Acute Liver Failure - PowerPoint PPT Presentation

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Acute Liver Failure

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... no RBC cast No nephrotoxic drugs Fluid challenge Spot Na and serum Na Serum and urine osmolality Urine output The stages of HE- West Haven criteria: Stage 0. – PowerPoint PPT presentation

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Title: Acute Liver Failure


1
Acute Liver Failure
2
Topics
  • Definitions of failure and classification
  • Aetiology- Acute versus acute on chronic
  • Basic diagnostic workup
  • Liver biopsy in the context
  • ACLF-Ethical dilemma- HDU admission
  • Treatment of complication
  • Hepatic encephalopathy
  • Renal failure
  • GI bleed
  • Infection
  • Coagulopathy
  • Aetiology specific treatment
  • Organ support
  • Liaison with Transplant centre

3
  • The mortality rate for acute liver failure ranges
    between 56 and 80

4
Abnormal LFT is NOT ALF
  • Dear Doctor
  • Patients bilirubin is 600 and has liver failure-
    kindly urgently see
  • Family was told transplant may be necessary

5
Formal diagnosis of acute liver failure
  • An increase in PT by 4-6 seconds (INRgt1.5)
  • And the development of hepatic encephalopathy
    (HE).
  • In a patient without pre-existing cirrhosis and
    with an illness of less than six months duration.

6
  • 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

7
aCLF
  • This entity is quite common- background of
    cirrhosis. Innocent precipitating event
    culminates in MOF
  • Events
  • Toxins (alcohol!)
  • Vascular (hypotension- GI bleed, dehydration,
    Portal vein thrombosis)
  • Infection (SBP)
  • HCC

8
  • ACLF-Ethical dilemma- HDU admission

9
For patients with aCLF
  • Young age
  • First presentation
  • Reversible pathology- sepsis, GI bleeding or
    severe hepatitis
  • A trip to ITU is a life changing experience to
    some alcoholics

10
Few definitions
  • Hyperacute- lt7days
  • Acute - gt7days lt21days
  • Subacute- gt21days lt6months
  • FHF- not used

11
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12
Diagnostics
  • Good history- difficult if HE

13
Initial Laboratory Analysis- general
  • Prothrombin Time/INR
  • Blood Chemistry
  • Sodium, potassium, chloride, bicarbonate,
    calcium, magnesium, phosphate, AST, ALT, alkaline
    phosphatase, GGT, total bilirubin, albumin,
  • Creatinine, urea
  • Glucose
  • Arterial blood gas
  • Arterial lactate
  • Full blood count
  • Blood type and screen
  • Ammonia (arterial if possible)
  • HIV status
  • Amylase and lipase

14
Diagnostics- specific
  • Paracetamol (acetaminophen) level
  • Toxicology screen
  • Viral hepatitis serologies
  • Anti-HAV IgM,
  • HBSAg, anti-HBc IgM,
  • anti-HEV,
  • anti-HCV
  • CMV
  • EBV
  • VZ/HZ
  • Ceruloplasmin level
  • Pregnancy test
  • Autoimmune markers- ANA, ASMA, Immunoglobulin
    levels
  • Doppler US- ischaemic vs thrombosis

15
Liver biopsy
  • Importance of early biopsy- severity and
    aetiology
  • Particularly useful in Hep B, AIH, Alcoholic
    hepatitis, differentiate between ALF and aCLF
  • Transjugular route

16
www.gastrotraining.com
17
  • Urgent OLT is the only life saving therapy
  • The main role of intensive care therapy is
    multi-organ support

18
All Liver transplants
  • CLD 60
  • Malignancy- 10
  • ALF- 10 ( Paracetamol)
  • Cholestasis - 10-20

19
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21
Paracetamol Overdose
  • Phase I 0-24h
  • Anorexia, nausea and vomiting, malaise
  • LFT derrangement at 12h
  • Phase II 18-72h
  • RUQ pain
  • LFT derrangment
  • Phase III 72-96h
  • Centrilobar necrosis
  • Liver failure
  • Phase IV 4d-3wk
  • Recovery, transplant or death
  • No chronic state

22
When to pick up the phone
  • D2-
  • pH lt7.3
  • INRgt3
  • Cr gt200
  • Hypoglycaemia
  • D3-
  • HE
  • Crgt200
  • INR gt4.5
  • D4-
  • Any rise in INR
  • Cr gt250
  • HE

23
DefinitionHRS
  • ARF in a patient
  • CLD, severe alcoholic hepatitis or ALF from any
    cause
  • End-stage of reduction in renal perfusion induced
    by increasingly severe hepatic injury.

