Esophageal varices are portosystemic collateral vessels formed by dilation of the submucosal venous plexus of the esophagus due to portal hypertension. They develop in 50% of cirrhosis patients, and bleeding occurs in 25-35% of patients with varices. Variceal bleeding is one of the most important causes of mortality in cirrhosis (15-20% mortality/episode). Varices develop when portal venous pressure exceeds 12 mmHg. On CT, they appear as enhancing serpiginous vascular structures in the distal esophageal wall. Submucosal serpiginous filling defects are characteristic on barium.
Age Range
30-80
Peak Age
55
Gender
Male predominant
Prevalence
Common
Portal hypertension (usually due to cirrhosis) increases pressure in the portal venous system. When portal pressure exceeds 12 mmHg, portosystemic collateral pathways open. Portal blood is diverted to systemic circulation via the left gastric vein (coronary vein) → esophageal submucosal venous plexus → azygos/hemiazygos veins pathway. Progressive dilation of submucosal veins forms esophageal varices. Varices are most prominent in the distal esophagus because this region is the main drainage area of the left gastric vein. They appear as enhancing tubular structures on CT because these dilated veins are filled with contrast. The variceal wall is thin and fragile — rupture risk and life-threatening bleeding exist with mechanical stress (swallowing, coughing) or increased portal pressure.
Serpiginous, lobulated filling defects in the distal esophagus on barium, formed by dilated submucosal veins. Varices become more prominent with Valsalva maneuver. This appearance is the classic barium finding of portal hypertensive esophageal varices.
Enhancing serpiginous tubular structures in the distal esophageal wall on portal venous phase. Varices are submucosal and may appear as wall thickening. Varices show maximum enhancement in portal venous phase. Variceal diameter is proportional to bleeding risk.
Report Sentence
Serpiginous enhancing vascular structures in the distal esophageal wall on portal venous phase; consistent with esophageal varices.
Dilated venous collateral vessels around the esophagus (paraesophageal region). Paraesophageal varices are separate from submucosal varices and localized outside the adventitia. Left gastric vein dilation (>5 mm) is associated. Azygos vein dilation (>10 mm) indicates increased systemic venous drainage.
Report Sentence
Dilated venous collateral vessels in the periesophageal region with left gastric vein dilation; consistent with portal hypertensive collateral circulation.
Serpiginous, lobulated submucosal filling defects in the distal esophagus on barium. Varices create a 'string of beads' or 'worm track' appearance not coated by barium. Varices become more prominent with Valsalva maneuver. May decrease with Mueller maneuver.
Report Sentence
Serpiginous submucosal filling defects in the distal esophagus; consistent with esophageal varices.
Uphill varices (distal 2/3): portal hypertension origin, most common type. Downhill varices (proximal 1/3): superior vena cava obstruction origin, rare. In downhill varices, varices are seen in the upper esophagus accompanied by mediastinal mass/SVC syndrome findings.
Report Sentence
Varices in the distal/proximal esophagus; the localization is consistent with uphill/downhill variceal pattern.
In active variceal bleeding, leakage of enhancing blood into the esophageal lumen (active extravasation). High-density blood is seen within the lumen. Intramural hematoma may be associated. Active bleeding focus can be detected on emergency multiphase CT.
Report Sentence
Active contrast extravasation from esophageal varices into the lumen; consistent with active variceal bleeding — URGENT endoscopic intervention required.
Serpiginous structures showing flow voids in the distal esophageal wall on T2-weighted sequences. High signal may be seen in slow-flow areas. Contrast-enhanced MR angiography demonstrates variceal anatomy in detail. Advantageous for follow-up without radiation exposure.
Report Sentence
Serpiginous vascular structures with flow voids on T2 in the distal esophageal wall; consistent with esophageal varices.
Criteria
Portal hypertension origin, distal 2/3 of esophagus.
Distinct Features
Most common type (95%+). Cirrhosis, portal vein thrombosis. Gastric varices may be associated.
Criteria
SVC obstruction origin, proximal 1/3 of esophagus.
Distinct Features
Mediastinal mass, SVC syndrome findings. Lung cancer, lymphoma. Rare (<5%).
Criteria
Both esophageal and gastric varices together. GOV1: lesser curvature, GOV2: fundus.
Distinct Features
GOV2 has higher bleeding risk. TIPS or BRTO should be considered. Sarin classification used.
Distinguishing Feature
SCC shows asymmetric solid mass with mucosal destruction; varices are serpiginous tubular structures with intact mucosa
Distinguishing Feature
Esophagitis shows diffuse mucosal thickening; varices are focal serpiginous vascular structures with portal HT signs
Distinguishing Feature
Leiomyoma is a solid, homogeneously enhancing single mass; varices are multiple, serpiginous vascular structures enhancing in portal phase
Distinguishing Feature
Fibrovascular polyp is intraluminal pedunculated mass; varices are submucosal serpiginous filling defects changing with Valsalva
Urgency
emergentManagement
interventionalBiopsy
Not NeededFollow-up
6-monthActive variceal bleeding is a life-threatening emergency — mortality 15-20%/episode. Urgent endoscopic band ligation or sclerotherapy is applied. Primary prophylaxis: non-selective beta-blockers (propranolol/nadolol) or prophylactic band ligation. TIPS (transjugular intrahepatic portosystemic shunt) for refractory bleeding. Liver transplantation is the definitive treatment for portal hypertension. CT demonstrates variceal anatomy, paraesophageal collaterals, and portal system pathology — critical for TIPS planning and bleeding risk assessment.
Esophageal varices are one of the most common causes of life-threatening upper GI bleeding. Prophylactic band ligation or beta-blocker therapy (propranolol/nadolol) reduces bleeding risk. Acute bleeding is managed with endoscopic band ligation + vasopressin/octreotide + antibiotics. TIPS is considered for refractory cases.