Esophageal varices: symptoms and treatment

Esophageal varices are not just a "vein problem," but a serious complication that most often occurs against the background of liver cirrhosis or portal hypertension.

Classification of the disease according to ICD-10

In the International Classification of Diseases, 10th Revision (ICD-10), esophageal varices are coded as I85.0 — "Esophageal varices without bleeding" and I85.1 — "Esophageal varices with bleeding." These codes belong to the section "Diseases of the circulatory system," subsection "Varicose diseases of veins." It is important to understand: ICD-10 does not consider esophageal varices as an independent disease, but always associates it with the underlying pathological process — more often with portal hypertension (code K76.6). Therefore, when filling out medical documentation, the doctor must indicate both the primary cause (for example, liver cirrhosis — K74.6), and the secondary complication — esophageal varices.
This has practical significance: if the medical history only states "esophageal varices," but does not indicate that it is due to portal hypertension, the insurance company may refuse to pay for treatment. And during hospitalization, the code for the primary disease determines the type of department and therapy protocol. There is also a separate code for gastric varices in ICD-10 (I85.2), which often coexists with esophageal varices — the so-called "gastroesophageal varices," and its presence sharply increases the risk of recurrent bleeding after endoscopic treatment.

History of the disease and interesting historical facts

The first description of esophageal varices dates back to the works of the ancient Greek physician Galen (2nd century AD), who noted "nodular vessels in the throat area" in patients with ascites and jaundice. However, the true nature of the pathology remained a mystery until the 19th century. In 1840, French pathologist Jean Lécaine first established a link between splenomegaly, ascites, and dilated esophageal veins — he called it "portal hypertension," although the mechanism was unclear.
A real breakthrough occurred in the 1930s when American surgeon Ralph Blalock developed a method for measuring pressure in the portal vein through the spleno-renal anastomosis. This allowed for a quantitative assessment of the degree of portal hypertension and explained why the esophageal veins dilate: the pressure in the portal system exceeds 10 mm Hg, and blood seeks "detours" — through the esophageal veins, which connect to the inferior vena cava system. An interesting fact: in the USSR in the 1950s, at the clinic of Academician N.N. Petrov (St. Petersburg), the world's first specialized service for the prevention of bleeding from varicose veins was established — they were the first to apply ligation of veins through an endoscope, even before the advent of modern sclerosing agents.
Another curious point: in military medicine during the Great Patriotic War, doctors noticed that soldiers with chronic liver diseases (often due to hepatitis A or toxic exposure) experienced a sharp increase in the frequency of esophageal bleeding under conditions of stress and malnutrition. This became one of the triggers for studying the role of environmental factors in the progression of portal hypertension.

Epidemiology (statistics of disease occurrence)

According to the World Health Organization (WHO, 2024), the global prevalence of liver cirrhosis is about 0.27% of the population, and among individuals over 50 years old — up to 1.2%. At the same time, esophageal varices are found in 30–60% of these patients depending on the stage of the disease. In Russia, the situation is more complicated: according to statistics from the Ministry of Health of the Russian Federation (2025), about 120,000 new cases of liver cirrhosis are registered annually, and almost 70,000 of them are diagnosed with esophageal varices. The dynamics among young people is particularly alarming: over the past 5 years, the number of patients aged 30–40 with this complication has increased by 28% — the main reason is the rise in alcohol consumption and the spread of viral hepatitis C (although its prevalence is decreasing thanks to new antiviral drugs).
As for mortality: without preventive treatment, the first episode of bleeding from esophageal varices ends in death in 20–30% of cases. Even with timely hospitalization and modern therapy, mortality during the acute period remains at 10–15%. However, if a patient undergoes preventive endoscopic ligation, the risk of recurrent bleeding decreases to 15–20% within a year. The table below contains summary data on epidemiology:

Note: the majority of patients learn about esophageal varices only after the first bleeding — that is, already at the stage of complications. This indicates that screening in at-risk groups (for example, in chronic hepatitis or ascites) should be mandatory, not optional.

