Cirrhosis Flashcards
Definition
End-stage of chronic liver damage with replacement of normal liver architecture with diffuse fibrosis and nodules of regenerating hepatocytes.
Decompensation of cirrhosis
· Cirrhosis is considered DECOMPENSATED if it becomes complicated by any of: o Ascites o Jaundice o Encephalopathy o GI bleed
· Decompensation can be precipitated by infection, GI bleeding, constipation, high-protein meal, electrolyte imbalances, alcohol and drugs, tumour development or portal vein thrombosis
Aetiology/Risk factors
· Chronic alcohol misuse (most common in the UK)
· Chronic viral hepatitis (hep B/C - most common worldwide)
· Autoimmune hepatitis
· Drugs (e.g. methotrexate, hepatotoxic drugs)
· Inherited o a1-antitrypsin deficiency o Haemochromatosis o Wilson's disease o Galactosaemia o Cystic Fibrosis
· Vascular
o Budd-Chiari Syndrome
o Hepatic Venous Congestion
· Chronic Biliary Diseases
o PBC
o PSC
o Biliary atresia
· Unknown: 5-10%
· Non-Alcoholic Steatohepatitis (NASH)
o Associated with obesity, diabetes, total parenteral nutrition, short bowel syndromes, hyperlipidaemia and drugs (e.g. amiodarone, tamoxifen)
Presenting symptoms (early)
· Early non-specific symptoms: o Anorexia o Nausea o Fatigue o Weakness o Weight loss
Presenting symptoms (decreased liver synthetic function)
o Easy bruising
o Abnormal swelling
o Ankle oedema
Presenting symptoms (reduced detoxification function)
o Jaundice
o Personality change
o Altered sleep pattern
o Amenorrhoea
o Galactorrhoea
Presenting symptoms (portal hypertension)
o Abdominal swelling
o Haematemesis
o PR bleeding or melaena
3 symptoms to remember for portal hypertension:
Visible veins on abdomen
Splenomegaly
Ascites
Epidemiology
One of the top 10 causes of death worldwide
Signs on physical examination
These are all signs of chronic liver disease
· Asterixis · Bruises · Clubbing · Dupuytren's contracture · Palmar erythema · Jaundice · Gynaecomastia · Leukonychia · Parotid enlargement · Spider naevi · Scratch mark (from cholestatic pruritis) · Ascites · Enlarged liver (may be shrunken in the later stages) · Testicular atrophy · Caput medusae · Splenomegaly
Investigations (bloods)
o FBC: low platelets + Hb = because of hypersplenism as a result of portal hypertension
o LFTs - may be normal but often get:
· High AST, ALT, ALP, GGT and bilirubin
· Low albumin
o Clotting: prolonged PT
o Serum AFP (alpha-fetoprotein = tumour marker for liver cancer):
· Raised in chronic liver disease
· High levels may suggest hepatocellular carcinoma
Investigations (to determine cause)
o Viral serology
o a1-antitrypsin
o Caeruloplasmin
· This is a copper-carrying complex that is LOW in Wilson’s disease
o Iron studies: serum ferritin, iron, total iron binding capacity (TIBC) - check for haemochromatosis
o Anti-mitochondrial antibody (PBC)
o ANA, ASMA (autoimmune hepatitis)
Investigations (ascitic tap)
o MC&S - check for infection
o Biochemistry (protein, albumin, glucose, amylase)
o Cytology
o IMPORTANT: ascitic tap with neutrophils > 250/mm3 = spontaneous bacterial peritonitis (SBP)
Investigations (liver biopsy)
o Performed either:
· Percutaneously
· Transjugular - if clotting deranged or ascitic
o Histopathological features of cirrhosis:
· Periportal fibrosis
· Loss of normal liver architecture
· Nodular appearance
o Grade - indicates degree of inflammation
o Stage - degree of architectural distortion (from mild portal fibrosis –> cirrhosis)
Investigations (imaging)
· Imaging
o US, CT or MRI - to detect complications such as: · Ascites · HCC · Hepatic or portal vein thrombosis · Exclude biliary obstruction
o MRCP (if PSC suspected)
· Endoscopy
o To examine varices
Investigations (Child-Pugh grading)
· Child-Pugh Grading - score for estimating the prognosis in chronic liver disease/cirrhosis. It is based on 5 factors:
o Albumin o Bilirubin o PT o Ascites o Encephalopathy
· Cirrhosis can be divided into Classes using the Child-Push grading system:
o Class A: 5-6
o Class B: 7-9
o Class C: 10-15
Management plan
· Treat the CAUSE if possible
· Avoid alcohol, sedatives, opiates, NSAIDs and drugs that affect the liver
· Nutrition is important
· Enteral supplements should be given
· NG feeding may be indicated
Management plan (treating complications - encephalopathy)
· Treat infections
· Exclude GI bleed
· Use lactulose and phosphate enemas
§ Normally, the liver breaks down ammonia that is absorbed in the GI tract, however, in Cirrhosis the ammonia can go through the liver without being broken down and exert toxic effects on the brain
§ IMPORTANT: lactulose reduces the absorption of ammonia from the gut
§ This helps prevent encephalopathy caused by ammonia reaching the brain
· Avoid sedation
Management plan (treating complications - ascites)
· Diuretics (spironolactone with/without furosemide)
· Dietary sodium restriction
· Therapeutic paracentesis (with human albumin replacement)
· Monitor weight
· Fluid restrict if plasma sodium < 120 mmol/L
· Avoid alcohol and NSAIDs
Management plan (treating complications - spontaneous bacterial peritonitis)
· Antibiotics (e.g. cefuroxime and metronidazole)
· Prophylaxis against recurrent SBP with ciprofloxacin
Management plan (treating complications - surgical)
· Consider TIPS (transjugular intrahepatic portosystemic shunt) - this helps reduce portal hypertension
§ However, it may precipitate encephalopathy because it is providing a route for blood from the GI tract to bypass the liver
· Liver transplantation is the only curative method
Possible complications
· Portal hypertension with ascites
· Hepatic encephalopathy
· Variceal haemorrhage
· SBP (spontaneous bacterial peritonitis)
· HCC (hepatocellular carcinoma)
· Renal failure (hepatorenal syndrome)
· Pulmonary hypertension (hepatopulmonary syndrome)
Prognosis
· Depends on aetiology and complications
· Generally poor prognosis
o Overall 5 year survival = 50%
o If ascites, 2 year survival = 50%
