Hepatic encephalopathy

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Hepatic Encephalopathy : 

Hepatic Encephalopathy Dr .Umamaheshwara rao

Hepatic encephalopathy (HE) : 

Hepatic encephalopathy (HE) a reversible neuro-psychiatric state a complication of liver failure pathogenesis is not understood fully derangement of neurotransmitter system and metabolic system

Pathogenesis : 

Pathogenesis No single metabolic derangement accounts for HE. Failure of hepatic clearance of gut derived substances. Hepatocellular failure or shunting. Altered aminoacid metabolism. Accumulation of unmetabolized ammonia 2ry to poor hepatic function or shunt. Production of false neurotransmitters. Activation of GABA-Benzo receptors by endogenous ligands. Altered cerebral metabolism. Disturbed activity of Na/K ATPase.

Pathogenesis : 

Pathogenesis Scarring of liver( cirrhosis) Obstruction of the passage of blood (liver) portal hypertension Portal-systemic anastomoses ("shunts“) Bypasses liver Return to heart Toxic substances enters brain Impending hepatic coma

Classification of hepatic encephalopathy : 

Classification of hepatic encephalopathy (World Congress of Gastroenterology 1998 in Vienna ) Type A (=acute) describes hepatic encephalopathy associated with acute liver failure; Type B (=bypass) is caused by portal-systemic shunting without associated intrinsic liver disease; Type C (=cirrhosis) occurs in patients with cirrhosis .

Classification of hepatic encephalopathy : 

Classification of hepatic encephalopathy Type Aetiological factors A(20%) Viral hepatitis, Alcoholichepatitis, Drug reacns &overdose. B(100%) Portal systemic shunt, Dietary protein intake, Intestinal bacteria. C(75%) Diuresis, Haemorrhage,Paracentesis, Diarrhoea,Surgery,Sedatives, Sepsis,Constipation.

Neurotansmitters implicated in HE : 

Neurotansmitters implicated in HE Ammonia and Glutamate Manganese, Mercaptans,Phenols, False neurotransmitters GABA and Endogenous BZD Others :Serotonin,Nitric oxide

Ammonia and Glutamate : 

Ammonia and Glutamate Ammonia is produced from breakdown of proteins, amino acids, purines, pyrimidines. Liver converts ammonia to urea and glutamate by urea cycle In HE, blood NH3 by 90% also brain levels There is no urea cycle in the brain & NH3 is removed by diff pathway NH3 leads to CMR and BBB permeability to NH3

Ammonia and Glutamate …contd : 

Ammonia and Glutamate …contd Hepatic encephalopathy increase in cerebral ammonia astrocyte damage reduced glutamate receptors glutamine accumulates

Ammonia and Glutamate …contd : 

Ammonia and Glutamate …contd SOURCE : intestinal protein/bacteria reduced hepatic removal reduced muscle metabolism NH3 EFFECTS: Astrocyte damage glutamine accumulates BBB permeability (ICP)

Manganese &false neurotransmitters : 

Manganese &false neurotransmitters Blood & Brain Mn levels increased in CLF Normally produced dopamine & catecholamines mediated neuroamines are inhibited by false neurotransmitters (tyramine,octopamine) Plasma levels of aromatic a.a & branched chain a.a

GABA & Endogenous BZD : 

GABA & Endogenous BZD GABA is principal inhibitory amine It binds to specific GABA receptor in postsynaptic memb Receptor also has binding site for BZD &barbiturates GABA & Endogenous BZD are high in plasma &CSF of liver failure pts These leads to hyperpolarisation &neuroinhibition

Symptoms & Signs : 

Symptoms & Signs Earliest manifestations of hepatic encephalopathy is 'day-night Reversal‘ Impairment in spatial perception Changed cognitive function –mild confusion to coma Flapping tremor (asterixis ) Exaggerated deep tendon reflexes &sustained ankle clonus

Acute liver failure : 

Acute liver failure (Depending on onset of encephalopathy & onset of jaundice) Hyperacute - less than 7days Acute - 7 to 28 days Subacute - 28days to 6months Chronic - more than 6 months

Investigations : 

