Hepatic encephalopathy is a syndrome of altered mental status and neurological dysfunction seen in patients with liver disease. It progresses from confusion to coma and can potentially lead to permanent neurological damage. It is caused by the impaired ability of the diseased liver to metabolize toxic substances like ammonia, which then crosses the blood-brain barrier and is absorbed by astrocytes in the brain, causing them to swell. Treatment focuses on reducing ammonia levels through medications like lactulose and rifaximin that alter bowel bacteria to prevent ammonia reabsorption.

1. GMC

2.  HE is the syndrome of disordered consciousness and
altered neuromuscular activity that is seen in
patients with liver disease.
 As it progresses , confusion is followed by coma
 And very rarely chronic HE give rise to
hepatocerebral degeneration (cerebellar dysfunction,
dementia, parkinsonian syndromes)

3.  Drugs
 Dehydration
 Portosystemic shunting
 Infection
 Hypokalemia
 Constipation
 High protein diet

5.  This process is impaired in hepatic encephalopathy,
either because the hepatocytes are incapable of
metabolizing the waste products
or because portal venous blood bypasses the liver through
collateral circulation or a shunt
 Ammonia crosses the blood–brain barrier and is absorbed
and metabolized by the astrocytes
 Astrocytes use ammonia when synthesizing glutamine
from glutamate. The increased levels of glutamine lead to
an increase in osmotic pressure in the astrocytes, which
become swollen.

6. Numerous other abnormalities have been described
in hepatic encephalopathy-
 Benzodiazepine -like compounds have been
detected at increased levels
 abnormalities in the GABA neurotransmission
system
 depletion of zinc and accumulation
of manganese may play a role
 inflammation elsewhere in the body may
precipitate encephalopathy through the action
of cytokines and bacterial lipopolysaccharide on
astrocytes.

8.  Usually shows a flapping tremor i.e. aterixis and a
sweet musty odor to breath – fetor hepaticus

9. Inability to perform simple mental arithmetic tests

10. Inability to draw simple objects i.e. constructional
apraxia

11.  Diagnosis is usually made clinically
 Arterial ammonia is usually increased in patients
with HE, but it is not a sensitive and specific test for
HE
 EEG shows
high amplitude low frequency waves and triphasic
waves
 CT/MRI

12.  Intracranial bleed – EDH, SDH
 Drug or alcohol intoxication
 Delirium tremens/ alcohol withdrawal
 Hypoglycemia
 Primary psychiatric disorders
 Wernicke’s encephalopathy

13.  Lactulose – 15 to 3O ml x TDS , increased gradually
until the bowels are moving twice or thrice daily
 Lactulose degraded by intestinal bacteria to form
lactic acid and acetic acid and reduces the pH of
colonic content
 Ammonia gets converted to ammonium ions, which
are not easily absorbed and remain trapped in lumen

14.  Rifaximin – 4OO mg x TDS/ 5oo mg x BD
non absorbed antibiotic , acts by reducing the
bacterial content of bowel
 Neomycin 5OO-1OOO mg xTDS
 Other therapies currently under further
investigation include
L-ornithine-L-aspartate
Zinc supplements