Management of Liver Disease Complications PDF

Summary

This document discusses the management of hepatic encephalopathy, a syndrome of disordered consciousness and neuromuscular activity seen in patients with acute or chronic liver failure. Treatment focuses on reducing hyperammonemia through dietary protein restriction, colon cleansing, and medication.

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Part 2 2: Ma anageme ent of L iver Dis sease Co omplica ations █ MAN...

Part 2 2: Ma anageme ent of L iver Dis sease Co omplica ations █ MAN NAGEMEN NT OF HEP PATIC EN NCEPHALO OPATHY Definittion and pathogenesis Hepatic c encephalopathy is the syndrome of disordered d con- sciousn ness and neuromu uscular activityy seen in n patients s with acute o or chronic liver failure e. The failing liver cannot metabo- m mmonia and lize am a benzoodiaze- pines-llike med diators (G GABA- ansmitters) generatted by like tra the inntestinal bacteria. These toxins a are shunte S causing encephalo ed directly to the CNS opathy. gement: Treatment Manag T is aimed a at reductio on of hype erammone emia: Diet: – Protein reestriction to t decreasse formatio on of ammo onia by inttestinal bac cteria. – VVegetablee protein is s better tole erated tha an animal protein. p – TThe rationa ale and beenefit of die etary prote ein restriction is conttroversial. Ene emas: clea ansing of the colon n is a rap pid and efffective meethod to remove moniagenic substrates. It can b amm be done with w lactulosse or tape water. Lac ctulose: – It is syntheetic non-ab bsorbable disaccharride. In the e colon, it iis transformed by bacteria intto lactic an acids → ↓ pH nd acetic a p of the co olonic med dium leadin ng to: – Inhibitio on of intes eria → ↓ pro stinal bacte oduction of o ammoniaa. – ↑ transsport of ammonia from blood to intestinal lum men wherre it is converrted to the poorly abssorbed am mmonium io on. – Osmotic laxation → ↑ excrettion of ammonium io on. – It is admin nistered ora ally or as eenema (for patients in n coma). – A Adverse effects: e rellatively saffe drug. Ora al antibiotiics: Neo omycin: – It is non-absorbable aminoglyccoside antibiotic. 262 – It ↓ blood ammonia by killing intestinal bacteria that generate ammonia. – It is used in a dose of 1-2 g 4 times daily orally or as retention enema. – Small amounts of neomycin may be absorbed (~1%) and result in ototoxicity and nephrotoxicity especially in patients with renal impairment. Other antibiotics: – Metronidazole acts on anaerobic bacteria. It is the preferred option if there is fear from adverse effects of neomycin (but given for short term). – Rifaximin: is non-absorbable and better tolerated antibiotic. █ MANAGEMENT OF VARICEAL BLEEDING DUE TO PORTAL HYPERTENSION ▌Management of acute bleeding Fresh blood transfusion. Acid suppression with omeprazole (80 mg) to minimize HCl irritation. i.v. vasopressin or its analogues:  Vasopressin: – It produces mesenteric VC leading to  portal venous flow and pressure. – It can produce systemic VC (coronary, cerebral, limb, etc), so it is better combined with i.v. nitroglycerine to reduce systemic and coronary VC. – The vasopressin/nitroglycerine combination is rarely used now.  Terlipressin: – It is synthetic analog of vasopressin that is released in a slow and sustained manner allowing more sustained hemodynamic effects with fewer systemic side effects than vasopressin. Prophylactic antibiotics: to prevent infectious complications after GI hemorrhage. The preferred antibiotic is i.v. ceftriaxone 1 gm/day for 7 days. Endoscopic sclerotherapy: injection of the varices with a sclerosing agent to induce fibrosis and obliteration. ▌Prevention of re-bleeding (prophylaxis):  Beta-blockers (propranolol 40 mg twice daily). It ↓ portal BP through: – They ↓ COP → ↓ portal blood flow. – They cause unopposed α- action → VC of the splanchnic vascular bed.  H2 blockers or PPIs: to prevent gastroduodenal erosions.  Metoclopramide: to enhance gastric evacuation and  LES pressure. 263

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