Acute liver failure
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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


Acute liver failure

Suspect ALF?..........Admit to ICU


Etiology of alf

Etiology ofALF

  • Acute viral hepatitis (A - E)

  • Mushroom poisoning

  • Acetaminophen

  • Acute fatty liver of pregnancy

  • Chemical agents


Acute liver failure

  • 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


Acute liver failure

Etiology ofALFin 342 Cases(University Hospital, London UK)

Drugs-OverdoseOther

Acetaminophen 250Wilson’s 3

Ecstasy 2Fatty liver of pregnancy 7

Lymphoma/

Viral Hepatitis malignant infiltrate 7

HAV 8Sepsis 2

HBV 8Budd-Chiari 5

Non A-E 28Ischemia 9

Miscellaneous 6

Idiosyncratic Drug Reactions

Lamotrigine, cyproterone, NSAID,

chloroguine, rifampin/ INH

halothane, flucloxacillin


U s alf study group 2003 308 patients 73 women

U.S. ALF STUDY GROUP 2003 (308 Patients, 73% Women)


Acute liver failure

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 HBc100%

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 damageincreased risk

    of infection

    Failure of

    clearance

    Endotoxemia

    Gut leak

    MOFActivation of

    macrophages

    Tissue CirculatingRelease of

    Hypoxiachangescytokines

    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


    Outcome results u s alf study group

    OUTCOME RESULTS U.S.ALFSTUDY GROUP


    Approach to suspected alf

    Approach to SuspectedALF

    • Etiology and Pathogenesis

    • Evaluation and Diagnosis

    • Complications

    • Management

    • Prognosis

    • Current and future treatment

    • approaches


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