n.
Longitudinal, superficial venous varices at the lower end of the esophagus that are prone to ulceration and massive bleeding.
| Medical Dictionary: esophageal varices |
Longitudinal, superficial venous varices at the lower end of the esophagus that are prone to ulceration and massive bleeding.
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| Wikipedia: Esophageal varices |
| Esophageal varices | |
|---|---|
| Classification and external resources | |
Gastroscopy image of esophageal varices with prominent cherry-red spots |
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| ICD-10 | I85. |
| ICD-9 | 456.0-456.2 |
| DiseasesDB | 9177 |
| MedlinePlus | 000268 |
| eMedicine | med/745 radio/269 |
| MeSH | D004932 |
In medicine (gastroenterology), esophageal varices are extremely dilated sub-mucosal veins in the lower esophagus. They are most often a consequence of portal hypertension, commonly due to cirrhosis; patients with esophageal varices have a strong tendency to develop bleeding.
Esophageal varices are diagnosed with endoscopy.[1]
Contents |
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 superior vena cava. These veins have no part in the development of esophageal varices. The remaining blood from the esophagus is drained away via the superficial veins lining the esophageal mucosa, which drain into the coronary vein (left gastric vein) which in turn, drains directly into the portal vein. These superficial veins (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.[2] A gradient greater than 5 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 anastomosis, leading to esophageal varices. Splenic vein thrombosis is a rare condition which causes esophageal varices without a raised portal pressure. Splenectomy can cure the variceal bleeding due to splenic vein thrombosis.
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.
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:
In cases of refractory bleeding, balloon tamponade with Sengstaken-Blakemore tube may be necessary, usually as a bridge to further endoscopy or treatment of the underlying cause of bleeding (usually portal hypertension). Methods of treating the portal hypertension include: transjugular intrahepatic portosystemic shunt (TIPS), or a distal splenorenal shunt procedure or a liver transplantation.
Nutritional supplementation is not necessary if the patient is not eating for four days or less.[3]
Terlipressin and octreotide have also been used.[4]
Ideally, patients with known varices should receive treatment to reduce their risk of bleeding.[5] The non-selective β-blockers (e.g., propranolol, timolol or nadolol) and nitrates have been evaluated for secondary prophylaxis. Non-selective β-blockers are preferred because they decrease both cardiac output and splanchnic blood flow. The effectiveness of this treatment has been shown by a number of different studies.[6]
Unfortunately, non-selective β-blockers do not prevent the formation of esophageal varices.[7]
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