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ACUTE LIVER FAILURE. Milton G. Mutchnick, M.D. Professor of Medicine Chief, Division of Gastroenterology Wayne State University School of Medicine. Acute Liver Failure. Rapid deterioration of liver function resulting in altered mentation and

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acute liver failure
ACUTE LIVER FAILURE

Milton G. Mutchnick, M.D.

Professor of Medicine

Chief, Division of Gastroenterology

Wayne State University

School of Medicine

acute liver failure1
Acute Liver Failure

Rapid deterioration of liver function

resulting in altered mentation and

coagulopathy in a patient without preexisting cirrhosis and with an illness of less than 26 weeks duration.

acute liver failure aka
Acute Liver Failure….AKA
  • Fulminant hepatic failure
  • Fulminant hepatitis
  • Subfulminant liver failure
  • Subacute hepatic necrosis
  • Subacute liver failure
  • Hyperacute liver failure
index of suspicion for alf
Index of Suspicion forALF
  • Clinical signs of moderate to severe hepatitis
  • Laboratory findings including an increase in the prothrombin time of 4-6sec.(INR ≥ 1.5).
  • Altered sensorium

INR ≥ 1.5 + Altered Mental Status = ALF

etiology of alf
Etiology ofALF
  • Acute viral hepatitis (A - E)
  • Mushroom poisoning
  • Acetaminophen
  • Acute fatty liver of pregnancy
  • Chemical agents
slide7
Drug-induced hepatitis
  • Budd-Chiari Syndrome
  • VOD of liver
  • Wilson’s disease
  • AIH
alf etiologies
Viral

Drug

Poisoning

Ischemia

VOD

Malignant Infiltrate

Wilson’s Disease

Microvesicular steatosis

AIH

Hyperthermia

OLT

Partial hepatectomy

ALFEtiologies
slide9
Etiology ofALFin 342 Cases(University Hospital, London UK)

Drugs-Overdose Other

Acetaminophen 250 Wilson’s 3

Ecstasy 2Fatty liver of pregnancy 7

Lymphoma/

Viral Hepatitis malignant infiltrate 7

HAV 8 Sepsis 2

HBV 8 Budd-Chiari 5

Non A-E 28Ischemia 9

Miscellaneous 6

Idiosyncratic Drug Reactions

Lamotrigine, cyproterone, NSAID,

chloroguine, rifampin/ INH

halothane, flucloxacillin

slide11
Viral
  • Acute Hepatitis A-E
  • Reactivation of HBV
  • Chemotherapy
  • Immunosuppresion
  • Herpes simplex
  • Varicella-Zoster
  • EBV
acute hav and alf
Acute HAV andALF
  • ALF uncommon
  • Frequency 0.01% - 0.1% in
  • jaundiced patients
  • ALF occurs early
  • Survival (transplant- free) 75%
  • Age related survival
acute hbv and alf
Acute HBV andALF
  • HBV alone or with HDV co-infection
  • (rare)
  • Transplant-free survival is 23%
  • Overall survival 77% because of
  • transplantation
hbv markers in alf
HBV Markers inALF

IgM Anti HBc 100%

HBsAg 90%

HBV DNA (Abbott) 10%

*Absence of HBsAg favors better

prognosis (47% v 17%).

