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Hepatic encephalopathy 2012 presentation

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Hepatic encephalopathy 2012 presentation

  1. 1. 7 December, 2014 Phase 2 medicine posting PRESENTER: MUSA IKO MODURATOR: DR BANCY
  2. 2.   Introduction  Epedimiology  Classification  Aetiopathogenesis  precipitant  Clinical features  Differential diagnosis  Investigation  Treatment 7 December, 2014 Outline
  3. 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. 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. 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. 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. 7.   Disorder of astrocyte function Ammonia hypothesis  Accumulation of neurotoxic substances (FNT)  GABA hypothesis 7 December, 2014 Aetiopathogenesis
  8. 8. FNTs & HE  phenylethanolamine octopamin NA Dopamine 7 December, 2014 competitive Reticular formation: maintain excitation of cerebral cortex Nerve pulse transfer↓ coma
  9. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 20. 7 December, 2014

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