Hepatic encephalopathy is due to rise in ammonia levels in blood
Etiopathogenesis :
- Increased ammonia level in blood (Most important)
- Increase in short chain fatty acids
- Rise in methionine level
- Rise in false neurotransmitters like octopamine
- Increased conversion of tryptophan to inhibitory neurotransmitter serotonin
- Increased sensitivity of CNS neurones to GABA (inhibitory neurotransmitter)
- Increased conversion of tryptophan to inhibitory neurotransmitter serotonin
- Ratio of aromatic amino acids (phenylalanine, tyrosine and tryptophan) to branched-chain
amino acids (leucine, isoleucine and valine) is raised - Excessive manganese deposition in the basal ganglia
- Increased circulating levels of endogenous benzodiazepines
2 main factors- Liver failure and shunting of portal blood into systemic circulation bypassing the liver.
Signs and symptoms :
- Disturbed consciousness
- Inversion of sleep rhythm
- Slurred speech
- Musty odour in breath (fetor hepaticus)
- Personality changes (loss of family concern)
- Intellectual deterioration
- Flapping tremor in hands (asterixis)
- Constructional apraxia – Inability to reproduce simple diagrams with blocks
Diagnosis:
1.blood ammonia levels
2.electroencephalogram
3.dot join test
Treatment:
1.Lactulose
2.adequate protein intake
3.oxygen therapy
4.iv fluids
5.Antibiotics
–Mrunali Gondane