Incidence
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Aetiology	- pressure in the portal vein is normally 5-8 mmHg, with a small gradient via the liver to the hepatic vein - as portal pressure rises above 10-12 mmHg, the portal venous system dilates and forms collaterals with the systemic venous system at the gastro-oesophageal junction, the rectum, the left renal vein, the diaphragm, the retroperitoneum and the anterior abdominal wall (via the umbilical vein) - the oesophageal varices are the most prone to complications - portal hypertension can be classified according to site of obstruction: - prehepatic - due to blockage of the portal vein before the liver - intrahepatic - due to presinusodal or postsinusoidal distortion of liver architecture - posthepatic (rare) - venous blockage outside the liver Pathophysiology - during liver injury, stellate cells are activated and transform into myofibroblasts, with expression of a-actin - these contract in response to (the usual) vascular mediators -> abnormal blood flow and increased resistance - this leads to the changes of portal hypertension in both cirrhotic and precirrhotic livers - patients with cirrhosis have a hyperdynamic circulation; mediators induce peripheral and splanchnic vasodilatation -> plasma volume expansion with sodium retention Causes - prehepatic - portal vein thrombosis - intrahepatic - cirrhosis, hepatitis, idiopathic non-cirrhotic protal hypertension, schistosomiasis, partial nodular transformation, congenital hepatic fibrosis, myelosclerosis, granulomatia - posthepatic - Budd-Chiari syndrome, veno-occlusive disease, right heart failure, constrictive pericarditis
Presentation	- generally asymptomatic, ± large spleen - may present acutely with haematemesis or melaena from variceal haemorrhage - ascites - encephalopathy
Investigations	Acute bleed - bloods for group and crossmatch, Hb, PT, U&Es, LFTs
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Management	Management of variceal haemorrhage Initial management of acute variceal bleeding 1) Resuscitation - assess general condition, pulse and BP - i.v. access, bloods - restore volume with plasma expanders or, preferably, blood transfusion - prompt correction of hypovolaemia is important in cirrhotics as their baroreceptor reflex is impaired Urgent endoscopy - confirm diagnosis of varices - injection sclerotherapy or banding - this arrests bleeding in 80% of cases and reduces the incidence of rebleeding - 15-20% of bleeding is due to gastric varices; results of sclerotherapy under these conditions are poor Vasoconstrictor therapy - aim is to restrict portal inflow by constricting the splanchnic arterial bed - octreotide 50 µg bolus followed by 50 µg/hour infusion for 48 hours; octreotide is safe, has few systemic side-effects, and is as effective as ballon tamponade - vasopressin 25 u/hour via central venous catheter (reduces risk of leakage and necrosis); should not be given to those with ischaemic heart disease; nitrates enhance efficacy and reduce side-effects, which include abdominal colic, defaecation and facial pallor; terlipressin is a longer-acting alternative Balloon tamponade - used if sclerotherapy is impossible or unsuccessful, or if vasoconstrictor therapy has failed or is contraindicated - Sengstaken-Blakemore tube passed into stomach; gastic balloon is inflated with air and pulled back - oesophageal balloon should be inflated if the gastric balloon does not stop bleeding by itself - successful in up to 90% of patients; very useful in first few hours of haemorrhage - complications include aspiration pneumonia, oesophageal rupture, mucosal ulceration (can be minimized with sucralfate 1 g qds); 5% mortality Management of acute rebleed - 50% rebleed within 10 days Endoscopy - repeat sclerotherapy Octreotide infusion for 3-5 days Transjugular intrahepatic portocaval shunt (TIPS) - guidewire is passed from jugular vein into the liver - an expandable metal shunt is passed over guidewire and forms a channed between the two venous systems - reduces sinusoidal and portal vein pressure - used when two sessions of sclerotherapy 24 hours apart fail to stop bleeding Emergency surgery - oesophageal transection and ligation of the bleeding vessels - used when other measures fail - especially when the bleeding varices are in the gastric fundus Prevention of recurrent variceal bleeding - following an acute bleed, there is a 60-80% risk of a re-bleed within 2 years; each of these re-bleeds has a 20% mortality Long-term injection sclerotherapy/banding - when performed at weekly intervalse, leads to obliteration of varices by fibrous tissue - varices return in 30-40% of cases each year - effect on survival is slight - sclerotherapy can cause oesophageal ulceration, mediastinitis and strictures ß-adrenoceptor blockade - oral propranolol reduces portal blood pressure by reducing cardiac output and causing unopposed constriction of splanchnic arteries - reduces frequency of rebleeding in patients with well-compensated disease Portosystemic shunting - associated with a significant reduction in re-bleeding, but also significant encephalopathy Consider liver transplant Prophylactic measures - non-selective ß-blockers, e.g. propranolol, should be prescribed to patients with cirrhosis and variced who have not bled
Prognosis	- prehepatic portal hypertension - these patients have normal liver function, hence prognosis following bleeding is excellent - overall mortality from variceal haemorrhage is 30% - however, in Child's grade C cirrhosis, this is 50%
Complications	- portosystemic encephalopathy can be precipitated by a large bleed

Hepatobiliary medicine

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