Acute Liver Failure

Question 1

When does Liver Failure occur?

Answer 1

Liver failure may occur suddenly in the previously healthy liver = acute hepatic failure.

More often it occurs as a result of decompensation of chronic liver disease = acute-on-chronic hepatic failure.

Question 2

Infectious Causes?

Answer 2

Viral hepatitis (esp b, c, cmv), yellow fever, leptospirosis.

Question 3

Drug Causes?

Answer 3

Paracetamol overdose, halothane, isoniazid.

Question 4

Toxin causes?

Answer 4

Amanita phalloides mushroom

Question 5

Vascular causes?

Answer 5

Budd–Chiari syndrome

Question 6

Misc causes?

Answer 6

Alcohol, primary biliary cirrhosis, haemochromatosis, autoimmune hepatitis, α‎1-antitrypsin deficiency, Wilson’s disease, fatty liver of pregnancy, malignancy, hellp syndrome (Haemolysis, Elevated Liver enzymes and Low Platelets; it is usually associated with pre-eclampsia

Question 7

Signs

Answer 7

Jaundice, hepatic encephalopathy, fetor hepaticus (smells like pear drops), asterixis/flap, constructional apraxia (cannot copy a 5-pointed star?).
Signs of chronic liver disease

Question 8

Blood tests

Answer 8

fbc (?infection,1 ?gi bleed), u&e,2 lft, clotting (↑pt/inr), glucose, paracetamol level, hepatitis, cmv and ebv serology, ferritin, α‎1-antitrypsin, caeruloplasmin, autoantibodies

Question 9

Microbiology

Answer 9

Blood culture; urine culture; ascitic tap for mc&s of ascites—neutrophils >250/mm3 indicates spontaneous bact-erial peritonitis

Question 10

Radiology

Answer 10

cxr; abdominal ultrasound; Doppler flow studies of the portal vein (and hepatic vein in suspected Budd–Chiari syndrome

Question 11

Managing Liver Failure

Answer 11

• Nurse with a 20° head-up tilt in itu. Protect the airway with intubation and insert an ng tube to avoid aspiration and remove any blood from stomach.
• Insert urinary and central venous catheters to help assess fluid status.
• Monitor t°, respirations, pulse, bp, pupils, urine output hourly. Daily weights.
• Check fbc, u&e (box 2), lft, and inr daily.
• 10% glucose iv, 1L/12h to avoid hypoglycaemia. Do blood glucose every 1–4h.

• Treat the cause, if known (eg gi bleeds, sepsis, paracetamol poisoning,
N-acetylcysteine probably does not help in non-paracetamol liver failure.112

• If malnourished, get dietary help: good nutrition can decrease mortality (eg carbohydrate-rich foods).113 Give thiamine and folate supplements
• Treat seizures with lorazepam
• Haemofiltration or haemodialysis, if renal failure develops
• Try to avoid sedatives and other drugs with hepatic metabolism
• Consider ppi as prophylaxis against stress ulceration, eg omeprazole 40mg/d iv/po.
• Liaise early with nearest transplant centre regarding appropriateness

Question 12

Treating ascites

Answer 12

Restrict fluid, low-salt diet, weigh daily, diuretics

if ascetic drain - give albumin

Question 13

Treating bleeding

Answer 13

Vitamin k 10mg/d iv for 3d, platelets, ffp + blood as needed ± endoscopy.

Question 14

Risk of infection

Answer 14

Ceftriaxone 1–2g/24h iv, not gentamicin (↑risk of renal failure).

Question 15

Treating encephalopathy

Answer 15

lactulose 30–50mL/8h + regular enemas to ↓numbers of nitrogen-forming gut bacteria; aim for 2–4 soft stools/d.

Question 16

Drugs to avoid

Answer 16

Avoid drugs that constipate (opiates, diuretics—↑risk of encephalopathy), oral hypoglycaemics, and saline-containing ivis. Warfarin effects are enhanced.

Question 17

hepatotoxic drugs

Answer 17

Paracetamol, methotrexate, isoniazid, azathioprine, phenothiazines, oestrogen, 6-mercaptopurine, salicylates, tetracycline, mitomycin.

Question 18

How does hepatic encephalopathy occur?

Answer 18

As the liver fails, nitrogenous waste (as ammonia) builds up in the circulation and passes to the brain, where astrocytes clear it (by processes involving the conversion of glutamate to glutamine). This excess glutamine causes an osmotic imbalance and a shift of fluid into these cells—hence cerebral oedema

Question 19

Grading encephalopathy

Answer 19

I Altered mood/behaviour; sleep disturbance (eg reversed sleep pattern); dyspraxia (“Please copy this 5-pointed star”); poor arithmetic. No liver flap.

II Increasing drowsiness, confusion, slurred speech ± liver flap, inappropriate behaviour/personality change (ask the family—don’t be too tactful).

III Incoherent; restless; liver flap; stupor, but not coma, which defines grade IV

Question 20

What is hepatorenal syndrome?

Answer 20

Cirrhosis + ascites + renal failure ≈ hrs—if other causes of renal impairment have been excluded. Abnormal haemodynamics causes splanchnic and systemic vasodilatation, but renal vasoconstriction. Bacterial translocation, cytokines and mesenteric angiogenesis cause splanchnic vasodilatation, and altered renal auto-regulation is involved in the renal vasoconstriction.

Question 21

Types of HRS?

Answer 21

HRS 1 is a rapidly progressive deterioration in circulatory and renal function (median survival <2wks), often triggered by other deteriorating pathologies. Terlipressin replenishes hypovolaemia. Haemodialysis may be needed.

HRS 2 is a more steady deterioration (survival ∼6 months). Transjugular intrahepatic portosystemic stent shunting is the best option for most (tips,

Question 22

Paracetamol-induced liver failure

Answer 22

• Arterial pH <7.3 24h after ingestion Or all of the following:

Or all of the following:

• Prothrombin time (pt) >100
• Creatinine >300µmol/L
• Grade III or IV encephalopathy

Question 23

Non-paracetamol liver failure

Answer 23

• pt >100s Or 3 out of 5 of the following:

1 Drug-induced liver failure

2 Age <10 or >40yrs old

3 >1wk from 1st jaundice to encephalopathy

4 PT >50s

5 Bilirubin ≥300µmol/L118