Varices are dilated veins in the distal esophagus or proximal stomach caused by elevated pressure in the portal venous system, typically from cirrhosis. They may bleed massively but cause no other symptoms. Diagnosis is by upper endoscopy. Treatment is primarily with endoscopic banding and IV octreotide. Sometimes a transjugular intrahepatic portosystemic shunting procedure is needed.
Portal hypertension (see Portal Hypertension) results from a number of conditions, predominantly liver cirrhosis. If portal pressure remains higher than inferior vena caval pressure for a significant period, venous collaterals develop. The most dangerous collaterals occur in the distal esophagus and gastric fundus, causing engorged, serpentine submucosal vessels known as varices. These varices partially decompress portal hypertension but can rupture, causing massive GI bleeding. The trigger for variceal rupture is unknown, but bleeding almost never occurs unless the portal/systemic pressure gradient is > 12 mm Hg. Coagulopathies caused by liver disease may facilitate bleeding. See also the American College of Gastroenterology's practice guidelines on Variceal Hemorrhage in Cirrhosis.
Symptoms and Signs
Patients typically present with sudden, painless, upper GI bleeding, often massive. Signs of shock may be present. Bleeding is usually from the distal esophagus, less often from the gastric fundus. Bleeding from gastric varices also may be acute but is more often subacute or chronic.
Bleeding into the GI tract may precipitate portal-systemic encephalopathy in patients with impaired hepatic function.
Both esophageal and gastric varices are best diagnosed by endoscopy, which may also identify varices at high risk of bleeding (eg, those with red markings). Endoscopy is also critical to exclude other causes of acute bleeding (eg, peptic ulcer), even in patients known to have varices; perhaps as many as one third of patients with known varices who have upper GI bleeding have a nonvariceal source.
Because varices are typically associated with significant hepatic disease, evaluation for possible coagulopathy is important. Laboratory tests include CBC with platelets, PT, PTT, and liver function tests. Bleeding patients should have type and cross-match for 6 units of packed RBCs.
In about 40% of patients, variceal bleeding stops spontaneously. Previously, mortality was > 50%, but even with current management, mortality is at least 20% at 6 wk. Mortality depends primarily on severity of the associated liver disease rather than on the bleeding itself. Bleeding is often fatal in patients with severe hepatocellular impairment (eg, advanced cirrhosis), whereas patients with good hepatic reserve usually recover.
Surviving patients are at high risk of further variceal bleeding; typically, 50 to 75% have recurrence within 1 to 2 yr. Ongoing endoscopic or drug therapy significantly lowers this risk, but the overall effect on long-term mortality seems to be marginal, probably because of the underlying hepatic disease.
Management of hypovolemia and hemorrhagic shock is as described (see Fluid resuscitation) and see Shock and Fluid Resuscitation. Patients with coagulation abnormalities (eg, elevated INR) should be given 1 to 2 units of fresh frozen plasma and 2.5 to 10 mg vitamin K IM (or IV if severe). Patients with known cirrhosis with GI bleeding are at risk of bacterial infection and should receive antibiotic prophylaxis with norfloxacin or ceftriaxone.
Because varices are invariably diagnosed during endoscopy, primary treatment is endoscopic. Endoscopic banding of varices is preferred over injection sclerotherapy. At the same time, IV octreotide (a synthetic analog of somatostatin, which may also be used) should be given. Octreotide increases splanchnic vascular resistance by inhibiting the release of splanchnic vasodilator hormones (eg, glucagon, vasoactive intestinal peptide). The usual dose is a 50-μg IV bolus, followed by infusion of 50 μg/h. Octreotide is preferred over previously used agents such as vasopressin and terlipressin, because it has fewer adverse effects.
If bleeding continues or recurs despite these measures, emergency techniques to shunt blood from the portal system to the vena cava can lower portal pressure and diminish bleeding. A TIPS procedure is the emergency intervention of choice. TIPS is an invasive radiologic procedure in which a guidewire is passed from the vena cava through the liver parenchyma into the portal circulation. The resultant passage is dilated by a balloon catheter, and a metallic stent is inserted, creating a bypass between the portal and hepatic venous circulations. Stent size is crucial. If the stent is too large, portal-systemic encephalopathy results because of diversion of too much portal blood flow from the liver. If the stent is too small, it is more likely to occlude. Surgical portacaval shunts, such as the distal spleno-renal shunt, work by a similar mechanism but are more invasive and have a higher immediate mortality.
Mechanical compression of bleeding varices with a Sengstaken-Blakemore tube or one of its variants causes considerable morbidity and should not be used as primary management. However, such a tube may provide life-saving tamponade pending decompression with a TIPS or surgical procedure. The tube is a flexible NGT with one gastric balloon and one esophageal balloon. After insertion, the gastric balloon is inflated with a fixed volume of air, and traction is applied to the tube to pull the balloon snugly against the gastroesophageal junction. This balloon is often sufficient to control bleeding, but if not, the esophageal balloon is inflated to a pressure of 25 mm Hg. The procedure is quite uncomfortable and may result in esophageal perforation and aspiration; thus, endotracheal intubation and IV sedation are often recommended.
Liver transplantation can also decompress the portal system but is a practical option only for patients already on a transplant list.
Long-term medical therapy of portal hypertension (with β-blockers and nitrates) is discussed elsewhere (see Treatment). Treatment of portosystemic encephalopathy may be needed (see Treatment).
Last full review/revision September 2012 by Parswa Ansari, MD
Content last modified November 2012