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    Acute Liver Failure

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    Acute liver failure can have high mortality rates between 56-80%. A thorough history, exam, and lab work is needed to identify the cause which varies worldwide. Paracetamol toxicity is a common cause in western countries. Some etiologies like autoimmune hepatitis have low survival without liver transplant so prompt specialist referral is important. While hepatic encephalopathy was historically a main cause of death, supportive treatments for complications have improved outcomes.

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    Acute Liver Failure

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    pascalmugodo
    7 views39 pages
    Acute liver failure can have high mortality rates between 56-80%. A thorough history, exam, and lab work is needed to identify the cause which varies worldwide. Paracetamol toxicity is a common cause in western countries. Some etiologies like autoimmune hepatitis have low survival without liver transplant so prompt specialist referral is important. While hepatic encephalopathy was historically a main cause of death, supportive treatments for complications have improved outcomes.

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    Acute liver failure can have high mortality rates between 56-80%. A thorough history, exam, and lab work is needed to identify the cause which varies worldwide. Paracetamol toxicity is a common cause in western countries. Some etiologies like autoimmune hepatitis have low survival without liver transplant so prompt specialist referral is important. While hepatic encephalopathy was historically a main cause of death, supportive treatments for complications have improved outcomes.

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    Download as ppt, pdf, or txt
    7 views39 pages

    Acute Liver Failure

    Uploaded by

    pascalmugodo
    Acute liver failure can have high mortality rates between 56-80%. A thorough history, exam, and lab work is needed to identify the cause which varies worldwide. Paracetamol toxicity is a common cause in western countries. Some etiologies like autoimmune hepatitis have low survival without liver transplant so prompt specialist referral is important. While hepatic encephalopathy was historically a main cause of death, supportive treatments for complications have improved outcomes.

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    Acute Liver

    Failure
    MUTUA W. MUTHEU
    Topics

     Definitions of failure and classification


     Aetiology- Acute versus acute on chronic
     Basic diagnostic workup
     Treatment of complication
     Hepatic encephalopathy
     Coagulopathy
     Specialist centre referral
     Organ support
    The mortality rate for acute liver failure ranges between 56% and 80%
     UK incidence of cirrhosis 17 per 100,000
     Prevalence of cirrhosis is 76 per 100,000
     ALF incidence is 1-6 per million per year
    Formal diagnosis of acute liver failure

     An increase in PT by 4-6 seconds (INR>1.5)

     And the development of hepatic encephalopathy (HE).

     In a patient without pre-existing cirrhosis and with an illness of less than


    six months duration.
    Definition; Jaundice to HE

     Hyperacute- <7days

     Acute - >7days <21days

     Subacute- >21days <6months

     FHF- not used


    Stages of Hepatic Encephalopathy:

    Stage 0. Lack of detectable changes in personality or


    behaviour. Asterixis absent.

    Stage 1. Trivial lack of awareness. Shortened attention


    span. Impaired addition or subtraction. Hypersomnia,
    insomnia, or inversion of sleep pattern. Euphoria or
    depression. Asterixis can be detected.

    Stage 2. Lethargy or apathy. Disorientation.


    Inappropriate behaviour. Slurred speech. Obvious
    asterixis.

    Stage 3. Gross disorientation. Bizarre behaviour.


    Semistupor to stupor. Asterixis generally absent.

    Stage 4. Coma.
    Worldwide cause varies
    Diagnostics:

     Good history-
    difficult if HE
    Diagnosis and Initial
    Evaluation ALF
     HISTORY:
     Family members with liver disease?
     Recent cold sores
     Onset of jaundice
     Work environment- toxic agents
     Hobbies/travel
     Herbal products/dietary supplements
    Initial Laboratory Analysis

     Prothrombin time/INR
     Chemistries
     Liver enzymes
     Arterial blood gas
     Paracetamol level, Toxicology screen
     Viral hepatitis serologies (anti-HAV IgM,
    HBsAg, anti-HBc IgM, anti-HEV, anti-HCV, HCV
    RNA , HSV1 IgM, VZ/HS, EB, CMV)
    Initial Laboratory Analysis

