The most common presentation is hematemesis and there could also be melena. Other symptoms are abdominal pain, dysphagia, odynophagia, and other features of liver disease or underlying medical condition. They could also present in confusion secondary to hepatic encephalopathy. On physical examination, patient will be pale, hypotensive and could be in shock, with reduced urine output, and could be unconscious/subconscious. There would also be signs of liver disease and signs of overwhelming infection might also be seen.

• Intermittent Claudication

  claudication - Arteriovenous fistula - Hereditary hemorrhagic telangiectasia - Spider angioma - Dissection ( Carotid artery, Vertebral artery ) Veins, lymphatic vessels and lymph nodes Thrombosis / Phlebitis / Thrombophlebitis ( Deep vein thrombosis, [wikidoc.org]

  claudication and impotence) and in 6 patients (6 percent) in the placebo group (1 each had impotence, hypotension, depression, heart failure, nodal rhythm, and bronchospasm) (P 0.006). [doi.org]

• Localized Edema

  Localized edema and superficial venous engorgement (signs of SVC occlusion) were each observed in four of eight patients. [ncbi.nlm.nih.gov]

• Stridor

  Three days later, the patient developed sudden dyspnea with stridor during inspiration under sedation with an intravenous injection of low-dose flunitrazepam prior to receiving additional treatment and was aroused with intravenous flumazenil, after which [ncbi.nlm.nih.gov]

• Hematemesis

  We herein report a case of a 50-year-old male with hematemesis due to the rupture from esophageal varices coexisting with multiple liver tumors metastasizing from sigmoid colon cancer. [ncbi.nlm.nih.gov]

• Melena

  Abstract Esophageal varices is one of the most important comorbidity related liver cirrhosis, patients usually presented with hematemesis, melena, or both, ultimately 20% is the mortality during the first attack, hence we aimed to investigate the incidence [ncbi.nlm.nih.gov]

  Patients without acute bleeding liver cirrhosis symptoms; dysphagia; anaemia (microcytes) – sign of previous bleeding; previous hematemesis and/or melena. [wikilectures.eu]

  Objective: hematemsis-bloody vomitus, either bright red (indicate fresh blood) or "coffee ground" (indicate older blood that has been in the stomach long enough for gastric juices to act on it) melena (occult blood in stool) peripheral edema Idicators [quizlet.com]

• Black Stools

  A 58-year-old man with hepatitis B cirrhosis noticed black stools and underwent an endoscopy at a community hospital. The presence of esophageal varices (EVs) was confirmed, but the bleeding point was not found. [ncbi.nlm.nih.gov]

  Ballooning of blood vessels (veins) may cause vessels to rupture causing: vomiting of blood, tarry black stools. If large volume of blood is lost sign of shock will develop. [quizlet.com]

  Signs and Symptoms of Esophageal Varices Signs and Symptoms of Esophageal Varices may include the following: Lightheadedness Bloody stools Abdominal pain Hematemesis (blood in vomit) Shock or faintness due to blood loss Black stools If you or someone [eatingdisorderhope.com]

  Exams and Tests Your health care provider will do a physical exam which may show: Bloody or black stool (in a rectal exam) Low blood pressure Rapid heart rate Signs of chronic liver disease or cirrhosis Tests to find the source of the bleeding and check [account.allinahealth.org]

• Blood in Stool

  Objective: hematemsis-bloody vomitus, either bright red (indicate fresh blood) or "coffee ground" (indicate older blood that has been in the stomach long enough for gastric juices to act on it) melena (occult blood in stool) peripheral edema Idicators [quizlet.com]

  The most feared situation is a rupture of the varices that causes massive hemorrhage with blood vomiting and presence of black tarry blood in stool ( melena ). Without urgent medical assistance, the patient bleeds relatively quickly to death. [health-tutor.com]

• Coffee Ground Emesis

  Patients with upper gastrointestinal (GI) bleeding—bleeding that originates in the esophagus and stomach, rather than in the intestines—can look for the following signs and symptoms: Vomiting bright red blood or coffee-ground emesis (very dark and granular [verywellhealth.com]

