Management Team

Oesophageal varices

Overview

Oesophageal varices, i.e., expanded oesophageal veins, primarily occur in response to elevated blood pressure in the portal vein that transports blood from the intestines and spleen to the liver. This elevated portal vein pressure (a condition known as portal hypertension) causes blood to be rerouted through smaller veins, including those in the oesophagus, which can become engorged and prone to rupture. Oesophageal varices are a serious medical condition because if they rupture, they can lead to severe bleeding, which can be life-threatening.

As specified above, the predominant cause of oesophageal varices is portal hypertension, and therefore, all factors that cause portal hypertension are also the factors responsible for oesophageal varices; these include:

  • Cirrhosis of the liver: In cirrhosis, the blood-filtering ability of the liver is impaired, leading to an increase in portal vein pressure.
  • Chronic liver diseases: Chronic conditions like viral hepatitis, fatty liver disease, or alcoholic liver disease can cause progressive liver damage that culminates in cirrhosis, which leads to portal hypertension.
  • Portal vein thrombosis: Blood clots formed in the portal vein obstruct normal blood flow, causing increased blood pressure in the portal venous system, ultimately leading to varices.
  • Schistosomiasis: In certain geographies, particularly parts of Africa and Asia, liver flukes are common. Upon infection (schistosomiasis), the eggs of these parasites get lodged in various tissues, especially liver, and trigger an inflammatory reaction that leads to hypertension, thereby contributing to varices.
  • Congenital abnormalities: Rarely, portal hypertension can be caused by congenital conditions such as portal vein malformations.

Initially, oesophageal varices are asymptomatic (no noticeable symptoms); however, later on, the varices begin to bleed. The observed symptoms are mostly of the complications. The symptom trends for these conditions have been described below. 

  • Uncomplicated oesophageal varices (no bleeding):
    • None or mild symptoms: In many cases, oesophageal varices are asymptomatic and are only discovered during an endoscopy or imaging study for another condition (e.g., liver disease).
    • Signs of liver disease: Patients with oesophageal varices often have signs of liver failure, like yellow skin (jaundice), excess fluid in the abdomen (ascites), and enlarged spleen (splenomegaly).
  • Bleeding oesophageal varices (most serious complication):
    • Hematemesis (vomiting blood): The most dramatic and dangerous symptom of bleeding oesophageal varices is vomiting bright red blood or coffee-ground-like material (which indicates partially digested blood).
    • Melena: Black, tarry stools, indicating the presence of digested blood from varices that have bled into the stomach.
    • Hypovolemic shock: When varices rupture and bleed heavily, the person can go into shock. Symptoms of shock include:
      1. Dizziness or fainting
      2. Pale or cold extremities
      3. Rapid heartbeat (tachycardia)
      4. Low blood pressure (hypotension)
      5. Confusion or altered mental status due to loss of blood.

Oesophageal varices are often suspected in cases of chronic liver disease or portal hypertension and confirmed through a variety of tests; these include:

  • Endoscopy (gastroscopy):
    • Esophagogastroduodenoscopy or EGD: This is the best diagnostic modality for oesophageal varices. During the procedure, a camera bound to a fine tube is endoscopically guided via the mouth to visualise the interior of the oesophagus and assess the size and severity of any varices. This modality can also detect signs of bleeding or red spots on varices, which indicate a higher risk of rupture.
  • Imaging:
    • Doppler ultrasound: This technique can assess the flow of blood through the liver and portal vein, which helps in diagnosing portal hypertension.
    • CT and MRI: These techniques can determine the severity of portal hypertension or any complications, such as a portal vein thrombosis.
    • Endoscopic ultrasound: This technique can be used to assess the varices in more detail, especially if there is bleeding risk.
    • Liver function tests: These tests help diagnose the underlying liver disease that might be causing portal hypertension and include:
      1. Liver enzyme tests (ALT, AST, ALP)
      2. Bilirubin tests
      3. Prothrombin time assessment (to assess clotting function)
      4. Albumin tests

  • Prevention of bleeding (primary prophylaxis):
    • Non-specific beta-blockers (e.g., propranolol or nadolol): These medications reduce portal hypertension and lower the risk of variceal bleeding. Further, they reduce blood flow to the oesophagus, helping prevent varices from expanding or rupturing.
    • Endoscopic variceal ligation (EVL): This technique involves stopping blood flow and preventing rupture by ligating the varices using a small rubber band. It is often employed for larger varices or high-risk patients.
    • Endoscopic sclerotherapy: In this technique, variceal shrinkage and sealing is induced by introducing a sclerosing agent into the varices. This modality is not employed very often but may be an option for some patients.
  • Acute bleeding (emergency treatment):
    • Stabilisation: The first step after bleeding is patient stabilisation via fluid resuscitation (IV fluids or blood transfusions) to manage blood loss and restore blood pressure.
    • Endoscopic treatment: Once the patient is stabilised, EVL treatment of choice for acute bleeding varices is used to stop bleeding. If EVL is not successful, endoscopic sclerotherapy or balloon tamponade (a technique in which an endoscopically guided inflatable balloon is used to tamponade (compress) the bleeding varices) may be employed.
    • Pharmacologic therapy: Vasopressin or octreotide (somatostatin analogue) may be used to reduce portal pressure and control bleeding. These medications constrict blood vessels and help stop the bleeding.
    • Transjugular intrahepatic portosystemic shunt (TIPS): It may be used for refractory cases where bleeding cannot be controlled. TIPS involves implanting a stent between the portal and hepatic veins; this creates a shunt that allows blood to flow directly from the portal vein to the hepatic vein, thereby reducing portal pressure, and by extension, varices.
    • Surgery: In severe cases where other treatments fail, surgery (such as oesophageal devascularisation or a liver transplant) may be needed.

  • Regular monitoring for varices in individuals with liver disease, especially cirrhosis can help prevent varices.
  • Lifestyle changes (e.g., refraining from smoking and drinking) and managing hepatitis can diminish the risk of liver disease progression.
  • Prompt treatment of liver disease (including medications, lifestyle changes, and, in some cases, liver transplantation) can help prevent varices.
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