     Ceruloplasmin level
     Pregnancy test (females)
     Ammonia (arterial if possible)
     Autoimmune Markers (ANA, ASMA, Immunoglobulin
    levels )
    Liver biopsy for diagnostic dilemma

     Importance of early biopsy- severity and aetiology


     Particularly useful in Hep B, Autoimmune, Alcoholic hepatitis,
    differentiate between ALF and ACLF

     Transjugular route
    What are the potential
    outcomes?
     Recovery because of a successful
    intervention
     NAC for paracetamol toxicity
     Antivirals for acute hepatitis B

     Spontaneous recovery with


    supportive care
     Death

     Rescue by liver transplant (OLT)


    Aetiology outcome for ALF

    Transplant free survival >50%


    Hepatitis A, FLDP, paracetamol

    Transplant free survival <25%


    Autoimmune, HEB, Wilsons, mushroom, idiosyncratic drug
    All Liver transplants

     CLD – 60%
     Malignancy- 10%
     ALF- 10% ( Paracetamol)
     Cholestasis - 10-20%
    King’s College Criteria LT

     Acetaminophen-Induced
    ALF:
     Strongly consider OLT listing if:
     arterial lactate >3.5 mmol/L after early fluid resuscitation
     List for OLT if: pH<7.3 Or
     arterial lactate >3.0 mmol/L after adequate fluid
    resuscitation
     List for OLT if all 3 occur within a 24-hour period:
     1- presence of grade 3 or 4 hepatic encephalopathy
     2- INR >6.5
     3- Creatinine >3.4 mg/dL
    King’s College Criteria LT

    Non-acetaminophen:
     INR > 6.5 OR
     Any 3 of the following 5:
     Age < 10 or > 40
     Serum bilirubin > 300
     Jaundice to encephalopathy interval > 7 days
     INR > 3.5
     Unfavorable Etiology
     Non-A, non-B hepatitis, halothane, idiosyncratic drug
    reaction, Wilson’s
     Stage I – 0-24h
     Asymptomatic
     GI upset
     LFT derangement at 12h
     Stage 2 – 24-48h
     RUQ pain, tenderness
     LFT derrangment, bilirubin, PT
     Stage 3 – 48-96h
     Centrilobar necrosis
     Liver failure
     Stage 4
     Recovery, transplant or death
     No chronic state
    Encephalopathy
    HE- Four compatible theories

     Cerebral vasomotor dysfunction


     Oedema secondary to ammonia toxicity
     Inflammation due to SIRS
     putative benzodiazepine-like molecules
    The pathophysiology of HE

     Ammonia as a key factor in the


    pathogenesis of HE.
     Portal ammonia is derived from both the
     urease activity of colonic bacteria and the
     de-amidation of glutamine in the small bowel.
     The intact liver clears almost all of the
    portal vein ammonia, converting it into
    glutamine and preventing entry into the
    systemic circulation.
     Ammonia- astrocyte swelling in brain
    Cerebral Edema

     Degree of encephalopathy correlates w/ cerebral


    edema
     Grade I-II: rare
     Grade III: 25-35% risk risk
     Grade IV: 65-75% risk
     Uncal herniation
     Compromises cerebral blood flow  hypoxic brain
    injury
    Grade III/IV Encephalopathy

     Intubate trachea + ventilate


     Elevate head of bed
     Consider placement of ICP monitoring device
     Immediate treatment of seizures required; prophylaxis
    of unclear value
     Mannitol: use for severe elevation of ICP or first clinical
    signs of herniation
     Hypertonic saline to raise serum sodium to 145-155
    mmol/L
     Hyperventilation: effects short-lived; may use for
    impending herniation
    GCS –HE correlation

     Grade1- GCS 14-15


     Grade2- GCS 11-13- HDU

     Grade3- GCS 8-11 (Stupor or precoma)


     Grade4- GCS<8 (Coma)
    Lactulose is a first-line
    pharmacological treatment of
    HE.
     Lactulose – reaches colon, where
    bacteria will metabolize the lactulose
    to acetic acid and lactic acid.
     This lowers the colonic pH
     formation of the non-absorbable NH4+
    from NH3,
     Other effects like catharsis also
    contribute to the clinical effectiveness
    of lactulose.
    Lactulose

