bleeding was 0. 98, and the variceal pressure cutoff value was 25.3 mm Hg (1 mm Hg=0. 133 kPa) with both specificity and sensitivity of 91 %. Conclusion The level of variceal pressure is a major predictor for variceal bleeding in cirrhotic patients. Key words: Esophageal and gastric varices; Liver cirrhosis; Portal pressure

Variceal Hemorrhage.

Reducing morbidity and mortality from esophageal varices remains a challenge for physicians managing patients with chronic liver disease. For patients who have never bled from varices, prophylactic therapy with nonselective beta-blockers reduces the risk of initial variceal bleeding and bleeding-related death. Thus, patients with newly diagnosed cirrhosis should be considered for endoscopic variceal screening. All patients with Child's class B and C cirrhosis should be offered endoscopic screening, whereas those with Child's class A with evidence of portal hypertension (eg, platelet count less than 140,000 per milliliter, portal vein diameter larger than 13 mm, evidence of splenic varices on ultrasound) should be screened. The principal risk factors for variceal bleeding are variceal size, the presence of color changes on the variceal wall (indicative of decreased wall thickness), and degree of liver dysfunction. Patients with moderate or large sized varices and those with varices exhibiting color changes (eg, red wale marks, cherry red spots) should be treated with beta-blockers. Individuals without varices and those with small varices should undergo repeat endoscopy at approximately 2-year intervals. Patients unwilling or unable to take beta-blockers do not need to be screened. For patients with acute variceal bleeding, the combination of pharmacologic therapy plus endoscopic therapy is superior to either therapy alone. Octreotide is the drug most often used as initial therapy in the United States. Terlipressin is the preferred agent; however, it is not available in the United States. Endoscopy is performed as early as possible, and endoscopic injection sclerotherapy or endoscopic variceal band ligation is employed if variceal bleeding is confirmed or suspected. Endoscopic therapy should be repeated until the varices are obliterated completely. The addition of beta-blockers to endoscopic sclerotherapy or ligation may decrease the rate of rebleeding compared with receiving endoscopic treatment alone. Patients with bleeding refractory to combined medical plus endoscopic therapy should be considered for transjugular intrahepatic portosystemic shunts or shunt surgery.

Patients with ascites have higher variceal pressure and wall tension than patients without ascites

OBJECTIVE: It has been suggested that ascites is a risk factor for variceal bleeding. Recently, it has been demonstrated that total paracentesis decreases variceal pressure. However, no data are available showing the basal variceal pressure in patients with and without ascites. METHODS: We studied 76 cirrhotic patients, 49 with and 27 without ascites. Variceal pressure was measured by direct puncture. Variceal size, variceal pressure gradient, and variceal wall tension were also obtained. RESULTS: No demographic differences were observed between the groups. Child score was higher (9.7 ± 1.5 vs 7.8 ± 2.1, p < 0.001) and serum albumin lower (2.6 ± 0.6 vs 3.0 ± 0.7 mg %, p < 0.02) in ascitic than in nonascitic patients, respectively. Variceal pressure and variceal pressure gradient were significantly higher in patients with ascites than in those without ascites (25.0 ± 6 vs 20.4 ± 4.6 mm Hg, p < 0.001 and 18.75 ± 4.7 vs 13.70 ± 4.1 mm Hg, p < 0.0001, respectively). The variceal wall tension was significantly higher in patients with ascites (71.0 ± 25.1 mm Hg/mm) than in those without ascites (55.1 ± 22.1 mm Hg/mm, p < 0.03). No relationship was observed between variceal pressure gradient and liver function. Ascites patients included in Child-Pugh grade A+B presented a similar variceal pressure to Child C patients (18.5 ± 4.2 vs 19.3 ± 5.7 mm Hg, respectively, p = ns). In addition, no relationship was observed between variceal pressure gradient and etiology of cirrhosis. CONCLUSION: Our results demonstrate that patients with ascites have significantly higher variceal pressure and wall tension than patients without ascites. These results suggest that patients with ascites may be at risk for variceal bleeding.

Direct measurement of post-prandial portal haemodynamics in cirrhotic patients with a transjugular intrahepatic portosystemic stent-shunt.

Portal haemodynamics vary in response to eating and other stimuli, but any increase in portal venous pressure (PVP) in cirrhotic patients may be a risk factor for variceal bleeding. We directly assessed post-prandial splanchnic haemodynamics in cirrhotic patients with a transjugular intrahepatic portosystemic stent-shunt (TIPSS) in situ. A thermodilution catheter was inserted via the patent TIPSS into the portal vein in 12 cirrhotic patients. PVP,portal venous flow (PVF) (thermodilution method), portal vascular resistance (PVR), porto-atrial pressure gradient (PPG), heart rate, mean arterial pressure (MAP) and right atrial pressure (RAP) were measured. A 505 kcal meal was given and all haemodynamic measurements were repeated at 15 min intervals for 60 min. Following the meal, there was a significant rise in PVP from 11.2 +/- 1.5 to 14.0 +/- 1.9 mmHg at 15 min, and 14.0 +/- 1.8 mmHg at 30 min (P < 0.001); in PPG from 9.5 +/- 1.4 to 12.7 +/- 2.2 mmHg at 15 min and 12.7 +/- 2.1 mmHg at 30 min (P < 0.005); and in PVF from 1110.2 +/- 141.1 to 1543.2 +/- 227.6 ml/min at 30 min (P < 0.01). PVR feil from 0.08 +/- 0.01 to 0.05 +/- 0.01 RU at 30 min (P < 0.05). Heart rate increased from 77 +/- 4.1 to 80.5 +/- 5.4 bpm at 15 min (p < 0.05), but MAP and RAP remained unchanged. In cirrhotic patients with TIPSS, significant changes in portal haemodynamics occur at 15-30 min following a meal, with minimal effect on systemic haemodynamics. This model offers a new technique to directly assess the causes for and possible treatments of post-prandial splanchnic hyperaemia in cirrhosis.

