Portal hypertension
DEFINITION AND HAEMODYNAMICS
Portal hypertension is a pathological rise in portal venous pressure. The hepatic venous pressure gradient (HVPG) is the difference between wedged and free hepatic venous pressures; normal is approximately 1–5 mmHg. Clinically significant portal hypertension is generally HVPG ≥10 mmHg in sinusoidal cirrhosis; variceal bleeding risk rises as pressure increases, commonly above 12 mmHg.
CAUSES AND CLASSIFICATION
Prehepatic causes include portal vein thrombosis and splenic vein thrombosis. Intrahepatic causes include presinusoidal disease (e.g. schistosomiasis), sinusoidal cirrhosis and postsinusoidal disease. Posthepatic causes include Budd–Chiari syndrome, right heart failure and constrictive pericarditis. Cirrhosis is the commonest cause in many settings.
PATHOPHYSIOLOGY AND COLLATERALS
Fibrosis, regenerative nodules and sinusoidal endothelial dysfunction increase intrahepatic resistance. Splanchnic vasodilatation increases portal inflow and drives collateral formation. Portosystemic collaterals develop at the gastro-oesophageal junction (varices), rectum, umbilicus (caput medusae) and retroperitoneum. Splenic congestion causes splenomegaly and hypersplenism. Increased lymph formation and renal sodium retention contribute to ascites.
CLINICAL FEATURES AND INVESTIGATIONS
Presentation may be asymptomatic or include splenomegaly, thrombocytopenia, ascites, abdominal wall collaterals, haemorrhoidal/rectal varices and upper GI bleeding with haematemesis or melaena. Doppler ultrasound assesses portal vein patency, flow direction, collaterals and splenic size. Endoscopy identifies and grades oesophageal/gastric varices. CT/MRI maps thrombosis and collaterals. HVPG is the reference haemodynamic measurement in selected cases. Investigate the underlying cause and liver reserve.
MANAGEMENT OF VARICES AND BLEEDING
Primary prophylaxis for high-risk oesophageal varices uses a non-selective beta-blocker (e.g. carvedilol or propranolol) or endoscopic variceal ligation, selected according to patient factors. Acute bleeding is an emergency: protect airway when indicated, establish IV access, use cautious resuscitation and a restrictive red-cell transfusion strategy in most patients, start vasoactive therapy (e.g. terlipressin or octreotide) and prophylactic antibiotics, and perform urgent endoscopy with band ligation. Failure of control may require balloon tamponade or an oesophageal stent as a bridge and rescue TIPS. Secondary prophylaxis usually combines beta-blocker and repeated ligation.
OTHER COMPLICATIONS AND SURGICAL OPTIONS
Ascites is managed with sodium restriction, diuretics, paracentesis and selected TIPS. TIPS reduces portal pressure but may precipitate encephalopathy or cardiac decompensation. Surgical portosystemic shunts are now reserved for selected situations where expertise and anatomy support them. Treat portal vein thrombosis according to extent, chronicity and bleeding risk. Liver transplantation is definitive for suitable patients with end-stage liver disease. Complications include variceal haemorrhage, hypersplenism, ascites, SBP and encephalopathy.