1. Hepatic Encephalopathy
PIMA CONVENTION MARCH 2010 AIMC
Dr Muzaffar Mehdi
Senior Resident MD Gastroenterology Shaikh Zayed Hospital Lahore

2. Definition
Hepatic encephalopathy (HE) is a complex
metabolic mental state disorder with a spectrum
of reversible neuropsychiatric abnormalities seen
in patients with severe acute or chronic liver
dysfunction after exclusion of other brain
diseases

3. Epidemiology
•Exact data regarding incidence and prevalence is lacking
• 70% of patients with liver cirrhosis, while clinically
unremarkable have pathologic changes on EEG and
psychometric tests.MHE
•Prevalence of minimal HE is 53.3% in patients with extra hepatic
portal vein obstruction
•Approximately 50% of patients with liver cirrhosis
develop HE after surgical portosystemic bypass procedures
•After placement of a TIPS approximately one third of patients
develops HE.

4. Classification
Type Description Subcategory Subdivision
A Encephalopathy associated with _____ ______
acute liver failure
B Encephalopathy with porto-systemic _____ ______
bypass and no
intrinsic hepatocellular disease
C Encephalopathy associated with Episodic •Percipated
•Spontaneous
cirrhosis or portal •Recurrent
hypertension ⁄ porto-systemic shunts Persistent •Mild
•Severe
Minimal •Treatment dependent

5. Clinical Detection Relationship Of HE
Subtypes

6. Etiology and Pathogenesis
• liver cirrhosis with reduced functional hepatic mass
underlies the development /HCC
• Triggered by precipitating factors
Drugs Portosytemic
Incresed NH3 Hypovolumia
•Tranqulizers shunts
• Increased /hepatic hypoxia
•Narcotic •Spontaeous
protien intake •Overdiuresis
analegesics •Surgical
• Constipation •Large volume
•Diuretics •TIPS
• GI bleeding paracentesis
• Blood TX •Diarrhoea •Electrolyte
• Infections vomiting Imbalance
• Sepsis •Circulatory •Hypokalemia
• Renel failure shock •Hyponateremia
•Metabolic acidosis
/ alkolosis

7. Factors Involved In HE development
•Neurotoxins (Ammonia,GABA,Maganese )
•Impaired astrocyte functions
•Dysfunction of blood brain barrier
•Imbalance of amino acids
•False neurotransmitters

8. Ammonia Theory

9. Clinical Manifestations & Diagnosis :MHE
•Clinically normal
•No mental deficit
•Normal verbal ability
• Deficit in attention ,visual perception, memory
function, and learning
•Impaired daily activities / driving
•Only sophisticated tests such as
EEG,CFF,ICT,NCT,DST,BDT,CDR,RBANS
• Neuroimaging : SPECT ,MRI,MRS.DWI

10. Manifestations & Diagnosis :MHE
Number Connection Test (NCT) Draw a star
Time to
complete____________________
End
6 10 25
4
7 9 23
5 Begin 1 11
14
3 8 24
2 Sample handwriting
13 12
17
15 16 22
18 21
19 20

11. Clinical Manifestations : OHE
Detailed physical examination to place according to
WHC for management
•R/O FND
•Hypereflexia
•Positive Babinski’s sign
•Asterixis
•Parkinsonian symptoms
•Hepatic mylopathy spastic paraparesis

12. West-Haven criteria for HE: OHE
Stage Consciousness Intellect and Neurological
behaviour findings
0 Normal Normal Normal examination; if
impaired psychomotor
testing, then MHE
1 Mild lack of awareness Shortened attention Mild asterixis or
span; impaired
addition or subtraction
tremor
2 Lethargic Disoriented; Obvious asterixis;
inappropriate slurred speech
behaviour
3 Somnolent but Gross Muscular rigidity
arousable disorientation; and clonus;
bizarre behaviour Hyper-reflexia
4 coma Coma Decerebrate
posturing

