Esophageal and Gastric Varices

Morphology
tortuous dilated veins lying primarily within the submucosa of the distal esophagus and proximal stomach; venous channels directly beneath the esophageal epithelium may also become massively dilated. The net effect is irregular protrusion of the overlying mucosa into the lumen, although vertices are collapsed in surgical or postmortem specimens. When the varix is unruptured, the mucosa may be normal, but often it is eroded and inflamed because of its exposed position. Variceal rupture produces massive hemorrhage into the lumen, as well as suffusion of the esophageal wall with blood. In this instance the overlying mucosa appears ulcerated and necrotic. If rupture has occurred in the past, venous thrombosis and superimposed inflammation may be present.

Etiology: PORTAL HYPERTENSION

the elevation of the hepatic venous pressure gradient (HVPG) to >5 mmHg caused by a combination of two simultaneously occurring hemodynamic processes: (1) increased intrahepatic resistance to the passage of blood flow through the liver due to cirrhosis and regenerative nodules, and (2) increased splanchnic blood flow secondary to vasodilatation within the splanchnic vascular bed. Cirrhosis is the most common cause of portal hypertension in the United States, and clinically significant portal hypertension is present in >60% of patients with cirrhosis. Portal vein obstruction may be idiopathic or can occur in association with cirrhosis or with infection, pancreatitis, or abdominal trauma.

Clinical features: ESOPHAGEAL

Usually produce no symptoms until they rupture, producing massive hematemesis
Factors leading to rupture of a varix are unclear; however, the following are likely to play roles: silent inflammatory erosion of underlying thinned mucosa increased tension in progressively dilated veins vomiting with increased vascular hydrostatic pressure

Cirrhosis and varices

Approximately one-third of patients with histologically confirmed cirrhosis have varices. Approximately 5 15% of cirrhotics per year develop varices, and it is estimated that the majority of patients with cirrhosis will develop varices over their lifetime. Roughly one-third of patients with varices will develop bleeding.

Clinical features: GASTRIC

Develop in the setting of portal hypertension but less often than esophageal varices. Most lie between 2-3cm of the gastroesophageal junction, arising from longitudinally placed submucosal veins. They often appear as masslike, tortuous and winding elevations of the mucosa in the cardia or fundus Due to their deep submucosal or subserosal location and the normal color of the overlying mucosa, it may be difficult to distinguish varices from enlarged rugae or even malignancy.

Variceal bleeding
Patients with variceal hemorrhage have poorer outcomes than patients with other sources of UGIB. Factors that predict the risk of bleeding include:
the severity of cirrhosis the height of wedged-hepatic vein pressure the size of the varix the location of the varix certain endoscopic stigmata, including red wale signs, hematocystic spots, diffuse erythema, bluish color, cherryred spots, or white-nipple spots. tense ascites are also at increased risk for bleeding from varices.

Primary prophylaxis
Routine screening by endoscopy of all patients with cirrhosis:
Once varices that are at increased risk for bleeding are identified, then primary prophylaxis can be achieved either through nonselective beta blockade or by variceal band ligation.
Patients treated with beta blockers have a lower risk of variceal hemorrhage than those treated with placebo over 1 and 2 years of follow-up. There is also a decrease in mortality related to variceal hemorrhage. Unfortunately, overall survival was improved in only one study. Further studies have demonstrated that the degree of reduction of portal pressure is a significant feature to determine success of therapy. Therefore, it is has been suggested that repeat measurements of hepatic vein pressure gradients may be used to guide pharmacologic therapy; however, this may be cost prohibitive. Several studies have evaluated variceal band ligation and variceal sclerotherapy as methods for providing primary prophylaxis.

Treatment
local treatment of the bleeding vessel (if hemorrhage is present)
Local therapies, including endoscopic sclerotherapy, endoscopic band ligation, and balloon tamponade with a Sengstaken-Blakemore tube, effectively control acute hemorrhage in most patients and are the mainstay of acute treatment

treatment of the underlying portal hypertension

pharmacologic treatment, surgical shunts, or radiologically placed intrahepatic shunts

Treatment (cont d)
Endoscopic intervention is employed as first-line treatment to control bleeding acutely. Some endoscopists will use variceal injection therapy (sclerotherapy) as initial therapy, particularly when bleeding is vigorous. Variceal band ligation is used to control acute bleeding in over 90% of cases and should be repeated until obliteration of all varices is accomplished.

Treatment (cont d)
When esophageal varices extend into the proximal stomach, band ligation is less successful. In these situations, when bleeding continues from gastric varices, consideration for transjugular intrahepatic portosystemic shunt (TIPS) should be made.
creates a portosystemic shunt by a percutaneous approach under angiographic guidance to create a direct portocaval shunt. offers an alternative to surgery for acute decompression of portal hypertension. Encephalopathy can occur in as many as 20% of patients and is particularly problematic in elderly patients and in those patients with preexisting encephalopathy should be reserved for those individuals who fail endoscopic or medical management or who are poor surgical risks

Surgical esophageal transsection is a procedure that is rarely used and generally is associated with a poor outcome.

Local treatment: ENDOSCOPIC SCLEROTHERAPY

a sclerosing, thrombogenic solution is injected into or next to the esophageal varices controls acute hemorrhage in most patients but has a higher complication rate than band ligation

Local treatment: ENDOSCOPIC BAND LIGATION

When feasible, endoscopic band ligation is the preferred local therapy for control of active esophageal variceal bleeding and for subsequent eradication of esophageal varices In this technique a varix is suctioned into a cap fitted on the end of the endoscope, and a rubber band is then released from the cap, ligating the varix Acute hemorrhage can be controlled in up to 90% of patients, and complications (such as sepsis, symptomatic esophageal ulceration, or esophageal stenosis) are uncommon.

Local treatment: CYANOACRYLATE INJECTION

Bleeding from large gastric fundic varices is best treated by cyanoacrylate ("glue") injection, since band ligation or sclerotherapy of these varices are associated with a high rebleeding rate

Other treatment: MEDICAL

Prevention of further bleeding is usually accomplished with repeated variceal band ligation until varices are obliterated. Treatment of acute bleeding requires both fluid and blood product replacement. Use of vasoconstricting agents, usually somatostatin or Octreotide
Octreotide, a direct splanchnic vasoconstrictor, is given at dosages of 50 100 g/h by continuous infusion. Vasopressin was used in the past but is no longer commonly used.