Gastric Varices

Dilated submucosal veins in the gastric fundus or body from portal hypertension or splenic vein obstruction, draining mostly through a gastrorenal or splenorenal shunt; they bleed less often than oesophageal varices but bleed more severely.

• Classification by location: GOV1 (oesophageal varices continuing along the lesser curve), GOV2 (continuing along the greater curve into the fundus), IGV1 (isolated in the fundus), IGV2 (isolated elsewhere in the stomach or duodenum).
• Found in about 20% of patients with portal hypertension; bleeding risk is about 10 to 25% at 2 to 5 years (highest for fundal varices larger than 10 mm); bleeding carries a mortality of about 20 to 30% at 6 weeks and rebleeding of about 30 to 90% at 1 year without prevention.
• Causes: cirrhosis, schistosomiasis, portal vein thrombosis, and sinistral (left-sided) portal hypertension from splenic vein thrombosis due to pancreatitis, pancreatic tumour or splenic injury (isolated fundal varices with normal liver).
• Mechanism: raised portal pressure (or splenic vein pressure) pushes blood through short gastric and posterior gastric veins into large collaterals that have thinner walls, so they tolerate less wall stress.

Often asymptomatic; presents with haematemesis (large volume), melaena, shock, or anaemia; signs of chronic liver disease or of pancreatic disease and splenomegaly.

• Splenic vein thrombosis: epigastric pain history, pancreatitis, splenomegaly with preserved liver function.
• Differential diagnosis: oesophageal varices, peptic ulcer, erosive gastritis, portal hypertensive gastropathy, gastric antral vascular ectasia, Dieulafoy lesion, gastric tumour, fundic submucosal mass.
• Complications: massive haemorrhage, rebleeding, hepatic encephalopathy (large shunts), infection, renal injury, and glue embolisation (after cyanoacrylate injection).

Upper endoscopy shows tortuous bulging varices, often with a smooth, white or bluish surface and red spots, best seen with retroflexion in the fundus; differentiate from gastric folds and from tumour by CT or endoscopic ultrasound.

• CT or MR angiography: delineates the feeder and draining veins (gastrorenal or splenorenal shunt), splenic or portal vein thrombosis, liver morphology and tumour.
• Endoscopic ultrasound with Doppler: varix size, perforating veins, and flow to guide therapy.
• Blood tests: full blood count, INR, albumin, bilirubin, creatinine, electrolytes, group and crossmatch; hepatitis serology; schistosomiasis tests.
• Doppler ultrasound for portal and splenic vein patency.

Resuscitate and control bleeding, obliterate the varices, and treat the cause; therapy differs from oesophageal varices because band ligation is less effective for fundal varices.

• Acute bleeding:
  • Airway protection, two large-bore cannulae, restrictive transfusion (haemoglobin 70 to 80 g/L), and avoidance of over-transfusion.
  • Vasoactive drug for 2 to 5 days: terlipressin 2 mg IV every 4 hours for 48 hours then 1 mg every 4 hours, or octreotide 50 micrograms IV bolus then 50 micrograms/hour.
  • Ceftriaxone 1 g IV daily for up to 7 days; erythromycin 250 mg IV 30 to 120 minutes before endoscopy; lactulose 30 mL every 8 hours in encephalopathy risk.
  • Endoscopy within 12 hours: GOV1: band ligation of the bleeding varix every 2 to 4 weeks until eradication; GOV2 and IGV1: injection of cyanoacrylate glue (N-butyl-2-cyanoacrylate 0.5 to 1 mL per injection mixed with lipiodol in a 1:1 ratio, into the varix, with flushing, at one to three sites, up to 2 to 4 mL in total).
  • Bleeding not controlled: oesophagogastric balloon tamponade (a gastric balloon tube with a large gastric balloon for fundal varices, maximum 24 hours), then rescue transjugular intrahepatic portosystemic shunt with embolisation of the varices.
  • Pre-emptive shunt within 72 hours in high-risk patients (advanced cirrhosis).
• Obliteration (secondary prophylaxis):
  • Repeat glue injection every 2 to 4 weeks until obliteration (confirmed by endoscopic ultrasound or CT), then follow-up at 3 to 6 months.
  • Balloon-occluded retrograde transvenous obliteration through a gastrorenal shunt (sclerosant ethanolamine oleate 5% or foam polidocanol and balloon occlusion), preferred for isolated fundal varices with a large shunt and preserved liver function (watch for oesophageal varices worsening afterwards, which should be banded or treated).
  • Transjugular intrahepatic portosystemic shunt, with or without embolisation of gastric varices, for rebleeding, ascites or when a gastrorenal shunt is absent.
  • Beta blockers: propranolol 20 to 40 mg twice daily (heart rate 55 to 60 beats/min, maximum 160 mg daily without ascites) or carvedilol 6.25 mg once daily increasing to 6.25 mg twice daily, to reduce rebleeding (evidence is moderate).
• Primary prophylaxis: for GOV2 and IGV1 with large size (more than 10 mm) or red signs, propranolol 20 to 40 mg twice daily (heart rate 55 to 60 beats/min) or carvedilol 6.25 mg once daily increasing to 6.25 mg twice daily, and consider glue injection in selected high-risk patients; evidence is limited.
• Splenic vein thrombosis (sinistral portal hypertension): splenectomy or splenic artery embolisation cures the varices when the liver is normal; treat pancreatitis and anticoagulate only when there is a clear indication.
• Treat the cause: alcohol abstinence, hepatitis B (tenofovir 245 mg daily or entecavir 0.5 mg daily), hepatitis C (sofosbuvir-velpatasvir 400/100 mg daily for 12 weeks), schistosomiasis (praziquantel 40 mg/kg once), portal vein thrombosis (anticoagulation), and liver transplant assessment.
• Special groups: children (propranolol 1 mg/kg/day, glue injection by an experienced endoscopist, early referral); pregnancy (glue injection and octreotide, avoid terlipressin and balloon-occluded retrograde transvenous obliteration where possible); elderly (cautious beta blocker titration); renal impairment (avoid NSAIDs and aminoglycosides, albumin for hepatorenal syndrome); portal vein thrombosis (anticoagulation under specialist care).
• Red flags: haematemesis, shock, fever, confusion, rising creatinine, rebleeding within 5 days, pulmonary or cerebral symptoms after glue injection.
• Follow-up: endoscopy at 2 to 4 weeks until obliteration, then at 3 to 6 months and every 6 to 12 months; CT or endoscopic ultrasound to confirm obliteration; liver tests and ultrasound every 6 months in cirrhosis.