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Flashcards in Acute Liver Failure Deck (34)
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1
Q

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

A

Paracetamol poisoning

2
Q

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

A

70-80%

3
Q

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

A

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

4
Q

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

A

Hepatitis caused by an unidentified virus

5
Q

Acute liver failure is most commonly caused by what?

A

Decompensation of pre existing chronic liver disease

6
Q

What is this chronic decompensation called?

A

Acute-on-chronic hepatic failure

7
Q

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

A

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

8
Q

What are the classifications of fulminant liver failure?

A
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
9
Q

The risk of dangerous cerebral oedema decreases with what?

A

The longer it takes for encephalopathy to develop

10
Q

Signs of liver failure include…

A

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

11
Q

What blood tests would you do for liver failure?

A

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

12
Q

What microbiology tests would you do?

A

Blood culture, urine culture, ascetic tap

13
Q

What radiology would you do to investigate?

A

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

14
Q

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

A

Sepsis, hypoglycaemia, GI bleeds/varies, encephalopathy

15
Q

What is the management of liver failure?

A

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

16
Q

Why is high carb diet used?

A

To prevent hypoglycaemia

17
Q

Why are central venous and urinary catheters inserted?

A

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

18
Q

What is hepatorenal syndrome?

A

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

19
Q

What is the pathophysiology of HRS

A

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

20
Q

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

A

Rapid circulatory and renal dysfunction

Median survival is just 2 weeks

21
Q

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

A

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

22
Q

What treatments may be used in HRS?

A

Dialysis and combined liver and kidney transplant

23
Q

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

A

Lorazepam

24
Q

What drugs should be avoided?

A

Sedatives and any others that require hepatic metabolism

25
Q

How is the following complication treated?

Cerebral oedema

A

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

26
Q

How is the following complication treated?

Ascites

A

Restrict fluid and salt intake, weigh daily, diuretics

27
Q

How is the following complication treated?

Bleeding

A

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

28
Q

How is the following complication treated?

Infection (blind treatment)

A

Ceftriaxone NEVER gentamicin as it contributes to renal failure

29
Q

How is the following complication treated?

Hypoglycaemia

A

Give glucose

30
Q

How is the following complication treated?

Encephalopathy

A

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

31
Q

When is prognosis worst?

A

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

32
Q

What are the grades of hepatic encephalopathy?

A

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

33
Q

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

A

Warfarin so monitor and adapt levels as required

34
Q

What is the definition of acute liver failure?

A

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