Acute liver failure Flashcards

1
Q

What is acute liver failure?

A

Rapid onset of liver dysfunction without prior disease. Generally lasting less than 6 months.

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2
Q

What are the main functions of the liver?

A
Protein metabolism, Lipid metabolism
Carbohydrate metabolism
Imunological defence
Bilirubin metabolism
Hormone and drug metabolism
Bile acid secretion
Storage
Protein synthesis
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3
Q

What are the true liver function tests?

A

Bilirubin, albumin and prothrombin. MOST important as they are prognostic markers

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4
Q

What are the liver ‘damage’ liver function tests?

A

GGT, AKP, ALT/AST and bilirubin

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5
Q

What percentage of patients with cirrhosis have normal LFTs?

A

17%

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6
Q

What are the features of acute liver failure?

A

1) Encephalopathy,
2) Coagulopathy (prolonged prothrmbin time)
3) Jaundice

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7
Q

What are the common symptoms of acute liver failure?

A
None!
Jaundice
Lethargy
nausea
Itchy
Pain (capsule stretching)
Abnormal LFTs
Anorexia
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8
Q

What are the causes of acute liver failure?

A

1) Viral (Hep A-E, CMV, EBV and toxoplasmins)
2) Drugs (many)
3) Shock liver
4) Cholangitis
5) Alcohol
6) Malignancy
7) Chronic liver disease
8) Paracetamol
RARE: Budd Chiarri, AFLP, Cholestasis of pregnancy

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9
Q

What is Shock liver?

A

Inadequate perfusion of the liver. (Hypotention- check the vascular patency of the hepatic artery)

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10
Q

What is Budd Chiarri?

A

Occlusion of hepatic veins which drain the liver.

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11
Q

What is AFLP?

A

Acute fatty liver disease of pregnancy

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12
Q

When you ask a patient about paracetamol what else should you ask?

A

Preparations
OTC drugs which contain paracetamol.
Even 4g/day for 2 weeks can change liver function.

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13
Q

What are the directly toxic causes of liver failure?

A

Drugs, alcohol, virus and hypoperfusion (shock liver)

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14
Q

What are the immunologic causes of liver failure?

A

Primary Billary Cirrhosis

Autoimmune hepatitis

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15
Q

What are the nutritional causes of liver failure?

A

NASH, Malnutrition, refeeding syndrome.

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16
Q

What are the genetic causes of liver failure?

A

Wilsons disease and haemachromatosis (insidious onset and can present with HHC)

17
Q

What are the investigations to consider in acute liver failure?

A
Bilirubin, Prothrombin, Albumin.
LFTs
Ultrasound including vascular
Virology
Immunological serology
Rarely a liver biopsy.
18
Q

When is a liver biopsy indicated?

A

Struggling to get a clear diagnosis or looking at the patients prognosis

19
Q

Acute liver failure history?

A

Duration
Drugs (OTC, illicit, herbal and food supplements)
Alcohol, unusual hobbies, travel, sexual history.

20
Q

What is the treatment for acute liver failure?

A

Supportive. Rest 3-6 months.
Fluids and NO alcohol.
Increase calories (high protein, low fat)
Observe for FHF

21
Q

What is puritus and what is the cause?

A

Severe itching of the skin caused by increase in bilirubin- often post hepatic picture.

22
Q

What is the treatment for puritus?

A

Sodium bicarbonate bath
Cholestyramine (prevents bile salt reabsorption)
Uresodeoxycholic acid (reduces cholesterol absorption)

23
Q

What are the metabolic considerations in acute liver failure? WHat should people be eating?

A

Patients are in a hypermetabolic state and require increased nutritional requirements but are often not hungry.
35-40 calories/Kg/day
1.2-1.5g protein/kg/day.
Monitor K, PO4 and Mg for signs of refeeding syndrome.
Monitor blood glucose for hyper/hypoglycemia
Consider NG feeding in some patients

24
Q

What are the features of a hepatic drug reaction?

A

Occurs about 6 weeks post exposure- the first effect may not have been noticed.
Often the liver is predisposed. Eg NASH.
Caused by any drug, many mechanisms and variation in LFT abnormalities.
Effects CP450 => free radiacl production and lipid peroxidation.

25
Q

How does paracetamol toxicity come about?

A

Paracetamol is metabolised to NAPQI (toxic) as it comsumes most of the GLUTATHIONE. Glutathione is usually recycled in the liver but when bound to NAPQI it is not.

26
Q

How is Paracetamol toxicity treated?

A

NAC is given which is the precursor to glutathione. You need to give it faster then it is being used.

27
Q

What are the common drugs which cause liver reactions?

A

Co-amoxiclav, Flucloxacillin, NSAIDs
Fat burners/protein powders
Paracetamol containing drugs
(statins can change LFts but don’t normally cause liver damage.)

28
Q

What is Fulminant Hepatic failure?

A

Rapid development of encephalopathy in a previously normal liver

29
Q

What are the causes of FHF?

A

Paracetamol
Viral
Drugs
RARE: AFLP, mushrooms, malignancy, Wilsons disease, Budd Chiari

30
Q

What are the clinical features of fulminant hepatic failure?

A
Encephalopathy => cerebral oedema (may require decompression)
Spontaneous hypoglycemia
Coagulopathy
Circulatory failure
Renal failure => dialysis
Infection
31
Q

What is the treatment for fulminant hepatic failure?

A

Supportive: Fluids and Ionotropes to increase BP.
Renal replacement,
Manage raised Intra cranial pressure
Transplant

32
Q

What are the survival outcomes of fulminant hepatic failure?

A

75%, 65% if require transplant.

33
Q

What should you do if you suspect fulminant hepatic failure?

A

Refer quickly to a 24 hour transplant centre (Edinburgh)
Monitor closely (bloods every 6 hours)
If they need transplant get it within 24 hours (Die within 48-72 hours)
Consider intubating to reduce cerebral oedema and effects

34
Q

What are the guidelines for transplant called?

A

Kings Collage Criteria for Acetaminophen (paracetamol toxicity)
There are also guidelines for non paracetamol fulminant liver failure