Esophageal varices
From Wikipedia, the free encyclopedia
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| Gastroscopy image of esophageal varices with prominent red wale spots | |
| ICD-10 | I85 |
| ICD-9 | 456.0-456.2 |
| DiseasesDB | 9177 |
| MedlinePlus | 000268 |
| eMedicine | med/745 radio/269 |
In medicine (gastroenterology), esophageal varices are extremely dilated sub-mucosal veins in the esophagus. They are most often a consequence of portal hypertension, such as may be seen with cirrhosis.
Patients with esophageal varices have a strong tendency to develop bleeding.
Esophageal varices are diagnosed with endoscopy.
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[edit] Pathogenesis
The majority of blood from the esophagus is drained away via the esophageal veins, which drain deoxygenated blood from the esophagus to the azygos vein which in turn, directly drains into the inferior vena cava. These veins have no part in the development of esophageal varices. The remaining blood from the esophoagus is drained away via the superficial veins lining the esophagus interior, which drain into the coronary vein (left gastric vein) which in turn, drains directly into the portal vein. These superficial veins lining the esophagus interior (normally only approximately 1mm in diameter) become distended up to 1-2 cm in diameter in association with portal hypertension.
Normal portal pressure is approximately 9 mmHg compared to an inferior vena cava pressure of 2-6 mmHg. This creates a normal pressure gradient of 3-7 mmHg. If the portal pressure rises above 12mmHg, this gradient rises to 7-10 mmHg. A gradient greater than 10 mmHg is considered portal hypertension. At gradients greater than 10 mmHg, blood flow though the hepatic portal system is redirected from the liver into areas with lower venous pressures. This means that collateral circulation develops in the lower esophagus, abdominal wall, stomach and rectum. The small blood vessels in these areas become distended, becoming more thin-walled, and appear as varicosities. In addition, these vessels are poorly supported by other structures, as they are not designed for high pressures.
In situations where portal pressures increase, such as with cirrhosis, there is dilation of veins in the anastamosis, leading to esophageal varices.
Varices can also form in other areas of the body, including the stomach (gastric varices), duodenum (duodenal varices), and rectum (rectal varices). Treatment of these types of varices may differ.
[edit] Treatment and the role of endoscopy
In emergency situations, the care is directed at stopping blood loss, maintaining plasma volume, correcting disorders in coagulation induced by cirrhosis, and appropriate use of antibiotics (as infection is either concomitant, or a precipitant).
Therapeutic endoscopy is considered the mainstay of urgent treatment. Two main therapeutic approaches exist:
- Variceal ligation, or banding
- sclerotherapy
In cases of refractory bleeding, balloon tamponade may be necessary, usually as a bridge to further endoscopy, a transjugular intrahepatic portosystemic shunt (TIPS), or a distal splenorenal shunt procedure or a liver transplantation.
[edit] Prevention
Ideally, patients with known varices should receive treatment to reduce their risk of bleeding (Lebrec et al., 1981). The non-selective β-blockers (e.g., propranolol, timolol or nadolol) and nitrates have been evaluated for secondary prophylaxis. The effectiveness of this treatment has been shown by a number of different studies (Talwalkar JA & Kamath PS, 2004).
Unfortunately, non-selective β-blockers do not prevent the formation of esophageal varices (Groszmann RJ et al., 2005).
[edit] References
- Groszmann RJ, Garcia-Tsao G, Bosch J, et al. (2005). "Beta-Blockers to Prevent Gastroesophageal Varices in Patients with Cirrhosis". N Engl J Med 353 (21): 2254–2261. PMID 16306522.
- Lebrec D, Poynard T, Hillon P, Benhamou J-P (1981). "Propranolol for prevention of recurrent gastrointestinal bleeding in patients with cirrhosis: a controlled study". N Engl J Med 305: 1371–1374. PMID 7029276.
- Talwalkar JA, Kamath PS (2004). "An evidence-based medicine approach to beta-blocker therapy in patients with cirrhosis". Am J Med 116: 759–766. PMID 15144913.
[edit] See also
Other causes of GI bleeding include:
