Oesophageal varices

Definition

• Submucosal venous dilatation secondary to ↑portal pressures
• Not necessarily need to have a liver pathology—suspect if alcohol history
• Bleeding can be brisk, particularly if underlying coagulopathy 2° to loss of hepatic synthesis of clotting factors

Pathogenesis (from liver cirrhosis)

Progressive fibrosis and architectural reorganization of the liver (including nodule formation) → nodules produce contractile elements in the liver’s vascular bed → portal hypertension (from 9mmHg to 12mmHg) → arterial splanchnic vasodilation in response to portal hypertension (blood vessels supplying visceral organs) → hyperdynamic circulation (i.e. increased cardiac output, HR and decreased vascular resistance) → salt and water retention → increase portal flow → formation of collateral (porto-systemic collateral) between the portal and systemic systems e.g. in the lower oesophageal and gastric cardia → gastro-oesophageal varices develop once portal pressure is >10mmgHg (>12mmHg causes bleeding)

Variecs can also be found in the umbilicus (caput medusa, rare) and rectum

Causes

• Pre-hepatic
  • Thrombosis (portal or splenic vein)
• Intrahepatic
  • Cirrhosis (80%)
  • Schistosomiasis (commonest worldwide)
  • Sarcoid
  • Myeloproliferative disease
  • Congenital hepatic fibrosis
• Post hepatic
  • Budd-Chiari syndrome
  • Right heart failure
  • Constrictive pericarditis
  • Veno-occlusive disease

Management

Blood transfusion

Blood transfusion should be started when the haemoglobin level reaches 7 g/dL, and maintained between 7 g/dL and 9 g/dL (restrictive transfusion policy).[5][33][34] Blood transfusion above this threshold may increase mortality.[32]

All pateints with chirosis and variceal bleed

• Step 1: Terlipressin or Somatostatin (synthetic analogue of vasopressin → splanchnic arterial constriction, CI: IHD)
• Step 2: 7 day prophylactic antibiotics (all patients with chirosis and variceal bleed) to cover gram negative infection
• Step 3: Endoscopy (bang ligation or sclerotherapy) within 12 hours Band-ligation is superior to sclerotherapy

In selective patients with chirosis and variceal bleed

• Step 4: Early Transjugular Intrahepatic Portosystemic Shunting (TIPS) (esp. as rescue therapy if Step 1-3 fails, in high risk pateints Child-Pugh class C (with a score <14) or class B with active bleeding within 24-72 hours from admission ) A metal stent is passed over a guidewire in the internal jugular vein and then pushed into the liver substance under radiological guidance. A shunt is formed between the portal and hepatic vein, thus lowering the portal pressure.

• Step 3: if above fails, balloon tamponed with a Sengstaken-Blakemore tube (Risks: aspiration pneumonia, tissue necrosis, oesophageal rupture)

• Step 5: Surgery (oesophageal transection and ligation of varices) if all above fails.

Prevention:

Recurrence high so need prophylaxis (primary or secondary) to prevent re-bleed

• Propranolol as both primary and secondary prophylaxis
• Repeated courses of variceal banding
• TIPS or occasionally a surgical portosystemic shunt