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Hepatic encephalopathy

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Hepatic encephalopathy occurs when the liver fails to detoxify toxic substances, such as ammonia, which are then able to pass into the brain. This causes neurological symptoms ranging from mild confusion to coma. Precipitating factors include gastrointestinal bleeding, infections, and certain drugs. Treatment focuses on reducing ammonia production in the gut through lactulose, antibiotics, and low-protein diets. Correcting electrolyte imbalances and removing precipitating medications or infections are also important for management of hepatic encephalopathy.

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HEPATIC ENCEPHALOPATHY Dr. Reena Residant Ward 6
Definition It is a state of disordered CNS function, resulting from failure of liver to detoxify toxic agents because of hepatic insufficiency and porto-systemic shunt. It represents a reversible decrease in neurologic function. It occurs most often in patients with cirrhosis but also occur in acute hepatic failure.
Pathogenesis Ammonia formed by protein breakdown in GIT Liver liver dysfunction (abnormal) NH3 Passes BBB Hepatic encephalopathy. Other factors: Increase sensitivity to glutamine & GABA (inhibitory neurotransmitter) Increase circulating levels of endogenous benzodiazepines.
Pathogenesis (acute & chronic ) The basic cause is same in both forms but the mechanism is somewhat different Diminished detoxification of toxic intestinal nitrogenous compounds Increased in blood NH3 etc Toxic effect on brain Appearance of abnormal amines in systemic circulation Interference with neurotransmission
Endotoxins Ammonia. Mercaptans (degradation of methionine in the gut) Phenols. Free fatty acids. Gamma amino butyric acid(GABA) Octopamine.
Causes Chronic parenchymal liver disease: Chronic hepatitis. Cirrhosis. Fulminating hepatic failure: Acute viral hepatitis. Drugs. Toxins e.g. Wilsons Disease, CCL4. Surgical Portal-systemic anastomoses, - portacaval shunts, or Transjugular intrahepatic portal-systemic shunting [TIPS]).
Precipitating Agents (A) Increase Nitrogen Load (a) Constipation. (b) Gastro intestinal bleeding. (c) Excess dietary intake of protein & fatty acids. (d) Azotemia.
Precipitating Agents (B) Infections & Trauma (Surgery) (C) Electrolyte & Metabolic imbalance Hypokalemia. Alkalosis. Hypoxia. Hyponatremic.
Precipitating Agents (D) Drugs Diuretics. Narcotics, Tranquilizers, Sedatives.
Clinical Features A Disturbance in consciousness Disturbances in sleep rhythm. Impaired memory/ apraxia. Mental confusion. Apathy. Drowsiness / Somnolence. Coma.
B. Changes Personality Childish behavior. May be aggressive out burst. Euphoric. Foetor hepaticus Foulsmelling breath associated with liver disease due to mercaptans.
C Neurological signs: Flapping tremor / Asterixis (in pre coma). Exaggerated tendon reflex. Extensor plantar reflex.
Clinical Staging
Hepatic encephalopathy
Hepatic encephalopathy
Investigation Diagnosis is usually made clinically Routine Investigations - CBC, LFTS, Electolytes, Urea, Creatinine, Prothrombin time, Albumin , A/G ratio. Elevation of blood ammonia. EEG (Electroencephalogram) CSF & CT Scan Normal.
Differential Diagnosis Subdural Haematoma. Drug or Alcohol intoxication. Wernickes encephalopathy. Hypoglycaemia.
Management Supportive Treatment. Specific Treatment aims at: Decreasing ammonia production in colon Elimination or treatment of precipitating factors.
Hepatic encephalopathy
TREATMENT Hospitalize the patient. Maintain ABC. Identify and remove the precipitating factors. Iv fluid dextrose ,saline. Stop Diuretic Therapy. Correct any electrolyte imbalance. Ryle tube feeding & bladder catheterization. Reduce the ammonia (NH3) Load. Diet Restriction of protein diet. High glucose diet. Treat Constipation by Laxatives.
Lactulose Lactulose 15-30ml X 3 4 times a day- result aims at 2-4 stools/day. Rectal use is indicated when patient is unable to take orally. 300ml of lactulose in 700ml of saline or sorbitol as a retention enema for 30 60 min. May be repeated 4 6 hours.
