Management of Liver Disease Complications PDF

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CleanlyBoston

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Mansoura

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hepatic encephalopathy liver disease clinical pharmacology medical treatment

Summary

This document discusses the management of liver disease complications, focusing on hepatic encephalopathy, including dietary interventions, use of enemas, and lactulose for ammonia reduction. It also covers treatment options for variceal bleeding related to portal hypertension.

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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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