Acute Liver Failure Flashcards
Describe acute liver failure.
- Caused by severe liver injury with decline in hepatic function
- Characterised by jaundice, coagulopathy and hepatic encephalopathy in patients with no evidence of pre-existing liver disease
What is ‘acute on chronic liver failure’?
When usual symptoms of acute liver failure occur in a patient with pre-existing liver disease
What are the categories of acute liver failure and how can they be distinguished?
- HYPERACUTE - most severe coagulopathy. Least severe jaundice. Best chance of spontaenous recovery. Induced by HAV, HEV and Paracetamol
- ACUTE - Induced by HBV
- SUBACUTE - least severe coagulopathy. Most severe jaundice. Worst chance of spontaneous recovery. Non-paracetamol drug induced
What are the presenting symptoms and signs?
- Jaundice
- Pain and tenderness in right upper abdomen
- Nausea and vomiting
- Malaise
- Disorientation and confusion
- Drowsiness steadily progressing to coma in worst cases
At what point after initial presentation of jaundice is liver disease considered ‘chronic’?
28 weeks
What are the principal causes of acute live failure in the world and why is this less common in more developed countries?
- Drug-induced liver injury and hepatic viral infections
- Public health measures e.g vaccination, public awareness - reduced incidence of viral infections in more developed countries
Describe the drug-induced causes of acute liver failure.
- Most common cause is by paracetamol poisoning - risk groups include malnourished/alcoholic patients
- Greater risk of death from paracetamol when ingestion gradual over hours or days rather than large dose ingested in one go
Describe the viral causes of acute liver failure.
- Hep. A, B and E - responsible for most cases
- HBV - common cause in Japan and Sudan. Poor survival - particularly when infecction occurs alongside immunosuppression
- RARE - herpes simplex, EBV, adenovirus and cytomegalovirus
Describe idiosyncratic drug-induced liver injury.
- Very rarely progresses to acute liver failure
- Increased risk of death in elderly
- EXAMPLES: Ecstasy, NSAIDS, statins, chemotherapy, amoxicillin and tetracyclines
What are some other causes of acute liver failure?
- Sepsis
- Acute ischaemic hepatocellular injury - in patients with circulatory or respiratory failure
- Acute Budd-Chiari syndrome
- Autoimmune hepatitis
- Pregnancy - HELLP, pre-eclamptic liver rupture (both very rare)
What are some potential management pitfalls at presentation for patients with suspected acute liver failure?
- ALWAYS have a low threshold for recognising a case as either incipient or established ALF
- Confused and agitated case - these features can delay recognition
- Hyperacute presentations jaundice may be minimal or absent
- Subacute cases the presentation may be more suggestive of chronic than of acute disease
- Check for hypoglycaemia as cause for drowsiness rather than encephalopathy
What should be done upon presentation for someone with suspected acute liver failure? PART 1
- Initial history (where possible) & clinical examination to exclude cirrhosis, alcohol-induced liver injury or malignant infiltration.
- Initiate early discussions with tertiary liver/transplant centre even when not immediately relevant
- Assess carefully for features of hepatic encephalopathy
Determine the probable cause - this will guide treatment and prognosis
Assess suitability for liver transplant BUT contraindications should not preclude transfer to tertiary liver/transplant centre
Transfer to a specialized unit when:
INR >1.5 and/or
the onset of hepatic encephalopathy or other poor prognostic features
What should be done upon presentation for someone with suspected acute liver failure? PART 2
- Determine the probable cause - this will guide treatment and prognosis
- Assess suitability for liver transplant BUT contraindications should not preclude transfer to tertiary liver/transplant centre
- Transfer to a specialized unit when:
INR >1.5 and/or onset of hepatic encephalopathy or other poor prognostic features
What should be done upon presentation for someone with suspected acute liver failure? PART 3
- Maintain or restore intravascular volume to prevent or reduce organ failure
- Treat with N. acetylcysteine by IV infusion
- Check for encephalopathy which can progress rapidly, particularly in patients with hyperacute disease
- If encephalopathy is confirmed ADMIT TO AN ICU
What should be done upon presentation for someone with suspected acute liver failure? PART 4
- Consider early endotracheal intubation and sedation for airway control and oxygenation and to prevent inhalation pneumonia
- Monitor and correct low arterial blood pressure and check for evidence of sepsis
- IV antibiotics are often given pre-emptively
Describe N. Acetyl cysteine.