     For acute encephalopathy, lactulose (ingested


    or via nasogastric tube), 45 ml p.o.,

     Is followed by dosing every hour until


    evacuation occurs.
     Target -three soft bowel movements per day

     If response to disachharide is poor- add


    antibiotic (metronidazole or rifaximine after
    48Hrs) to reduce enteric bacterial mass.
    The coagulopathy of liver
    disease
     Failure to produce clotting factors II, V, VII and IX
     The degree of coagulopathy is a measure of severity of liver
    disease and of patient prognosis.
     Routine correction of coaguloapthy is therefore NOT
    indicated unless active bleeding or planned
    interventions require it
     Vitamin K: give at least one dose
     FFP: give only for invasive procedures or active bleeding
     Platelets: give only for invasive procedures or active bleeding
     Recombinant activated factor VII: possibly effective for invasive
    procedures
    Role of prophylactic
    antibiotic
     Only patients who have an episode of gastrointestinal
    bleeding
     or an episode of spontaneous bacterial peritonitis (SBP)
    have been shown to have a significant outcome benefit
    from prophylactic antibiotics.
    Role of NAC

     Efficacy of NAC is well established in


    paracetamol induced ALF
     Non PCM ALF – role of NAC is controversial
     However most recent studies has improved
    outcome
     175 patients of non PCM ALF received NAC
     Transplant free survival at 3 weeks was 52% in
    NAC group compared to 30% in placebo arm
    ( only with coma grade of 1-2)
     United States ALF study group- overall was 70%
    vs 66%
    Artificial liver??
    Extracorporeal Liver Assist
    Device (ELAD)
     Hepatocyte bioreactor- hepatoma cells cultivated on
    the exterior surface of semipermeable hollow fibres

     MARS (molecular adsorbent recirculating system)


    ELAD

     Both reduce the level of bilirubin, bile salt ammonia etc


     However no of patients dying or requiring liver
    transplant did not improve

    Devices remain experimental and large-


    scale phase two and three trials are
    awaited
    Case 2

     55yo Male, builder bricklayer


     PMH
     Alcohol abuse (abstinent)
     Recurrent ascites
     Oesophageal varices
     Meds
     Thiamine, vit B12, furosemide/amiloride, lactulose,
    propranolol
    Case 2

     PC
     Tired, fatigued, reversal of sleep wake pattern,
    generalized slowness,
     Exam
     Spider naevi, no asterixis, splenomegally, mild shifting
    dullness, INR 1.3, plt 115, Hb 14.5, MCV 101, alb 48, ALP
    110, ALT 32
     What next ?...
    Stages of Hepatic Encephalopathy:

    Stage 0. Lack of detectable changes in personality or


    behaviour. Asterixis absent.

    Stage 1. Trivial lack of awareness. Shortened attention


    span. Impaired addition or subtraction. Hypersomnia,
    insomnia, or inversion of sleep pattern. Euphoria or
    depression. Asterixis can be detected.

    Stage 2. Lethargy or apathy. Disorientation.


    Inappropriate behaviour. Slurred speech. Obvious
    asterixis.

    Stage 3. Gross disorientation. Bizarre behaviour.


    Semistupor to stupor. Asterixis generally absent.

    Stage 4. Coma.
    Acute on Chronic Liver Failure
    ACLF

     This entity is quite common- background of cirrhosis.


    Innocent precipitating event culminates in Massive
    Organ Failure (OF)
     Events
     Toxins (alcohol!)
     Vascular (hypotension- GI bleed, dehydration, Portal vein
    thrombosis)
     Infection (SBP)
    Summary
    • The mortality rate for acute liver failure ranges between 56% and 80%

    • Careful history taking and examination of lab results help identify


    patients

    • The commonest cause of acute liver failure in the western world is


    paracetamol toxicity

     Some causes have low survival without OLT, prompt referral…

    • Hepatic encephalopathy is no longer the main cause of death but it’s


    detection and management requires sophisticated cardiovascular and
    cerebral monitoring

    • Acute on Chronic Liver Failure

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