Acute liver failure
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Acute Liver Failure. Dr. Eduardo Martinez. Foie Gras. Foie gras  (pronounced  /fwɑːˈɡrɑː/  in English;  French  for "fat liver") is a  food product  made of the  liver  of a  duck  or  goose  that has been specially fattened. Functions of the Liver. Metabolic Carb metabolism

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Acute Liver Failure

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Acute liver failure

Acute Liver Failure

Dr. Eduardo Martinez


Foie gras

Foie Gras

  • Foie gras (pronounced /fwɑːˈɡrɑː/ in English; French for "fat liver") is a food product made of the liver of a duck or goose that has been specially fattened.


Functions of the liver

Functions of the Liver

  • Metabolic

    • Carb metabolism

    • Protein and lipoprotein metabolism

    • Fatty acid metabolism

    • Biotransformation of drugs

  • Storage

    • Glycogen

    • Vitamins A, D, E, and K

    • Iron and copper


Functions of the liver1

Functions of the Liver

  • Immunological function s

    • Synthesis of immunoglobulins

    • Phagocytosis by Kupffer cells

    • Filtration of bacteria

    • Degradation of endotoxins

  • Excretion of bilirubin and urea formation

  • Haematological functions

    • Blood reservoir

    • Haematopoiesis in the foetus


Acute liver failure

ALF

Syndrome that leads to MOF and death

Previously normal liver may fail within days

High grade encephalopathy, survival is <20%

Early death:

cerebral oedema, CVS collapse

Late death:

Sepsis , MOF


Definition and classifications

Definition and Classifications

ALF: Sd. defined by

Encephalopathy

Coagulopathy

Jaundice

Individual with previously normal liver


Definition and classifications1

Definition and Classifications

Fulminant Hepatic Failure

Potentially reversible condition

Consequence of severe liver injury

Encephalopathy appears within 8 wks. of initial Sx.

Absence of pre-existing liver ds.


Definition and classifications2

Definition and Classifications

King’s classification:

Hyperacute: encephalopathy within <7 days

Paracetamol, ischaemic, viral, toxins

Acute: 8-28 days

Subacute: 5-26 weeks

Seronegative, idiopathic, drug-related

Different etiology

Poorer prognosis


Etiology

Cause

Agent Responsible

Viral Hepatitis

Hep. A, B, D, E, CMV, HSV, seronegative hepatitis (14-25% in UK)

Drug-related

Dose-related, e.g.paracetamol; idiosyncratic reactions, e.g. anti-TB, statins, recreational drugs, anticonvulsants, NSAIDs, many others

Toxins

Carbon tetrachloride, amanita phalloides

Vascular events

Iscahemic hepatitis, veno-occlusive disease, Budd-Chiari, heatstroke

Other

Pregnancy-related liver disease, Wilson’s disease, lymphoma, carcinoma, trauma

Etiology


Etiology1

Etiology

Most common causes:

Worldwide:

Hepatotrophic viruses A-E

UK

Paracetamol overdose

Seronegative or non-A-E hepatitis

Idiosynchratic drug rxs. or Wilson’s ds.


Workup

Workup

Identify the etiology

Hx., examination, viral and autoimmune profiles

Bloods

FBC, EUC, CMP, coags, LFTs, drug levels

Abdo USG and CT

Vascular pattern, ascitis, splenomegaly


Workup1

Workup

Liver Bx.

Done by transjugular route

Mays suggest specific Dx.

Watch for sample from healthy liver

>50% necrosis assoc. with poor prognosis

Need to reverse coagulopathy before doing it


Pathophysiology

Pathophysiology

Hepatic encephalopathy

alteration in mental status and cognitive function occurring in the presence of liver failure

Liver failure leads to:

portal HTN

splachnic vasodilation

Hypoalbuminaemia

Reduced plasma oncotic pressure

Leads to ascitis and organ oedema


Pathophysiology1

Pathophysiology

Decreased intravascular volume

Kidneys try to “compensate” and retain Na+ and water making oedema worse

Also,

Gut-derived toxins reach the liver

Ammonia levels are often high

Correlation between ammonia and symptoms is poor


Clinical features

Clinical Features

Depend on the severity, which depends on:

Etiology

Speed of onset of symptoms

Non-specific

N&V, abdo pain

Neurological

Confusion, agitation, coma


Scale of hepatic encephalopathy

Scale Of Hepatic Encephalopathy

Grade

Level of Consciousness

Personality and Intellect

Neurologic Signs

Electroencephalogram (EEG) Abnormalities

0

Normal

Normal

None

None

Subclinical

Normal

Normal

Abnormalities only on psychometric testing

None

1

Day/night sleep reversal, restlessness

Forgetfulness, mild confusion, agitation, irritability

Tremor, apraxia, incoordination, impaired handwriting

Triphasic waves (5 Hz)

2

Lethargy, slowed responses

Disorientation to time, loss of inhibition, inappropriate behavior

Asterixis, dysarthria, ataxia, hypoactive reflexes

Triphasic waves (5 Hz)

3

Somnolence, confusion

Disorientation to place, aggressive behavior

Asterixis, muscular rigidity, Babinski signs, hyperactive reflexes

Triphasic waves (5 Hz)

4

Coma

None

Decerebration

Delta/slow wave activity


Clinical features1

Clinical Features

Mortality is higher for Grade III/IV

Mostly due to cerebral oedema

Occurs in 80% of pts. w/ALF

Due to lack of equilibration of osmotic gradient

30% of those have cerebellar tonsil and/or temporal lobe herniation causing death