• Protein S Deficiency

  Pretransplantation work-up revealed protein S deficiency. Results of liver function tests were normal. Upper endoscopy showed grade II to III EV in the upper and middle segments of the esophagus. [ncbi.nlm.nih.gov]

• Vein Disorder

  Da Wikimedia Commons, l'archivio di file multimediali liberi Jump to navigation Jump to search varici esofagee malattia umana Carica un file multimediale Wikipedia Istanza di malattia Sottoclasse di vein disorder, malattia dell'esofago, esophageal and [commons.wikimedia.org]

• Arthralgia

  The patient's first presentation was superior vena cava syndrome due to thrombosis followed by bipolar ulcers and arthralgia. He received warfarin, prednisolone and azathioprine. [ncbi.nlm.nih.gov]

• Laboratory investigations should include complete blood count which may show low hemoglobin level and platelet count. Blood should also be taken for clotting profile including INR. Renal and liver function tests should also be done and blood should be taken for grouping and cross-matching as patient may require transfusion. 
• Esophagogastroduodenoscopy is the main investigation for diagnosis of this condition. It will show the location and size of the varices. If it is unavailable, a Doppler ultrasound can be done. Although it is a poor second choice, it can demonstrate varices when done by a skilled handler [7]. 
• Barium swallow and portal vein angiography and manometry should also be conducted. A chest X-ray should be done to exclude the possibility of aspiration and look for underlying chest infections. Ascitic tap for microscopy and culture is necessary if there are suspicions of bacterial peritonitis.

• Gastric Varices

  The gastric varices disappeared after obliterating both the feeding and drainage vessels by means of intervention radiology. We thus, consider the occlusion of both the afferent and efferent vessels to be an effective treatment for gastric varices. [ncbi.nlm.nih.gov]

  From Wikidata Jump to navigation Jump to search Human disease Oesophageal varices Oesophageal varix Esophageal variceal ligation Variceal bleed Esophageal and gastric varices Acute variceal bleeding Oesophagus varices Bleeding esophageal varices Bleeding [wikidata.org]

• Total Bilirubin Increased

  After undergoing a variceal ligation, the serum total bilirubin increased from 4.0 mg/dL to 9.5 mg/dL, and the degree of liver failure worsened. She finally had to undergo a liver transplant. [ncbi.nlm.nih.gov]

• Treatment can be medical and surgical. Medical management involves the use of splanchnic vasoconstrictors (like vasopressin, somatostatin and non-cardioselective beta blockers), venodilators (like nitrates) or a combination of both.
• Surgical management include endoscopic sclerotherapy and variceal band ligation. Ligation provides better control of hemorrhage and better outcomes but may be difficult to perform in a patient with active hemorrhage [8]. 
• If the above steps fail, a transjugular intrahepatic portosystemic shunt (TIPS) is used [9]. 
• A balloon tamponade could be used where TIPS is unavailable. It is very effective in stopping hemorrhage but carries a high risk of rebleeding and major complications when the balloon is removed.
• Patient may present needing emergency attention and emergency management to secure airway, breathing and proper circulation should be instituted immediately.

There is a recurrence rate of about 70% and up to 33% of a recurring hemorrhage will result in death. The highest risk of fatality is during the first few days after the bleeding episode and the risk begins to decline progressively after 6 weeks. There is about 65% mortality in patients with esophageal varices that could be attributed to associated disorders of the renal, cardiovascular and immune system [6].

Esophageal varices are caused by anything that can cause portal hypertension. Such cause could be prehepatic like portal vein thrombosis, portal vein obstruction and increased splenic flow. It could also be intrahepatic like liver cirrhosis, hepatitis, idiopathic portal hypertension and congenital hepatic fibrosis and posthepatic like Budd-Chiari syndrome, compression from a tumor and constrictive pericarditis.

Factors are also present which increase the risk for variceal bleeding and they include malnutrition, alcohol intake, decompensation of liver disease, increased intraabdominal pressure, non-steroidal anti-inflammatory drugs (NSAIDs), bacterial infection and circadian rhythms [2].