- Complex anti-oxidant with immunological benefits
- Most useful in severe paracetamol poisoning
- Use even in non-paracetamol cases
- Very safe, so always give it
- Administer as early as possible
- Time between ingestion of paracetamol and treatment with NAC is critical and influences outcome
What is the standard regimen for N. Acetylcysteine IV?
- 150mg/kg over 15 minutes, then
- 50mg/kg over 4 hours, then
- 100mg/kg over 16 hours
- +/- 100mg/kg over 16 hours until the prothrombin time is improving
What would be done during subsequent care of a patient with suspected acute liver failure?
- Monitor for coagulopathy and encephalopathy
- Seek cause of liver injury - specific therapies may be available for some causes
- Avoid inappropriately prolonged investigation - organ transplantation not possible if multiorgan failure/sepsis develops
What is the treatmen algorithm for all patients with suspected acute liver failure?
- Assess for encephalopathy
- Liver transplantation assessment
- Neurological status monitoring for advanced encephalopathy
- Monitor blood glucose, electrolytes and cultures
What is the treatmen algorithm for patients in intensive care with suspected acute liver failure?
- Liaise with tertiary centre for transplants
- Intubation and sedation - monitor CVP
- Treat hypoglycaemia with iV glucose to target of 140 mg/dl
- Check sodium, potassium, phopshate and magnesium levels
- Check blood, urine and sputum cultures regularly
List some general support measures for suspected acute liver failure outside ICU.
- Cultures (respiratory, blood, urine)
- CXR, ECG, liver echography, possible CT imaging of abdomen and chest
- Monitoring of oxygen sats, BP, HR, PT, INR and neurological status
- NAC in early stages, glucose infusions, limit use of clotting factors unless active bleeding
- Avoid sedatives and hepatotoxic drugs
What are some issues to note in coagulopathy?
- Rapid changes in PT or INR are characteristic of ALF - PT/INR have significant prognostic value and are the best guides to liver function, severity and outcome in ALF cases
- Thrombocytopenia is often seen
- Abnormal INR does not necessarily translate to increased risk of bleeding - in most patients coagulation remains normal despite abnormal INR and PT
What criteria is used in staging of hepatic encephalopathy?
WEST HAVEN CRITERIA
List some additional clinical features of hepatic encephalopathy.
- Asterixis - hepatic flap
- Hepatic foetor
- Hyperacute- within 7 days of onset of jaundice (after paracetamol poisoning)
- Acute – develops 8-28 days after onset of jaundice (after viral or other drug-induced)
- Subacute – 4-12 weeks after onset of jaundice (any cause)
What are some danger signs in acute liver failure?
- In subacute ALF – low-grade encephalopathy has a poor prognosis
- In hyperacute ALF – high-grade encephalopathy has a poor prognosis
- Cerebral oedema causing intracranial hypertension contributes to the neurological complications of ALF and is a common cause of death in ALF
What is the proposed pathogenesis behind hepatic encephalopathy? PART 1
- Normal detoxification of ammonia to urea is impaired - increased levels of circulating ammonia.
- Ammonia increases intracellular osmolarity through its cerebral metabolism to glutamine
- Causes changes to neurotransmitter synthesis and to mitochondrial function
What is the proposed pathogenesis behind hepatic encephalopathy? PART 2
- Subsequent altered cerebral function and resultant cortical swelling.
- Cerebral oedema causes intracranial hypertension (ICH) and impaired conscious level.
- Affects one-third of cases who progress to grades 3 or 4 encephalopathy, mostly in the hyperacute group of ALF.
Describe the treatment of hepatic encephalopathy and the aims of treatment.
- Treatment focuses on prevention of infection, control of circulating ammonia and its cerebral metabolism - lower risk of ICH
- Moderate hypothermia - slow body metabolism and systemic ammonia production. Avoid fever and consequent increased metabolism
- Osmotherapy with IV hypertonic fluids e.g saline and mannitol
- Transplantation - best chances of survival when encephalopathy/oedema occur
What is the most common cause of acute liver failure in the following areas:
- USA, UK and Western Europe
- Developing world
- Paracetamol poisoning
- Viral infections