Mechanism of action of Lactulose A non-absorbable disaccharide. It produces osmosis of water- Diarrhea. It reduces pH of colonic content & thereby prevents absorption of NH3. It converts NH3- NH4 that can be excreted.
Treat the GIT & other Infections Antibiotics: Rifaximin Broad spectrum antibiotic, recently approved in humans for HE. Negligible systemic absorption. Shown to decrease hospitalizations and length of stay as compared to lactulose in humans. DOSE: 550 mg orally B.I.D
Metronidazole : 250mg orally T.D.S Neomycin : 0.5 1 g orally 6 or 12 hours for 7 days. Side effects: Ototoxicity, nephrotoxicity. Vancomycin : 1 g orally B.I.D
DIET With held dietary protein during acute episode if patient cannot eat. Oral intake should be 60 80 g/day as tolerated. Vagetable protein is better tolerated than meat protein. G.I.T bleeding should be controlled 120ml of magnesium citrate by mouth or NG tube every 3 4 hours until stool free of blood.
Stimulation of metabolic ammonia metabolism: Sodium benzoate 5 g orally twice a day. L-ornithine-L-aspartate 9 g orally thrice a day. L-acyl-carnitine aspartate 4 g orally daily. Zinc sulphate 600mg/day in divided doses.
Correct amino acid metabolic imbalance Infusion or oral administration of BCAA (branched-chain amino acid) Its use is unnecessary except in patient who are intolerant of standard protein supplements. GABA/BZ complex antagonist: Flumazenil ( particularly if patient has been given banzodiazepines ) Opiods & sedatives should be avoided.
Acarbose 留 glucosidase inhibitor. Under study. Other Therapies: Prebiotics & probiotics. Extracorporeal albumin dialysis ( MARS) Liver transplant.
PROGNOSIS Acute hepatic encephalopathy may be treatable. Chronic forms of the disorder often keep getting worse or continue to come back. Both forms may result in irreversible coma and death. Approximately 80% (8 out of 10 patients) die if they go into a coma. Recovery & the risk of the condition returning vary from patient to patient
REFERENCES Davidsons Principles & Practice of Medicine- 21st edition. Harrisons Principles of internal Medicine-10th & 17th edition. Current Medical Diagnosis & Treatment 2014 edition.
Hepatic encephalopathy

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Hepatic encephalopathy

  • 2. Definition It is a state of disordered CNS function, resulting from failure of liver to detoxify toxic agents because of hepatic insufficiency and porto-systemic shunt. It represents a reversible decrease in neurologic function. It occurs most often in patients with cirrhosis but also occur in acute hepatic failure.
  • 3. Pathogenesis Ammonia formed by protein breakdown in GIT Liver liver dysfunction (abnormal) NH3 Passes BBB Hepatic encephalopathy. Other factors: Increase sensitivity to glutamine & GABA (inhibitory neurotransmitter) Increase circulating levels of endogenous benzodiazepines.
  • 4. Pathogenesis (acute & chronic ) The basic cause is same in both forms but the mechanism is somewhat different Diminished detoxification of toxic intestinal nitrogenous compounds Increased in blood NH3 etc Toxic effect on brain Appearance of abnormal amines in systemic circulation Interference with neurotransmission
  • 5. Endotoxins Ammonia. Mercaptans (degradation of methionine in the gut) Phenols. Free fatty acids. Gamma amino butyric acid(GABA) Octopamine.
  • 6. Causes Chronic parenchymal liver disease: Chronic hepatitis. Cirrhosis. Fulminating hepatic failure: Acute viral hepatitis. Drugs. Toxins e.g. Wilsons Disease, CCL4. Surgical Portal-systemic anastomoses, - portacaval shunts, or Transjugular intrahepatic portal-systemic shunting [TIPS]).
  • 7. Precipitating Agents (A) Increase Nitrogen Load (a) Constipation. (b) Gastro intestinal bleeding. (c) Excess dietary intake of protein & fatty acids. (d) Azotemia.
  • 8. Precipitating Agents (B) Infections & Trauma (Surgery) (C) Electrolyte & Metabolic imbalance Hypokalemia. Alkalosis. Hypoxia. Hyponatremic.