24
  1. Sinusoidal portal hypertension, in the presence
    of severe hepatic decompensation
  2. Leads to splanchnic and systemic
    vasodilatation-role of NO
  3. Decreased effective arterial blood volume
  4. Activation of RAS, and vasopressin aimed at
    restoring arterial filling pressure.
  5. Renal vasoconstriction increases counterbalanced
    by the intrarenal prostaglandins.
  6. When this balance is lost renal hemodynamics
    worsens, and hepatorenal syndrome develops

25
  • Terlipressin
  • NSBB

26
HRS
  • Major criteria
  • Chronic or acute hepatic disease and liver
    failure with portal hypertension
  • Serum creatinine level gt133 micromoles/L
  • Absence of shock, ongoing bacterial infection,
    recent use of nephrotoxic drugs, excessive fluid
    or blood loss
  • No sustained improvement in renal function after
    volume expansion with 1.5 L isotonic saline
    solution
  • No Proteinuria (Proteinlt500 mg/day) and no
    ultrasonographic evidence of renal tract or
    parenchymal disease
  • Minor criteria
  • Urine volume lt500 mL/day
  • Urine sodium lt10 mEq/L
  • Urine osmolality greater than plasma osmolality
  • Urine red blood cell count lt50 per high-power
    field
  • Serum sodium lt130 mEq/L

27
Classification of HRS
  • Type I is defined by a rise in creatinine level
    to over 221 micromoles/L in less than 2 weeks
  • Median survival of 2 weeks
  • Type II is defined as less severe renal
    insufficiency it is principally characterized by
    ascites that is resistant to diuretics.
  • Median survival of 3-6 months.

28
Vasoactive Medical treatment
  • Terlipressin bolus(0.5mg/4h)-increase every 3
    days if no response to 1-2mg/4h
  • Given until creatinine normalizes or for 15 days
  • Albumin 1g/kg on day1( one bag of HAS contains
    20grams)
  • 20-60g/d thereafter

29
Step by step guide
  • Normal renal us
  • Normal urine dipsix no RBC cast
  • No nephrotoxic drugs
  • Fluid challenge
  • Spot Na and serum Na
  • Serum and urine osmolality
  • Urine output

PRERENAL HRS ATN
Spot Na lt10 lt10 gt30
Urine sediment Nil Nil Positive
Fluid challenge Responds Nil Nil
30
The stages of HE- West Haven criteria
  • 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 ordepression. 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.

31
HE- Four compatible theories
  • Cerebral vasomotor dysfunction
  • Oedema secondary to ammonia toxicity
  • Inflammation due to SIRS
  • putative benzodiazepine-like molecules

32
The pathophysiology of HE
  • A large body of work points at ammonia as a key
    factor in the pathogenesis of HE.
  • Portal ammonia is derived from both the urease
    activity of colonic bacteria and the deamidation
    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

33
  • Patients with grade II HE should be managed in a
    HDU environment.
  • Grades III and IV HE requires definitive airway
    protection and appropriate monitoring.
  • Grade IV HE is strongly associated with elevated
    levels of serum ammonia, a high incidence of
    raised intracranial pressure and the development
    of uncal herniation.

34
GCS HE correlation
  • Grade1- GCS 14-15
  • Grade2- GCS 11-13- HDU
  • Grade3- GCS 8-11 (Stupor or precoma)
  • Grade4- GCSlt8 (Coma)

35
  • In acute and chronic liver disease, increased
    arterial levels of ammonia are commonly seen.
  • However, correlation of blood levels with mental
    state in cirrhosis is inaccurate.

36
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.

37
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.

38
  • If patient is refusing oral lactulose prescribe
    phosphate enemas TDS!
  • An excessively sweet taste, flatulence, and
    abdominal cramping are the most frequent
    subjective complaints with this drug.

39
The coagulopathy of liver disease
  • Failure to produce clotting factors II, V, VII
    and IX
  • Failure of the diseased liver to clear activated
    clotting factors.
  • Degree of hypersplenism and thrombocytopaenia
    often adds to the coagulopathy, especially if
    disseminated intravascular coagulation (dic) also
    co-exists.
  • 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

40
Sepsis
  • Infection may be the initiating event of liver
    failure,
  • Intercurrent sepsis is also a common problem .
  • Impaired immune function, in part secondary to
    reduced complement factor production and
  • Impaired neutrophil, leukocyte and monocyte
    function, can result in delayed presentation of
    clinical signs of infection.
  • The interventions required for diagnosis and
    management of liver disease also increase patient
    vulnerability to invasive infection.

41
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.

42
In presence of sepsis
  • Choice of antibiotic should be guided by local
    microbiological surveillance.
  • The high incidence of mycoses - low threshold for
    antifungal.
  • Regular microbiological surveillance

43
Role of NAC
  • Efficacy of NAC is well established in PCM
    induced ALF
  • Non PCM ALF role of NAC is controversial
  • 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

44
  • Artificial liver??

45
Extracorporeal Liver Assist Device (ELAD)
  • Hepatocyte bioreactor- hepatoma cells cultivated
    on the exterior surface of semipermeable hollow
    fibres
  • MARS (molecular adsorbent recirculating system)

46
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

47
Summary
  • The mortality rate for acute liver failure
    ranges between 56 and 80
  • The main role of intensive care therapy is
    multi-organ support
  • The commonest cause of acute liver failure in
    the western world is paracetamol toxicity
  • Hepatic encephalopathy is no longer the main
    cause of death but its detection and management
    requires sophisticated cardiovascular and
    cerebral monitoring
  • Hepatorenal failure is due to the complex
    interplay between splanchnic, renal and systemic
    circulatory responses to liver failure.
    Terlipressin has been shown to be of use in its
    treatment
  • Novel hepatic replacement therapies are under
    development but definitive studies as to their
    efficacy are, as yet, unpublished.
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