Esophageal varices

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Resident
Survival
Guide
Esophageal varices
Gastroscopy image of esophageal varices with prominent red wale spots
ICD-10 I85
ICD-9 456.0-456.2
DiseasesDB 9177
MedlinePlus 000268
MeSH D004932

Template:Search infobox Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Overview

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.[1]

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 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.[2] 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.

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.

Treatment

Recommendations for the treatment of Esophageal Varices (DO NOT EDIT)

The following is from clinical practice guidelines published in 2007 by the American Association for Study of Liver Diseases and American College of Gastroenterology.[3]

Patients with Cirrhosis and No Varices:

“
  1. In patients with cirrhosis who do not have varices, nonselective beta-blockers cannot be recommended to prevent their development.
  2. In patients who have compensated cirrhosis and no varices on the initial EGD, it should be repeated in 3 years. If there is evidence of hepatic decompensation, EGD should be done at that time and repeated annually.
 ”

Patients with Cirrhosis and Small Varices That Have Not Bled:

“
  1. In patients with cirrhosis and small varices that have not bled but have criteria for increased risk of hemorrhage (Child B/C [see Table 2 in the original guideline document for Child-Pugh classification of the severity of cirrhosis] or presence of red wale marks on varices), nonselective beta-blockers should be used for the prevention of first variceal hemorrhage.
  2. In patients with cirrhosis and small varices that have not bled and have no criteria for increased risk of bleeding, beta-blockers can be used, although their long-term benefit has not been established.
  3. In patients with small varices that have not bled and who are not receiving beta-blockers, EGD should be repeated in 2 years. If there is evidence of hepatic decompensation, EGD should be done at that time and repeated annually. In patients with small varices who receive beta-blockers, a follow-up EGD is not necessary.
 ”

Patients with Cirrhosis and Medium/Large Varices That Have Not Bled:

“
  1. In patients with medium/large varices that have not bled but have a high risk of hemorrhage (Child B/C [see Table 2 in the original guideline document] or variceal red wale markings on endoscopy), nonselective beta-blockers (propranolol or nadolol) or EVL may be recommended for the prevention of first variceal hemorrhage.
  2. In patients with medium/large varices that have not bled and are not at the highest risk of hemorrhage (Child A patients [see Table 2 in the original guideline document] and no red signs), nonselective beta-blockers (propranolol, nadolol) are preferred and EVL should be considered in patients with contraindications or intolerance or non-compliance to beta-blockers.
  3. If a patient is placed on a nonselective beta-blocker, it should be adjusted to the maximal tolerated dose; follow-up surveillance EGD is unnecessary. If a patient is treated with EVL, it should be repeated every 1-2 weeks until obliteration with the first surveillance EGD performed 1 to 3 months after obliteration and then every 6 to 12 months to check for variceal recurrence.
  4. Nitrates (either alone or in combination with beta-blockers), shunt therapy, or sclerotherapy should not be used in the primary prophylaxis of variceal hemorrhage.
 ”

Patients with Cirrhosis and an Acute Episode of Variceal Hemorrhage:

“
  1. Acute gastrointestinal (GI) hemorrhage in a patient with cirrhosis is an emergency that requires prompt attention with intravascular volume support and blood transfusions, being careful to maintain a hemoglobin of ~8 g/dL.
  2. Short-term (maximum 7 days) antibiotic prophylaxis should be instituted in any patient with cirrhosis and GI hemorrhage. Oral norfloxacin (400 mg twice a day [BID]) or intravenous ciprofloxacin (in patients in whom oral administration is not possible) is the recommended antibiotic. In patients with advanced cirrhosis intravenous ceftriaxone (1 g/day) may be preferable particularly in centers with a high prevalence of quinolone-resistant organisms.
  3. Pharmacological therapy (somatostatin or its analogues octreotide and vapreotide; terlipressin) should be initiated as soon as variceal hemorrhage is suspected and continued for 3 to 5 days after diagnosis is confirmed.
  4. EGD, performed within 12 hours, should be used to make the diagnosis and to treat variceal hemorrhage, either with EVL or sclerotherapy.
  5. Transjugular intrahepatic portosystemic shunt (TIPS) is indicated in patients in whom hemorrhage from esophageal varices cannot be controlled or in whom bleeding recurs despite combined pharmacological and endoscopic therapy.
  6. Balloon tamponade should be used as a temporizing measure (maximum 24 hours) in patients with uncontrollable bleeding for whom a more definitive therapy (e.g., TIPS or endoscopic therapy) is planned.
 ”

Patients with Cirrhosis Who Have Recovered from Acute Variceal Hemorrhage:

“
  1. Patients with cirrhosis who survive an episode of active variceal hemorrhage should receive therapy to prevent recurrence of variceal hemorrhage (secondary prophylaxis).
  2. Combination of nonselective beta-blockers plus EVL is the best option for secondary prophylaxis of variceal hemorrhage.
  3. The nonselective beta-blocker should be adjusted to the maximal tolerated dose. EVL should be repeated every 1-2 weeks until obliteration with the first surveillance EGD performed 1 to 3 months after obliteration and then every 6 to 12 months to check for variceal recurrence.
  4. TIPS should be considered in patients who are Child A or B (see Table 2 in the original guideline document) who experience recurrent variceal hemorrhage despite combination pharmacological and endoscopic therapy. In centers where the expertise is available, surgical shunt can be considered in Child A patients.
  5. Patients who are otherwise transplant candidates should be referred to a transplant center for evaluation.
 ”

Medical Therapy

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 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.

