ALF CLF Flashcards
Definition of acute liver failure
Acute liver failure is a syndrome of acute liver dysfunction without underlying chronic liver disease.
ALF characterised by + Key presentations
Coagulopathy
HE
3 subtypes of ALF
- Hyperacute: HE within 7 days of noticing jaundice. Best prognosis as much better chance of survival and spontaneous recovery.
- Acute: HE within 8-28 days of noticing jaundice
- Subacute: HE within 5-12 weeks of noticing jaundice (ALF may be defined up to 28 weeks). Worst prognosis as usually associated with shrunken liver and limited chance of recovery.
Epidemiology of ALF
ALF is the primary indication for liver transplantation in around 8% of cases within Europe.
Acute liver injury (ALI): severe acute liver injury from a primary liver aetiology. Characterised by impaired liver function but hepatic encephalopathy is absent, unlike in ALF that cause ALF
- Viral (Hepatitis A, B and CMV) - most common worldwide
- Other infections e.g. yellow fever, leptospirosis, EBV
- Drug-induced liver injury - paracetamol and non-paracetamol (e.g. alcohol, anti-depressants, NSAIDs)
- Wilsons
- Budd chiari
- Toxin induced
Secondary liver injury (SLI): similar to ALI but no evidence of a primary liver insult that cause ALF
- Ischaemic hepatitis
- Liver resection(post-hepatectomy liver failure)
- Severe infection(e.g. malaria)
- Malignancy infiltration(e.g. lymphoma)
- Heat stroke
ALF pathophysiology
DIrect liver insult > massive hepatocyte necrosis and apoptosis > liver doesnt carry out normal function
As ALF progresses what happens
hyperdynamic circulatory state with low systemic vascular resistance due to a profound inflammatory response
Causes poor peripheral perfusion and multi-organ failure
Marked cerebral oedema occurs in ALF what does this lead to
Morbidity and mortality in ALF
Due to hyperammonaemia causing cytotoxic oedema and increased cerebral BF
S + S of ALF
- HE - altered mental status, confusion
- Jaundice
- Right upper quadrant pain(variable)
- Hepatomegaly
- Ascites
Primary investigations of ALF
FBC
U&Es
LFTs
Blood Glucose
LDH
ABG
Imaging for ALF
- Ultrasound - to see liver size and underlying liver pathology
- Doppler ultrasound - to assess patency of hepatic and portal veins
- Chest x-ray
- CT abdomen and pelvis - examine liver architecture, volume, vascular integrity etc
Management of ALF
- Treat underlying cause
- Good nutrition - thiamine and folate supplementation
Major complications of ALF
- Acute kidney injury/ hepatorenal syndrome
- Metabolic disturbance
- Hypoglycaemia
- Haemorrhage (e.g. GI Bleeding)
- Cerebral dysfunction (e.g. seizures, irreversible brain injury).
- Patients are at risk of high output cardiac failure due to low vascular resistance from the widespread inflammatory response.
- Sepsis
Definition of CLD
Chronic liver disease is caused by repeated insults to the liver, which can result in inflammation, fibrosis and ultimately cirrhosis.
CLD is generally defined as progressive liver dysfunction for six months or longer. The end result of chronic liver disease is cirrhosis, which describes irreversible liver remodelling.
Epidemiology
- CLD represents the fourth commonest cause of years of life lost in those aged under 75.
- In England and Wales an estimated 600,000 patients have CLD.
Aetiology of CLD
- Alcohol
- Viral(Hepatitis B, C)
- Inherited(Alpha-1-antitrypsin deficiency, Wilson’s disease, Hereditary haemochromatosis)
- Metabolic(Non-alcohol fatty liver disease / Non-alcoholic steatohepatitis)
- Autoimmune(Autoimmune hepatitis)
What happens overtime in CLD
inflammation (hepatitis), fatty deposits (steatosis) and scarring (fibrosis)
normal liver architecture is replaced by fibrotic tissue and regenerative nodules.
End result is cirrhosis
2 types of Cirrhosis
Compensated= Asymptomatic - liver carries out normal function despite damage
Decompensated= Multiple complications
Complications of Decompensated
- Coagulopathy(reducing clotting factor synthesis)
- Jaundice(impaired breakdown of bilirubin)
- Encephalopathy(poor detoxification of harmful substances)
- Ascites(poor albumin synthesis and increased portal pressure due to scarring)
- Gastrointestinal bleeding(increase portal pressure causing varices)
Signs of CLD
Splenomegaly
Palmar erythema
Gynaecomastia
Spider naevi
Signs of decompensated liver disease
- Encephalopathy:confusion, often present with a flapping tremor (asterixis)
- Ascites:fluid within the peritoneal cavity
- Jaundice:yellow pigmentation of skin and sclera
- GI bleeding: variceal bleeding or slow oozing from portal hypertensive gastropathy
- Coagulopathy: may see marked bruising due to raised INR
Investigations for CLF
- LFTs - Raised AST and ALT
- FBC - thrombocytopenia
- USS
- CT MRI
GS for CLF
Liver biopsy
Management of CLF
- Treat underlying pathology e.g. alcohol cessation, removal of offending medications or use of anti-viral therapies in chronic hepatitis.
- Transplantation based on patient’s ‘United Kingdom model for end-stage liver disease’ (UKELD) score
Treatment of ascites
- develops due to a combination of portal hypertension and loss of oncotic pressure (hypoalbuminaemia).
- Aldosterone antagonists:e.g. spironolactone (can be combined with loop diuretics i.e. furosemide).
- Paracentesis:percutaneous drainage of ascites
GI bleeding
- due to oesophageal varices secondary to portal hypertension
- Beta blockers to reduce portal hypertension
- Endoscopic variceal band ligation - for variceal haemorrhage
Spontaneous bacterial peritonitis
- Infection within the ascitic fluid
- Antibiotics
- Human albumin solution - draws fluid out peritoneum. Helps to prevent acute kidney injury and hepatorenal syndrome
Complications of CLF
- Hepatic encephalopathy
- Ascites
- Gastrointestinal bleeding(i.e. variceal bleed)
- Bacterial infections(i.e. SBP)
- Acute kidney injury
- Hepatocellular carcinoma
