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Liver & GIT

7 out of 10

All are precipitating factors of hepatic encephalopathy except? (LQ)

A Hypophosphatemia

B Hypomagnesemia

C Hyponatremia

D Hyperkalemia

Ans. D Hyperkalemia

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:

a. GI bleeding (most common precipitating factor)

b. Excess dietary protein

c. Azotemia

d. Constipation

2. Electrolyte and metabolic abnormality:

a. Hypokalemia

b. Alkalosis , Hypoxia,

c. Hypovolemia

d. Hyponatremia

3. Drugs

Sedatives, Excess diuretics

4. Others

Infection, Surgery, Superimposed acute liver disease, porto systemic shunt, progressive liver disease

Clinical features of hepatic encephalopathy– The diagnosis should be considered when four major factors are present:

1) Macrographia is an early feature. Trail making test

2) Neurological signs – asterixis, rigidity, hyper reflexia, extensor planters

3) Symmetric, high voltage, triphasic slow waves (2-5 per second) on EEG

a. Disturbances of sleep with reversal of sleep/wake cycles is one of the earliest sign of encephalopathy.

b. Alteration in personality, mood disturbances, confusion, changes in hand writing are also seen.

c. Fetor hepaticus – musty odor of breath and urine is due to mercaptans.

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)

Extra Edge:

Trail making test (Ref. Hari-18th, pg. 2602)

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.

Extra Edge:

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

Complications of hepatic encephalopathy

1. Metabolic

a. Hypoglycemia

b. Hypophosphatemia

c. Hypokalemia

d. Hypomagnesemia

e. Hyponatremia

2. Acid base

a. Resp alkalosis

b. Metabolic acidosis

3. Hematological

a. Aplastic anemia

b. Coagulopathy

c. DIC

4. CNS

a. Cerebral oedema

b. Seizure

5. Multiorgan failure

a. Pancreatitis

b. Pulmonary oedema

c. Shock

d. ATN

e. Sepsis

f. Hepato renal syndrome

Clinical stages of hepatic encephalopathy:


Mental status




Euphoria, depression, slurred speech mild


Triphasic wave


Confusion, sleep disorder


Triphasic wave


Lethargy, moderate confusion


Triphasic wave


Marked confusion, incoherent speech, Stupor


Triphasic wave




Delta wave


1. Decreasing ammonia production - Agents used are:

a. Lactulose – acts by:

i. Causing osmotic diarrhea

ii. Metabolism of lactulose by colonic bacteria result in acid pH that favour conversion of ammonia to poorly absorbed ammonium ions.

b. Direct effect on bacterial metabolism causing decrease in ammonia production.

Antibiotics – by causing gut bacteria suppression.

e.g. Neomycin, ampicillin

c. 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 (Hari-18th ed., Pg. 2602)

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