View clinical trials related to Esophageal and Gastric Varices.
Filter by:Gastrointestinal bleeding is a common complication of liver cirrhosis which caused by esophageal and gastric varices. The risk of bleeding from gastric varices is relatively low. However, the bleeding is usually significant and severe. Current guidelines recommend endoscopic glue injection as the first line of treatment for gastric variceal bleeding. Although this technique has been shown to be effective, it is associated with many severe adverse events including systemic embolization, fever, chest pain, and even death. The rate of hemostasis has been reported to be as high as 91-100% but the rebleeding rate from gastric varices still present. Endoscopic ultrasound (EUS) guided therapy has recently been introduced as a more effective and safer option than endoscopic therapy for gastric varices. EUS-guided therapy includes EUS guided Cyanoacrylate injection alone or in combination with EUS-guided coiling. It offers the advantage of directly visualizing the varices and delivering targeted therapy. A standard endoscopic examination only allows the evaluation of superficial varices. The use of Endoscopic ultrasound facilitates evaluation of peri-gastric and perforating vessels, which are directly involved in variceal development. EUS also facilitates accurate placement of the coil and preserves the naturally formed splenorenal shunt. Balloon-occluded retrograde transvenous obliteration(BRTO) has been reported to achieve satisfactory bleeding control rates for isolated gastric varices with High hemostasis rates and low rebleeding rate. Despite all these promising results, there are scarce studies describing and comparing the efficacy of EUS-guided therapy and BRTO in patients with gastric varices. Further prospective comparative studies are needed.
Non-alcoholic fatty liver disease (NAFLD) is defined as accumulation of fat in the liver which is not related to either alcohol excess or other causes such viral infection, immune-mediated, or medication related which can lead to fibrosis and later-on, cirrhosis. Over the last years NAFLD related liver cirrhosis has become the commonest cause of chronic liver disease worldwide. Portal hypertension is the major complication caused by increased splanchnic blood flow which leads to development of oesophageal varices (OV). Almost all of the patients with portal hypertension can develop OV sometime in their life and one third of those will bleed, hence identifying the presence of OV is a an important aspect of diagnostic workup of these patients with portal hypertension. Upper digestive camera test/endoscopy is the only means to diagnose and grade OV but endoscopy is an invasive procedure and its cost effectiveness for screening is also questionable. These limitations and the ever-increasing workload on endoscopy units has led many researchers to identify some parameters that can non-invasively diagnose OV. Researchers have proposed use of platelet count/spleen diameter ratio, liver stiffness on Fibroscan among many non-invasive tools to predict OV in patients with portal hypertension with success. Recently criteria proposed in Baveno VI conference, (Baveno-IV Criteria) recommended that screening endoscopy can be avoided in patients with compensated advanced chronic liver disease (cACLD) with liver stiffness measurement (LSM) less than 20 kPa and a platelet count more than than 150,000/μL with an expanded Baveno-IV criteria suggesting platelet count >110 × 109 cells/L and LSM <25 kPa can spare even more endoscopies with a risk of missing varices needing treatment (VNT) being minimal.
In the Western world, liver cirrhosis is a significant issue. Acute variceal bleeding (AVB) is a considerable complication of cirrhosis associated with high mortality. Still, the combination of endoscopic variceal ligation and terlipressin-like treatment decreases the risks of rebleeding and mortality. This therapy with terlipressin usually was used for 72 hours. However, there are some studies demostrating that using terlipressin for 24 hours could control variceal bleeding with fewer side effects.
A prospective, randomized controlled study on whether re-education after discharge can reduce the rebleeding rate after endoscopic treatment of esophageal and gastric varices in patients with liver cirrhosis
The aim of this study is to compare the efficacy of 2-days versus 5-days octreotide infusion after endoscopic therapy in preventing early esophageal varices rebleed in patients with cirrhosis.
