Acute Liver Failure

Question 1

What is the most common cause of fulminant liver failure in the UK?

Answer 1

Paracetamol poisoning

Question 2

What percentage of fulminant liver failure is attributed to drugs?(paracetamol, NSAIDs, antidepressants, halothane, rifimpacin)

Answer 2

70-80%

Question 3

Name some of the other causes of liver failure…(name 7)

Answer 3

Hepatitis, herpes simplex, ecstasy, mushrooms, herbal remedies, ischeamic hepatitis, budd-chiari syndrome, surgical shock, Wilson’s disease, Reye’s syndrome, malignant infiltration and massive bacterial infection

Question 4

Those who a cause cannot be found are labeled as having what?

Answer 4

Hepatitis caused by an unidentified virus

Question 5

Acute liver failure is most commonly caused by what?

Answer 5

Decompensation of pre existing chronic liver disease

Question 6

What is this chronic decompensation called?

Answer 6

Acute-on-chronic hepatic failure

Question 7

How is fulminant liver failure different I.e. The one caused by paracetamol poisoning etc

Answer 7

Fulminant hepatic failure is a clinical syndrome resulting from massive necrosis of hepatocytes leading to a severe drop in liver function

Question 8

What are the classifications of fulminant liver failure?

Answer 8

Hyper-acute = encephalopathy within 7d of jaundice onset
Acute = encephalopathy within 8-28d of jaundice onset
Sub-acute = encephalopathy within 5-26 weeks of jaundice onset

Question 9

The risk of dangerous cerebral oedema decreases with what?

Answer 9

The longer it takes for encephalopathy to develop

Question 10

Signs of liver failure include…

Answer 10

Jaundice, hepatic encephalopathy, fetor hepaticus (pear drops smell on breath), asterixis (liver flap), constructional apraxia (e.g. cannot copy a 5 pointed star)

Signs of chronic liver failure - acute on chronic failure

Question 11

What blood tests would you do for liver failure?

Answer 11

FBC, U+E, LFT, clotting (increase PTT/INR), glucose, paracetamol levels, hepatitis and CMV/EBV serology, ferritin, alpha trypsin, caeruloplasmin antibodies

Question 12

What microbiology tests would you do?

Answer 12

Blood culture, urine culture, ascetic tap

Question 13

What radiology would you do to investigate?

Answer 13

CXR, abdominal USS, Doppler flow studies of portal vein (and hepatic vein of buds chiari suspected)

Question 14

What 4 complications should you be wary of when managing liver failure?

Answer 14

Sepsis, hypoglycaemia, GI bleeds/varies, encephalopathy

Question 15

What is the management of liver failure?

Answer 15

Surpportive - ITU, 20 degree head tilt, NG tube feeding to prevent aspiration infections, insert venous+urinary catheters, monitor closely with reg tests, high carb diet, give thiamine and folate supplements

Question 16

Why is high carb diet used?

Answer 16

To prevent hypoglycaemia

Question 17

Why are central venous and urinary catheters inserted?

Answer 17

To allow hourly fluid status checks to make sure the patient isn’t developing Hepatocytes renal syndrome especially

Question 18

What is hepatorenal syndrome?

Answer 18

Cirrhosis+ascites+renal failure when other renal impairment causes have been excluded

Question 19

What is the pathophysiology of HRS

Answer 19

Abnormal haemodynamics causes splanchic and systemic vasodilation but renal vasoconstriction! This causes pre renal kidney failure

Question 20

HRS is split into two types, what occurs in type 1 and what is the prognosis?

Answer 20

Rapid circulatory and renal dysfunction

Median survival is just 2 weeks

Question 21

Type 2 HRS, what occurs and what is the prognosis?

Answer 21

Circulatory and renal dysfunction but at a much slower and steadier rate
Median survival of 6 months

Question 22

What treatments may be used in HRS?

Answer 22

Dialysis and combined liver and kidney transplant

Question 23

What is done to treat the seizures due to encephalopathy in liver failure?

Answer 23

Lorazepam

Question 24

What drugs should be avoided?

Answer 24

Sedatives and any others that require hepatic metabolism

Question 25

How is the following complication treated?

Cerebral oedema

Answer 25

IV mannitol (20%) (osmotic balance agent for reducing fluid buildup in the brain) and hyperventilate

Question 26

How is the following complication treated?

Ascites

Answer 26

Restrict fluid and salt intake, weigh daily, diuretics

Question 27

How is the following complication treated?

Bleeding

Answer 27

Vitamin K and platelets. FFP, blood and endoscopy as required

Question 28

How is the following complication treated?

Infection (blind treatment)

Answer 28

Ceftriaxone NEVER gentamicin as it contributes to renal failure

Question 29

How is the following complication treated?

Hypoglycaemia

Answer 29

Give glucose

Question 30

How is the following complication treated?

Encephalopathy

Answer 30

ITU, 20 degree head tilt, lactulose and regular enemas to prevent buildup of nitrogen forming bacteria

Question 31

When is prognosis worst?

Answer 31

If patient has grade 3/4 encephalopathy, >40yrs old, albumin below 30g/L, high INR/PTT, drug induced, chronic decompensation worse than fulminant

Question 32

What are the grades of hepatic encephalopathy?

Answer 32

1: altered mood/behaviour, sleep disturbance, dyspraxia, poor arithmetic but NO liver flap
2: drowsiness, confusion, slurred speech, inappropriate behaviour (collateral history) may have liver flap
3: incoherent, restless, liver flap, stupor
4: COMA

Question 33

What drug’s effects will be amplified by liver failure?

Answer 33

Warfarin so monitor and adapt levels as required

Question 34

What is the definition of acute liver failure?

Answer 34

Onset of hepatic decompensation with encephalopathy, coagulation disturbance and jaundice within 6 months of onset of symptoms (which will have been jaundice)