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Hepatic Encephalopathy

Hepatic encephalopathy is a complex neuro-psychiatric syndrome characterized by disturbances in consciousness and behaviour, personality changes, fluctuating neurologic signs, asterixis and distinctive electro encephalographic changes.
Biochemical bases of hepatis encephalopathy.
Normally CO2 combines with NH3 in liver and makes urea. But as liver is not functioning than CO2 does not combine with NH3. It is NH3 which is the main cause of hepatic encephalopathy. 
Precipitating factors:
  1. Increased nitrogen load:
    1. GI bleeding (most common precipitating factor)
    2. Excess dietary protein
    3. Azotemia
    4. Constipation
  2. Electrolyte and metabolic abnormality:
    1. Hypokalemia
    2. Alkalosis, Hypoxia,
    3. Hypovolemia
    4. Hyponatremia
  3. Drugs
    Sedatives, Excess diuretics
  4. Others
    Infection, Surgery, Superimposed acute liver disease, porto systemic shunt, progressive liver disease
Clinical features – The diagnosis should be considered when four major factors are present:
  1. Macrographia is an early feature. Trail marking test is done
  2. Neurological signs – asterixis, rigidity, hyper reflexia, extensor planters
  3. Symmetric, high voltage, triphasic slow waves (2-5 per second) on ECG
    1. Disturbances of sleep with reversal of sleep/wake cycles is one of the earliest sign of encephalopathy.
    2. Alteration in personality, mood disturbances, confusion, changes in hand writing are also seen.
    3. Fetor hepaticus – musty odor of breath and urine is due to mercaptans.
Complications of hepatic encephalopathy
  1. Metabolic
    1. Hypoglycemia
    2. Hypophosphatemia
    3. Hypokalemia
    4. Hypomagnesemia
    5. Hyponatremia
  2. Acid base
    1. Resp alkalosis
    2. Metabolic acidosis
  3. Hematological
    1. Aplastic anemia
    2. Coagulopathy
    3. DIC
  4. CNS
    1. Cerebral oedema
    2. Seizure
  5. Multiorgan failure
    1. Pancreatitis
    2. Pulmonary oedema
    3. Shock
    4. ATN
    5. Sepsis
    6. Hepato renal syndrome
Clinical stages of hepatic encephalopathy:
Stage Mental status Asterixis EEG
1. Euphoria, depression, slurred speech mild +/- Triphasic wave
2. Confusion, sleep disorder + Triphasic wave
3. Lethargy, moderate confusion + Triphasic wave
4. Marked confusion, incoherent speech, Stupor + Triphasic wave
5. Coma - Delta wave
Laboratory features:
  1. Serum ammonia level are elevated
  2. CSF is normal
  3. CT scan of brain shows cerebral edema in stage IV
  4. Typical EEG abnormalities. (Symmetrical triphasic high voltage slow wave 2-5/sec)
Important Points

Trail making test

  1. A helpful measure of hepatic encephalopathy is a careful mental status examination and use of the trail-making test, which consists of a series of 25 numbered circles that the patient is asked to connect as rapidly as possible using a pencil.
  2. The normal range for the connect-the-dot test is 15–30 s; it is considerably delayed in patients with early hepatic encephalopathy.

Coagulation factors as Laboratory Prognostic markers in patients with acute liver failure include the following:

  1. Prothrombin time (Kings’ criteria)
  2. Factor V levels (Clinch’s criteria)
  3. INR


  1. Decreasing ammonia production - Agents used are:
    1. Lactulose – acts by:
      1. Causing osmotic diarrhea
      2. Metabolism of lactulose by colonic bacteria result in acid pH that favour conversion of ammonia to poorly absorbed ammonium ions.
    2. Direct effect on bacterial metabolism causing decrease in ammonia production.
      Antibiotics – by causing gut bacteria suppression.
      e.g. Neomycin, ampicillin
    3. Biochemical neutralization of ammonia:
      Sodium benzoate. Especially in lactulose resistant cases.
  2. Flumazenil – antagonizes endogenous benzodiazepines.
  3. Mannitol to reduce cerebral edema.
  4. For seizures – short acting benzodiazepines are used – oxazepam, midazolam, paraldehyde.

Recent Advances New antibiotic being used in hepatic encephalopathy – Rifaximin (Ref. Hari. 18th ed., Pg - 2602)


CHILD PUGH CLASSFICATION OF CIRRHOSIS (To assess severity of Cirrhosis is based on)
Factor (Ref. Hari. 18th ed., Pg- 2526)
  1. S.Bilirubin (mg%)
  2. S.Albumin (g%)
  3. Ascites
  4. Neurological disorder
  5. PT/INR
Recent Advances (Ref. Hari. 18th ed., Pg- 2526)
  1. Recently the Child-Pugh system has been replaced by the model for end-stage liver disease (MELD) score for assessing the need for liver transplantation. 
  2. The MELD score is a prospectively derived scoring system designed to predict prognosis of patients with liver disease and portal hypertension. 
  3. It is calculated using three noninvasive variables-
    1. PT (INR)
    2. Serum bilirubin,
    3. Serum creatinine


Important Points:
Summary of Clinical Features of Hepatic Failure (LQ 2012)
Jaundice Its an almost invariable finding
Hypoalbuminemia Predisposes to peripheral edema
Hyper ammonemia Plays a role in cerebral dysfunction
Fetor hepaticus Characteristic musty or sweet and sour body odour (caused due to production of mercaptans by the action of gastrointestinal bacteria on the sulfur containing amino acids methionine)
Palmar erythema,
Spider angiomas

Caused due to impaired estrogen metabolism (AIPG 12)
Caused due to hyperestrogenemia
Susceptibility to failure of multiple organ system Respiratory failure with pneumonia and sepsis may combine with renal failure
Coagulopathy Attributed to impaired hepatic synthesis of blood clotting factors II, VII, IX and X. The resultant bleeding tendency leads to massive GIT hemorrhage.
Hepatic encephalopathy - Regarded as a disorder of neurotransmission in the CNS and neuromuscular system and appears to be elevated with blood ammonia level which impair neuronal function and promote generalized edema.
- It is associated with only minor morphologic changes in the brain and encephalopathy is reversible if underlying hepatic condition can be corrected.
Hepatorenal syndrome Appearance of renal failure in patients with severe chronic liver disease, in whom there are no intrinsic morphological or functional causes of renal failure.


Extra Edge
Terry's nails (LQ 2012)
  1. It is a physical finding in which fingernails and/or toenails appear white with a characteristic "ground glass" appearance, with no lunula. 
  2. The condition is thought to be due to a decrease in vascularity and an increase in connective tissue within the nail bed. 
  3. It is seen in
    1. hepatic failure M/C cause,
    2. Cirrhosis,
    3. diabetes mellitus,   
    4. congestive heart failure,
    5. hyperthyroidism,
    6. malnutrition

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