Hepatic encephalopathy 2012 presentation
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Hepatic encephalopathy 2012 presentation
- 1. 7 December, 2014 Phase 2 medicine posting PRESENTER: MUSA IKO MODURATOR: DR BANCY
- 2. Introduction Epedimiology Classification Aetiopathogenesis precipitant Clinical features Differential diagnosis Investigation Treatment 7 December, 2014 Outline
- 3. Introduction spectrum of neuropsychiatric abnormalities in patients with liver dysfunction, after exclusion of other known brain disease is a potentially reversible, or progressive, neuropsychiatric syndrome characterized by changes in cognitive function, behaviour, and personality, as well as by transient neurological symptoms and characteristic EEG patterns associated with acute and chronic liver failure. 7 December, 2014
- 4. Clinical spectrum ranges from minor signs of altered brain function to deep coma. It occurs in approximately 30-45% of patients with cirrhosis and 10-50% of patients with TIPS, while minimal HE affects approximately 20-60% of patients with liver disease. prevalence of minimal hepatic encephalopathy detectable on formal neuropsychological testing is 60–80%; 7 December, 2014 Epidemiology
- 5. Hippocrates (460-370 BC) described a patient with hepatitis who ‘barked like a dog, could not be held and said things which could not be comprehended’. Giovanni Battista Morgagni (1682–1771) reported in 1761 that it was a progressive condition.[15] West Haven classification was formulated by Prof Harold Conn and colleagues at Yale University while investigating the therapeutic efficacy of lactulose 7 December, 2014 History
- 6. Classification of HE Type A: HE associated with Acute liver failure Type B: HE associated with portal-systemic Bypass, no intrinsic hepatocellular disease Type C: HE associated with Cirrhosis and portal hypertension or portal-systemic shunts: Episodic HE: precipitated, spontaneous, recurrent Persistent HE: mild, severe, treatment-dependent Minimal HE 7 December, 2014
- 7. Disorder of astrocyte function Ammonia hypothesis Accumulation of neurotoxic substances (FNT) GABA hypothesis 7 December, 2014 Aetiopathogenesis
- 8. FNTs & HE phenylethanolamine octopamin NA Dopamine 7 December, 2014 competitive Reticular formation: maintain excitation of cerebral cortex Nerve pulse transfer↓ coma
- 9. --major inhibitory neurotransmitter Evidence Patients: GABA-ergic tone ↑ Flumazenil related research Causes Decreased hepatic metabolism of GABA Gut wall permeability ↑ Advanced HE 7 December, 2014 GABA hypothesis
- 10. Glucose choline Pyruvate AcetylCoA Lactic acid acetylcholine Oxaloacetat Citrate α-ketoglutatrate Succinate NADH NAD+ ATP ADP Glutamate Glutamine NADH GABA NAD+ NADH NAD+ CoA ④ ⑤ ⑥ ⑦ NH3 NH3 Early Later 7 December, 2014
- 11. GABA in CNS ↑ ＋ GABA/ BZ•receptor/Chloride Ionophore Complex ↑ Cl – increase in neuron membrane •hyperpolarization Inhibitory postsynaptic potential Coma 7 December, 2014 GABA & HE
- 12. Clinical features Symptoms Change in personality, emotion, consciousness Inability to concentrate Confusion Disorientation Drowsiness Slurring of speech Coma Signs Asterixis Constructional aprasia Hyper-reflexia Bilateral planter extensor responses Inability to perform simple mental arithematic task 7 December, 2014
- 13. Clinical grading of HE Clinical grade Clinical signs Flapping tremor Infrequent at this stage Alert, euphoric, occasionally depression. Poor concentration, slow mentation and affect, reversed sleep rhythm. Grade 1 (prodrome) Drowsiness, lethargic, Easily elicited inappropriate behavior, disorientation. Grade 2 (impending coma) Stuporose but easily rousable, Usually present marked confusion, incoherent speech Grade 3 (early coma) Coma, unresponsive but may Usually absent respond to painful stimulus Grade 4 (deep coma) 7 December, 2014
- 14. Clinical patterns of HE in CLD Type Features No easily identifiable clinical features. EEG changes present Minimal Discrete episode with full recovery within 4 weeks precipitated or spontaneous. Acute Treatment responsive Persistent Severe Chronic 7 December, 2014
- 15. Precipitant of HE Metabolic Drugs Others alteration Nitrogen products GI bleeding Hypokalemia Opiates Infections Hyperazotemia Alkalosis Benzodiazepines Surgery Constipation Hypoxia Diuretics Renal failure High-protein diet Hyponatremia Sedatives Short fatty acids Superimposed hepatic injury H. Pylori Hyperkalemia Phenol Uraemia Dehydration Alcohol Rarely,hepatoma and/or vascular occlusion Porto-systemic Hypoglycemia shunt creation (7i Dneccelumdbeirn, 2g01 4TIPPS)
- 16. 7 December, 2014 Differential diagnosis Severe hyponatremia Respiratory failure Severe sepsis Intracranial bleed Acute alcoholism Wernicke’s encephalopathy Status epilepticus Zinc deficiency Drug overdose Hypoglycemia Post ictal CNS sepsis Delirium tremens Hepato-lenticular degeneration (Wilson’s disease) Functional psychoses
- 17. • Urea, crt, electrolyte • Increased blood NH3 • CSF – Usually clear and under normal pressure – May be increased protein conc. but cell count is normal – Glutamic acid and glutamine may be increased Electroencephalogram High amplitude Low frequency waves Triphasic waves CT/MRI 7 December, 2014 Investigations
- 18. Correct the precipitant Lactulose (15-30 mL 8-hourly) Haloperidol as sedative Antibiotics: neomycin Neomycin (1-4 g 4-6-hourly, metronidazole Zinc sulfate, zinc acetate 600mg Sodium benzoate, sodium phenybutyrate Avoid medication that depress the CNS Diet that contain vegetable protein than animal protein 7 December, 2014 Treatment
- 19. Davidson’s:principles and practice of medicine; 21st ed,UK, London, 2010 www.medscape.com/reference/hepatic_encephalop athy Kumar and Clark: clinical medicine 7 December, 2014 References
- 20. 7 December, 2014