Liver Failure Flashcards

1
Q

Define Liver Failure

A

Severe liver dysfunction characterise by jaundice, hepatic encephalopathy and coagulopathy

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2
Q

What are the classifications of Liver Failure (by onset)

A

Hyperacute: jaundice + encephalopathy <7 days

Acute: jaundice + encephalopathy 1-4 weeks of onset

Subacute: jaundice + encephalopathy within 4-12 weeks

Acute-on-chronic: Acute deterioration (decompensation) in patients with CLD

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3
Q

Aetiology of Liver Failure

A

Paracetamol overdose (most common in UK/US)
Viral hepatitis (esp. B)
Drug reactions e.g. anti-TB, anti-microbial
Autoimmune hepatitis
Budd-Chiari syndrome
Malignancy
Haemochromatosis
Wilson’s
Alpha-1 antitrypsin deficiency
NAFLD
Pregnancy-related e.g. fatty liver of pregnancy/HELLP syndrome

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4
Q

Symptoms of Liver Failure

A

Triad of encephalopathy, jaundice and coagulopathy

±
Fever
Nausea and vomiting
Jaundice
Abdominal pain
Malaise

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5
Q

Signs of Liver Failure on examination

A

Jaundice
Encephalopathy (impaired awareness, sleep alterations, shortened attention span, anxiety, personality change, disorientation, hyperreflexia)
Liver asterisks/flap
Fetor hepaticus
Ascites and splenomegaly
RUQ tenderness

CLD signs: palmar erythema, dupuytren’s contracture, gynaecomastia, bruising, spider naevi

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6
Q

Investigations for Liver Failure

A

LFTs: enzymes are raised (AST/ALT very high in paracetamol od) | bilirubin high | albumin reduced
Clotting: PT prolonged
FBC: WCC raised in infection |anaemia if bleeding
U+Es: check for renal failure
ESR/CRP: may be raised
ABG: often a metabolic acidosis (esp. in paracetamol od) | elevated lactate (esp. in paracetamol od)

Find the cause: Paracetamol level | urine toxicology | viral serology | ANA/SMA/AMA | Caeruloplasmin | Iron studies | Pregnancy test

USS liver: hepatosplenomegaly, hepatic surface modularity
CT abdomen
Doppler scanning hepatic/portal vein: check for Budd-chiari syndrome

Ascitic fluid tap: check for SBP
Electroencephalogram

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7
Q

Management for Liver Failure

A
  1. Intensive care + ABCDE
  2. Assessment for liver transplant (King’s College Hospital Criteria)
  3. Treat the cause
  4. Monitoring
  5. Manage the complications
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8
Q

How are the following causes of liver failure treated:
Paracetamol
Herpes
Pregnancy
Autoimmune
Hepatitis B
Budd-chiari
Wilson’s

A

Paracetamol: N-Acetycysteine 140mg/kg

Herpes: acyclovir

Pregnancy: Deliver the foetus

Autoimmune: Methylprednisolone

Hepatitis B: Oral nucleoside

Budd-chiari: Antiocagulation (LMWH) ± TIPS

Wilson’s: Plasmapheresis

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9
Q

What is the King’s College criteria for liver transplant

A

Paracetamol induced:
Arterial pH <7.3 24h after ingestion OR
- Pro-thrombin time >100s
- AND creatinine >300µmol/L
- AND grade III or IV encephalopathy

Non-paracetamol induced:
Prothrombin time >100s OR
Any three of:
- Drug-induced liver failure
- Age under 10 or over 40 years
- 1 week from 1st jaundice to encephalopathy
- Prothrombin time >50s
- Bilirubin ≥300µmol/L.

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10
Q

Complications of liver failure

A

Hepatic encephalopathy
Coagulopathy
Infection: Bacterial infection occurs in up to 80% of patients, and fungal infection in around 30%.
Renal failure (hepatorenal syndrome)
Metabolic disorders
Cerebral oedema
GI bleeding
Hypoglycaemia
Respiratory failure
Acid-base disturbance

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11
Q

How are the complications of liver failure managed

Encephalopathy
SBP
Coagulopathy
Hypoglycaemia
Cerebral oedema
Fenal failure

A

Encephalopathy -> lactulose and phosphate enemas
Antibiotic and antifungal prophylaxis
Hypoglycaemia treatment
Treat coagulopathy -> IV vit K, FFP, platelet infusion
Protect gastric mucosa -> PPI or sulfacralfate
Avoid any sedatives or drugs metabolised by the liver
Cerebral oedema: Nurse patient sat 30 degrees, reduce intracranial pressure by IV mannitol
Renal failure -> haemofiltration and nutritional support

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12
Q

Prognosis for liver failure

A

ALF secondary to paracetamol overdose is associated with favourable prognosis if treated (75% recover without transplantation)
ALF due to idiosyncratic drug-induced liver injury and hep B has much lower rate of spontaneous recovery (21-40%)
Fulminant presentation of Wilson’s disease carries much higher risk of mortality

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