Introduction to Esophageal Varices in Children

Portal hypertension is defined as an elevation of portal venous pressure to levels 10–12 mm Hg higher than pressures present in the inferior vena cava. Decompression of this hypertension through portosystemic collateral circulation via the coronary vein, in conjunction with the left gastric veins, gives rise to esophageal varices. Most esophageal varices are “uphill varices”; less commonly, those that arise in the absence of portal hypertension and with superior vena cava (SVC) obstruction are termed “downhill varices.” Their treatment is directed at the underlying cause of the SVC abnormality.

Clinical Presentation:
Hemorrhage from esophageal varices is the major cause of morbidity and mortality due to portal hypertension. Presentation is with significant hematemesis and melena; whereas most patients have liver disease, some children with entities such as extrahepatic portal venous thrombosis may have been previously asymptomatic. Any child with hematemesis and splenomegaly should be presumed to have esophageal variceal bleeding until proven otherwise.

Diagnosis:
Varices are occasionally seen on fluoroscopic barium contrast studies, but upper endoscopy is preferred because it provides definitive diagnosis as well as therapy for acute bleeding episodes via either sclerotherapy or band ligation.

Treatment:
Treating children with varices with prophylactic sclerotherapy with the goal of preventing an initial hemorrhage can decrease the incidence of esophageal bleeding. Treated patients may bleed from congestive gastropathy, and no improvement in survival rate may be seen. Nonselective ? blockade, such as with propranolol, has also been used to prevent variceal bleeding. Endoscopic variceal ligation in adults reduces the risk of first-time variceal bleeding when compared with untreated controls as well as patients treated with ? blockade; a decrease in mortality is only noted in comparison to the control group