Total Volume Paracentesis Decreases Variceal Pressure, Size, and Variceal Wall Tension in Cirrhotic Patients

It has been suggested that ascites is a risk factor for variceal bleeding in cirrhotic patients. However, no data of total volume paracentesis (TVP) effects on variceal hemodynamics has yet been published. The aim of this study was to investigate the effects of TVP on variceal pressure, size, and tension in cirrhotic patients. Before sclerotherapy, 18 cirrhotic patients with grade II esophageal varices were studied. The following measurements were performed on 12 patients at basal condition and after TVP: inferior vena cava pressure, esophageal pressure (EP), and intravariceal pressure (IVP) by direct punction and variceal size at endoscopy. The same measurements were performed at basal condition and 1 hour later without TVP on the other 6 patients used as a control group. Variceal pressure gradient (VPG) and variceal wall tension (WT) were calculated. Paracentesis and intra– abdominal pressure were obtained with a direct punction. No demographic differences were observed between both groups. Paracentesis produced a significant reduction of IVP (from 25.6 ± 2.4 to 17.9 ± 2.1 mm Hg, means ± SEM, –30%, P &lt; .05), VPG (from 16.6 ± 2.4 to 10.8 ± 1.4 mm Hg, –35%, P &lt; .05). TVP also reduced variceal size (from 9 ± 0.3 to 5.6 + 0.4 mm, –38%, P &lt; .05) and WT (from 75.3 ± 11.6 to 30 ± 4.7 mm Hg. mm, –60%, P &lt; .05). Intra–abdominal pressure decreased from 18 ± 2.2 to 4 ± 0.9 mm Hg ( P &lt; .05), and IVC decreased from 15.5 ± 2.4 to 5.7 ± 1.5 mm Hg ( P &lt; .05). No significant differences were observed in mean arterial pressure and heart rate. The mean ascitic fluid removed was 8 ± 0.71 L. No significant difference between measurements was observed in the control group. Our results show that TVP significantly decreases variceal pressure and tension. These results suggest that ascites removal can be useful in the treatment of variceal bleeding in cirrhotic patients.

Total volume paracentesis decreases variceal pressure, size, and variceal wall tension in cirrhotic patients

It has been suggested that ascites is a risk factor for variceal bleeding in cirrhotic patients. However, no data of total volume paracentesis (TVP) effects on variceal hemodynamics has yet been published. The aim of this study was to investigate the effects of TVP on variceal pressure, size, and tension in cirrhotic patients. Before sclerotherapy, 18 cirrhotic patients with grade II esophageal varices were studied. The following measurements were performed on 12 patients at basal condition and after TVP: inferior vena cava pressure, esophageal pressure (EP), and intravariceal pressure (IVP) by direct punction and variceal size at endoscopy. The same measurements were performed at basal condition and 1 hour later without TVP on the other 6 patients used as a control group. Variceal pressure gradient (VPG) and variceal wall tension (WT) were calculated. Paracentesis and intra- abdominal pressure were obtained with a direct punction. No demographic differences were observed between both groups. Paracentesis produced a significant reduction of IVP (from 25.6 +/- 2.4 to 17.9 +/- 2.1 mm Hg, means +/- SEM, -30%, P < .05), VPG (from 16.6 +/- 2.4 to 10.8 +/- 1.4 mm Hg, -35%, P < .05). TVP also reduced variceal size (from 9 +/- 0.3 to 5.6 + 0.4 mm, -38%, P < .05) and WT (from 75.3 +/- 11.6 to 30 +/- 4.7 mm Hg. mm, -60%, P < .05). Intra-abdominal pressure decreased from 18 +/- 2.2 to 4 +/- 0.9 mm Hg (P < .05), and IVC decreased from 15.5 +/- 2.4 to 5.7 +/- 1.5 mm Hg (P < .05). No significant differences were observed in mean arterial pressure and heart rate. The mean ascitic fluid removed was 8 +/- 0.71 L. No significant difference between measurements was observed in the control group. Our results show that TVP significantly decreases variceal pressure and tension. These results suggest that ascites removal can be useful in the treatment of variceal bleeding in cirrhotic patients.(Hepatology 1997 Jan;25(1):59-62)