## Distinguishing Variceal vs Non-Variceal Bleeding in Cirrhosis **Key Point:** The endoscopic appearance is the gold standard discriminator between variceal and non-variceal sources of bleeding in portal hypertension. ### Endoscopic Findings | Feature | Oesophageal Varices | Portal Hypertensive Gastropathy | |---------|-------------------|--------------------------------| | **Appearance** | Dilated submucosal veins; may show red wale signs, cherry-red spots, or adherent clots | Diffuse mucosal erythema, "mosaic" or "snake-skin" pattern; no discrete vessels | | **Bleeding pattern** | Brisk, often massive; visible vessel or clot in varix | Slow oozing; no discrete bleeding point | | **Endoscopic discrimination** | **Presence of visible vessel/clot within varix** | Absence of discrete vascular lesion | **High-Yield:** The presence of a visible vessel or adherent clot *within* a variceal lesion is the single best endoscopic discriminator and predicts high rebleeding risk (Forrest Ia/Ib). This finding mandates urgent variceal ligation or sclerotherapy. ### Why Other Features Are Non-Discriminatory **Clinical Pearl:** Coagulopathy (elevated PT, thrombocytopenia) and signs of portal hypertension (ascites, splenomegaly) are present in *both* variceal and non-variceal bleeding in cirrhosis — they reflect underlying liver disease, not the bleeding source. Bilirubin and albumin levels reflect synthetic function and do not distinguish bleeding source. ### Management Implication Identification of a visible vessel or clot in a varix on endoscopy determines the need for: - Immediate variceal ligation (preferred) or sclerotherapy - Octreotide infusion - Prophylactic antibiotics (ceftriaxone) In contrast, gastropathy is managed medically with beta-blockers and PPI therapy, without endoscopic intervention.
Sign up free to access AI-powered MCQ practice with detailed explanations and adaptive learning.