Esophageal varices
Other names	Esophageal varix, oesophageal varices
Gastroscopy image of esophageal varices with prominent cherry-red spots andwale signs
Specialty	Gastroenterology,Hematology,Hepatology (liver disease)
Symptoms	vomiting blood,passing black stool
Complications	Internal bleeding,hypovolemic shock,cardiac arrest
Causes	portal hypertension (high blood pressure in theportal vein and the associated blood vessels in the hepatic, or liver-based, circulation)
Diagnostic method	Endoscopy

Esophageal varices are extremelydilated sub-mucosalveins in the lower third of theesophagus.^[1] They are most often a consequence ofportal hypertension,^[2] commonly due tocirrhosis.^[3] People with esophageal varices have a strong tendency to develop severebleeding which left untreated can befatal. Esophageal varices are typically diagnosed through anesophagogastroduodenoscopy.^[4]

The upper two thirds of theesophagus are drained via theesophageal veins, which carry deoxygenated blood from the esophagus to theazygos vein, which in turn drains directly into thesuperior vena cava. These veins have no part in the development of esophageal varices. The lower one third of the esophagus is drained into the superficial veins lining the esophageal mucosa, which drain into theleft gastric vein, which in turn drains directly into theportal vein. These superficial veins (normally only approximately 1 mm in diameter) become distended up to 1–2 cm in diameter in association with portal hypertension.^{[citation needed]}

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.^[5] A gradient greater than 5 mmHg is consideredportal hypertension. At gradients greater than 10 mmHg, blood flowing through the hepatic portal system is redirected from the liver into areas with lower venous pressures. This means thatcollateral circulation develops in the loweresophagus, abdominal wall,stomach, andrectum. The small blood vessels in these areas become distended, becoming more thin-walled, and appear asvaricosities.^{[citation needed]}

In situations where portal pressures increase, such as withcirrhosis, there is dilation of veins in theanastomosis, leading to esophageal varices.^[3] 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.^{[citation needed]}

Varices can also form in other areas of the body, including thestomach (gastric varices),duodenum (duodenal varices), andrectum (rectal varices). Treatment of these types of varices may differ. In some cases,schistosomiasis also leads to esophageal varices.^{[citation needed]}

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 includesnecrosis andulceration of the mucosa. Evidence of past variceal hemorrhage includes inflammation andvenous thrombosis.^{[citation needed]}

In some circumstances, people with known varices should receive treatment to reduce their risk of bleeding.^[6] The non-selectiveβ-blockers (e.g.,propranolol,timolol ornadolol) and nitrates (e.g.,isosorbide mononitrate (IMN) have been evaluated for secondary prophylaxis. Non-selective β-blockers (but not cardioselective β-blockers likeatenolol) 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.^[7]

However, non-selective β-blockers do not prevent theformation 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]

Esophageal varices may lead to severeupper gastrointestinal bleeding. In emergency situations, care is directed at stopping blood loss, maintaining plasma volume, correcting disorders in coagulation induced by cirrhosis, and appropriate use ofantibiotics such asquinolones orceftriaxone. 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)^{[citation needed]}

Therapeuticendoscopy is considered the mainstay of urgent treatment. The two main therapeutic approaches are variceal ligation (banding) andsclerotherapy.^{[citation needed]}

In cases of refractory bleeding,balloon tamponade with aSengstaken–Blakemore tube may be necessary, or the use of a fully-covered esophagealself-expandable metallic stent, usually as a bridge to further endoscopy or treatment of the underlying cause of bleeding (i.e.: portal hypertension). Esophageal devascularization operations such as theSugiura procedure can also be used to stop complicated bleeding. Methods of treating the portal hypertension include:transjugular intrahepatic portosystemic shunt (TIPS),distal splenorenal shunt procedure, orliver transplantation.^{[citation needed]}

Nutritional supplementation is necessary if the person has been unable to eat for more than four days.^[10]

Terlipressin andoctreotide for one to five days have also been used.^[11]

• Esophagus disorders
• Diseases of veins, lymphatic vessels and lymph nodes
• Medical emergencies

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