Esophageal varices
From Wikipedia, the free encyclopedia
| 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]
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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 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.
[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 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 (50mcg bolus IV followed by 25-50mcg/h IVF for 1 to 5 days) have also been used.[4]
[edit] Prevention
Ideally, patients with known varices should receive treatment to reduce their risk of bleeding.[5] The non-selective β-blockers (e.g., propranolol 10mg PO TID, timolol or nadolol 20mg PO OD) and nitrates (e.g. isosorbide mononitrate (IMN) 20mg BD to TID) have been evaluated for secondary prophylaxis. Non-selective β-blockers (but not cardioselective β-blockers like atenolol) are preferred because they decrease both cardiac output by β1 blockade and splanchnic blood flow by blocking vasodilating β2 receptors at splanchnic vasculature. 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]
[edit] See also
[edit] References
- ^ Biecker E, Schepke M, Sauerbruch T (2005). "The role of endoscopy in portal hypertension". Dig Dis 23 (1): 11–7. doi:. PMID 15920321.
- ^ Arguedas M (2003). "The critically ill liver patient: the variceal bleeder". Semin Gastrointest Dis 14 (1): 34–8. PMID 12610853.
- ^ de Lédinghen V, Beau P, Mannant PR, et al. (1997). "Early feeding or enteral nutrition in patients with cirrhosis after bleeding from esophageal varices? A randomized controlled study". Dig. Dis. Sci. 42 (3): 536–41. doi:. PMID 9073135.
- ^ Abid S, Jafri W, Hamid S, et al. (March 2009). "Terlipressin vs. octreotide in bleeding esophageal varices as an adjuvant therapy with endoscopic band ligation: a randomized double-blind placebo-controlled trial". Am. J. Gastroenterol. 104 (3): 617–23. doi:. PMID 19223890. http://dx.doi.org/10.1038/ajg.2008.147.
- ^ 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. doi:. PMID 15144913.
- ^ 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. doi:. PMID 16306522.
[edit] See also
[edit] External links
- Treatment of Esophageal Varices - World Gastroenterology Organisation (WGO)
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