Esophageal varices account for up to 30% of all cases of upper gastrointestinal hemorrhage and they are seen in over 50% of patients with liver cirrhosis. Annually, up to 8% of patient with liver cirrhosis develop esophageal varices and the varices are large enough to have a risk of bleeding in about 3% of those that develop it. Up to 30% of patients with small varices will progressively develop large varices and are also therefore at a risk of bleeding. The mortality rate from esophageal variceal bleed is about 20% at 6 weeks although, in up to 40% of patients, bleeding stops spontaneously [3].

Portal hypertension develops in liver disease as a consequence of an increase in vascular resistance at either the prehepatic, intrahepatic or posthepatic levels. An increase in portal venous flow also contributes to the hypertension. Esophageal varices develop as the pressure in the portal vein continues to increase. The varices are small on the outset but as the hyperdynamic circulation increases, blood flow through the varices also increases and this raises the tension within the wall. When the expanding force exceeds the maximal wall elastic limit, there is rupture which will cause variceal hemorrhage. If the pressure in the portal vein does not reduce, then there is a risk of recurrence [4] [5].

There is no known method to prevent the formation of esophageal varices. Newly diagnosed patients with liver cirrhosis should be screened for varices. Varices can be treated with beta blockers and esophageal band ligation to significantly reduce the risk of bleeding [10].

Esophageal varices are porto-systemic collaterals. They are vascular channels that link the portal and systemic venous system and they form as a result of portal hypertension and are mostly seen in the lower one-third of the esophagus. The rupture of esophageal varices and subsequent bleeding is a major complication of portal hypertension. It is usually associated with a high mortality rate [1].

• Definition: Esophageal varices are dilated veins usually located at the lower end of the esophagus. They are usually as a result of liver disease which causes the pressure in the veins of the liver to increase. This condition could lead to death if these vessels rupture.
• Cause: The main causes are anything that will cause a liver disease. Some risk factors for formation of varices include chronic alcoholism, anything that will cause increased intraabdominal pressure, aspirin, NSAIDs, malnutrition and bacterial infections.
• Symptoms: The main symptoms is vomiting of pure blood and there could also be blood in the stool. Other symptoms are abdominal pain and pain on swallowing. There could also be symptoms arising due to the underlying liver disease like yellowness of the eyes and skin.
• Diagnosis: Diagnosis is usually confirmed by an endoscopic examination. This involves looking directly into the esophagus with a small camera. Ultrasound could be done if this is not available. Special X-rays and imaging of the blood vessels can also be done. Laboratory tests are done to check the blood level and cells, to check the kidney and liver function and also to prepare for possible blood transfusion.
• Treatment: Treatment involves the use of drugs to try and reduce the pressure in these veins. Surgery can also be done to either shrink the veins or tie them up to reduce the risk of bleeding.

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3. Gore RM, Livine MS, eds. Textbook of Gastrointestinal Radiology. 2nd ed. Philadelphia, Pa: WB Saunders Co; 2000:454-63, 2082
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5. de Franchis R, Primignani M. Why do varices bleed?. Gastroenterol Clin North Am. Mar 1992;21(1):85-101.
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7. Liu CH, Hsu SJ, Liang CC, Tsai FC, Lin JW, Liu CJ, et al. Esophageal varices: noninvasive diagnosis with duplex Doppler US in patients with compensated cirrhosis. Radiology. Jul 2008;248(1):132-9
8. Garcia-Pagan JC, Bosch J. Endoscopic band ligation in the treatment of portal hypertension. Nat Clin Pract Gastroenterol Hepatol. Nov 2005;2(11):526-35.
9. Conn HO. Portal hypertension, varices, and transjugular intrahepatic portosystemic shunts. Clin Liver Dis. Feb 2000;4(1):133-50, vii.
10. Krige JE, Shaw JM, Bornman PC. The evolving role of endoscopic treatment for bleeding esophageal varices. World J Surg. 2005;29:966-73.