This document discusses hepatic encephalopathy, which is a potentially reversible disturbance in brain function caused by liver disease or portal-systemic shunting. It defines and classifies hepatic encephalopathy, discusses potential precipitating factors, describes methods of grading its severity including the West Haven criteria, and outlines treatment approaches including reducing nitrogenous toxins from the gut, improving extra-intestinal ammonia elimination, and counteracting abnormalities in central neurotransmission.

1. Abdomonal Examination
(Hepatic Encephalopathy)
By:
Dr. Mohamed Naguib Abdalla,
M.D.
Lecturer of Internal Medicine
Cairo University

2. Definition
Potentially reversible disturbance in central
nervous system function secondary to hepatic
insufficiency or portal-systemicshunting.
This broad definition reflects a spectrum of
neurologic manifestations, ranging from subtle
alterations in neuropsychological tests to
appearance of deep coma, brain edema, and
intracranial hypertension.

3. Classification:
a. Encephalopathy associated with acute
liver failure (type A, for acute).
b. Encephalopathy associated with portal-
systemic bypass and no intrinsic
hepatocellular disease (type B, for By-
pass).
c. Encephalopathy associated with cirrhosis
and portal hypertension and/or portal-
systemic shunts (type C, for cirrhosis).

4. Subgroups:
We can divide type C further into:
c.1. Episodic HE. Subdivided into
precipitated and spontaneous, depending
on the presence of precipitating factors.
``Recurrent encephalopathy'‘ refers to the
occurrence of at least two episodes of
episodic HE within 1 year.

5. c.2. Persistent HE. Includes cognitive deficits that
impact negatively on social and occupational
functioning, and is subdivided into mild and severe.
Treatment-dependent persistent HE is a subgroup
in which overt symptoms develop promptly after
discontinuing medication.
c.3. Minimal HE. Refers to abnormalities of cognition,
affection/emotion, behavior, or bioregulation that
are not usually detected by regular clinical
examination; diagnosis requires specific
neuropsychological and neurophysiological tests.

6. Precipitating Factors
A) Gut Factors:
 Constipation
 High protein intake,
 Upper gastrointestinal bleeding

7. Precipitating Factors (cont.)
B) Electrolyte/ Water Imbalance:
 Vomiting,
 Diarrhea,
 Diuretic treatment,
 Renal failure,
 Paracentesis

8. Precipitating Factors (cont.)
C) Infection:
 Chest,
 Urinary,
 Spontaneous bacterial peritonitis

9. Precipitating Factors (cont.)
D) Drugs:
 Hypnotic/sedative drugs,
 Alcohol
E) Severe factors affecting major metabolic
functions:
 Hypoxia,
 Hypotension,
 Hypoglycemia

10. Grading
 The two most useful and
recommended methods of grading
HE are based on clinical findings.
The West Haven criteria are a
semiquantitative classification that
groups HE in four stages, covering
the whole spectrum of HE except
minimal HE.

11.  Thus, stage I includes trivial lack of
awareness, euphoria, anxiety, shortened
attention span, and impairment of skills
such as addition or subtraction;
 stage II is characterized by lethargy, time
disorientation, obvious personality
change, and inappropriate behavior;

12.  stage III includes somnolence to
semistupor but responsiveness to
stimuli, confusion, gross
disorientation, and bizarre
behavior; and
 Stage IV is coma and no response
to noxious stimuli.

13.  The Glasgow coma scale, initially developed for
patients with neurotrauma, is less subject to
observer variability, but its use has not been
validated in metabolic encephalopathies.
 It measures the response to eye opening, verbal
behavior, and motor responsiveness, and
quantifies neurologic impairment in a continuous
numerical scale.
 It is mainly useful for evaluation of advanced
stages of HE.

14.  The portal-systemic encephalopathy index,
which combines assessment of mental state,
arterial ammonia, electroencephalography,
number connection test, and estimation of
degree of asterixis, is another method that has
been extensively used to grade HE.
 However, a consensus has been recently
reached indicating that it is not adequate for
clinical followup evaluation and it is not
recommended for clinical trials.

15. Flapping Tremors
Clinical Presentation
Infrequent at this stage
Alert, euphoric, occasionally depression
Poor concentration, slow mentation and
affect, reversed sleep rhythm
Grade 1
(prodrome)
Easily elicited
Drowsiness, lethargic, inappropriate
behavior, disorientation
Grade 2
(impending
Coma)
Usually present
Stuporous but easily rousable, marked
confusion, incoherent speech
Grade 3
(Early Coma)
Usually absent
Coma, unresponsive but may respond to
painful stimulus
Grade 4
(Deep Coma)

16. Treatment
A) General Measures:
1. Special nursing staff to avoid harm.
2. Adequate hydration and nutrition during period
of altered mental state.
3. Identification and removal of precipitating
factors.
4. Early diagnosis and management of infection,
GI hemorrhage, renal impairment, electrolyte,
constipation….etc
5. Intubation in stage III or IV

17. Treatment
A) General Measures:
1. Special nursing staff to avoid harm.
2. Adequate hydration and nutrition during period
of altered mental state.
3. Identification and removal of precipitating
factors.
4. Early diagnosis and management of infection,
GI hemorrhage, renal impairment, electrolyte,
constipation….etc
5. Intubation in stage III or IV

18. Treatment
B) Reduction of Nitrogenous Load from the Gut:
1. Prolonged periods of dietary protein restriction
should be avoided.
2. Preferably from vegetable and dairy sources
rather than animal protein.
3. Nonabsorbable disaccharides, such as lactulose
and lactitol, remain the first-line pharmacological
treatment of HE.
4. Lactitol and lactulose enemas have been also
shown effective.

19. 5. Antibiotics as they reduce ammonia-producing
bacteria in the colon:
- Neomycin
- Metronidazole
- Also, vancomycin or rifaximin

20. C) Improvement of Extraintestinal Elimination of
Ammonia:
1. Zinc is a cofactor in all enzymes of the urea cycle,
thus administration of zinc acetate to improve
ureagenesis may be specially indicated in patients
with associated malnutrition
2. Ornithine-aspartate provides substrates for the
urea cycle in the liver as well as for the synthesis
of glutamine via transamination.

21. D) Counteracting Abnormalities of Central
Neurotransmission:
1. Intravenous administration of flumazenil (esp. if
benzodiazepine ingestion is suspected).
2. Bromocriptine to correct abnormalities of
dopaminergic neurotransmission, it is indicated
only for the treatment of chronic encephalopathy.
3. Administration of intravenous and oral solutions of
branched-chain amino acids (???).

22. E) Manipulation of Splanchnic Circulation:
 In HE caused by congenital portal-systemic shunts
and in those patients with severe HE after
placement of a transjugular intrahepatic
portosystemic stent shunt.
 Occlusion or reduction of the shunt via surgery or
via interventional radiology should be considered.
 This may be also an option in selected patients with
cirrhosis and large spontaneous portal-systemic
shunts, if they present with recurrent episodes of
HE without precipitating factors.

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