HEPATIC

ENCEPHALOPATHY
DEEPA MERIN KURIAKOSE
ASSISTANT PROFESSOR
GOVT COLLEGE OF NURSING, KOTTAYAM
DEFINITION

• A condition that causes temporary

worsening of brain function in
people with advanced liver disease.
• Altered level of consciousness as a
result of liver failure.
• Onset : Gradual or sudden
• Possibly reversible with treatment.
 Definition

• Hepatic encephalopathy or
portosystemic encephalopathy is a
reversible syndrome of impaired
brain function occuring in patients
with advanced liver failure.
• Decreased metabolism of ammonia
may be the mechanism causing
brain dysfunction in liver failure
Etiology

• Liver failure
• Cirrhosis of liver
• Fulminant hepatitis caused
by viruses, drugs or toxins
Causes

• Excessive nitrogen load:

• GI Bleeding eg., from esophageal
varices
• High-protein diet
• Kidney failure(inability to excrete
nitrogen containing waste products
such as urea)
• Constipation
Causes
• Electrolyte or metabolic
disturbance:
• Hyponatremia & hypokalemia
• Alkalosis
• Hypoxia
• Dehydration, Fluid restriction
• Azotemia
• Diarrhea, vomiting
Causes

• Drugs & Medications:

• Sedatives such as benzodiazepines,
narcotics,
• Analgesics
• Antipsychotics,
• Diuretics
• Alcohol intoxication
 Causes

• Infection :
• Urinary tract infection
• Spontaneous bacterial pneumonitis
• Others :
• Surgery, shock
• Hypoxia
• Progession of liver disease
• Alcoholic hepatitis
• Creation of transjugular intrahepatic portosystemic
shunt(TIPS)
 Pathophysiology
• Reversible biochemical disturbance of brain
functions- Progressive liver cell failure to detoxify
noxious agents from gut and shunting of portal
blood directly into systemic circulation(portocaval
shunts) are two major determinants in the
development of encephalopathy.
• Nitrogenous substances including ammonia are
major contributory factors
• In liver failure, the nitrogenous waste products are
not metabolised and even enter the portosystemic
circulation to reach the brain.
 Pathophysiology cont..d

• Activation of inhibitory
neurotransmitter system,e.g.
aminobutyric acid, increased blood
levels of aminoacids, mercaptans
and fatty acids
• Blood brain barrier is disrupted in
cirrhosis leading to development of
cerebral edema
 Stages of Hepatic Encephalopathy
• West Haven Grading System
• Grade 0: Minimal HE- Minimal changes in memory,
concentration and intellectual functioning
• Grade 1: Mild HE- Short attention span, mood changes
like depression or irritability & sleep problems.
• Grade 2: Moderate HE- May keep forgetting things,
have no energy & exhibit inappropriate behaviour,
slurred speech, trouble in doing mental tasks such as
basic math, hands might shake & have difficulty
writing.
 Stages of HE (cont..d)

• Grade 3: Severe HE- Confused,

disoriented, extremely sleepy, but can
still be woken up, May be unable to do
basic mental tasks, feel extremely
anxious and act strangely
• Grade 4 : Coma
• The last stage of HE when the person
becomes unconscious and slips into
coma.
 Clinical manifestations

• Impaired cerebration : Earliest features are

reduced alertness, restlessness, behavioural
changes,mania, bizarre handwriting,
disturbance in sleep rhythm, drowsiness,
confusion, disorientation, yawning,
constructional apraxia. In late stages,
convulsions may occur and the patient
develops coma.
 Clinical signs
• Moderate to severe jaundice and cerebral features
of encephalopathy
• Fetor hepaticus(sweety odour due to methyl
mercaptans)
• Flapping tremors seen on stretched or extended
hands
• Signs of cirrhosis and portal hypertension
• Neurological signs in the form of chorea and
spasticity of limbs. Other features such as
fever,tachycardia, hyperventilation,hypotension
may be present.
 Diagnosis
• Clinical evaluation
• Psychometric evaluation : reveal subtle
neuropsychiatric deficits in attention, working
memory, psychomotor speed and visuospatial ability.
• High blood ammonia levels
• EEG : can detect changes in cortical cerebral activity
across the spectrum of HE. Shows diffuse slow-wave
activity, even in mild cases.
• MRI & CT : To rule out other conditions such as brain
tumors
 Management

• Cornerstone of HE management
• Controlling precipitating factors in the
management of overt HE is of paramount
importance. Nearly 90% of patients can be
treated with just correction of the
precipitating factor.
• Protein intake is limited to 20 to 40 g/day
 Treatment
• Non-absorbable disaccharides
• Lactulose syrup 25ml every 1-2 hours until atleast 2 soft
or loose bowel movements per day are produced. Given
orally or via a rectal enema. Creates an acidic environment
in the bowel that causes the ammonia to leave the blood
stream and enter the colon. Also has a laxative effect.

• Antibiotics
• Rifaximin – Cognitive improvement & Ammonia
lowering. Efficacious in maintaining remission and reducing
hospitalization
 Second line treatments

• Neomycin orally every 4-6 hours.

• Daily renal function studies are
monitored when neomycin is administered
Metronidazole 500mg to 1.5gm/day for 1
week
• Restriction of medications that are toxic
to the liver is another important
treatment.
 Other therapies
• Metabolic ammonia scavengers
• Ornithine phenylacetate
• Glyceryl phenylbutyrate
• Oral branched-chain amino acids(B CAA) improve the
manifestations of episodic HE.
• L-ornithine L-aspartate (L OLA) : I/V preparation showed
improvement in psychometric testing and postprandial venous
ammonia levels in persistent HE.
• Probiotics
• Flumazenil : transiently improves mental status in overt HE
• LIVER TRANSPLANTATION in Recurrent Hepatic Encephalopathy.
 Nursing Management
• Protecting the patient with an altered
mental status from harm are a priority
• Many patients with hepatic
encephalopathy need to be sedated to
prevent from doing harm to themselves or
to others.
• Oxazepam, Diazepam(Valium),
Lorazepam(Ativan) must be used
judiciously
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