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Karan - MBBS Year 1: Gastrointestinal Week 3 > Acute Liver Failure > Flashcards

Acute Liver Failure Flashcards

1
Q

Describe acute liver failure.

A
  • 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
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2
Q

What is ‘acute on chronic liver failure’?

A

When usual symptoms of acute liver failure occur in a patient with pre-existing liver disease

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3
Q

What are the categories of acute liver failure and how can they be distinguished?

A
  • 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
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4
Q

What are the presenting symptoms and signs?

A
  • Jaundice
  • Pain and tenderness in right upper abdomen
  • Nausea and vomiting
  • Malaise
  • Disorientation and confusion
  • Drowsiness steadily progressing to coma in worst cases
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5
Q

At what point after initial presentation of jaundice is liver disease considered ‘chronic’?

A

28 weeks

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6
Q

What are the principal causes of acute live failure in the world and why is this less common in more developed countries?

A
  • 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
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7
Q

Describe the drug-induced causes of acute liver failure.

A
  • 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
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8
Q

Describe the viral causes of acute liver failure.

A
  • 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
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9
Q

Describe idiosyncratic drug-induced liver injury.

A
  • Very rarely progresses to acute liver failure
  • Increased risk of death in elderly
  • EXAMPLES: Ecstasy, NSAIDS, statins, chemotherapy, amoxicillin and tetracyclines
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10
Q

What are some other causes of acute liver failure?

A
  • 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)
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11
Q
A
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11
Q

What are some potential management pitfalls at presentation for patients with suspected acute liver failure?

A
  • 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
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12
Q

What should be done upon presentation for someone with suspected acute liver failure? PART 1

A
  • 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
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13
Q

What should be done upon presentation for someone with suspected acute liver failure? PART 2

A
  • 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
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14
Q

What should be done upon presentation for someone with suspected acute liver failure? PART 3

A
  • 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
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15
Q

What should be done upon presentation for someone with suspected acute liver failure? PART 4

A
  • 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
16
Q

Describe N. Acetyl cysteine.

A
  • 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
17
Q

What is the standard regimen for N. Acetylcysteine IV?

A
  • 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
18
Q

What would be done during subsequent care of a patient with suspected acute liver failure?

A
  • 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
19
Q

What is the treatmen algorithm for all patients with suspected acute liver failure?

A
  • Assess for encephalopathy
  • Liver transplantation assessment
  • Neurological status monitoring for advanced encephalopathy
  • Monitor blood glucose, electrolytes and cultures
20
Q

What is the treatmen algorithm for patients in intensive care with suspected acute liver failure?

A
  • 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
21
Q

List some general support measures for suspected acute liver failure outside ICU.

A
  • 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
22
Q

What are some issues to note in coagulopathy?

A
  • 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
23
Q

What criteria is used in staging of hepatic encephalopathy?

A

WEST HAVEN CRITERIA

24
Q

List some additional clinical features of hepatic encephalopathy.

A
  • 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)
25
Q

What are some danger signs in acute liver failure?

A
  • 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
26
Q

What is the proposed pathogenesis behind hepatic encephalopathy? PART 1

A
  • 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
27
Q

What is the proposed pathogenesis behind hepatic encephalopathy? PART 2

A
  • 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.
28
Q

Describe the treatment of hepatic encephalopathy and the aims of treatment.

A
  • 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
29
Q

What is the most common cause of acute liver failure in the following areas:
- USA, UK and Western Europe
- Developing world

A
  • Paracetamol poisoning
  • Viral infections

Karan - MBBS Year 1: Gastrointestinal Week 3 (9 decks)

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