Varices are dilated anastamoses between the portal and systemic venous systems which form in an attempt to decompress the portal venous system when the pressure within undergoes sustained elevation. Those in the lower oesophagus or gastric body are prone to rupture because they are thin-walled and lie just below the mucosa.
Portal pressure is a function of resistance in the portal venous system and the flow of blood through it. In cirrhosis, portal venous resistance is increased, and inflow of blood is increased by splanchnic vasodilatation and elevation of cardiac output. Variceal bleeding is increasingly likely as the pressure gradient between the portal and systemic venous systems rises beyond 12 mmHg.
Up to 50% of patients with portal hypertension bleed from oesophageal or gastric varices and half die from complications of their first bleed. Hypovolaemia must be corrected with plasma expanders and blood transfusion. Sepsis is common; the incidence rises from 20% at 48 hours to over 60% at 7 days and antimicrobial prophylaxis should be given with ciprofloxacin (lg/day). Some 70% will stop bleeding spontaneously but over half re-bleed within 10 days.
Acute variceal bleeding
Management involves measures directed at the varices and also to reduce portal pressure by pharmacological methods and blood shunting procedures.
Direct treatment of varices by endoscopy is preferred. Band ligation, in which the varices are strangulated by application of small elastic bands has fewer complications than sclerotherapy, which involves injecting sclerosant into and around the varices but may lead to oesophagitis, stricture or embolisation of sclerosant. Either technique can control bleeding in about 90% of patients, and rebleeding is reduced if this direct treatment is combined with reduction of portal pressure (see below).
Direct pressure on varices can be applied by inserting an inflatable triple-lumen (Sengstaken) tube which abuts the gastro-oesophageal junction, and controls bleeding in 90%; rebleeding is common when the tube is withdrawn and its use may be accompanied by aspiration, oesophageal ulceration or perforation.
Reduction of portal pressure. Vasopressin (anti-duiretic hormone, see p. 711), in addition to its action on the renal collecting ducts (through V2 receptors), constricts smooth muscle (Vj receptors) in the cardiovascular system (hence its name), and particularly in splanchnic blood vessels, so reducing blood flow in the portal venous system. Unfortunately, coronary vasoconstriction can also occur, and treatment has to be withdrawn from 20% of patients because of myocardial ischaemia. Glyceryl trinitrate (transdermally, sublingually, or intravenously) reduces the cardiac risk and, advantageously, further reduces portal venous resistance and pressure.
Vasopressin is rapidly cleared from the circulation and must be given by continuous i.v. infusion. The synthetic analogue, terlipressin (triglycyl-lysine-vasopressin) is now preferred. This prodrug (or hormogen) is converted in vivo to the vasoactive lysine vasopressin which has biological activity for 3-4 hours, and is effective by bolus injections 4-hourly, usually for 48-72 hours. It is a useful adjunct to endoscopic therapy and reduces rebleeding.
Somatostatin and its synthetic analogue octreotide reduce portal pressure by decreasing splanchnic blood flow. Octreotide has the advantage of a longer duration of action so that it can be given as a bolus injection rather than the constant intravenous infusion needed for administration of somatostatin. Its can be used as an alternative to terlipressin, having similar efficacy and indications for use.
Patients who continue to bleed despite the above measures require surgery (ligation or transection of varices) or placement of a stent between intrahepatic branches of the portal and (systemic) hepatic veins under radiological control. The latter is now the technique of choice for the 10-15% of patients with acute bleeding resistant to conventional treatment, and also for long-term management of patients who are difficult to help by other methods (see below).
Endoscopic therapy as (above), preferably by band ligation, and repeated at weekly intervals until all varices are obliterated, is currently the treatment of choice; it reduces the incidence of rebleeding by 50-60%.
Pharmacological therapy. Nonselective p-blockers, e.g. propranolol or nadolol, reduce cardiac output (Pj receptor antagonism) and induce splanchnic vasoconstriction (p2 receptor antagonism allowing unopposed a-adrenergic vasoconstriction). Recurrent bleeding is reduced by about 40%. As propranolol is extensively extracted in a single pass through the liver, its systemic availability may be unpredictable in patients with cirrhosis and portal hypertension due to variations in hepatic blood flow and portal/ systemic shunts. Ideally, the dose of propranolol (given b.d.) should be adjusted by measuring the portal/systemic venous pressure gradient; if this is not feasible, the resting pulse rate is monitored, aiming at a 25% reduction. Decreased cardiac output can exacerbate impaired renal function and fluid retention. Nadolol, having a longer duration of action, is given only once daily.
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Your heart pumps blood throughout your body using a network of tubing called arteries and capillaries which return the blood back to your heart via your veins. Blood pressure is the force of the blood pushing against the walls of your arteries as your heart beats.Learn more...