13. Stages of Hepatic Encephalopathy

14. Differential Diagnosis
Metabolic Intracranial Meningeal Psychiatric
encephalopathies lesions irritation
•Hypoxia
diseases
•Bleeding •Meningitis
•Ethonol
•Electrolyte subdural •Encepalitis
imbalance subarachnoidal •Seizure
•Ketoacidosis intracerebral disorders
•CO2 narcosis •Tumor
•Psychoactive •Abscess
drugs •Vascular
•Salicylate toxicity
accident
•Wilson disease

15. Course And Prognosis
•Develops rapidly few hours – 1-2 days
•Mortality in grade IV is 80%
•Death usually due to brain herniation / edema ICH
•Type C develops slowly – undulating course /
recurrence
•Neuropsychiatric manifestations are reversible
•Can lead to permanent damage with dementia, extra
pyramidal signs, cerebellar degeneration,myelopathy
with spastic paraplegia, peripheral polyneuropthy
•Liver TX can reverse all changes

16. Treatment Objectives
1.Normalization of neurological functions
2.Elimination of precipitating factors
3. lowering ammonia level

17. Hepatic Encephalopathy Precipitants

18. Treatment Options for Hepatic Encephalopathy
Treatment Chronic encephalopathy Acute encephalopathy
option
Lactulose 15-45ml 2-4 times Oral /NG 30-45 ml /hourly Oral /NG
until 2-3 bowel movements /day until bowel movement and
clinical improvement
Retention Enema 300 ml +
water2-6 hrly/improvement
Rifaxamin 1100 –1200 mg/day oral 8-12hrly 1100 –1200 mg/day 8-12hrly
Neomycin 1-4 gm /day oral 1-2 gm 4-6 /hrly oral/NG
Metronidazole 250 mg oral 12 hrly Oral 250 mg oral 12 hrly O/NG
Sodium benzoate 5 gm / oral twice a day
Bromocriptine
Surgery Obliteration of portosystemic LIVER TRANSPLANT
anastomosis ,Surgical shunt
LIVER TRANSPLAANT

19. Mechanism Of Action of Drugs
Lactulose
BRAIN Acarbose
ABX
UREA
LOLA LIVER
NH3 GUT
MUSCLE
KIDNEY
Glutamine

20. Actions Of Lactulose

21. Management of Hepatic Encephalopathy
Episodic encephalopathy Persistent Encephalopathy Minimal encephalopathy
Exclude other causes
First line options 1. No established indication
Nutritional support
• Identify precipitating for treatment
3. Dairy and vegetable
factor 2. Consider changes daily
based diet
• Nutrional management activeties (avoid driving)
4. Consider BCAA
• Reduce dietry protiens 3. In selected patients
5. Lactulose/Lactitol
• Enterl nutrtion Lactulose /lactitol
6. Zinc supplementation
• Zinic supplementation Dietry intervention
7. Interventional radiology
• Lactulose/lactitol vegetable based diet
search large portosytemic
.probiotics
2nd line options shunts occlud / reduce
• ABX TIPS diameter
• LOLA NH3 lowering agents
• Acarbose, probiotics, 9. ABX
• l –carnitine 10. LOLA
• Flumazinal 11. Bromocriptine
OLT evaluation

22. Prophylaxis Of New Episodes
1. Control of precipitating factors
2. Nutritional support
3. Adequate protein intake with dairy and
vegetable based diets
4. Vitamins
5. Zinc supplementation
6. Lactulose /lactitol as needed
7. OLT evaluation

23. Nutritional measures in patient with acute HE
SUFFICENT CALORIC SUPPLY
30 k cal /kg body weight /day
RESTRICTION OF DIETRY PROTIEN
Day 1-5 20-30 g/day
Then 1-2 g/kg body weight /day
INCREASED OF GLUCOSE (LIPID) CALORIES
10% glucose 1-2 L/day
BRANCHED CHAINED AMINO ACID ( BCAA)
0.2-1.2 G/KG body weight i.v/day
REPLACEMENT OF VITAMINS AND TRACE
ELEMENTS
Vitamin B complex
Vitamin K
Zinc

24. Thanks