Hepatic encephalopathy is a neuropsychiatric syndrome that occurs secondary to liver disease and portosystemic shunting. It is caused by toxic metabolites like ammonia that bypass the liver and affect the brain. Clinical features range from subtle personality changes to confusion, coma, and death in acute liver failure. Treatment involves identifying and removing precipitants, providing nutrition support, antibiotics, and procedures to reduce ammonia levels like lactulose. Prognosis depends on the underlying liver disease severity.

1. HEPATIC ENCEPHALOPATHY
IJATUYI OLUWATOMISIN

2. OUTLINE
• Introduction
• Epidemiology
• Pathogenesis
• Clinical features
• Management
• Conclusion
• References

3. INTRODUCTION
• Hepatic encephalopathy a.k.a portosystemic encephalopathy (PSE) is
a chronic neuropsychiatric syndrome that is often secondary to
cirrhosis.
• Acute hepatic encephalopathy can occur in acute hepatic failure .
• It can also arise in portal hypertensive patients due to spontaneous
‘shunting’, or in those with surgical or TIPS shunts.
• It is sometimes the cardinal presentation in acute liver failure

4. EPIDEMIOLOGY
• The exact incidence is unknown.
• M:F is thesame
• It can occur in individuals of any age who have acute or chronic liver
disease
• 24 % - 53% of patients with a portosystemic shunt develop HE
• It is most often associated with cirrhosis-70%

5. PATHOGENESIS
• The portal blood bypasses the liver via collaterals, and ‘toxic’ metabolites pass directly to
the brain to produce encephalopathy.
• Ammonia-induced alteration of brain neurotransmitter balance, especially at the
astrocyte–neurone interface, is considered to be the leading pathophysiological
mechanism.
• Other implicated substances are free fatty acids and mercaptans; accumulation of false
neurotransmitters (octopamine) or activation of the γ-aminobutyric acid (GABA)
inhibitory neurotransmitter system may also be responsible.
• Increased blood levels of aromatic amino acids (tyrosine and phenylalanine) and reduced
branched-chain amino acids (valine, leucine and isoleucine) also occur.

6. PRECIPITANTS
• High dietary protein
• GI hemorrhage
• Constipation
• Infection (SBP)
• Fluid & electrolyte derangement
• Drugs
• Portosystemic shunts
• Surgery
• Hepatocellular carcinoma

7. CLINICAL FEATURES
• The patient becomes increasingly drowsy and comatose.
• Chronically, there is a disorder of personality, mood and intellect, with a reversal of
normal sleep rhythm.
• The patient is irritable, confused and disorientated, and has slow, slurred speech.
• Nausea, vomiting and weakness.
• There is hyper-reflexia and increased tone.
• Coma occurs as the encephalopathy becomes more marked.
• Convulsions are very rare, but if they do occur, other causes must be considered.

8. • Signs include:
• fetor hepaticus
• asterixis
• constructional apraxia
• decreased mental function

9. MANAGEMENT
• Diagnosis is clinical!
• History
• Examination
• Investigations
• EEG shows diffuse decrease in the frequency of the normal α-waves (8–13 Hz)
to 1.5–3 Hz and eventual development of delta waves. These changes occur
before coma supervenes.
• Visual evoked responses also detect subclinical encephalopathy.
• Arterial blood ammonia

10. TREATMENT
• Identify and remove the possible precipitating cause.
• Give purgation and enemas
• Maintain nutrition, if necessary via a fine-bore nasogastric tube, and do not restrict
protein for more than 48 h.
• Give antibiotics. Rifaximin,Metronidazole .Neomycin should be avoided.
• Stop or reduce diuretic therapy.
• Give intravenous fluids as necessary
• Treat infection.
• Increase protein in the diet to the limit of tolerance as encephalopathy improves.

11. Grading of Hepatic Encephalopathy (West Haven
Criteria)
Grade Neurological Manifestations
0 No alteration in consciousness, intellectual function,
personality or behaviour
1 Trivial lack of awareness, euphoria or anxiety; short attention
span, cognitive defects
2 Lethargy or apathy, disorientation for time, personality
change, inappropriate behaviour
3 Somnolence to semi-stupor, confusion; responds to noxious
stimuli, gross disorientation, bizarre behaviour
4 Coma, no response to noxious stimuli

12. Conventional EEG Grading of Hepatic Encephalopathy
Grade 0: Normal, regular alpha rhythm
Grade 1: Irregular background activity (alpha  and theta 
rhythm)
Grade 2: Continuous theta activity, occasionally delta  activity
Grade 3: Prevalence of theta activity, transient polyphasic
complexes of spikes and slow waves
Grade 4: Continuous delta  activity, abundant complexes of
spikes & slow waves
Quero JC & Herrerias GJM. Clinica Chimica Acta, 2006

13. DIFFERENTIALS
• Intracranial hemorrhage
• Drug or alcohol intoxication
• Delirium tremens/alcohol withdrawal
• Psychiatric disorders
• Hypoglycemia
• Neurological Wilson’s disease
• Post-ictal state

14. PROGNOSIS
• Acute encephalopathy in acute hepatic failure has a very poor prognosis
associated with that of the disease itself.
• In cirrhosis, chronic HE adversely affects prognosis but the course is very
variable.
• Very rarely with chronic portosystemic shunting, an organic syndrome with
cerebellar signs or choreoathetosis develops, as well as myelopathy leading
to a spastic paraparesis due to demyelination. These patients require
referral to a liver transplant centre.

15. CONCLUSION

16. REFERENCES

17. THANK YOU FOR LISTENING

18. QUESTIONS?