Investigations CSF analysis :cell count,protein, glutamatic acid Electroencephalogram :b/l synchronous slowing of waves Evoked potentials Brain scans Magnetic resonance spectroscopy Neuropathology

Treatment of Hepatic encephalopathy : 

Treatment of Hepatic encephalopathy Broadly divided into 3 areas Identification & treatment of ppt factors Interventions to reduce the production of & absorption of gut derived ammonia & other toxins Prescription of agents to modify neurotransmitters

Reduction of absorption and production of ammonia : 

Reduction of absorption and production of ammonia Protein restriction to 20g/day then increase 10g /3-5 days and evaluate tolerance. Supplementation with vegetable protein is important in patients with low tolerance.(Related to fiber/protein ratio) Reduction of endogenous (intestinal cells shedding) and dietary ammoniagenics by cathartics (Lactulose and Lactitol). Dose titrated to 2-4 loose/acidic stools/day generally requiring 30-60grams/day. Lactulose (10-30ml tid): 1- Decreases Intestinal PH. Favors growth of non-urease producing bacteria. 2- Promotes movement of ammonia from blood to bowel and decreased absorption. Lactilol (0.3-0.5g/kg/day)–responds more quickly,less diarrhoea & flatulence

Reduction of absorption and production of ammonia : 

Reduction of absorption and production of ammonia Antibiotics : Neomycin (4-6 gr /day )for 5-7 days in acute cases reduces ammonia formation in GIT (careful in RF) Metronidazole(200 mg Qid ) Rifaximin, or brand name Xifaxan, a derivative of rifamycin at a dose of 400 mg taken orally 3 times a day was as effective as lactulose or lactilol at improving hepatic encephalopathy symptoms. Similarly, rifaximin was as effective as neomycin and paromomycin. Rifaximin was better tolerated than both the cathartics and the other nonabsorbable antibiotics. . There are also concerns regarding the cost-effectiveness of the medication. Purgation by enemas esp phosphate Repopulation of bowel with non urease producing bacteria. Erradication of H. pylori.

Other support : 

Other support Supplementation with ornithine-aspartate to provide substrates for ammonia detoxification Reduction of false neurotransmitters Formulas rich in branched chain a.a and low in aromatic a.a. Decreased activity of dopaminergic neurotransmitters taken care with bromocriptine or levodopa Controversial results in the use of Flumazenil to block GABA-Benzo receptor (Increased endogenous production of benzo-like ligands).

Slide 24: 

Management in Acute Liver Failure : HE rapid in onset and associated with cerebral edema in later stages. ALF with stage 3-4 HE should undergo elective ventilation , sedation with fentanyl, and paralysis if needed to avoid surges in ICP 2ry to psycomotor agitation(propofol). Mannitol is the mainstay of therapy for cerebral edema in these cases. Acetylcysteine and PGI2 have also proven beneficial. Avoidance of hyopglycemia is paramount

Other options : 

Other options Shunt occlusion Hepatic support(MARS) Hepatic transplantation

Molecular adsorbent recirculating system(MARS) : 

Molecular adsorbent recirculating system(MARS) MARS is a device used to perform albumin liver dialysis. The basic technical concept is based on conventional HD It is a liver support system developed to support excretory liver function It uses an albumin enriched dialysate to facilitate the removal albumin bound toxin(ABT)

Schematic drawing of the molecular adsorbent recirculating system : 

Schematic drawing of the molecular adsorbent recirculating system

USES OF MARS : 

USES OF MARS Acute fulminant liver failure Acute on chronic liver failure (acute hepatorenal synd) ALF with extensive liver resection for tumour As temporary support in spontaneous recovery following abalative liver surgery Liver transplant pt with primary graft dysfunction

ISSUES TO RESOLVED(MARS) : 

ISSUES TO RESOLVED(MARS) Optimal timing of initiation & intensity of MARS Optimum dose of albumin liver dialysis Better approach b/w continous or intermittent

References : : 

References : R.D.Miller.Miller’s anaesthesia ,6th ed 2005, P-2209-2229. Sheila sherlock & James dooley.Diseases of the liver & biliary system,11th ed,P-93-110. H .K. Tan: Hepatic excretory-assist device. Ann Acad Med Singapore 2004;33:329-335.

Slide 31: 

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