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Acute (fulminant) hepatic failure
It is a rare syndrome in which hepatic encephalopathy results from a sudden severe impairment of hepatic function. It must occur within 8 weeks of onset of the precipitating illness In the absence of evidence of pre-existing liver disease
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Clinical grading of hepatic encephalopathy
Hepatic encephalopathy is the cardinal manifestation of acute hepatic failure. Clinical grading of hepatic encephalopathy Clinical grade Clinical signs Grade 1 Poor concentration, slurred speech, slow mentation, disordered sleep rhythm Grade 2 Drowsy but easily rousable, occasional aggressive behavior, lethargic Grade 3 Marked confusion, drowsy, sleepy but responds to pain & voice, gross disorientation Grade 4 Unresponsive to voice, may or may not respond to painful stimuli, unconscious
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Fulminant hepatic failure
Hepatic encephalopathy include the following: Reduced alertness & poor concentration Behavioral abnormalities e.g. restlessness, aggressive outbursts & mania Confusion Disorientation Inversion of sleep rhythm Slurred speech Yawning Hiccup Convulsions
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Fulminant hepatic failure
Flapping tremor (asterixis) is characteristic for cases of acute hepatic failure but may be absent. Cerebral edema: Produce increased intracranial pressure This results in: Unequal or abnormally reacting pupils Fixed pupils Hypertensive episodes Bradycardia Hyperventilation Profuse sweating Local or general myoclonus Focal fits Decerebrate posturing Papiledema Right hypochondrial pain (occasionally)
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Fulminant hepatic failure
Examination can reveal: Jaundice Fetor hepaticus Initially the liver is enlarged (later may become impalpable) Splenomegaly (uncommon) Ascites & edema (late features)
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Fulminant hepatic failure
Investigations to determine the cause of acute hepatic failure: Toxicology screen of blood & urine IgM anti-HBc IgM anti-HAV. Anti-HEV, HCV, CMV, herpes simplex, EBV Ceruloplasmin, serum copper, urinary copper Autoantibodies: ANF, AMA, ASMA, LKM. Ultrasound of liver & Doppler of hepatic veins
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Adverse prognostic criteria in acute hepatic failure
Paracetamol overdose: pH < 7.3 at or beyond 24 hours following the overdose OR Serum creatinine >300 μmol/l, prothrombin time >100 seconds and encephalopathy grade 3 or 4 Non-paracetamol cases: Prothrombin time >100 seconds Any THREE of the following: Jaundice to encephalopathy time > 7 days Age < 10 yrs or > 40 yrs Indeterminate or drug-induced causes Bilirubin > 300 μmol/l Prothrombin time > 50 seconds These adverse prognosis criteria predict a mortality rate of ≥ 90%
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Observations in fulminant hepatic failure
Neurological: Conscious level Pupils Size Equality Reactivity Fundi: Papiledema Plantar responses Cardiorespiratory: Pulse Blood pressure Central venous pressure Respiratory rate Fluid balance: Input: Oral Intravenous Output: Hourly urine output 24 hours sodium output Vomiting Diarrhea
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Observations in fulminant hepatic failure
Blood analysis: Arterial blood gases Peripheral blood count (including platelets) Creatinine, urea Na, K, HCO3, Ca, Mg Glucose (2-hourly in acute phase). Prothrombin time Infection surveillance: Cultures: Blood Urine Throat Sputum Canula sites Chest radiograph Temperature
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Complications of acute hepatic failure
Encephalopathy Cerebral edema Respiratory failure Hypotension Hypothermia Infection Bleeding Pancreatitis Renal failure Metabolic: Hypoglycemia Hypokalemia Hypocalcemia Hypomagnesemia Acid-base disturbance
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Management Conservative treatment Intensive care unit
Role of N-acetylecystein therapy Liver transplantation
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Chronic liver failure Chronic liver failure is a syndrome complex that can occur as a consequence of insidious destruction of the hepatocytes. It is more commonly precipitated by a number of events such as variceal hemorrhage or infection. Liver cirrhosis results from progressive and widespread death of liver cells associated with inflammation and fibrosis.
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Causes of cirrhosis Any cause of chronic hepatitis Alcohol
Primary biliary cirrhosis Primary sclerosing cholangitis Secondary biliary cirrhosis (stones, strictures) Hemochromatosis Wilson’s disease α-1 antitrypsin deficiency Cystic fibrosis
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Pathophysiology Recurrent or persistent hepatocyte death:
Viral hepatitis Alcohol Prolonged biliary damage or obstruction: Primary biliary cirrhosis Sclerosing cholangitis Post-surgical biliary stricture Stone Persistent blockage to the venous return: Veno-occlusive disease Budd Chiari syndrome
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World wide the most common causes of cirrhosis are:
Viral hepatitis Prolonged, excessive alcohol consumption
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Clinical features of hepatic cirrhosis
Hepatomegaly (although the liver may be small) Jaundice Ascites Circulatory changes: Spider telangiectasia Palmar erythema Cyanosis Endocrine changes: Loss of libido Loss of hair Men: gynecomastia, testicular atrophy, impotence Women: breast atrophy, irregular menses, amenorrhea Hemorhagic tendency: Bruises, purpura, epistaxis, menprrhagia Portal hypertension: Splenomegaly Collateral vessels Variceal bleeding Fetor hepaticus Hepatic (portasystemic) encephalopathy Other features: Pigmentation Digital clubbing Low grade fever
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Stigmata of chronic liver disease
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Gynecomastia in male patient with liver cirrhosis
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Ascites with dilated blood vessels
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Ascites with everted umbilicus
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Spontaneous bruises in patient with cirrohsis
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Hepato-splenomegaly
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Spider naevi (telangeicatasia) in patient with alcoholic cirrhosis
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Spider nevi Spider nevi
Notice fading of peripheral capillaries after pressing the central arteriole Spider nevi
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Palmar erythema
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Duputyrine contracture
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Management This includes:
Treatment of any cause The maintenance of nutrition Treatment of the complications of liver cirrhosis. Chronic liver failure due to liver cirrhosis can also be treated by orthotopic liver transplantation.
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Indications for orthoptopic liver transplantation
Cholestatic form of cirrhosis especially that is due to primary biliary cirrhosis Alcoholic cirrhosis (the patient must has capacity for abstinence) Cirrhosis due to hepatitis C virus Rarer indications include: α -1 antitrypsin deficiency Hemachromatosis
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Signs of liver failure pointing to transplantation
Sustained or increased jaundice Bilirubin > 100 mmol/l in cholestatic diseases like primary biliary cirrhosis Ascites or hepatic encephalopathy not responding readily to medical therapy Hypoalbuminemia Albumin < 30g/l Additional indications: Fatigue & lethargy affecting the quality of life. Intractable itching in cholestatic disease Recurrent variceal bleeding
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Main contraindications for liver transplantation
Sepsis AIDS Extrahepatic malignancy Active alcohol or other substance misuse Marked cardiorespiratory dysfunction Survival at 1 year after transplantation is about 80% and the prognosis thereafter is good
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