• Acute and Chronic Liver Disease

    by  • 11/05/2013 • Gastroenterology • 0 Comments

    Acute hepatitis:

    1. Non-specific term for acute, self-limiting liver inflammation
    2. p/c: jaundice, nausea, anorexia, RUQ pain, fever, fatigue, orange urine, occasional substantial intrahepatic cholestasis (=white stools)
    3. Causes:
      1. o Common = viral hepatitis A/B, EBV, drug reactions (=paracetamol)
      2. o Uncommon = autoimmune hepatitis
      3. o Rare = Wilson’s disease, toxins
    4. Ix:
      1. o LFTs: measure hepatic enzymes (=transaminases), measure cholestatic enzymes (= alk phos), measure synthetic function tests (=prothrombin, albumin)
      2. o Tests to determine cause = viral serology, immunoglobulins, autoantibody profile, copper levels
      3. o Liver USS = exclude structural lesions (neoplasms, biliary disease)
    5. Mx: stop all potentially harmful drugs

     

    Fulminant liver failure:

    1. Describes liver failure with hepatic encephalopathy (AND REDUCED CONSCIOUSNESS) within 8 weeks
    2. p/c:
      1. o Encephalopathy: progressive deterioration in cognitive function from a shortened attention span through to a reversal of sleep pattern and deep coma. clinical sign = metabolic flap/asterixis.
      2. o Jaundice: depending on rate of deterioration
      3. o Haemorrhage: maybe confined to GI or occur widely as result of haemostatic failure
      4. o Fever, small liver, acidotic, coagulopathies, brisk reflexes, pre-renal renal failure, hypotensive (vasodilated circulation).
    1. Ix:
      1. o Prothrombin time: important prognostic marker for liver synthetic function
      2. o Blood glucose: hypoglycaemia is an ominous sign
      3. o Electrolytes: renal impairment relates to acute tubular necrosis on admission. Unlikely to reflect genuine hepatorenal syndrome
      4. o ABGs: metabolic acidosis is a poor prognostic sign
      5. o Paracetamol level: should be measured in all cases. Most common cause of fulminant liver failure in UK. It is ameniable to medical Tx (=N-acetylcysteine)
    2. Mx:
      1. o Airway management: those with progressive coma should undergo early intubation and ventilation, especially if between hospital transfer occurs
      2. o Optimize circulatory state: pts have a hyperdynamic circulation with lowered systemic vascular resistance. the degree of volume depletion on admission is often underestimated
      3. o N-acetylecysteine: antidote for paracetamol OD, but evidence also shows it may benefit all patients with fulminant hepatitis
      4. o H2-receptor antagonists and sucralfate: to decrease chance of GI bleeding
      5. o Indications for liver transplant:
      6. o In paracetamol poisoning:
      7. pH <7.3
      8. INR >6.5
      9. Creatinine >300umol/L
      10. In other pathologies (viruses/drugs):
      11. INR >6.5
      12. And any 3 of the following:
      13. Age <10 or >40
      14. Jaundice for 7/7 before encephalopathy
      15. Bilirubin >300
      16. INR >3.5

     

    Chronic liver disease:

    1. Many liver pathologies follow an indolent course and present with clinical features of cirrhosis
    2. Compensated cirrhosis implies a relatively well patient, whereas those who have decompensated are often v unwell
    3. p/c: long-term low grade damage results in progressive liver fibrosis = reduced liver cell mass and portal HTN. Weakness, anorexia, muscle/adipose tissue loss, GI bleeding, ascites (+complicated spontaneous bacterial peritonitis), jaundice, encephalopathy
    4. Also: low BP, spider naevi (upper body only), gynaecomastia, hypersplenism, easy bruising, palmar erythema, clubbing, oedema, piles, caput medusa, small liver, metabolic flap
    5. Problems caused by reduced liver cell mass:
      1. o Encephalopathy: often a subtle sign in most patients with liver disease is encephalopathy = reduced attention span (clinically proven by a ‘trail test’), reversed sleep pattern (=insomnia and daytime somnolence). Metabolic flap may be found. As encephalopathy advances = pt develops constructional dyspraxia and progresses to hepatic coma.
      2. o Portosystemic shunting may worsen encephalopathy
      3. o Loss of lean body mass: most evident at shoulders, often hidden by accumulation of water (oedema)
      4. o Coagulopathy
    1. Portal HTN:
      1. o Caused by: RHF, Budd-Chiari syndrome (=hepatic vein thrombosis), portal vein thrombosis, cirrhosis, schistosomiasis, vinyl chloride poisoning, idiopathic.
    2. Complications of portal HTN
      1. o Varices: form at sites of portosystemic communication (oesophagus/rectum). GI bleeding (sometimes torrential) may be first presentation of chronic liver disease and can provoke decompensation
      2. o Ascites: result of high portal pressure, low albumin, and Na retention. It is always important to exclude spontaneous bacterial perontinitsi (SBP)
    3. Ix
      1. o Confirm cirrhosis
      2. o Assess:
      3. Haematology: Hb may be low (due to bleeding and hypersplenism), PTT may be prolonged (due to synthetic failure and DIC)
      4. Biochemistry: if causative agent has been removed, AST and LDH levels will be normal – despite established cirrhosis
      5. o Autoimmune: assess immunoglobulins
      6. o Iron studies: for haemochromatosis and Cu levels for Wilson’s disease
      7. o Viral serology: hep B/C
      8. o Liver biopsy: to confirm cirrhosis
    4. Mx:
      1. o Identify and tx cause of initial clinical decompensation: drugs/sepsis/hypokalaemia/other electrolyte disturbances/GI bleeding/hepatoma
    5. Tx of acute complications:
      1. o Variceal bleeding: blood products, endoscopy with band ligation or sclerosant injection. Vasoconstrictors (=glypressin) as a short-term measure. In overwhelming haemorrhage = balloon tamponade (=Sengstaken-Blakemore tube). Can also try = acute percutaneous portosystemic shunting and trans-jugular intrahepatic portosystemic stent shunt. Long-term, b-blockers reduce the risk of haemorrhage.
      2. o Ascites: spironolactone and salt restriction
      3. o Encephalopathy: minimise absorption of dietary nitrogen (protein restriction, bowel evacuation using lactulose, non-absorbable Abx).
    6. Prognosis:
      1. o Related to Child-Pugh class (scored by a table of values for bilirubin, albumin, ascites, encephalopathy, nutrition).
      2. o If cause is known, tx can often restore good function – even if cirrhosis exists
      3. o Hepatoma – complicates longstanding cirrhosis. Frequent liver USS and AFP measurements are indicated for early tumour detection
      4. o Refractory disease may require transplantation 
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