1. Hepatic encephalopathy/ Portal-systemic encephalopathy /hepatic coma
Hepatic encephalopathy is a neuropsychiatric syndrome caused by hepatic insufficiency
It represents a reversible decrease in neurologic function, based upon the disorder of metabolism which are caused by severe decompensated liver disease
“Portal-systemic encephalopathy” - patients with portal hypertension abnormal shunting of blood
It occurs most often in patients with cirrhosis but also occur in acute hepatic failure.

2. Causes:
Chronic parenchymal liver disease:
Chronic hepatitis:
Cirrhosis.
 Fulminating hepatic failure:
Acute viral hepatitis
Drugs
Toxins e.g. Wilson’s Disease, CCL4,
Surgical Portal-systemic anastomoses, - portacaval shunts, or Transjugular intrahepatic portal-systemic shunting [TIPS]).

3. Factors precipitating hepatic encephalopathy:
Metabolic stress
Infection
Electrolyte imbalance, especially hypokalemia;
Dehydration , Renal failure
Diuretic drugs,
Disorders that increase gut protein
GI bleeding
High-protein diet
Nonspecific cerebral depressants
alcohol, sedatives, analgesics

4. Pathogenesis
Absorbed products – detoxified in Liver
PSS – toxic substances enter systemic circulation - Which are toxic to brain
Other factors
Increase sensitivity to GABA (inhibitory neurotransmitter)
Increase circulating levels of endogenous benzodiazepines

5. 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
Dr S Chakradhar

6. Endotoxins of HE
Ammonia
Mercaptans - degradation of methionine in the gut
Phenols
Free fatty acids

7. Ammonia Production
Small intestine: degradation of glutamine produced NH3
Large intestine: Breakdown of Urea and proteins by normal flora
Muscles: proportion to muscle work
Kidney: increased production when hypokalemia and diuretic therapy
Liver: detoxified ammonia into urea
Brain can also detoxified ammonia into glutamine

8. Clinical Features of hepatic encephalopathy:
A Disturbance in consciousness
Disturbances in sleep rhythm.
Impaired memory/ apraxia
Mental confusion.
Apathy.
Drowsiness / Somnolence 
Coma.

9. B. Changes Personality
Childish behavior.
May be aggressive out burst.
Euphoric.
Foetor hepaticus – Foul–smelling breath associated with liver disease due to mercaptans

10. C Neurological signs:
Flapping tremor / Asterixis (in pre coma).
Exaggerated tendon reflex.
Extensor plantar reflex.

11. Clinical stages of hepatic Encephalopathy

12. Investigations
Diagnosis is usually made clinically
No Pathognomonic liver function abnormality
Elevation of blood ammonia
Hypokalaemia
EEG (Electroencephalogram)
CSF & CT Scan – Normal
Other Routine Investigations - TC, DC, ESR, Hb, Na, k, Urea, Creatinine, Prothrombin time

13. Differential Diagnosis
Subdural Haematoma
Drug or Alcohol intoxication
Wernicke’s encephalopathy
Hypoglycaemia

14. Treatment
Hospitalization is mandatory
ABC maintain
Remove the cause & precipitating factors
IV fluid dextrose saline & Inj. Thiamine
Maintenance of fluid, electrolytes & calorie
Diet – Restriction of protein diet
High glucose diet
Avoid constipation – Lactulose 15-20ml X 3 times a day
Antibiotics :
Neomycin
Ampicillin
Metronidazole
Inj. Vitamin K

15. Mechanism of action of Lactulose:
Osmotic laxative effect.
It reduces pH of colonic content & thereby prevents absorption of NH3.
Incorporates nitrogen into bacteria