Genetic predisposition to this disease

There is no direct "gene for esophageal varices" — it is a secondary complication, so genetics plays an indirect but important role here. The most studied genes affect the development of the underlying disease — liver cirrhosis or portal hypertension. For example, a mutation in the gene HFE (on chromosome 6) leads to hereditary hemochromatosis — an excess of iron in the liver, which in 70 % of cases ends with cirrhosis and, consequently, esophageal varices. Another example is a mutation in the gene ATP7B, responsible for Wilson's disease: in it, copper accumulates in the liver, causing inflammation and fibrosis.
There is also data on the polymorphism of the gene PNPLA3 (patatin-like phospholipase 3): carriers of the variant rs738409 (G-allele) have a 3 times higher risk of developing fatty hepatitis and cirrhosis at the same level of alcohol or obesity. A study published in "Genetics" (2023) showed that such patients develop esophageal varices 2–3 years earlier than those without this mutation.
Important: genetic testing is not routine when esophageal varices are suspected, but if the patient has a family history of hemochromatosis, Wilson's disease, or early cirrhosis, molecular screening should be considered. This is especially relevant for young people without obvious causes of liver damage (for example, without alcoholism or viral hepatitis). In such cases, genetic analysis helps to diagnose earlier than irreversible fibrous transformation develops.

Risk factors for the development of this disease

Risk factors can be divided into two groups: those that provoke the underlying disease (portal hypertension) and those that accelerate the formation and progression of esophageal varices. The first group includes:

• Chronic viral hepatitis B and C — the main cause of cirrhosis in the world; in Russia, hepatitis C remains the leader (up to 45% of cirrhosis cases);
• Alcohol addiction — daily consumption of more than 60 g of pure ethanol (≈ 150 ml of vodka) for 10 years leads to cirrhosis in 10–20% of men;
• Non-alcoholic fatty liver disease (NAFLD) — especially when combined with obesity and type 2 diabetes;
• Autoimmune hepatitis and primary biliary cholangitis — rare but severe forms, rapidly progressing to cirrhosis.

The second group includes factors that increase pressure in the portal vein or damage the vein wall:

• Increased intra-abdominal pressure — in ascites, obesity, pregnancy, or chronic cough (for example, in bronchial asthma);
• Sharp increase in blood pressure — hypertensive crisis can provoke a vein rupture;
• Intake of NSAIDs (ibuprofen, diclofenac) — they reduce the protection of the esophageal mucosa and increase the risk of erosions;
• Consumption of coarse, spicy, or hot food — mechanical damage to the vein wall;
• Smoking — nicotine causes vasospasm and enhances the fibrous reaction in the liver.

Special attention to combined factors. For example, a patient with cirrhosis who smokes and takes ibuprofen for headaches has a 5 times higher risk of bleeding than the same patient without these habits. That is why in our clinic we always conduct a "risk analysis" before prescribing any medication — even a harmless analgesic.

Diagnosis of this disease

Diagnosis begins not with instruments, but with history. If a patient has cirrhosis, ascites, an enlarged spleen, or "spider veins" on the skin — there are already grounds to suspect esophageal varices. But the key method — esophagogastroduodenoscopy (EGDS). This is not just a "stomach examination," but a detailed study assessing the size, location, and condition of the veins. The doctor uses the classification by Paquet (or the more modern one by the Japanese Research Society for Portal Hypertension), where varices are assessed by three parameters: diameter (small — up to 5 mm, medium — 5–10 mm, large — >10 mm), color (blue — less dangerous, red — high risk of bleeding) and the presence of "red spots" or "spiders" — signs of increased fragility.
Laboratory tests do not directly reveal varices, but help assess liver function and the degree of portal hypertension:

• Platelets — in portal hypertension they are reduced (< 100×10⁹/l);
• Albumin and PTI — reflect the synthetic function of the liver;
• Ultrasound with Doppler — allows measuring the blood flow velocity in the portal vein and identifying collaterals;
• CT or MRI of the abdominal cavity — if necessary, to assess the volume of veins and exclude tumor causes of portal hypertension.

