Hepatic encephalopathy (HE) is defined as a neuropsychiatric syndrome in patients with liver dysfunction, characterized by personality changes, intellectual impairment and decreased level of consciousness (after exclusion of brain disease). •Its mainly due to liver failure or portosystemic shunting of blood. •Portosystemic shunting is divertion of portal blood into the systemic circulation through portosystemic collateral vessels (liver is bypassed). •Shunting can either be surgical / spontenious.

1. HEPATIC
ENCEPHALOPATHY
DR KAWANA MUKELABAI
MBChB, BSc_hb
07/07/2023

2. Objectives
• Define hepatic encephalopathy
• Know pathophysiology of disease
• Types and grades of HE
• Investigation
• DDX
• Common precipitating factors
• treatment

3. introduction
• Hepatic encephalopathy (HE) is defined as a neuropsychiatric
syndrome in patients with liver dysfunction, characterized by
personality changes, intellectual impairment and decreased
level of consciousness (after exclusion of brain disease).
• Its mainly due to liver failure or portosystemic shunting of
blood.
• Portosystemic shunting is divertion of portal blood into the
systemic circulation through portosystemic collateral vessels
(liver is bypassed).
• Shunting can either be surgical / spontenious.

4. pathology
• Neurotoxins absorbed from the GIT into the blood
• NH3
• Glutamine
• Nitrogen
• GABA

5. Pathophysiology
• Cirrhosis
• → ↓ hepatic metabolism and portosystemic
shunt → accumulation of neurotoxic metabolites,
including ammonia (NH3) → excess glutamine and swelling
produced by astrocytes → cerebral edema and ↑ intracranial
pressure → neurological deterioration
• Metabolic effects:
• Hypokalemia → shift of K+ ions out of the cells → shift
of H+ ions into the cells to
maintain electroneutrality→ intracellular acidosis → tubular cells
produce more ammonia → neurological deterioration
• Metabolic alkalosis → decreased H+ ion availability → decreased
conversion of ammonia to ammonium (NH4
+) → increased levels
of ammonia → diffuses freely through the blood-brain
barrier → neurological deterioration

6. Types and grades of HE
• Hepatic encephalopathy can either be Overt (OHE) or Covert
(CHE), CHE normally has poor outcomes.
1. Type A- associated with acute liver failure ( normally
episodic)
2. Type B- due to portosystemic bypass (no liver/
hepatocellular disease)
3. Type C- associated with liver Cirrhosis and Portal
hypertension or portosystemic shunting. Can be episodic,
persistent or minimal but normally persistent.

7. Grading of symptoms of HE
1. Grade 0
no changes, patient has no features of HE.
2. Grade 1
• Trivial lack of awareness
• Short attention span mild confusion
• Inversion of sleep pattern ( normally sleeps during the day and awake
during the night)
• Euphoria
3. Grade 2
• Lethargy or apathy
• Inappropriate behavior
• Slurred speech
• Obvious asterixis
• Disoriented (mainly to time)
• Moderate confusion

8. Grading of symptoms of HE
con…
1. Grade 3
• Marked confusion
• Arousable somnolence
• Disoriented
• Amnesia
• Incomprehensible speech
• Grade 4
• Coma

9. Precipitating factors
• Renal failure
This leads to decreased clearance of urea, ammonia and
nitrogenous wastes and compounds .
• GI Bleeding.
Blood in the GIT results in increased NH3 and nitrogen absorption
from the Gut.
• Hemorrhage
Blood loss predisposes to kidney hypo-perfusion and impaired renal
function.
• Blood Transfusion (BT)
May result in mild hemolysis and increase the blood NH3 levels.
• Infections
Increase blood NH3 levels due to renal impairment and increased
tissue catabolism.

10. Precipitating factors con…
• Constipation
Increases intestinal production & absorption of NH3.
• Medication
Drugs that act on the CNS (opiates, benzodiazepines,
antidepressants and antipsychotic agents.) may worsen hepatic
encephalopathy.
• Diuretic therapy
Hypokalemia and alkalosis facilitate the conversion of NH3+ to NH3
• Dietary protein overload

11. DDX
• Intracranial lesions
Such as subdural hematoma, intracranial bleeding, stroke, tumors and abscess.
• Infections
e.g. meningitis, encephalitis
• Metabolic enceohalopathy
e.g. hypoglycemia, electrolyte imbalance, anoxia, hypercapnia and uremia.
• Hyperammonemia from other causes,
Such as ureterosigmoidostomy and inherited urea cycle disorder.
• Toxin encephalopathy from alcohol intake such as;
Alcohol intoxication, withdrawal and Wernicke's encephalopathy.
• Toxin encephalopathy from drugs;
Such as sedatives, hypnotics, anti depressants, antipsychotic agents and
salicylates.
• Organic brain syndrome
• Post seizure encephalopathy

12. Management
• General principles
 Diagnosis of hepatic encephalopathy is largely clinical and based on
ruling out alternate explanations for altered mental status.
 It is critical to identify the precipitating factor (e.g., GI bleeding)
 The diagnosis of covert hepatic encephalopathy requires psychometric
testing, which is usually carried out by a specialist.
• Initial evaluation
 Physical examination
 Assessment of mental status (e.g., orientation, mini mental state,
Glasgow coma scale.)
 Evaluation of asterixis.
 LAB TEST
 CBC, BMP: Rule out hypoglycemia, hyponatremia, uremia, ketoacidosis,
and hypercalcemia.
 CRP, WBC count, blood cultures, urinalysis and culture: evaluation for
underlying infection.
 Blood alcohol: rule out alcohol intoxication.
 Ammonia level: low/ normal level may be helpful to rule out hepatic
encephalopathy.

13. Management cont….
• Additional evaluation
Imaging:
 Chest x-ray to rule out infection
 Consider an abdominal ultrasound to assess for ascites and PVT.
 Consider CT or MRI head to rule out alternate etiology.
Psychometric tests (e.g., number of connection test): usually
carried out by specialists to quantify the severity of hepatic
encephalopathy.

14. Treatment
General measures
• Avoid further insult(e.g., hepatotoxic medictions, alcohol).
• Treat precipitating factors (e.g., hypovolemia, constipation, GI
bleeding, electrolyte disturbances).
• Liver transplant is the ultimate treatment in cirrhosis.
Pharmacotherapy
• Lactulose: a synthetic non absorbable disaccharide (laxative)
• Dosage 15- 35ml
• 1st line treatment for hepatic encephalopathy
• Improves symptoms of hepatic encephalopathy by decreasing the
absorption of ammonia in the bowel.
• M.O.A: Lactulose is converted to lactic acid by intestinal flora
acidification in the gut  conversion of ammonia (NH3) to
ammonium (NH4+) ammonium is excreted in the feces
decreased blood ammonia concentration.

15. Treatment cont….
• Rifaximin
• Dosage: 550 mg BD PO.
• Is a non absorbable antibiotic that act by reducing the bacterial
content of the bowel (reducing the number of ammonia
producing bacteria).
• May be added to lactulose if a second episode occurs to prevent
recurrent episodes of hepatic encephalopathy.
• Neomycin
• Dosage: upto 4mg daily PO in divided doses usually for 5 – 7 days
to reduce gut flora
• Consider iv VIT K if prothrombin time is prolonged.
• Replace animal based protein with vegetable based proteins.

16. THANK YOU