Esophageal Varices

Esophageal varices are venous varices localized in the submucosal layer of esophagus. They are direct consequence of portal hypertension. All the patients with esophageal varices are at the risk of acute bleeding, which can cause be fatal. The most common cause of portal hypertension and esophageal varices is liver cirrhosis. 30–60% of patients with liver cirrhosis are at the risk of esophageal varices bleeding^[1]. Rebleeding is very often (60–100% patients with anamnesis of previous variceal bleeding will rebleed in 2 years)^[1].

Contents 1 Pathogenesis 2 Localization 3 Clinical features 3.1 Patients without acute bleedeng 3.2 Patients with acute bleeding 4 Diagnostic 5 Therapy 5.1 Conservative therapy 5.2 Acute bleeding therapy 6 Links 6.1 Related articles 6.2 External links 6.3 References

edit Pathogenesis

Higher blood pressure in portal vein expands in all the veins that carry blood to the portal vein. There are anatomical junctions between venae gastricae (→ portal vein) and venae esophageae (→ superior vena cava) The junctions are called portocaval anastomoses. Because of the higher venous pressure are these junctions more opend and the pressure can expand to esophageal veins too. Esophageal veins are localized in submucosis, over the muscular layer of esophagus. There is scope for the development of varices, which can expand into lumen of esophagus. Their perforation and bleeding is just a question of time.

The esophageal varices bleeding is common in portal pressure higher than 12 mmHg^[2]. Normal venous pressure in portal vein is 5–10 mm Hg^[1].

edit Localization

These varices are usually localized in distal part of esophagus. They can be found in higher level of esophagus or stomach too. The bleeding is most often in gastroesophageal junction^[2].

edit Clinical features

edit Patients without acute bleedeng

• liver cirhosis symptomes;
• dysphagia;
• anaemia (microcytes) – sign of previous bleeding;
• previous hematemesis and/or melena.

edit Patients with acute bleeding

• hematemesis (then melena);
• hypotension;
• other signs of hemorrhagic shock^[1].

edit Diagnostic

Gastroscopy is the only diagnostic method, which can prove existance of esophageal varices (visualization) and bring therapeutic solution in the same moment.^[1]

edit Therapy

edit Conservative therapy

All the patients with esophageal varices which are not in direct danger of bleeding or patients with portal hypertension without significant varices should be treated for portal hypertension. All the patients with portal hypertension will develop varices (sooner or later…). The therapy of portal hypertension includes:

• nonselective β-blockers (propranolol, nadolol);
• TIPS – transjugular intrahepatic porosystemic shunt (which is not conservative therapy of course).

edit Acute bleeding therapy

Every patient suspected of esophageal varices bleeding should be hospitalized in ICU and treated like every patient with massive blood loss:

• central and peripheral intravenous catheter;
• blood loss replacement (but carefully – it can increase portal blood pressure);
• vasopressin – for vasoconstriction in splanchnical circulation;
• antibiotic prophylaxis – these patients are at risk of infection.^[2][1]

Acute gastroscopy is necessary! It can be the only solution how to stop bleeding.

The endoscopic treatment methods are:

• endoscopic variceal ligation (EVL), almost replaced other endoscopic methodes;
• baloon tamponade (Sengstaken-Blakemore or Minnesota);
• endoscopic sclerosis of varices.^[2]

Other treatment method is acute TIPS or surgical shunt (decompression of portal system).^[2]

edit Links

edit Related articles

• Portal Hypertension
• Gastroscopy

edit External links

• Esophageal varices ligation - images

edit References

1. ↑ ^{a b c d e f} ČEŠKA, Richard, et al. Interna. 1. edition. Prague : Triton, 2010. 855 pp. pp. 433-434. ISBN 978-80-7387-423-0.
2. ↑ ^{a b c d e} KASPER, Dennis L – FAUCI, Anthony S – LONGO, Dan L, et al. Harrison's principles of Internal Medicine. 16th edition. New York : McGraw-Hill Companies, Inc, 2005. 2607 pp. pp. 1892-1896. ISBN 0-07-139140-1.