HEPATIC ENCEPHALOPATHY

PRESENTER :Dr.Ch.Priyanka ( DNB junior resident)

MODERATOR : DR.THIRUPATHI REDDY ( Associate
professor,MD,General Medicine)
• DEFINITION : Hepatic encephalopathy is
defined as a spectrum of neuropsychiatric
abnormalities in patients with liver
dysfunction,after exclusion of brain disease.

• It represents a reversible decrease in neurologic

function, based upon the disorders of
metabolism which are caused by severe
decompensated liver disease

• It occurs most often in patients with cirrhosis but

also occur in acute hepatic failure.
Causes:
•Chronic parenchymal liver disease:
Chronic hepatitis
Cirrhosis
• Fulminating hepatic failure:
Acute viral hepatitis
Drugs
Toxins e.g. Wilson’s Disease, CCL4, Mushroom.

•Surgical Portal-systemic anastomoses

- portacaval shunts, or
- Transjugular intrahepatic portal-systemic shunting (TIPS).
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
Types of HE
PATHOPHYSIOLOGY
 Clinical features
Symptoms Signs
• hypersomnia-earliest feature • Asterixis (flapping
• progress to inversion of sleep tremor)
pattern • Constructional apraxia
• Change in personality, emotion,
• Hyper-reflexia
consciousness
• Inability to concentrate • Bilateral planter extensor
• Confusion responses
• Disorientation • Inability to perform
• Drowsiness simple mental
• Slurring of speech arithematic task
• Coma • Hypertonia
• Fetor hepaticus
 Constructional apraxia
Number connection test

Useful, reliable, sensitive bedside tests.

Helps to assess degree of encephalopathy and response to treatment.
Grade Intellectual Function Neuromuscular Function
0 normal normal
minimal Normal examination Minor abnormalities of visual
findings; subtle changes in work or perception or on psychometric or
driving number tests

1 Personality changes, Tremor and incoordination

attention deficits, irritability,
depressed state
2 Changes in sleep-wake Asterixis, ataxic gait, speech
cycle, lethargy, mood and abnormalities (slow and slurred)
behavioral changes,
cognitive dysfunction
3 Altered level of Muscular rigidity, nystagmus,
consciousness clonus, Babinski sign,
(somnolence), confusion, hyporeflexia
disorientation, and amnesia
4 Stupor and coma Oculocephalic reflex,
unresponsiveness to noxious
stimuli

West Haven Criteria

 Spectrum of Neurocognitive Impairment in Cirrhosis (SONIC)
classification

Classification Mental status Special tests Asterexis

Unimpaired(Grade 0) Not impaired normal absent

Covert HE (Grade 1) Not Impaired abnormal absent

Overt HE(Grade2,3&4) Impaired abnormal Present(absent in

coma)
Differential diagnosis :
1. Intracranial lesions  subdural hematoma,Intracranial
bleeding,stroke,tumour,abscess
2. Infections  Meningitis,encephalitis,intracranial abscess
3. Metabolic encephalopathy hypoglycemia,Electrolyte
imbalance,anoxia,uremia,hypercarbia
4. Toxic encephalopathy(alcohol intake) alcohol
intoxication,alcohol withdrawal,wernicke’s encephalopathy
5. Toxic encephalopathy(drugs)Sedative
hypnotics,antidepressants,antiosychotics,salicylates
6. Hyperammonemia other causesureterosigmoidostomy,inherited
urea cycle disorders
7. Organic brain syndrome
8. Post seizure encephalopathy
Approach :
• Approch to a patient with hepatic encephalopathy depends upon
the severity of mental status changes and certainty of the
diagnosis.
• General management recommendations :
• Exclude nonhepatic causes of altered mental function
• Chech arterial ammonia levels in the initial assesment of a
hospitalized patient with cirrhosis and with impaired mental
function
• Precipitants of hepatic encephalopathy should be corrected
• Avoid medications that depress central nervous system
function,especially benzodiazepines
• Patients with severe encephalopathy(grade 3/4),who are at risk for
aspiration,should undergo prophylactic endotracheal intubation.
 Investigations
• Diagnosis is usually made clinically
• Elevated blood ammonia-in 90% cases.(N= 11-35 mmol/L)
• Routine Investigations – Hb%, TC, DC, ESR, RBS, Na+, K+
(decreased), B.Urea, S.Creatinine, Prothrombin time.
• Investigations to suggest liver disease- abnormal  LFT
and USG s/o CLD, and ideally liver biopsy.
• EEG - High amplitude, Low frequency waves, Triphasic waves
• CSF - Protein may increased,cell count normal.
• CT Scan - usually normal
• Visual evoked potential abnormailties in initial stages.
 MANAGEMENT
• Supportive Treatment
• Specific Treatment aims at-
– Decreasing ammonia production in colon
– Elimination or treatment of precipitating factors.
 TREATMENT
• Hospitalization is mandatory
• Maintain ABC
• Ryle’s tube feeding and bladder catheterization
• Remove the cause & precipitating factors if known
• IV fluids 25% Dextrose & Inj. Thiamine 100 mg iv OD
• Maintenance of fluid, electrolytes & calories
• Diet – High glucose diet, Restriction of protein diet(not
recommended now) vegtable protien and dairy protein
can be allowed.
• Inj. Vitamin K -10 mg iv OD
• Avoid constipation – Lactulose 15-30ml X 3 times a day
atleast 2-4 stools/day.
• Antibiotics :
Neomycin-causes ototoxicity and renal failure
Ampicillin
Metronidazole – peripheral neuropathy
• Rifaximin- 550 mg x BD
• Rifaximin-only used as a second-line treatment if lactulose is
not effective or poorly tolerated. When added to lactulose,
the combination of the two may be more effective than each
component separately.
• Liver Transplantation
 LOLA
• A preparation of L-ornithine and L-aspartate (LOLA) is used to
decrease ammonia by increaseing the generation
of urea through the urea cycle.
• It may be combined with lactulose and/or rifaximin if these
alone are ineffective.
• Dosage- tab.150 mg orally TID
• Inj. 5 gm iv infusion QID
• Sachets 5 gm tid
• It is contra indicated if serum cretinine > 3 mg/dl.