Acute Liver Failure

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CAUSES:

• Acute viral hepatitis of all types but rare with hepatitis A
• Drugs –all hepatotoxic drugs especially acetaminophen
• Pregnancy with hepatitis
• Wilson’s disease
• Poisons – carbon tetrachloride,phosphorous, poisonous fungi (amanita phalloides)
• Reye’s syndrome (fatty liver with encephalopathy in children)
• Shock, hyperemia and hypothemia.

 

PATHOLOGY:

There is extensive parenchymal necrosis of the liver. In acute fulminant liver failure, it is estimated that only less than 30% liver cells appear viable. Fatty degeneration can be seen in hepatitis associated with pregnancy or Reye’s syndrome.

 

SYMPTOMS:

• CEREBRAL: poor alertness, disturbed concentration, behavioral changes , drowsiness, confusion , disorientation , disturbed sleep pattern , slurred speech , convulsions and coma.
• JAUNDICE: Bilirubin more than 20 mg carries poor prognosis. It is associated with fever,vomiting. Hypoglycemia can occur.
• FETOR HEPATICUS: it is an ammonical odor in patient’s breath and is due to methyl mercaptan.
• FLAPPING TREMORS: a flap on extended hands is visible but may be lost in deep comatosed patients.
• LIVER DULLNESS: the liver span is reduced to shrinkage of liver. Liver is just slightly enlarged only in initial cases.
• BLEEDING DIATHESIS: in some patients, purpura or severe gastrointestinal bleeding occurs and it may occur from any site and evident in the form of epistaxis, black colored gastric aspirate , purpura ecchymosis or from a punctured site .
• SIGNS OF PORTAL HYERTENSION: Ascites, oedema are usually absent.Splenomegaly is unusual.
• NEUROLOGICAL: Cerebral oedema is seen in 80% patients who die.

 

INVESTIGATIONS:

• BILIRUBIN: is raised – both unconjugated and conjugated fractions are high.
• SERUM TRANSAMINASES: are raised. Hence fall of SGOT and SGPT in acute hepatic coma constitutes a bad prognostic parameter. Serum alkaline phosphate levels are normal.
• SERUM ALBUMIN: normal to low.
• PROTHROMBIN TIME: will be increased.
• LEUCOCYTOSIS: occurs without an evidence of an infection.
• URINE: may contain urobilinogen, bilirubin.
• EEG: is done to grade the hepatic encephalopathy.
• SERUM AMMONIA: levels are usually high.
• USG OF LIVER: shows reduced liver size.

 

TREATMENT:

• No sedation is given until the patient is irritable. Only a small dose of phenobarbitone or 5mg of I.V diazepam may be given.
• Care of comatosed patient: care of back, bowel,bladder,skin, respiration, pulse and BP.
• Barrier nursing care with proper disposal of excreta.
• V. vitamin K, 10 mg daily for 3 days with I.V. vitamin C 500mg daily in the drip to prevent bleeding, if PTI is prolonged. Blood transfusion is given in severe bleeding.
• V. H2 blockers – ranitidine 50mg twice a day to prevent GIT bleeding.

 

ENCEPHALOPATHY TREATMENT:

• Withdrawal of protein intake from all sources.
• Sterilization of gut with neomycin 1gm orally after every 6 hours.
• Increased faecal output of nitrogen by changing the bacterial flora with lactulose, 30-60 ml orally after every 2-3 hours till a lose stool is produced.
• L-dopa, bromocriptine with some success have been tried.
• Repeated bowel/colonic wash should be attempted to evacuate the colon off its contents so as to reduce the ammonia formation from breakdown of proteins by coliform bacteria.
• Hypokalemia, hypomagnesaemia should be corrected and their levels are to be monitored.
• Infections are treated with parenteral amoxycillin and gentamicin or ceftriaxone.
• Corticosteroids are of no help.
• Cerebral oedema is reduced by 20% mannitol I.V.

 

PREVENTION:

• Maintaining a healthy weight.
• Maintaining a good hygiene.
• Vaccination against hepatitis A and hepatitis B.
• Avoid medicines overdose such as paracetamol.
• Avoid alcohol as much as you can
• Avoid any drug usage
• Have a balanced diet that includes essential phospholipids.