Hepato encephalopathy


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Hepato encephalopathy

  1. 1. Hepatic Encephalopathy PIMA CONVENTION MARCH 2010 AIMC Dr Muzaffar Mehdi Senior Resident MD Gastroenterology Shaikh Zayed Hospital Lahore
  2. 2. DefinitionHepatic encephalopathy (HE) is a complexmetabolic mental state disorder with a spectrumof reversible neuropsychiatric abnormalities seenin patients with severe acute or chronic liverdysfunction after exclusion of other braindiseases
  3. 3. Epidemiology•Exact data regarding incidence and prevalence is lacking• 70% of patients with liver cirrhosis, while clinicallyunremarkable have pathologic changes on EEG andpsychometric tests.MHE•Prevalence of minimal HE is 53.3% in patients with extra hepaticportal vein obstruction•Approximately 50% of patients with liver cirrhosisdevelop HE after surgical portosystemic bypass procedures•After placement of a TIPS approximately one third of patientsdevelops HE.
  4. 4. ClassificationType Description Subcategory SubdivisionA Encephalopathy associated with _____ ______ acute liver failureB Encephalopathy with porto-systemic _____ ______ bypass and no intrinsic hepatocellular diseaseC Encephalopathy associated with Episodic •Percipated •Spontaneous cirrhosis or portal •Recurrent hypertension ⁄ porto-systemic shunts Persistent •Mild •Severe Minimal •Treatment dependent
  5. 5. Clinical Detection Relationship Of HE Subtypes
  6. 6. Etiology and Pathogenesis• liver cirrhosis with reduced functional hepatic mass underlies the development /HCC• Triggered by precipitating factors Drugs Portosytemic Incresed NH3 Hypovolumia •Tranqulizers shunts • Increased /hepatic hypoxia •Narcotic •Spontaeous protien intake •Overdiuresis analegesics •Surgical • Constipation •Large volume •Diuretics •TIPS • GI bleeding paracentesis • Blood TX •Diarrhoea •Electrolyte • Infections vomiting Imbalance • Sepsis •Circulatory •Hypokalemia • Renel failure shock •Hyponateremia •Metabolic acidosis / alkolosis
  7. 7. Factors Involved In HE development•Neurotoxins (Ammonia,GABA,Maganese )•Impaired astrocyte functions•Dysfunction of blood brain barrier•Imbalance of amino acids•False neurotransmitters
  8. 8. Ammonia Theory
  9. 9. Clinical Manifestations & Diagnosis :MHE •Clinically normal •No mental deficit •Normal verbal ability • Deficit in attention ,visual perception, memory function, and learning •Impaired daily activities / driving •Only sophisticated tests such as EEG,CFF,ICT,NCT,DST,BDT,CDR,RBANS • Neuroimaging : SPECT ,MRI,MRS.DWI
  10. 10. Manifestations & Diagnosis :MHENumber Connection Test (NCT) Draw a starTime tocomplete____________________ End 6 10 25 4 7 9 23 5 Begin 1 11 143 8 24 2 Sample handwriting 13 12 1715 16 22 18 2119 20
  11. 11. Clinical Manifestations : OHEDetailed physical examination to place according toWHC for management•R/O FND•Hypereflexia•Positive Babinski’s sign•Asterixis•Parkinsonian symptoms•Hepatic mylopathy spastic paraparesis
  12. 12. West-Haven criteria for HE: OHEStage Consciousness Intellect and Neurological behaviour findings0 Normal Normal Normal examination; if impaired psychomotor testing, then MHE1 Mild lack of awareness Shortened attention Mild asterixis or span; impaired addition or subtraction tremor2 Lethargic Disoriented; Obvious asterixis; inappropriate slurred speech behaviour3 Somnolent but Gross Muscular rigidity arousable disorientation; and clonus; bizarre behaviour Hyper-reflexia4 coma Coma Decerebrate posturing
