This describes a syndrome of neuropsychiatric symptoms and signs, including coma, which may develop in severe liver disease and liver failure.
CAUSES
Liver failure may occur from several causes. These include:
• Viral hepatitis
• Cirrhosis of the liver
• Fatty liver of pregnancy
• Drugs - halothane, isoniazid, paracetamol overdose
• Terminal phase of chronic cholestasis
Precipitating factors include:
• Hypotension
• Infection
• Electrolyte imbalance
• Sedatives
• Increased gastrointestinal tract (GIT) protein load e.g. heavy GIT bleeding
• Alcoholic binge
Although there are several causes whose clinical features certainly differ, the overall clinical picture and treatment are similar, irrespective of the aetiology.
SYMPTOMS
• Jaundice
• Fever
• Disturbed consciousness which progresses as follows: disorder of sleep, hypersomnia and inversion of sleep rhythm, apathy and eventually coma
• Personality changes
SIGNS
• Intellectual deterioration
• Cyanosis
• Fetor hepaticus
• Speech impairment
• Neurological abnormalities - asterixis (a flapping tremor) indicates precoma and strongly supports the diagnosis of encephalopathy; inability to draw or construct objects e.g. a 5 pointed star
• Stigmata of chronic liver disease (for example ascites, gynaecomatia, palmar erythema, parotid enlargement, testicular atropy and spider naevi)
• Coma
Clinical grading of encephalopathy
• Confused. Altered mood or behaviour psychometric defects
• Drowsy with inappropriate behaviour
• Stuporous but speaking and obeying simple commands
• Inarticulate speech and marked confusion
• Coma
Acute encephalopathy may appear spontaneously with precipitating factors, usually in a patient with chronic liver disease in the terminal stages.
INVESTIGATIONS
• FBC, differential
• Liver function tests
• Blood urea and electrolytes
• Hepatitis Bs Ag
• Prothrombin time (INR)
• Blood glucose
• Electroencephalogram (EEG)
TREATMENT (Acute Phase)
Medical treatment of encephalopathy includes the recognition and correction of precipitating factors.
Non-Pharmacological Treatment
• Place in the coma position if unconscious
• Daily tap water enemas may be used to further reduce enteric bacteria
• Avoid protein feeds, sedatives and drugs metabolized by the liver. Increase protein intake slowly on recovery.
• Give nutrition as glucose, maintain fluid and electrolyte balance.
• Monitor temperature, pulse and respiratory count, blood pressure (BP), pupils, urine output, blood glucose, INR, urea and electrolytes, liver function tests, EEG (if available) and blood cultures.
Pharmacological Treatment
(Evidence rating: C)
• Prevent worsening coma by emptying the bowel with Magnesium sulphate, oral, 15 mls 3 times daily. Aim for 2 soft stools/day and no diarrhoea.
• Give Neomycin, oral, 1 g every 6 hours or Metronidazole, oral, 400 mg 8 hourly a day and Lactulose 30-50 mls 3 times daily
• If the patient starts bleeding, or INR is elevated give Vitamin K (Phytomenadione), IV, 10 mg/day for 2-3 days. SLOWLY AND CAUTIOUSLY Platelets, fresh frozen plasma and blood should be given as needed.
• Measure blood glucose regularly e.g. every 12 hours until acute phase over. Give 5% Glucose, IV, if levels fall below 2 mmol/L.
• Treat any infection that may be present.
TREATMENT (Maintenance Phase)
• Limit protein to level of tolerance
• Ensure at least one free bowel movement daily with Lactulose, oral, 10-30 mls 3 times daily or Magnesium sulphate 30 mls 3 times a day. The aim is to produce acid stools without diarrhoea
• Revert to management of acute encephalopathy if symptoms worsen
