What causes gastric varices?

Causes of Gastric Varices

Gastric varices primarily develop as a result of portal hypertension, which can occur due to cirrhosis or non-cirrhotic causes such as splenic vein occlusion or thrombosis. 1, 2

Primary Mechanisms

1. Portal Hypertension Due to Cirrhosis

• Portal pressure increases due to:
  • Structural resistance: Architectural distortion of the liver from fibrous tissue and regenerative nodules (70-80% of increased resistance) 1
  • Active intrahepatic vasoconstriction: Accounts for 20-30% of increased resistance, primarily due to decreased endogenous nitric oxide production 1
  • Increased portal venous inflow: Results from splanchnic arteriolar vasodilation 1
  • Insufficient portal decompression: Collaterals have higher resistance than normal liver 1

2. Splenic Vein Occlusion (Sinistral Portal Hypertension)

• Causes localized portal hypertension without cirrhosis 2
• Blood from spleen is diverted through collateral vessels, forming varices primarily in gastric fundus 2
• Common etiologies include:
  • Pancreatic disorders (cancer, chronic pancreatitis, pseudocysts)
  • Thrombophilic disorders
  • Myeloproliferative disorders
  • Various malignancies (lymphoma, gastric cancer, renal cancer)
  • Post-surgical complications 2

Classification of Gastric Varices

Gastric varices are classified based on their location and relationship to esophageal varices:

1. Gastroesophageal varices (GOV):

   • GOV1: Extension of esophageal varices along lesser curvature (most common, ~74%) 1
   • GOV2: Extension of esophageal varices into gastric fundus 1

2. Isolated gastric varices (IGV):

   • IGV1: Located in fundus without esophageal varices 1
   • IGV2: Located in other regions of stomach or duodenum 1

Anatomical Drainage Routes

Gastric varices typically drain through two main portosystemic collateral systems:

1. Gastroesophageal (azygous) venous system:

   • Gastric varices contiguous with esophageal varices
   • Drains into azygos vein and ultimately superior vena cava 3

2. Gastrophrenic venous system:

   • Gastric varices connect to left inferior phrenic vein
   • Drains into left renal vein or inferior vena cava
   • Often forms spontaneous gastrorenal shunts 3, 4

Clinical Significance

• Gastric varices occur in approximately 20% of patients with portal hypertension 1, 5
• Less prevalent than esophageal varices but associated with higher mortality when bleeding occurs 1
• Risk factors for gastric variceal bleeding include:
  • Size of varices (large/medium > small)
  • Location (IGV1 > GOV2 > GOV1)
  • Presence of red spots on varices
  • Severe liver dysfunction (Child C > B > A) 1
• Unlike esophageal varices, gastric varices can bleed at lower portal pressure gradients, likely due to frequent spontaneous gastrorenal shunts 5

Important Considerations

• Proper diagnosis requires both endoscopy and cross-sectional imaging (contrast-enhanced CT or MRI) 1, 2
• Treatment approach differs based on the type of gastric varices and underlying cause
• GOV1 should be managed similar to esophageal varices, while fundal varices (GOV2, IGV1) require different approaches 1, 5
• Understanding the drainage pathways is crucial for selecting appropriate treatment options 3

Recognizing the specific cause of gastric varices is essential for determining the optimal management strategy and preventing potentially life-threatening bleeding complications.