  13. 13. Stages of Hepatic Encephalopathy
  14. 14. Differential Diagnosis Metabolic Intracranial Meningeal Psychiatric encephalopathies lesions irritation•Hypoxia diseases •Bleeding •Meningitis•Ethonol•Electrolyte subdural •Encepalitisimbalance subarachnoidal •Seizure•Ketoacidosis intracerebral disorders•CO2 narcosis •Tumor•Psychoactive •Abscessdrugs •Vascular•Salicylate toxicity accident•Wilson disease
  15. 15. Course And Prognosis•Develops rapidly few hours – 1-2 days•Mortality in grade IV is 80%•Death usually due to brain herniation / edema ICH•Type C develops slowly – undulating course /recurrence•Neuropsychiatric manifestations are reversible•Can lead to permanent damage with dementia, extrapyramidal signs, cerebellar degeneration,myelopathywith spastic paraplegia, peripheral polyneuropthy•Liver TX can reverse all changes
  16. 16. Treatment Objectives1.Normalization of neurological functions2.Elimination of precipitating factors3. lowering ammonia level
  17. 17. Hepatic Encephalopathy Precipitants
  18. 18. Treatment Options for Hepatic EncephalopathyTreatment Chronic encephalopathy Acute encephalopathyoptionLactulose 15-45ml 2-4 times Oral /NG 30-45 ml /hourly Oral /NG until 2-3 bowel movements /day until bowel movement and clinical improvement Retention Enema 300 ml + water2-6 hrly/improvementRifaxamin 1100 –1200 mg/day oral 8-12hrly 1100 –1200 mg/day 8-12hrlyNeomycin 1-4 gm /day oral 1-2 gm 4-6 /hrly oral/NGMetronidazole 250 mg oral 12 hrly Oral 250 mg oral 12 hrly O/NGSodium benzoate 5 gm / oral twice a dayBromocriptineSurgery Obliteration of portosystemic LIVER TRANSPLANT anastomosis ,Surgical shunt LIVER TRANSPLAANT
  19. 19. Mechanism Of Action of Drugs Lactulose BRAIN Acarbose ABX UREALOLA LIVER NH3 GUT MUSCLE KIDNEY Glutamine
  20. 20. Actions Of Lactulose
  21. 21. Management of Hepatic Encephalopathy Episodic encephalopathy Persistent Encephalopathy Minimal encephalopathy Exclude other causesFirst line options 1. No established indication Nutritional support• Identify precipitating for treatment 3. Dairy and vegetable factor 2. Consider changes daily based diet• Nutrional management activeties (avoid driving) 4. Consider BCAA• Reduce dietry protiens 3. In selected patients 5. Lactulose/Lactitol• Enterl nutrtion Lactulose /lactitol 6. Zinc supplementation• Zinic supplementation Dietry intervention 7. Interventional radiology• Lactulose/lactitol vegetable based diet search large portosytemic .probiotics2nd line options shunts occlud / reduce• ABX TIPS diameter• LOLA NH3 lowering agents• Acarbose, probiotics, 9. ABX• l –carnitine 10. LOLA• Flumazinal 11. Bromocriptine OLT evaluation
  22. 22. Prophylaxis Of New Episodes1. Control of precipitating factors2. Nutritional support3. Adequate protein intake with dairy and vegetable based diets4. Vitamins5. Zinc supplementation6. Lactulose /lactitol as needed7. OLT evaluation
  23. 23. Nutritional measures in patient with acute HE SUFFICENT CALORIC SUPPLY 30 k cal /kg body weight /day RESTRICTION OF DIETRY PROTIEN Day 1-5 20-30 g/day Then 1-2 g/kg body weight /day INCREASED OF GLUCOSE (LIPID) CALORIES 10% glucose 1-2 L/day BRANCHED CHAINED AMINO ACID ( BCAA) 0.2-1.2 G/KG body weight i.v/day REPLACEMENT OF VITAMINS AND TRACE ELEMENTS Vitamin B complex Vitamin K Zinc
  24. 24. Thanks