Higher frequency ALF with mutant

HBV form

drug induced alf
Drug InducedALF
  • Many drugs implicated
  • Acetaminophen
  • Halothone and derivatives
  • INH/ Rifampin
  • Tricyclics/ MAO inhibitors
  • Phenytoin/ NSAID
  • Increased risk: acetaminophen (as little as
  • 2gms) + ETOH median dose: 13 gm
  • Increased risk if drug continued after
  • jaundice appears
poisoning and alf
Poisoning andALF
  • Amanita mushrooms (amanatoxins)
  • - LD = 50 gms (3 mushrooms)
  • - Toxins not destroyed by cooking
  • - Rapid onset of HE in 4-8 days
  • following severe emesis and diarrhea
  • Solvents - chlorinated hydrocarbons
  • Herbal remedies
  • Yellow phosphorus
ischemic hepatitis and alf
Ischemic Hepatitis and ALF
  • Liver cell necrosis - massive
  • scale
  • Cardiac tamponade
  • Acute heart failure
  • Pulmonary embolus
  • Hepatic artery thrombosis
obstruction of hepatic veins and alf
Obstruction of Hepatic Veins andALF
  • Budd-Chiari syndrome and thrombosis of hepatic veins
  • VOD - Post BMT Chemotherapy, Irradiation
massive malignant infiltration of the liver
Massive Malignant Infiltration of the Liver
  • Attributed to ischemic
  • changes
  • Leukemia, lymphoma
  • Malignant histiocytosis
  • Metastatic Replacement
other etiologic causes of alf
Other Etiologic Causes ofALF
  • Wilson’s Disease
  • can be presenting feature
  • usually in patients <20 yrs
  • can occur if patient discontinued
  • D-penicillamine for a few years
other etiologies 2
Other Etiologies (2)
  • Microvesicular steatosis
    • Acute fatty liver of pregnancy
    • Reye’s syndrome
    • Drug Induced - Valproic acid
  • AIH
  • May appear as an acute hepatitis
  • on initial presentation
  • More common if anti-LKMI antibody present
  • ASMA usually not present
other etiologies 3
Other Etiologies (3)
  • Hyperthermia (Heat stroke)
  • Direct thermal injury
  • Hepatic ischemia due to
  • -DIC
  • -Perfusion defect
  • OLT
  • Poor presentation of donor liver
  • Acute graft rejection
  • Thrombosis - hepatic artery, hepatic
  • vein, portal vein
  • Partial hepatectomy
  • Removal of 80% or more of healthy liver Removal of 50% or less in hepatic dysfunction
evaluation diagnosis of impending alf
Evaluation & Diagnosisof ImpendingALF

History! History! History!

Sexual contacts

IDU

Risk Factors

Pregnancy Mushrooms

Medications Travel Toxic exposures

history
HISTORY
  • Family members with liver disease?
  • Recent cold sores
  • Onset of jaundice
  • Work environment- toxic agents
  • Hobbies
  • Herbal products/dietary supplements
physical exam
Physical Exam

Determine presence or absence

of pre-existing liver disease

Hepatic tenderness

Hepatic decompensation

laboratory tests 1
Laboratory Tests(1)
  • Drug screening
  • ALT, AST, Alk Phos, Glu,

Bilirubin

  • Lytes, Albumin, Mg, Phos.,
  • CBC with differential
  • Coags: PT, PTT
  • Anti HAV IgM
  • Anti HBc IgM/ Anti HBsAg/
  • Anti-HCV
laboratory tests 2
Laboratory Tests (2)
  • If under 35 years of age

Ceruloplasmin

Serum & urine copper

  • Arterial blood gas
  • Arterial lactate
  • Pregnancy test
  • Autoimmune markers – ANA, ASMA, Ig levels
  • HIV status
  • Amylase & lipase
liver biopsy
Liver Biopsy

Reserved for diagnostic dilemma -

AIH, HS

(Transjugular approach)

diagnosis of alf
Diagnosis ofALF
  • Hallmarks - occurs simultaneously or in
  • succession
  • Altered mentation
      • Clinical
      • EEG
      • Arterial Ammonia
  • Coagulopathy
  • PT 4 sec prolonged (INR≥ 1.5)
  • Arterial pH<7.3 if acetaminophen ingested (cause for immediate transfer for OLT)
management of alf 1
Management ofALF(1)
  • Directed towards prevention of complications
  • ICU setting
  • Central line(s)-10% dextrose
  • Pulmonary artery pressure and CO
  • Inform Transplant Service and transfer with
  • onset of HE
  • Monitor VS and urinary output (Foley)
  • strict I&O
  • Laboratory Testing every 4-6hr
  • electrolytes, BUN, creatinine, CBC, platelets,
  • PT, PTT, ALT, AST, T. bilirubin, Alk Phos, Albumin
management 2
Management (2)
  • Maintain gastric pH above 5
  • - protonix IV
  • Preparation for endotracheal intubation
  • Prepare to initiate monitoring intracranial
  • pressure
  • Enteral feeding tubes for grade 3 or 4 coma
cerebral edema cerebral perfusion pressure
Cerebral EdemaCerebral Perfusion Pressure

