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Clinical features
Jaundice, hypoalbuminemia, hyperammonemia
Fetor hepaticus (a peculiar body odor related to
mercaptan formation)
Hyperestrogenemia : palmar erythema, spider
angiomas of the skin (one or two are normal esp. in
pregnancy), hypogonadism, Gynecomastia
Complications
Cirrhosis (1)
Cirrhosis (2)
Three characteristics
Fibrosis : delicate bands or broad septa from portal
triad to central vein or c vein to c vein.
Fibrosis - irreversible and result in Portal HTN
Inflammation
(Hepatitis)
Fibrosis
(Cirrhosis)
LIVER CIRRHOSIS
Major causes :
Alcohol - (60-70%) called ASH (common in western)
Cryptogenic cirrhosis called NASH
Viral hepatitis B & C (tropical countries)
Loss of hair
Hyperpigmentation
Jaundice
Spidernaevi (neck, upper chest (front-back), upper
arm)
Gynaecomastia,testes atrophi,disturbance of
periodicity
Ascites
Liver palm
White nail
palmar erythema
Spider angiomas
Complications of cirrhosis
Portal hypertension
Varices, ascites, hypersplenism
Synthetic dysfunction
Coagulopathy, encephalopathy hepaticum
Immunodeficiency, infection spontaneus bacterial
peritonitis
Hypoalbumine, malnutrition
Hepato-cellular carcinoma
Hepato-renal syndrome
Hepatic Encephalopathy
Disorder of CNS & neuromuscular transmission
Disturbances of consciousness & sleep, (behavioral
abnormalities, confusion, stupor, coma, death)
EEG changes, limb rigidity and Hyperreflexia,
Seizures & asterixis (a flapping tremor of
outstretched hands)
Pathogenesis : Severe loss of Hepatocellular function
& Exposure of the brain to excess ammonia levels
Etiology
Fulminant hepatic failure due to acute
hepatocellular necrosis
Acute severe viral hepatitis, drug/toxin, acute fatty
liver of pregnancy
Non-Nitrogenous
Encephalopathy
Uremia/azotemia
Sedative
Gastrointestinal bleeding
Dehydration
Benzodiazepines
Metabolic alkalosis
Hypoxia
Hypokalemia
Hypoglycemia
Constipation
Excessive dietary protein
Infection
Hypothyroidism
Anemia
Pathogenesis (1)
Toxic materials derived from nitrogeneous substrate in
the gut and bypass the liver
Postulated factors/mechanisms:
Ammonnia neurotoxicity
Synergistic neurotoxins
Excitatory inhibitory neurotransmitters and plasma
amino acid imbalance hypothesis
-Aminobutyric acid hypothesis
Synergistic neurotoxins
Ammonia
Mercaptans fetor hepaticus
Short-chain fatty acids
Phenols
Pathohistology
Clinical manifestation(1)
Clinical manifestation(2)
In chronic liver disease
Insidious onset
Characterized by subtle and/or intermittent changes in
consciousness, personality, intelligence speech
Disturbed consciousness: slowness, somnolence,
Disorientation, confusion, deep coma
Personality changes: Childishness, irritability
Intellectual deterioration : inability to produce simple
designs with blocks or matches, Reitan trail-making test,
Daily writing chart
Speech: slow, slurred, monotonous voice
Flapping tremor (asterixis)
Fetor hepaticus
Differential diagnosis
Hypoglycemia
Uremia
Diabetic ketoacidosis
Nonketotic hyperosmolar syndrome
Subdural hematoma
Cerebrospinal infection
Treatment
Strategy for the management of HE
Identify and correct the precipitating cause(s)
Initiate ammonia-lowering therapy
Minimize the potential medical complications of
cirrhosis and depressed consciousness
Essential management
Bleeeding : it must be controlled
Azotemia : rehydration, attention to other prerenal
factors
Eliminate sedative/tranquilizers/similar drugs
Decreasing
nitrogen
load
Decreasing
ammonia
production
Decreasing
absorption
of enteric
toxins
Management
Supportive care
Correction of fluid, electrolyte, glucose, acid-alkaline
abnormalities
Management of cerebral edema, bacteremia
Initiate ammonia-lowing therapy
Bowel cleaning
Antibiotics : Neomycin: 2~4g/D (4~6g/D), Metronidazol:
0.2g qid as effective as neomycin
Dietary protein restriction: 40-60 g/day
Lactulosa
Administration of BCAAs: oral or parenteral administration
Livert ransplantation