Esophageal varices

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Esophageal varices
Classification and external resources

Gastroscopy image of esophageal varices with

prominent cherry-red spots
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 (or oesophageal varices) are extremely dilated submucosal veins in the lower third [1] of the 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.[2]

Contents

1 Pathogenesis
2 Treatment
3 Prevention
4 Histology
5 See also
6 References
7 External links

Pathogenesis
The majority of blood from the esophagus is drained via the esophageal veins, which carry deoxygenated blood
from the esophagus to the azygos vein, which in turn drains directly into the superior vena cava. These veins
have no part in the development of esophageal varices. The remaining blood from the esophagus is drained into
the superficial veins lining the esophageal mucosa, which drain into the left gastric vein (coronary vein), which
in turn drains directly into the portal vein. These superficial veins (normally only approximately 1 mm in
diameter) become distended up to 12 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 12 mmHg, this gradient

rises to 7-10 mmHg.[3] A gradient greater than 5 mmHg is considered portal hypertension. At gradients greater
than 10 mmHg, blood flow through 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 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 that 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 some cases,
schistosomiasis also leads to esophageal varices.

Treatment

Esophageal varices seven days after banding, showing ulceration at the site of banding
In emergency situations, care is directed at stopping blood loss, maintaining plasma volume, correcting
disorders in coagulation induced by cirrhosis, and appropriate use of antibiotics (usually a quinolone or
ceftriaxone, as infection by Gram-negative strains is either concomitant or a precipitant).
Blood volume resuscitation should be done promptly and with caution. The goal should be hemodynamic
stability and hemoglobin of over 8 g/dl. Resuscitation of all lost blood leads to increase in portal pressure
leading to more bleeding. Volume resuscitation can also worsen ascites and increase portal pressure. (AASLD
guidelines)
Therapeutic endoscopy is considered the mainstay of urgent treatment. The two main therapeutic approaches
are variceal ligation or banding and sclerotherapy.
In cases of refractory bleeding, balloon tamponade with a Sengstaken-Blakemore tube may be necessary,
usually as a bridge to further endoscopy or treatment of the underlying cause of bleeding (usually portal
hypertension). Esophageal devascularization operations such as the Sugiura procedure can also be used to stop
complicated variceal bleeding. Methods of treating the portal hypertension include: transjugular intrahepatic
portosystemic shunt, 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.[4]
Terlipressin and octreotide (50-g bolus intravenously followed by 25-50 g/h IVF for 1 to 5 days) have also
been used.[5]

Prevention

In ideal circumstances, patients with known varices should receive treatment to reduce their risk of bleeding.[6]
The non-selective -blockers (e.g., propranolol 10 mg PO TID, timolol or nadolol 20 mg PO OD) and nitrates
(e.g. isosorbide mononitrate (IMN) 20 mg BD to TID) have been evaluated for secondary prophylaxis. Nonselective -blockers (but not cardioselective -blockers like atenolol) are preferred because they decrease both
cardiac output by 1 blockade and splanchnic blood flow by blocking vasodilating 2 receptors at splanchnic
vasculature. The effectiveness of this treatment has been shown by a number of different studies.[7]

However, non-selective -blockers do not prevent the formation of esophageal varices.[8]

When medical contraindications to beta-blockers exist, such as significant reactive airway disease, then
treatment with prophylactic endoscopic variceal ligation is often performed. [9]

Histology

Axial CT showing esophageal varices in liver cirrhosis with portal hypertension

Dilated submucosal veins are the most prominent histologic feature of esophageal varices. The expansion of the
submucosa leads to elevation of the mucosa above the surrounding tissue, which is apparent during endoscopy
and is a key diagnostic feature. Evidence of recent variceal hemorrhage includes necrosis and ulceration of the
mucosa. Evidence of past variceal hemorrhage includes inflammation and venous thrombosis.

See also

Gastric varices
Intestinal varices
Esophagitis
Mallory-Weiss syndrome

Peptic ulcer
Caput medusae
Portal hypertensive gastropathy

References
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4.
5.

6.
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8.
9.

Rubin's Pathology: Clinicopathologic Foundations of Medicine edited by Raphael Rubin, David

S. Strayer, Emanuel Rubin, page 612
Biecker E, Schepke M, Sauerbruch T (2005). "The role of endoscopy in portal hypertension".
Dig Dis 23 (1): 117. doi:10.1159/000084721. PMID 15920321.
Arguedas M (2003). "The critically ill liver patient: the variceal bleeder". Semin Gastrointest Dis
14 (1): 348. PMID 12610853.
de Ldinghen 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): 53641. doi:10.1023/A:1018838808396. 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): 61723. doi:10.1038/ajg.2008.147.
PMID 19223890.
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 (23): 1371
1374. doi:10.1056/NEJM198112033052302. PMID 7029276.
Talwalkar JA, Kamath PS (2004). "An evidence-based medicine approach to beta-blocker
therapy in patients with cirrhosis". Am J Med 116 (11): 759766. doi:10.1016/j.amjmed.2004.03.006.
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): 22542261.
doi:10.1056/NEJMoa044456. PMID 16306522.
Garcia-Tsao G, Sanyal AJ, Grace ND, Carey W; Practice Guidelines Committee of the American
Association for the Study of Liver Diseases; Practice Parameters Committee of the American College of
Gastroenterology. Prevention and management of gastroesophageal varices and variceal hemorrhage in
cirrhosis. Hepatology. 2007;46(3):922-938. PMID: 17879356