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