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 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 anastomosis, leading to esophageal varices.
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:
Nutritional supplementation is not necessary if the patient is not eating for four days or less.
Ideally, patients with known varices should receive treatment to reduce their risk of bleeding. 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.
Unfortunately, non-selective β-blockers do not prevent the formation of esophageal varices.
^ Biecker E, Schepke M, Sauerbruch T (2005). "The role of endoscopy in portal hypertension". Dig Dis23 (1): 11-7. PMID 15920321.
^ Arguedas M (2003). "The critically ill liver patient: the variceal bleeder". Semin Gastrointest Dis14 (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. PMID 9073135.
^ 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 Med305: 1371–1374. PMID 7029276.
^ Talwalkar JA, Kamath PS (2004). "An evidence-based medicine approach to beta-blocker therapy in patients with cirrhosis". Am J Med116: 759–766. 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 Med353 (21): 2254–2261. PMID 16306522.