The cumulative risk of refractory ascites is in the order of 20% within five years of the development of ascites. An elevated sinusoidal pressure is essential for the development of ascites, as fluid accumulation does not develop at portal pressure gradient below 8 mm Hg, and rising corrected sinusoidal pressure correlates with decreased 24-hour urinary excretion of sodium.More recently, it has been hypothesised that bacterial translocation associated with portal hypertension in cirrhosis and related pathogen-associated, molecular pattern activated innate immune responses lead to systemic inflammation.This is associated with vasodilatation as well as release of proinflammatory cytokines, reactive oxygen and nitrogen species, contributing to organ dysfunction.This activates sympathetic nervous system stimulating reabsorption of sodium in proximal,distal tubules, loop of Henle and collecting duct as well as the renin-angiotensin-aldosterone system, leading to sodium absorption from distal tubule and collecting duct.[5]Renal sodium retention and eventual free water clearance due to non-osmoticrelease of arginine-vasopressin and its action on V2 receptor in the collectingduct underlie the fluid retention associated with oedema and ascites in cirrhosis.The lowering of portal pressure using non selective beta blocker has also been shown to reduce the development of ascites, refractory ascites and hepatorenal syndrome.Furthermore, the effect of non slective beta blocker on intestinal permeability, bacterial translocation and inflammatory response has been proposed to mitigate the risk of developing spontaneous bacterial peritonitis.
The purpose of this study was to compare the effects of partial splenic artery embolization combined with endoscopic treatment and endoscopic treatment alone on portal hypertension in cirrhosis with hyperplenism or splenomegaly in esophageal and gastric varices.
Patients with chronic liver disease (CLD) are at risk of developing clinically significant portal hypertension (CSPH). In the Baveno VI consensus a new term "compensated advanced chronic liver disease (cACLD)'' has been proposed to better reflect that the spectrum of severe fibrosis and cirrhosis is a continuum in asymptomatic patients. Liver stiffness by TE is sufficient to suspect cACLD in asymptomatic subjects with known causes of CLD. TE values <10 kPa in the absence of other known clinical signs rule out cACLD; values between 10 and 15 kPa are suggestive of cACLD but need further test for confirmation; values >15 kPa are highly suggestive of cACLD. Patients with a liver stiffness <20 kPa and with a platelet count >150,000 have a < 5 % risk of having varices requiring treatment, and can avoid screening endoscopy. SSM can also predict the presence of CSPH and varices requiring treatment. Some studies have shown superiority of splenic stiffness over liver stiffness in predicting varices requiring treatment likely attributable to the better performance of SSM compared with LSM in more severe portal hypertension because it reflects better the hemodynamic component of portal hypertension. However, there are few studies on NAFLD and most are on viral hepatitis related cACLD. Moreover, very few studies are published on splenic stiffness from Indian subcontinent. Similarly baseline HVPG is an important predictor of disease progression patients of NAFLD related cACLD, but requires invasive hepatic vein catheterization. Hence, we intend to do the study assessing diagnostic utility of splenic and liver stiffness in predicting varices needing treatment in NAFLD related cACLD and compare from other noninvasive markers and its correlation with HVPG.
