Block 5: decompensated liver disease Flashcards
Decompensated cirrhosis: imaging and special tests
- MRI
- CT head
- Abdominal ultrasound
- Ascitic tap for culture and cell count
SAAG (serum to ascites albumin gradient)
- Identifies portal hypertension and is more accurate then protein based exudate
- You subtract the ascitic fluid albumin value from the serum albumin value, which should be obtained the same day. Don’t repeat after initial measurement
- ≥11g/l means there’s portal hypertension
- This is due to increased hydrostatic pressure within the blood vessels of the hepatic portal system, which in turn forces water into the peritoneal cavity but leaves proteins such as albumin within the vasculature.
Score for GI bleed
Glasgow-Blatchford score: assesses likelihood that you need endoscopy or a blood transfusion after an upper GI bleed
cirrhosis: Screening after a decompensation event
- Hepatocellular carcinoma: screening ultrasound and AFP every 6 months
- Ongoing review with addiction services to help maintain abstinence from alcohol and illicit drugs.
- Osteoporosis: Screen & treat
- Ascites & SBP: Monitor regularly for evidence of ascites & treat
- Variceal Haemorrhage: OGD at diagnosis of cirrhosis and every 2 years
Treatment follow decompensation event (cirrhosis)
- Beta-blocker (non-cardio-selective; carvedilol or propranol) as primary prevention of bleedingrebleed
- Viral Superinfection: Immunise for HAV and HBV (although this patient has already been exposed to HBV therefore would not require additional vaccination)
- Vitamin deficiencies: Treat (Vit B Co-strong & Thiamine)
Stages of alcohol related liver disease
- Steatosis: imbalance in triglyceride metabolism causing accumulation within hepatocytes
- Alcoholic hepatitis: inflammatory response causing neutrophilic infiltration and cytokine release. Jaundice, coagulopathy and encephalopathy
- Fibrosis and cirrhosis: chronic injury and inflammation activate hepatic stellate cells causing collagen deposition and fibrosis. Cirrhosis is causes by extensive fibrosis and formation of regenerative nodules
Symptoms of alcoholic liver disease
fatigue, malaise, abdominal pain, anorexia, weakness, nausea and/or vomiting
Clinical features of alcoholic hepatitis
- Jaundice (common)
- Right upper quadrant pain (common)
- Hepatomegaly: Generally an enlarged and smooth edge, but rarely tender to palpation
- Palmar erythema
- Peripheral oedema
- Clubbing
- Dupuytren’s contracture (present in 30% of patients with alcoholic liver disease)
- Pruritis: If there is cholestasis leading to bile salt deposition in skin
- Xanthomas
- Spider angioma: multiple increase disease severity
Oestrogenic effects of alcoholic hepatitis
- Gynaecomastiaand testicular atrophy (in males)
- Loss of body hair
- Amenorrhoea (in females)
- Loss of libido
Management of acute alcoholic hepatitis
- Glucocorticoids i.e. prednisolone
- Use Maddrey’s discriminant function (DF) to identify patients with severe acute alcoholic hepatitis: score above >32 indicates liver biopsy and corticosteroids
- Pentoxifylline can be used as an alternative to glucocorticoids if they are contraindicated (e.g. hepatitis B viral infection, tuberculosis, other serious infection)
Main causes of ALT >1000
drugs, ischaemia, viruses
Liver function
- Synthesis: proteins (including albumin), clotting factors, bile, lipids
- Metabolism: Bilirubin, carbohydrate drugs, waste products and toxin
Bilirubin
- Heme from haemoglobin breaks down into unconjugated bilirubin which is water insoluble, so travels around combines with albumin
- In the liver its combined glucoronic acid to make conjugated bilirubin which is water soluble
- Conjugated acid is excreted as bile acid, soted in the gallbladder and released in the small intestine causing lipid breakdown
- Most bile acid is reabsorbed in the Enterohepatic circulation
- Total serum bilirubin is usually <21
Unconjugated bilirubin: causes
- Elevated due to increased bilirubin production or decreased hepatic uptake/conjugation
- Causes of raised unconjugated bilirubin: Gilbert’s syndrome, haemolysis and drug relates (i.e. Rifampicicn)
Gilbert’s syndrome
- A genetic disorder where less of the enzyme that breaks down Bilirubin (UDP-glucuronyltransferase) is produced. It affects 5% of the population. There is an increase in the bilirubin often with fasting or concurrent illness.
- Confirmation of just a predominant unconjugated hyperbilirubinaemia makes the diagnosis of Gilbert’s syndrome virtually certain. This does not require any treatment and the patient can be completely reassured.
- Rarely does it cause a bilirubin above 68umol/L
Conjugated bilirubin
- Raised is usually a sign of liver disease which is acute or chronic in nature. Only increase when the liver has lost half of its excretory capacity
- Causes: obstruction in the common bile duct (gallstones, malignancy i.e. cholangiocarcinoma or Pancreatic cancer), Drugs (i.e. Penicillin), Primary sclerosing cholangitis, Primary biliary cirrhosis, hepatitis, cirrhosis
Alanine aminotransferase (ALT) or Aspartate aminotransferase (AST)
- ALT is more specific to liver. AST is found in cardiac, skeletal and renal tissue and red blood cells
- Raised with anabolic steroids, EBV, A fib causing low blood pressure, metabolic iron, acute/chronic Hepatitis, Excess iron (Haemochromatosis)
- Normal is <40. Its mild if the rise is <5, moderate if rise of 5-10, marked if >10
Common causes of acute and chronic hepatitis
- Alcohol – including chronic alcohol abuse and Alcoholic hepatitis
- Non-alcoholic fatty liver disease (NAFLD)
- Viral Hepatitis – both acute and chronic
- Autoimmune Hepatitis
- Drug toxicity
- Ischaemia – this can be due to anything which suddenly causes a patient’s blood pressure to drop
- Metabolic liver disease (Wilson’s / Haemochromatosis)
AST/ALT ratio indicating liver disease
An AST/ALT ratio of >2 in alcoholic liver disease; whilst an AST/ALT ratio of <1.0 would be more suggestive of non-alcoholic liver disease.