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Hepato encephalopathy
- 1. Hepatic Encephalopathy PIMA CONVENTION MARCH 2010 AIMC Dr Muzaffar Mehdi Senior Resident MD Gastroenterology Shaikh Zayed Hospital Lahore
- 2. Definition Hepatic encephalopathy (HE) is a complex metabolic mental state disorder with a spectrum of reversible neuropsychiatric abnormalities seen in patients with severe acute or chronic liver dysfunction after exclusion of other brain diseases
- 3. Epidemiology â˘Exact data regarding incidence and prevalence is lacking ⢠70% of patients with liver cirrhosis, while clinically unremarkable have pathologic changes on EEG and psychometric tests.MHE â˘Prevalence of minimal HE is 53.3% in patients with extra hepatic portal vein obstruction â˘Approximately 50% of patients with liver cirrhosis develop HE after surgical portosystemic bypass procedures â˘After placement of a TIPS approximately one third of patients develops HE.
- 4. Classification Type Description Subcategory Subdivision A Encephalopathy associated with _____ ______ acute liver failure B Encephalopathy with porto-systemic _____ ______ bypass and no intrinsic hepatocellular disease C Encephalopathy associated with ď§Episodic â˘Percipated â˘Spontaneous cirrhosis or portal â˘Recurrent hypertension â porto-systemic shunts ď§Persistent â˘Mild â˘Severe ď§Minimal â˘Treatment dependent
- 5. Clinical Detection Relationship Of HE Subtypes
- 6. Etiology and Pathogenesis ⢠liver cirrhosis with reduced functional hepatic mass underlies the development /HCC ⢠Triggered by precipitating factors Drugs Portosytemic Incresed NH3 Hypovolumia â˘Tranqulizers shunts ⢠Increased /hepatic hypoxia â˘Narcotic â˘Spontaeous protien intake â˘Overdiuresis analegesics â˘Surgical ⢠Constipation â˘Large volume â˘Diuretics â˘TIPS ⢠GI bleeding paracentesis ⢠Blood TX â˘Diarrhoea â˘Electrolyte ⢠Infections vomiting Imbalance ⢠Sepsis â˘Circulatory â˘Hypokalemia ⢠Renel failure shock â˘Hyponateremia â˘Metabolic acidosis / alkolosis
- 7. Factors Involved In HE development â˘Neurotoxins (Ammonia,GABA,Maganese ) â˘Impaired astrocyte functions â˘Dysfunction of blood brain barrier â˘Imbalance of amino acids â˘False neurotransmitters
- 9. Clinical Manifestations & Diagnosis :MHE â˘Clinically normal â˘No mental deficit â˘Normal verbal ability ⢠Deficit in attention ,visual perception, memory function, and learning â˘Impaired daily activities / driving â˘Only sophisticated tests such as EEG,CFF,ICT,NCT,DST,BDT,CDR,RBANS ⢠Neuroimaging : SPECT ,MRI,MRS.DWI
- 10. Manifestations & Diagnosis :MHE Number Connection Test (NCT) Draw a star Time to complete____________________ End 6 10 25 4 7 9 23 5 Begin 1 11 14 3 8 24 2 Sample handwriting 13 12 17 15 16 22 18 21 19 20
- 11. Clinical Manifestations : OHE Detailed physical examination to place according to WHC for management â˘R/O FND â˘Hypereflexia â˘Positive Babinskiâs sign â˘Asterixis â˘Parkinsonian symptoms â˘Hepatic mylopathy spastic paraparesis
- 12. West-Haven criteria for HE: OHE Stage Consciousness Intellect and Neurological behaviour findings 0 Normal Normal Normal examination; if impaired psychomotor testing, then MHE 1 Mild lack of awareness Shortened attention Mild asterixis or span; impaired addition or subtraction tremor 2 Lethargic Disoriented; Obvious asterixis; inappropriate slurred speech behaviour 3 Somnolent but Gross Muscular rigidity arousable disorientation; and clonus; bizarre behaviour Hyper-reflexia 4 coma Coma Decerebrate posturing
- 13. Stages of Hepatic Encephalopathy
- 14. Differential Diagnosis Metabolic Intracranial Meningeal Psychiatric encephalopathies lesions irritation â˘Hypoxia diseases â˘Bleeding â˘Meningitis â˘Ethonol â˘Electrolyte subdural â˘Encepalitis imbalance subarachnoidal â˘Seizure â˘Ketoacidosis intracerebral disorders â˘CO2 narcosis â˘Tumor â˘Psychoactive â˘Abscess drugs â˘Vascular â˘Salicylate toxicity accident â˘Wilson disease
- 15. Course And Prognosis â˘Develops rapidly few hours â 1-2 days â˘Mortality in grade IV is 80% â˘Death usually due to brain herniation / edema ICH â˘Type C develops slowly â undulating course / recurrence â˘Neuropsychiatric manifestations are reversible â˘Can lead to permanent damage with dementia, extra pyramidal signs, cerebellar degeneration,myelopathy with spastic paraplegia, peripheral polyneuropthy â˘Liver TX can reverse all changes
- 16. Treatment Objectives 1.Normalization of neurological functions 2.Elimination of precipitating factors 3. lowering ammonia level
- 18. Treatment Options for Hepatic Encephalopathy Treatment Chronic encephalopathy Acute encephalopathy option Lactulose 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/improvement Rifaxamin 1100 â1200 mg/day oral 8-12hrly 1100 â1200 mg/day 8-12hrly Neomycin 1-4 gm /day oral 1-2 gm 4-6 /hrly oral/NG Metronidazole 250 mg oral 12 hrly Oral 250 mg oral 12 hrly O/NG Sodium benzoate 5 gm / oral twice a day Bromocriptine Surgery Obliteration of portosystemic LIVER TRANSPLANT anastomosis ,Surgical shunt LIVER TRANSPLAANT
- 19. Mechanism Of Action of Drugs Lactulose BRAIN Acarbose ABX UREA LOLA LIVER NH3 GUT MUSCLE KIDNEY Glutamine
- 21. Management of Hepatic Encephalopathy Episodic encephalopathy Persistent Encephalopathy Minimal encephalopathy Exclude other causes First 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 .probiotics 2nd line options shunts occlud / reduce ⢠ABX TIPS diameter ⢠LOLA NH3 lowering agents ⢠Acarbose, probiotics, 9. ABX ⢠l âcarnitine 10. LOLA ⢠Flumazinal 11. Bromocriptine OLT evaluation
- 22. Prophylaxis Of New Episodes 1. Control of precipitating factors 2. Nutritional support 3. Adequate protein intake with dairy and vegetable based diets 4. Vitamins 5. Zinc supplementation 6. Lactulose /lactitol as needed 7. OLT evaluation
- 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. Thanks