Mean Arterial Pressure – ICP = Cerebral

Perfusion Pressure (CPP)

Ideal ICP<20-25mm Hg Ideal CPP>50-60mm Hg

Imazaki, et al

When CPP<40 for 2 hrs. 0 of 7 patients recovered

When CPP>50 6 of 8 patients recovered

Improved ICP first sign of spontaneous recovery

management 3
Management (3)

Cerebral Edema & Intracranial Hypertension

(Most serious complications of ALF)

Clinical signs of elevated ICP (Intracranial

Pressure)

-sluggish pupillary response

-increased limb-muscle tone

-none

Monitoring ICP

-usually reserved for grade 3 or 4 coma

-awaiting OLT

management 4
Management (4)

Cerebral Edema - General Measures

-quiet environment

-elevate head 10°-20°

-avoid sedation (use restraints)

-avoid Valsalva-like maneuvers

-mental status assessments q1-2h

-mannitol if signs of impending

uncal herniation (0.5mg/kg, lolus q4-8h)

when ICP<30-40mm

-assisted ventilation (in all grade 3 and 4)

multiple organ failure
Multiple Organ Failure

Hepatic damage increased risk

of infection

Failure of

clearance

Endotoxemia

Gut leak

MOF Activation of

macrophages

Tissue Circulating Release of

Hypoxia changes cytokines

TNF, IL-1, IL-6

Williams, Sem Liver Dis, Vol 16, No.4, 1996

management 5
Management (5)
  • Hemodynamic Complications include:
  • Hypotension, tachycardia, vascular volume decrease with capillary leak and vasodilation
  • Volume expansion (central line)
  • FFP or 4.5% albumin, 10% dextrose
  • Maintain pulmonary capillary wedge
  • pressure 12mm-14mm Hg
  • Minimize salt solutions (ascites,
  • interstitial accumulation)
  • Inotropic/pressor support(epi, norepi, dopamine),
  • but not vasopressin.
management 6
Management (6)
  • Coagulopathy/Bleeding Diathesis
  • FFP or platelets given in presence of bleeding
  • Conventional treatment of GI bleeding
  • DIC thrombocytopenia
  • Metabolic Complications
  • Prevent hypoglycemia
  • Phosphate and magnesium levels
  • monitored - replace early
  • Enteral feeding, 60gm protein/24 hrs
  • No role for high branched-chain AA
  • Monitor for lactic acidosis secondary to
  • tissue hypoxia, sepsis
role of cardiac index
Role of Cardiac Index
  • (CI = cardiac output/body surface area)
  • ALF associated with high CI
  • Presence of low CI (<4.5L/min)
  • is bad prognostic sign
  • Look for -
  • blood loss, pneumothorax
  • lactic acidosis, cardiac tamponade
management 7
Management (7)

Renal Failure

- In 42% to 82% of ALF

poor prognostic sign

- Rising creatinine and oliguria

- Metabolites of acetaminophen

are nephrotoxic leading to acute

renal failure similar to ATN and

loss of phosphate

-HRS

additional complications
Additional Complications
  • ARDS
  • Sepsis
  • - Severe complement deficiency
  • - Decreased PMN motility
  • - Decreased Kupffer cell function
  • and removal of endotoxins
  • - Increased levels of TNF and IL-6
prognostic factors
Prognostic Factors
  • Dependent on Etiology
  • Younger patients do better (<40 and >10)
  • Presence of cerebral edema
  • Delay between jaundice and HE of more
  • than 3 weeks - poorer prognosis
  • MOF - poor prognosis
current treatment
Current Treatment

Transplantation

temporary measures
Temporary Measures
  • Hemodialysis - no proven benefit on survival
  • Charcoal hemoperfusion - no proven benefit
  • Resins (Cation or anion - exchange) - not proven
  • Extracoporeal liver perfusions - may be bridge
  • to OLT
  • Hepatocyte transplants (peritoneum) - uncertain
  • Capillary hollow-fiber system - unproven,
  • ?bridge
approach to suspected alf
Approach to SuspectedALF
  • Etiology and Pathogenesis
  • Evaluation and Diagnosis
  • Complications
  • Management
  • Prognosis
  • Current and future treatment
  • approaches
ad