Varices

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.

• Endoscopy

• Evaluation for coagulopathy

(See also the American Society for Gastrointestinal Endoscopy's 2014 guidelines on the role of endoscopy in the management of variceal hemorrhage.)

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.

Bleeding Esophageal Varix

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Hemorrhage from a ruptured varix (arrow).

Image provided by David M. Martin, MD.

Because varices are typically associated with significant hepatic disease, evaluation for possible coagulopathy is important. Laboratory tests include complete blood count (CBC) with platelets, prothrombin time (PT), partial thromboplastin time (PTT), and liver tests. Bleeding patients should have type and cross-match for multiple (typically ≥ 6) units of packed red blood cells.

• Airway management and fluid resuscitation, including blood transfusion if needed

• Endoscopic banding (sclerotherapy second choice)

• IV octreotide

• Sometimes antibiotics

• Possibly a transjugular intrahepatic portosystemic shunting (TIPS) procedure

Airway management and fluid resuscitation, including transfusion if needed, are done to manage hypovolemia and hemorrhagic shock. Patients with coagulation abnormalities (eg, significantly elevated international normalized ratio [INR]) can be treated with 1 to 2 units of fresh frozen plasma, but this should be given cautiously because giving large volumes of fluid to patients who are not hypovolemic may actually promote bleeding from varices and is associated with higher mortality (1).

If a patient taking a nonselective beta-blocker (eg, propanolol) has active hemorrhage and hypotension, the beta-blocker should be stopped.

2). OctreotideOctreotide

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 nasogastric tube 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.

More recently, expandable metal esophageal stents have been used successfully to tamponade bleeding.

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 beta-blockers and nitrates) is discussed elsewhere. Treatment of portosystemic encephalopathy may be needed.

Splenectomy is done to treat gastric variceal bleeding due to splenic vein thrombosis (sometimes a sequela of pancreatitis).

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 weeks. 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 years. Ongoing endoscopic or drug therapy (ie, endoscopic banding or nonselective beta-blockers) significantly lowers this risk, but the overall effect on long-term mortality seems to be marginal, probably because of the underlying hepatic disease.

The following English-language resource may be useful. Please note that THE MANUAL is not responsible for the content of this resource.

1. American Society for Gastrointestinal Endoscopy: Guidelines on the role of endoscopy in the management of variceal hemorrhage (2014)

2. American Association for the Study of Liver Diseases: Portal hypertensive bleeding in cirrhosis: Risk stratification, diagnosis, and management: 2016 practice guidance (2016)