  • 9. Precipitating Agents (D) Drugs Diuretics. Narcotics, Tranquilizers, Sedatives.
  • 10. Clinical Features A Disturbance in consciousness Disturbances in sleep rhythm. Impaired memory/ apraxia. Mental confusion. Apathy. Drowsiness / Somnolence. Coma.
  • 11. B. Changes Personality Childish behavior. May be aggressive out burst. Euphoric. Foetor hepaticus Foulsmelling breath associated with liver disease due to mercaptans.
  • 12. C Neurological signs: Flapping tremor / Asterixis (in pre coma). Exaggerated tendon reflex. Extensor plantar reflex.
  • 16. Investigation Diagnosis is usually made clinically Routine Investigations - CBC, LFTS, Electolytes, Urea, Creatinine, Prothrombin time, Albumin , A/G ratio. Elevation of blood ammonia. EEG (Electroencephalogram) CSF & CT Scan Normal.
  • 17. Differential Diagnosis Subdural Haematoma. Drug or Alcohol intoxication. Wernickes encephalopathy. Hypoglycaemia.
  • 18. Management Supportive Treatment. Specific Treatment aims at: Decreasing ammonia production in colon Elimination or treatment of precipitating factors.
  • 20. TREATMENT Hospitalize the patient. Maintain ABC. Identify and remove the precipitating factors. Iv fluid dextrose ,saline. Stop Diuretic Therapy. Correct any electrolyte imbalance. Ryle tube feeding & bladder catheterization. Reduce the ammonia (NH3) Load. Diet Restriction of protein diet. High glucose diet. Treat Constipation by Laxatives.
  • 21. Lactulose Lactulose 15-30ml X 3 4 times a day- result aims at 2-4 stools/day. Rectal use is indicated when patient is unable to take orally. 300ml of lactulose in 700ml of saline or sorbitol as a retention enema for 30 60 min. May be repeated 4 6 hours.
  • 22. Mechanism of action of Lactulose A non-absorbable disaccharide. It produces osmosis of water- Diarrhea. It reduces pH of colonic content & thereby prevents absorption of NH3. It converts NH3- NH4 that can be excreted.
  • 23. Treat the GIT & other Infections Antibiotics: Rifaximin Broad spectrum antibiotic, recently approved in humans for HE. Negligible systemic absorption. Shown to decrease hospitalizations and length of stay as compared to lactulose in humans. DOSE: 550 mg orally B.I.D
  • 24. Metronidazole : 250mg orally T.D.S Neomycin : 0.5 1 g orally 6 or 12 hours for 7 days. Side effects: Ototoxicity, nephrotoxicity. Vancomycin : 1 g orally B.I.D
  • 25. DIET With held dietary protein during acute episode if patient cannot eat. Oral intake should be 60 80 g/day as tolerated. Vagetable protein is better tolerated than meat protein. G.I.T bleeding should be controlled 120ml of magnesium citrate by mouth or NG tube every 3 4 hours until stool free of blood.
  • 26. Stimulation of metabolic ammonia metabolism: Sodium benzoate 5 g orally twice a day. L-ornithine-L-aspartate 9 g orally thrice a day. L-acyl-carnitine aspartate 4 g orally daily. Zinc sulphate 600mg/day in divided doses.
  • 27. Correct amino acid metabolic imbalance Infusion or oral administration of BCAA (branched-chain amino acid) Its use is unnecessary except in patient who are intolerant of standard protein supplements. GABA/BZ complex antagonist: Flumazenil ( particularly if patient has been given banzodiazepines ) Opiods & sedatives should be avoided.
  • 28. Acarbose 留 glucosidase inhibitor. Under study. Other Therapies: Prebiotics & probiotics. Extracorporeal albumin dialysis ( MARS) Liver transplant.
  • 29. PROGNOSIS Acute hepatic encephalopathy may be treatable. Chronic forms of the disorder often keep getting worse or continue to come back. Both forms may result in irreversible coma and death. Approximately 80% (8 out of 10 patients) die if they go into a coma. Recovery & the risk of the condition returning vary from patient to patient
  • 30. REFERENCES Davidsons Principles & Practice of Medicine- 21st edition. Harrisons Principles of internal Medicine-10th & 17th edition. Current Medical Diagnosis & Treatment 2014 edition.