Nutritional supplementation is not necessary if the patient is not eating for four days or less.[4]


  • Esophageal varices seven days post banding, showing ulceration at the site of banding.

    Esophageal varices seven days post banding, showing ulceration at the site of banding.

Prevention

Ideally, patients with known varices should receive treatment to reduce their risk of bleeding.[5][6] 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 summarized in meta-analyses.[7] However, there may be a 'window effect':

Combining esophageal band ligation with β-blockers is better than either therapy alone.[5]

Unfortunately, non-selective β-blockers do not prevent the formation of esophageal varices.[10]

Variceal bleeding, prophylaxis

  • 1. Short-term antibiotic prophylaxis[11]
  • Preferred regimen (1): Norfloxacin 400mg PO bid for max. of 7 days
  • Preferred regimen (2): Ciprofloxacin 400mg IV q12h max. of 7 days (in patients in whom oral administration is not possible)
  • 2. In advanced cirrhosis and in a setting with high prevalence of quinolone-resistant organisms[11]
  • Preferred regimen: Ceftriaxone 1g IV q24h for max. of 7 days

References

  1. ↑ Biecker E, Schepke M, Sauerbruch T (2005). "The role of endoscopy in portal hypertension". Dig Dis. 23 (1): 11–7. PMID 15920321.
  2. ↑ Arguedas M (2003). "The critically ill liver patient: the variceal bleeder". Semin Gastrointest Dis. 14 (1): 34–8. PMID 12610853.
  3. ↑ Garcia-Tsao G, Sanyal AJ, Grace ND, Carey WD, Practice Guidelines Committee of American Association for Study of Liver Diseases. Practice Parameters Committee of American College of Gastroenterology (2007). "Prevention and management of gastroesophageal varices and variceal hemorrhage in cirrhosis". Am J Gastroenterol. 102 (9): 2086–102. doi:10.1111/j.1572-0241.2007.01481.x. PMID 17727436.
  4. ↑ 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.
  5. ↑ 5.0 5.1 Gonzalez R, Zamora J, Gomez-Camarero J, Molinero LM, Bañares R, Albillos A (2008). "Meta-analysis: Combination endoscopic and drug therapy to prevent variceal rebleeding in cirrhosis". Ann Intern Med. 149 (2): 109–22. PMID 18626050. Review in: ACP J Club. 2008 Nov 18;149(5):10
  6. ↑ 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&ndash, 1374. PMID 7029276.
  7. ↑ Pagliaro L, D'Amico G, Sörensen TI, Lebrec D, Burroughs AK, Morabito A; et al. (1992). "Prevention of first bleeding in cirrhosis. A meta-analysis of randomized trials of nonsurgical treatment". Ann Intern Med. 117 (1): 59–70. PMID 1350716.
  8. ↑ Qi XS, Bao YX, Bai M, Xu WD, Dai JN, Guo XZ (2015). "Nonselective beta-blockers in cirrhotic patients with no or small varices: A meta-analysis". World J Gastroenterol. 21 (10): 3100–8. doi:10.3748/wjg.v21.i10.3100. PMC 4356933. PMID 25780311.
  9. ↑ Mandorfer M, Bota S, Schwabl P, Bucsics T, Pfisterer N, Kruzik M; et al. (2014). "Nonselective β blockers increase risk for hepatorenal syndrome and death in patients with cirrhosis and spontaneous bacterial peritonitis". Gastroenterology. 146 (7): 1680–90.e1. doi:10.1053/j.gastro.2014.03.005. PMID 24631577.
  10. ↑ Groszmann RJ, Garcia-Tsao G, Bosch J, Grace ND, Burroughs AK, Planas R; et al. (2005). "Beta-blockers to prevent gastroesophageal varices in patients with cirrhosis". N Engl J Med. 353 (21): 2254–61. doi:10.1056/NEJMoa044456. PMID 16306522. Review in: ACP J Club. 2006 May-Jun;144(3):68
  11. ↑ 11.0 11.1 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 (2007). "Prevention and management of gastroesophageal varices and variceal hemorrhage in cirrhosis". Hepatology. 46 (3): 922–38. doi:10.1002/hep.21907. PMID 17879356.

See also


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