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Esophageal varices

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Esophageal varices
Esophageal varices

Esophageal varices are pathologically enlarged, twisted venous vessels located in the wall of the lower part of the esophagus, most commonly arising as a result of portal hypertension, which is increased pressure in the portal vein system. They are one of the most serious complications of liver cirrhosis and other diseases leading to impaired blood flow through the liver. Their presence may remain asymptomatic for a long time, but the rupture of a varix and massive bleeding into the gastrointestinal tract pose a direct threat to life. Diagnosis is based on endoscopic examination, and management includes both causal treatment of portal hypertension and prevention and therapy of bleeding.

Esophageal varices - causes

The main cause of esophageal varices is portal hypertension, which is an increase in pressure in the portal vein that carries blood from the abdominal organs to the liver. Under normal conditions, blood flows freely through the liver parenchyma. When resistance to flow increases, the body creates collateral circulation, including in the esophagus.

The most common causes of portal hypertension:

  • Liver cirrhosis (alcoholic, viral – HBV, HCV, metabolic, autoimmune),
  • Portal vein thrombosis,
  • Hepatic vein thrombosis (Budd-Chiari syndrome),
  • Massive liver fibrosis,
  • Tumors compressing the portal vein,
  • Congenital vascular disorders.

In the pathomechanism, the following occur:

  • Increased vascular resistance within the liver,
  • Increased splanchnic blood flow,
  • Formation of connections between the portal system and systemic veins (collateral circulation),
  • Dilation of esophageal submucosal veins.

The risk of developing varices increases with the advancement of liver cirrhosis (Child-Pugh classification). In patients with cirrhosis, varices are found in up to 50–70% of cases.

Esophageal varices - symptoms

Esophageal varices can remain asymptomatic for a long time. They are most often diagnosed during a planned gastroscopy performed in patients with diagnosed liver cirrhosis.

Symptoms usually appear only in the case of a complication – bleeding from the varix.

Typical symptoms of hemorrhage:

  • sudden, profuse vomiting of fresh blood (hematemesis),
  • coffee-ground vomit (partially digested blood),
  • tarry stools (melena),
  • drop in blood pressure,
  • accelerated heart rate,
  • dizziness, weakness,
  • in severe cases – hypovolemic shock.

The severity of bleeding can be very high – blood loss can be sudden and massive.

Factors increasing the risk of variceal rupture:

  • large size of varices (grade III),
  • presence of red signs on the surface of the varix (so-called red wale marks),
  • high portal pressure,
  • advanced liver failure.

The mortality rate of the first bleeding episode reaches 15–20%, and the risk of recurrence within a year is high without appropriate prophylaxis.

Varicose veins of the esophagus – can they be cured?

Esophageal varices are a consequence of hemodynamic disturbances within the portal system. This means that they are not treated in isolation from the cause, which is portal hypertension.

The possibility of a complete cure depends on:

  • the reversibility of the cause (e.g., acute thrombosis),
  • the degree of liver damage,
  • the effectiveness of the treatment of the underlying disease.

In the case of liver cirrhosis, the changes are chronic and progressive. Treatment focuses on:

  • reducing portal pressure,
  • preventing bleeding,
  • eliminating or reducing varices with endoscopic methods.

In selected cases, such as advanced cirrhosis with complications, the only radical method remains a liver transplant.

It is important to emphasize:

  • untreated varices do not regress spontaneously,
  • even after successful endoscopic therapy, they may recur,
  • regular endoscopic monitoring is necessary (every 1–3 years, depending on the degree of advancement).

Esophageal varices - treatment

Treatment of esophageal varices involves three main areas: primary prevention, treatment of acute bleeding, and secondary prevention.

1. Primary prevention (before the first bleeding)

It is used in patients diagnosed with varices who have not yet experienced a hemorrhage.

Methods:

  • Non-selective beta-blockers (e.g., propranolol, carvedilol) – they lower portal pressure,
  • Endoscopic variceal ligation (EVL).

2. Treatment of acute bleeding

A life-threatening condition requiring hospitalization.

Management includes:

  • Hemodynamic stabilization (fluids, blood transfusions),
  • Vasoconstrictor drugs (terlipressin, somatostatin),
  • Urgent endoscopy with variceal ligation,
  • In some cases – balloon tamponade,
  • Prophylactic antibiotic therapy.

In resistant situations, the following is used:

  • TIPS (transjugular intrahepatic portosystemic shunt) – creating an intrahepatic shunt to bypass portal hypertension.

3. Secondary prevention (after a bleeding episode)

  • Regular variceal ligation,
  • Continuous use of beta-blockers,
  • Monitoring liver function,
  • Treatment of the underlying disease.
Clinical Summary
Esophageal varices are a complication of chronic liver diseases and represent one of the most dangerous consequences of portal hypertension. It is crucial to:
perform early diagnostics in patients with cirrhosis,
conduct regular endoscopic monitoring,
implement effective pharmacological prophylaxis,
provide prompt treatment of bleeding.
 
From a medical perspective, this condition requires interdisciplinary care - involving a gastroenterologist, hepatologist, internist, and if necessary, a surgeon and transplant team.