To compare safety and efficacy of Endoscopic conventional technique (cyanoacrylate alone) to the EUS-guided injection technique (coil and cyanoacrylate) in the treatment of gastric varices. Methods: Patient recruitment: Patients would be recruited from the endoscopy centre prior to their scheduled endoscopic intervention. Study intervention :- Cyanoacrylate injection and EUS guided coil and glue injection The procedures would be performed by experienced endoscopists. The procedure would be performed under conscious sedation or monitored anaesthesia. The procedures would be performed by a therapeutic endoscope with the through the scope method. The endoscope would be used to reach the site of Varices. In Conventional technique treatment with cyanoacrylate the injection was performed using a 23-G sclerotherapy needle catheter (Interject®,Cook). One vial of N-butyl-2-cyanoacrylate (0.5 mL) was mixed with Lipiodol® in a 1:1 ratio, and injected intravesically as a 1 mL bolus. The injection was repeated until total hardening of the varix. In treatment with coil and cyanoacrylate once the gastric varix was identified, the total diameter of the vascular pseudotumor was measured and the puncture was made at the site of the widest varix. The puncture was performed using a 19 G needle (Expect®,Cook). The size of the coil used was selected based on the size of the widest varix in the pseudotumor; the size of the coil after release should not be greater than the caliber of the vessel. Following coil deployment, 2 mL of distilled water was injected, followed by one vial (0.5 mL) of N-butyl-2-cyanoacrylate mixed with Lipiodol in 1:1 ratio. Then, another 2 mL of distilled water was injected, and the needle was removed. COIL and GLUE: Cyanoacrylate injection remains the conventional treatment method. Since coils were first used to treat ectopic varices by Levy in 2008(6), this technique has been increasingly implemented into clinical practice. However, its higher cost has been a limiting factor in more widespread use. Depending on the ectasia of the varix the following coil was deployed: 8 mm x 20 cm, 10 mm x 20 cm, or 10 mm x 30 cm (Interlock-18 Fibered IDC Occlusion System,Cook). D.2.5 Randomization Patients were randomized into two groups: group I received standard endoscopic treatment with injection of a cyanoacrylate/Lipiodol (1:1) solution and group II received EUS-guided coiling and cyanoacrylate injection treatment A computer-based randomization list was generated with the online software Research Randomizer with 1:1 ratio (www.randomizer.org). An independent researcher not involved in this trial created the randomization list and sealed sequential opaque envelopes containing the random allocation sequence. The complete list generation occurred before the first enrollment. D.2.6 Post-procedural management After the procedure, EUS with Doppler flow evaluation was repeated to check the presence or absence of flow within the varix. The patients remained under observation in the GI endoscopy unit for at least one hour, being released if no complaint was reported. After endoscopic treatment, all patients underwent thoracic and abdomen computerized tomography (CT) scanning within one week, independent of the development of clinical symptoms.
Monitoring and Assessment: Transient Elastography will be performed in morning hours using the FibroScan apparatus (Echosens), which consists of a 5-MHz ultrasound transducer probe mounted on the axis of a vibrator. The tip of the transducer (M-or XL probe) will be covered with a drop of gel and placed perpendicularly in the intercostal space, with the patient lying in dorsal decubitus position with the right arm in the maximal abduction. Under control, in time motion and in A-mode, the operator will choose a liver portion within the right liver lobe, at least 6-cm thick and free of large vascular structures, and the gallbladder. Liver stiffness (LS) will be measured on a cylinder of hepatic tissue of 1 cm of diameter and 4 cm of length. For assessing the splenic stiffness (SS), the patient will be in supine position with left arm in maximum abduction. Ultrasonography will be used to identify and locate the spleen parenchyma, to choose the right place for SS measurement, and to measure the spleen diameter (long axis). Transducer will be placed in the left intercostal spaces, with location indicated by the ultrasound. A median value of 10 successful acquisitions, expressed in kPa, will be kept as a representative of the LS and SS measurements. The LS and SS measurement failure will be recorded when no value will be obtained after at least 10 shots. The results will be considered unreliable in the following circumstances: valid shots fewer than 10, success rate < 60%, or interquartile range / LS >30 %. Liver and splenic stiffness, LSPS score (LS measurement × spleen diameter / platelet count), Platelet count to spleen diameter ratio (PSR) will be calculated. Patient will also undergo upper g.i. endoscopy on same day. HVPG and TJLB will be done if indicated. The study will assess whether the stiffness scores correlate with presence of esophageal varices. Optimum cutoffs will be calculated for predicting the presence of esophageal varices. - Study design: A Cross-Sectional Study - Study period: 12 months - Sample size with justification: Consecutive Patients of ACLF from approval of study to 12 months. ACLF patients will be screened and eligible patients will be taken in to the study. - Intervention: Patients of ACLF will undergo upper g.i. endoscopy, liver and splenic stiffness measurement. HVPG and TJLB will be done in the patients only if clinically indicated.