Esophageal Varices – Symptoms and Treatment

Definition and Causes:

Esophageal varices are abnormal changes in the veins of the esophagus, where their openings widen, their walls ulcerate, and the vessels become twisted. This condition usually does not cause any symptoms but can be complicated by severe bleeding.

Prevalence:
About 50% of patients with liver cirrhosis suffer from esophageal varices. Bleeding from these veins poses a life-threatening risk if not promptly addressed. The incidence of bleeding from small dilated veins is approximately 4% per year, while the risk increases to about 15% with large vein dilation.

Despite advances in medicine in recent decades, bleeding from esophageal varices remains a serious problem due to the high mortality rate: the death rate ranges from about 10-20% within 6 weeks of the onset of bleeding.

Causes of Esophageal Varices:
Esophageal varices occur due to increased pressure in these vessels, often resulting from portal hypertension, which can also be caused by inferior vena cava obstruction.

Portal Hypertension: Refers to elevated blood pressure in the portal vein, which carries blood from the stomach, spleen, intestines, pancreas, and transports it to the liver. In a normal state, portal vein pressure is between 5-10 mmHg, but in portal hypertension, it rises to over 12 mmHg. This can be caused by various problems such as liver diseases like cirrhosis (the most common cause), chronic hepatitis, tumors, autoimmune diseases, and others.

Inferior Vena Cava Obstruction: Leads to variceal dilation in the upper and middle parts of the esophagus. Obstruction may result from blood clotting, severe pulmonary hypertension, thyroid gland tumor, Behçet’s disease, abnormal narrowing of esophageal muscles, mid-esophageal fibrosis, or surgical ligation of the inferior vena cava. The condition may also be related to venous shunts, for example, in patients with end-stage renal failure.

Risk Factors for Esophageal Varices Bleeding:

1. Portal Hypertension Crisis (Portal Hypertension Crisis): Increase in portal pressure to more than 44 mmHg.
2. Ulceration of the esophageal mucosa above the vessels due to reflux esophagitis.
3. Decreased blood clotting: International Normalized Ratio (INR) greater than 1.5 units, decreased platelet count.
4. Diameter of the portal vein more than 13 mm.

Symptoms of Esophageal Varices:

• Esophageal varices often do not present clear symptoms.
• Symptoms occur when damage to dilated vessels leads to bleeding.
• The first sign of bleeding is typically vomiting blood (hematemesis).

Bleeding Symptoms:

• Bleeding may cause symptoms such as nausea and vomiting blood.
• In cases of significant bleeding, symptoms like dizziness, weakness, excessive sweating, rapid heart rate, low blood pressure, and loss of consciousness may occur.
• Severe bleeding may coincide with gastric bleeding.
• Pain is typically absent during bleeding episodes.

Mechanism of Esophageal Varices in Portal Hypertension:

• Portal hypertension occurs due to liver cirrhosis.
• Cirrhosis leads to pressure on vessels in the liver and slows normal blood flow.
• Blood pressure increases in the portal vein system, pushing blood into smaller vessels.
• Blood flow direction in vessels changes, leading to the formation of collateral blood vessels.
• The left gastric vein plays a crucial role in the development of esophageal varices.
• Collateral vessels dilate and bend due to high blood pressure, increasing the risk of bleeding.

Three-Stage Classification:

First Stage:

• Mild dilation of veins above the mucous membrane surface (not exceeding 5 mm).

Second Stage:

• Dilated veins involve less than one-third of the esophagus passage distance (from 5 to 10 mm).

Third Stage:

• Dilated veins involve more than one-third of the esophagus passage distance (more than 10 mm).

Diagnosis of Esophageal Varices:
Medical History and Examination:

• In the absence of acute bleeding signs, the doctor collects the patient’s medical and life history.
• Inquiries may include liver diseases such as cirrhosis, alcohol consumption, exposure to hepatitis B, C, or D viruses, and long-term medication use.
  Examination:
• In the absence of specific signs during the examination.
• When bleeding occurs from dilated esophageal veins, the doctor may observe pallor of the skin and mucous membranes, low blood pressure, increased heart rate, and loss of consciousness.

Assessment of Bleeding:

• The doctor estimates its severity, identifies its source, and evaluates the prognosis.
• Any bleeding from the upper gastrointestinal tract in a patient with liver cirrhosis or signs of portal hypertension associated with variceal dilation should be treated as variceal bleeding until proven otherwise, aided by endoscopy examination.