Differential diagnosis is important: not every bleeding from the upper gastrointestinal tract is varicose. It is necessary to distinguish from:

• Erosive gastritis or duodenal ulcer;
• Esophageal cancer (especially in the case of solitary nodular varices);
• Telangiectasias (small vascular stars) in Osler–Weber–Rendu syndrome;
• Rupture of the cardiac section during vomiting (Mallory–Weiss syndrome).

If EGD is unavailable (for example, in an emergency situation), the clinic is guided by: vomiting "coffee grounds," melena, rapid drop in hemoglobin — all these are "red flags" for immediate transfer to a hospital.

Treatment

Treatment of esophageal varices is not the elimination of the veins themselves, but control over the cause (portal hypertension) and prevention of bleeding. The approach depends on the stage: preventive, emergency, or secondary (after bleeding).
Preventive treatment is applied to patients with large varices (diameter >5 mm) or the presence of "red spots." The main method — endoscopic ligation: through the gastroscope, the doctor places rubber bands at the base of the vein, compressing it. The procedure takes 10–15 minutes, without anesthesia (can be done under sedation), and is repeated every 2–4 weeks until the veins completely disappear. Effectiveness — 85–91% within a year.
If ligation is impossible (for example, with severe esophageal deformation), sclerotherapy is used — the introduction of a solution of ethyl alcohol or polidocanol into the vein, which causes the walls to stick together. The downside of the method is a higher risk of ulceration and rebleeding compared to ligation.
Emergency treatment of bleeding — this is the "fight for time". The algorithm is as follows:

1. Stabilization: introduction of a catheter into the central vein, blood transfusion, correction of coagulopathy;
2. Medication therapy: terlipressin (0.5–2 mg/hour IV) or somatostatin (250 mcg bolus + 250 mcg/hour) — they reduce pressure in the portal vein by 30–40 %;
3. Endoscopic intervention within 12 hours: ligation or sclerotherapy (in case of active bleeding — more often ligation);
4. If endoscopy is ineffective — temporary use of a Blakemore balloon tube (pressure on the veins through an inflatable balloon), but this is just a "bridge" to surgery.

Surgical treatment** is rarely used, but necessary in cases of recurrent bleeding or ineffectiveness of endoscopy. Options:

Esophageal varices are a disease of adults, but their manifestation strongly depends on age and the cause of the underlying process.
In young patients (under 40 years old) varices are more often associated with hereditary diseases (hemochromatosis, Wilson's disease), autoimmune hepatitis, or toxic damage (for example, from taking methotrexate or high doses of paracetamol). Here it is important: veins can dilate faster because the liver is still "compensating," and portal pressure rises rapidly. Bleeding in young people is often more massive — their vessels are more elastic, and rupture occurs suddenly.
In In patients aged 40–60 years, viral hepatitis and alcoholic cirrhosis prevail. At this age, varicose veins are more often detected against the background of already pronounced ascites and thrombocytopenia. Here it is important: they often ignore symptoms, considering them as "fatigue" or "nerves," and come to the clinic already with melena.
In elderly (over 65 years) Varicose veins are often associated with coronary artery disease, hypertension, and COPD. This complicates treatment: β-blockers can exacerbate bronchospasm, and terlipressin can cause a heart attack. Additionally, the elderly have a higher risk of "silent" bleeding — without vomiting, but with a rapid drop in hemoglobin and confusion. Therefore, in this group, we recommend more frequent monitoring — EGD every 4–6 months.
An interesting nuance: in menopausal women, the risk of varicose progression is higher due to decreased estrogen levels, which have a protective effect on the endothelial cells of blood vessels. Therefore, when planning hormone therapy for patients with cirrhosis, this factor should be taken into account.

