Endoscopic Variceal Ligation
Endoscopic Variceal Ligation - Related Videos
02:14
Underwater Endoscopic Injection Sclerotherapy for Gastroesophageal Varices
0 Views •
2025
Underwater endoscopic injection sclerotherapy might be a choice for patients with gastroesophageal varices (GEVs). The decreased peristalsis of the esophagus underwater can increase the success rate of intravascular injection and stabilize the vision.
04:09
Endoscopic Injection Sclerotherapy Assisted by Cyanoacrylate and Clips for Gastroesophageal Varices
0 Views •
2025
This protocol presents the management for gastroesophageal varices (GEVs) with endoscopic injection sclerotherapy assisted by cyanoacrylate and clips (CISC), which can improve the effectiveness of sclerotherapy and reduce complications.
01:24
Esophageal Varices-I: Introduction
0 Views •
2025
Esophageal varices are dilated, tortuous veins which are found mainly in the submucosa of the lower esophagus but which may also appear higher up or extend into the stomach. They develop due to increased pressure in the portal venous system, often as a result of liver cirrhosis. This condition scars and damages the liver, impeding normal blood flow through the portal vein. To compensate, blood seeks alternative pathways, forming fragile new vessels (varices) in the esophagus and stomach. These...
07:34
DNA Ligation Reactions
0 Views •
2023
In molecular biology, ligation refers to the joining of two DNA fragments through the formation of a phosphodiester bond. An enzyme known as a ligase catalyzes the ligation reaction. In the cell, ligases repair single and double strand breaks that occur during DNA replication. In the laboratory, DNA ligase is used during molecular cloning to join DNA fragments of inserts with vectors – carrier DNA molecules that will replicate target fragments in host organisms. This video provides an...
01:28
Esophageal Varices-II: Clinical Features and Management
0 Views •
2025
Esophageal varices often manifest as gastrointestinal bleeding episodes, presenting symptoms like hematemesis (vomiting of blood), hematochezia (passing fresh blood via the rectum), and melena (black, tarry stools). Other signs can include weight loss, anorexia, abdominal discomfort, jaundice, pruritus, altered mental status, and muscle cramps. In the initial assessment, a thorough review of the patient's medical history is vital to identify risk factors such as liver disease, alcohol abuse, or...
FAQs
During EVL, each varix is drawn into the endoscopic cap by suction. An elastic band is released around its base, compressing the vessel and interrupting local blood flow. The treated tissue then undergoes thrombosis, meaning clot formation, followed by sloughing and fibrosis. This sequence helps close the varix and limit bleeding.
The band creates an immediate mechanical obstruction, while thrombosis reinforces the loss of blood flow within the treated vein. Subsequent tissue sloughing removes the damaged varix, and fibrosis produces scar tissue at the site. Together, these delayed changes help maintain vessel closure after the elastic band is no longer the only source of compression.
EVL treats the local esophageal varices, but it does not remove the portal hypertension that contributed to their development. Continued high pressure can support the formation or enlargement of varices elsewhere or at later times. For this reason, controlling the underlying liver disease and portal hypertension remains an essential part of clinical management, particularly in cirrhosis.
During endoscopy, the clinician identifies an esophageal varix and positions a banding device over it. Suction draws the vein into a cap, and the device releases an elastic band around the captured tissue. The same process can be applied to additional varices during the session, allowing treatment of multiple bleeding risks through the endoscopic approach.
Clinicians use EVL in two major settings: controlling acute variceal hemorrhage and reducing the likelihood of recurrent bleeding. Its role is especially important when esophageal varices have developed in association with portal hypertension, including that caused by cirrhosis. The immediate goal is bleeding control, while repeated treatment and broader disease management support longer-term risk reduction.
A single session may not eliminate every clinically important varix or prevent future variceal development when portal hypertension persists. Follow-up endoscopy allows clinicians to reassess the esophagus and perform additional banding when needed. Repeated sessions therefore support ongoing reduction of bleeding risk, while management of the underlying liver disease addresses the continuing clinical cause.