Endoscopic Examination (EGD):

• This examination plays a crucial role in initial diagnosis and during treatment, occupying a central position in the treatment of active bleeding from dilated veins. Endoscopy allows detection of esophageal varices, determination of their location and size.

Confirmation of bleeding from dilated veins using endoscopic examination based on the following data:

1. Bleeding activity from the variceal node.
2. Yellowish mass covering the variceal node (called “white nipple”).
3. Blood clots covering the variceal node.
4. Variceal node and bleeding from the upper gastrointestinal tract without other clear sources of bleeding.

It is preferable to perform the examination within 12 hours of the onset of acute bleeding from dilated veins. Delaying endoscopy for more than 15 hours from the onset of bleeding increases the risk of death.

Differential Diagnosis:
Esophageal cancer, hiatal hernia, hemochromatosis, Wilson’s disease, schistosomiasis, hepatitis B and C, alcoholic cirrhosis, sarcoidosis.

Treatment of Esophageal Varices includes:

Medication:

• Use of drugs that reduce pressure in the portal vein, such as non-selective beta-blockers and others. Simvastatin has shown effectiveness in dilating hepatic blood vessels and reducing portal pressure.

Endoscopic Therapy:

• Endoscopic therapy includes sclerotherapy with endoscopic injection sclerotherapy (EIS) and endoscopic band ligation (EP). EIS involves injecting sclerosing agents directly into varices, causing damage to the lining and blood clot formation. EP is considered more effective and safer than EIS, as it involves ligating varices with a rubber band to reduce blood flow.
• Endoscopic therapy (EN) is repeated every 2-4 weeks until varices disappear or decrease to first-degree. EP is associated with a higher re-bleeding rate compared to EIS due to differences in mechanisms of action.

Transjugular Intrahepatic Portosystemic Shunt (TIPS):

• TIPS is a procedure where an artificial pathway (shunt) is created in the liver to divert blood flow from the portal vein to the hepatic vein. This reduces pressure in the portal vein and consequently reduces variceal dilation. The procedure is performed under fluoroscopic guidance.
• Studies show that the procedure is successful in 93–100% of cases, with a death rate ranging from 0–2%, and a 3–15% mortality rate within 30 days post-operation.
• The main drawback after TIPS is the risk of recurrent venous bleeding due to shunt occlusion or narrowing. To avoid this, monitoring of portal vein pressure gradient using ultrasound and Doppler is important, maintaining the pressure below 12 mm Hg. Routine monitoring tests using ultrasound and Doppler are recommended even for asymptomatic patients.

Prevention:

• To prevent recurrent bleeding, a combination of non-selective beta-blockers and endoscopic sclerotherapy (EP) is used. Non-selective beta-blockers can prevent re-bleeding even after variceal eradication using EP and can help prevent variceal recurrence. Studies have shown that the recurrence rate of bleeding in the combined treatment group is much lower than with endoscopic sclerotherapy alone. This indicates that non-selective beta-blockers are an effective secondary prevention measure, and other treatments such as TIPS should be considered only for patients who cannot tolerate non-selective beta-blockers.
• There was also an assumption that carvedilol could help prevent recurrent bleeding. However, the study showed that this drug does not surpass the effectiveness of EP, but in the group that took carvedilol, the survival rate was better, so further research is required.

Sources:

• Stiegmann G. V., Goff J. S., Sun J. H. et al. Endoscopic variceal ligation: an alternative to sclerotherapy. Gastrointest Endosc. 1989; 5: 431–434.
• Gonzalez R., Zamora J., Gomez-Camarero J. et al. Metaanalysis: Combination endoscopic and drug therapy to prevent variceal rebleeding in 34 cirrhosis. Ann Intern Med. 2008; 2: 109–122.
• De Franchis R. Revising consensus in portal hypertension: report of the Baveno V consensus workshop on methodology of diagnosis and therapy in portal hypertension. J Hepatol. 2010; 4: 762–768.
• Ansari P. Varicose veins of the esophagus. MSD Manual. 2021.
• Areia M., Romãozinho J. M., Ferreira M. et al. “Downhill” varices. A rare cause of esophageal hemorrhage. Rev Esp Enferm Dig. 2006; 5: 359–36.
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