Questions and Answers

Question 1: Can esophageal varices be treated without surgery?
Yes, in most cases — without surgery. Endoscopic ligation and drug therapy (β-blockers) allow for the condition to be controlled in 80–90% of patients. Complete "cure" is only possible with liver transplantation — but this is a last resort. The main thing is to prevent bleeding. If varices are detected at an early stage and all recommendations are followed (regular EGDs, taking medications, abstaining from alcohol), the patient can live 10 or more years without complications.
Question 2: Why is aspirin not allowed for esophageal varices?
Aspirin is acetylsalicylic acid, which suppresses platelet aggregation. In a patient with portal hypertension, the platelet level is already low (due to splenic "sequestration"), and adding aspirin sharply increases the risk of bleeding — not only from the esophagus but also from the stomach or intestines. Even one tablet can become a trigger. Instead of aspirin, paracetamol (at a dose of no more than 2 g/day) is used for pain, but only after consulting a doctor.
Question 3: What foods are prohibited for esophageal varices?
It is not the foods themselves that are prohibited, but the ways they are consumed:

• Coarse fiber (raw carrots, cabbage, nuts) — can scratch the wall of the vein;
• Spicy, sour, very hot dishes — irritate the mucosa;
• Alcohol in any form — even beer increases pressure in the portal vein;
• Strong coffee and energy drinks — cause vasospasm and increase blood pressure.

Fractional nutrition is recommended (5–6 times a day), soft food (purees, cereals, boiled meat), dish temperature — no higher than 40 °C.
Question 4: Can esophageal varices disappear on their own?
No. Veins do not "narrow" on their own. The only case is if the cause of portal hypertension is completely eliminated (for example, curing viral hepatitis C and achieving regression of fibrosis). But even then, the veins remain a "memory" — they can expand again upon relapse. Therefore, even after normalizing liver indicators, the patient must be monitored for at least 2 years.

Typical mistakes and how to avoid them

Mistake #1: "I don't feel anything — so everything is fine."
Esophageal varices do not give symptoms until the moment of bleeding. Patients with cirrhosis should undergo esophagogastroduodenoscopy at least once a year — even if there are no complaints. Example: a 52-year-old man, drank "on weekends," did not treat hepatitis C, refused esophagogastroduodenoscopy "because he feels good." After 8 months — vomiting blood, resuscitation, death. This can be avoided: create a schedule for examinations and attach it to the refrigerator.
Mistake #2: Self-administration of NSAIDs for joint pain.
Ibuprofen, diclofenac, nimesulide — all of them irritate the mucosa and reduce coagulability. Instead, use paracetamol (if there is no liver failure) or local gels (for example, finalgon). Be sure to consult a gastroenterologist before taking any medication.
Mistake #3: Refusal of β-blockers due to "low blood pressure."
Patients often say: "My blood pressure is 100/60, why do I need propranolol?". But here, systemic blood pressure is not important, but the pressure in the portal vein. β-blockers specifically lower it, and the dose is adjusted so that the heart rate does not drop below 55 beats per minute. If you feel weakness — do not stop the medication, but consult a doctor for dose adjustment.
Mistake #4: Ignoring diet and eating regimen.
Even after successful ligation, the veins remain fragile. One serving of hot peppers or a piece of hard bread can lead to rupture. Keep a diary — write down everything you eat and note when you experienced discomfort or heartburn. This will help identify triggers.

Conclusion

Esophageal varices are not a sentence, but a signal: your liver is working at its limit, and the body is looking for alternative pathways. The main thing is not to wait for bleeding, but to act in advance. If you have cirrhosis, ascites, or chronic hepatitis — get an upper gastrointestinal endoscopy today, not "when you have time." Ligation is safe, effective, and available in most city hospitals. β-blockers are cheap, time-tested medications that save lives. And most importantly: you are not alone. In our clinic, we help over 200 patients with this diagnosis every month — and most of them live full lives, work, enjoy, and see their grandchildren. Remember: esophageal varices are not a disease, but a consequence. Treat the cause, control your blood pressure, take care of yourself — and you will be able to keep the situation under control for many years.