We’re now better at treating cerebral oedema


Clinical features2

Clinical Features

Elevated ICP

HTN, bradycardia, blown pupils: occur late

CTB won’t tell you

ICP monitor is best way of knowing

CVS changes

Similar to sepsis

Might be due to infection


Clinical features3

Clinical Features

Renal failure

Oliguric

Poor prognosis

Except with paracetamol overdose where it has a good prognosis

Impaired immunity

Decreased complement synthesis, Kupffer cell dysfunction, poor neutrophil adhesion and superoxide production


Clinical features4

Clinical Features

Increased susceptibility to infection

80% of pts. have bacteriologically proven infections

Major sepsis is contributor to death in 20% of cases

Staph. aureus 70% of gram (+)

E. Coli most common gram (-)

C. albicans in 30% of pts.


Monitoring

Monitoring

Pts. need HDU/ICU

Need CVC and continuous IBP monitoring and IDC

Baseline ABG and lactate

Lactate >3mmo/L after adequate resus has same sensi. and speci. for death as The King’s College Hospital criteria


Prognosis

Prognosis

Early indicators of prognosis in fulminant hepatic failure.

O'Grady JG, Alexander GJ, Hayllar KM, Williams R.

Gastroenterology. 1989 Aug;97(2):439-45.

King’s Collage Hospital Criteria

Originally devised as prognostic criteria to predict patient survival without liver transplant

Now used as selection criteria for potential liver transplant recipients


Kch criteria

KCH Criteria

  • Other patients

    • Prothrombin time >100 seconds orThree of the following variables:

    • Age <10 yr or >40 yr

    • Jaundice >7 days before encephalopathy

    • PT > 50s

    • Bilirubin > 300mmol/L

Patients with paracetamol toxicity

pH <7.3 (7.25 if given NAC)

Or

all three of the following:

Prothrombin time >100s

Serum creatinine level >300 μmol/l

Grade III or IVencephalopathy


Kch criteria1

KCH Criteria

  • Positive predictive value for ICU death without transplantation of 0.98

  • Negative predictive value of 0.82


Treatment

Treatment

Intensive care of patients with acute liver failure: recommendations of the U.S. Acute Liver Failure Study Group.

Stravitz RT, Kramer AH, Davern T, Shaikh AO, Caldwell SH et al.

Critical Care Medicine 2007; 35: 2498-508


Treatment1

Treatment

Adult U.S. Acute Liver Failure Study Group

Data from

23 liver transplant centers

>1,110 pts.

In 2005 convened to

review literature on management

Care of pts. w/high ICPs

Compare practices of different centers


General management

General Management

Admit to hospital and HDU/ICU

When evidence of ALF

E.g.: INR>1.5

D/W:

Physician

Intensivist

Nearest transplant center

Regarding best time to refer


General management1

General Management

Etiology-specific treatment

Studies only for paracetamol overdose

NAC regardless of time of overdose

IV if Grade I encephalopathy

Hypotension

Any other reason PO NAC is not tolerated

HELLP or acute fatty liver of pregnancy

Tx. Is immediate delivery


General management2

General Management

NAC

150mg/kg IV in 200ml NS over 15-60mins

50mg/kg IV over 4hrs

100mg/kg IV over 16hrs

Total dose: 300mg/kg over 20hrs

Infusion recommended until there is evidence of improved hepatic function rather than time or paracetamol levels


Management of complications

Management of Complications

Hepatic encephalopathy and hyperammonaemia

Infections

Sedation and analgesia

Bleeding diathesis

Nutrition

Seizures

Circulatory dysfunction


Encephalopathy

Encephalopathy

Standard treatment:

Lactulose

Watch for:

Abdo distension

Oesophageal varices will need a scope

Avoid intravascular depletion

Non-absorbable ATBs

Neomycin not recommended by ALFSG because of nephrotoxicity


Infection prophylaxis and surveillance

Infection prophylaxis and surveillance

Infection is one of main causes of death in ALF

Most common sites:

Lung

Urinary tract

Blood

Most common M.O.

Gram (+) cocci: Staph aureus

Gram (-) rods: E. coli

Fungi: candida


Infection prophylaxis and surveillance1

Infection prophylaxis and surveillance

Empirical ATBs are recommended by ALFSG when:

Surveillance cultures reveal significant isolates

Advanced stage (III/IV) encephalopathy

Refractory hypotension

SIRS

3rd gen. Cephalosporin or Timentin, Vancomycin, Fluconazole


Sedation and analgesia

Sedation and analgesia

Agitation contributes to raised ICP

Propofol vs. Benzos

Both increase GABA neurotransmission, therefore may exacerbate encephalopathy

Propofol decreases ICP and wears off quickly

Opioids

Shorter acting are preferable

When there is concommitant ARF, avoid morphine or pethidine due to metabolite accumulation


Correction of bleeding diathesis

Correction of bleeding diathesis

Pts. with ALF are by definition coagulopathic

Low plts. and fibrinogen, Vit. K deficient

Spontaneous bleeding is rare

Very difficult to obtain complete correction

ALFSG recommends aiming for:

INR 1.5

Plts. 50,000


Correction of bleeding diathesis1

Correction of bleeding diathesis

Prophylactic FFP not recommended

Obscures the trend of PT as prognostic marker

Cryo recommended when fibrinogen low

When FFP fails to correct PT/INR, then recombinant factor VIIa can be given

Should be given before planned procedures

Avoid in patients with risk of thrombotic complication

MI, DVTs, etc.


Correction of bleeding diathesis2

Correction of bleeding diathesis

UGI bleeding

reduced by H2 antagonists or PPIs

TEDS and Scuds


Nutrition

Nutrition

ALF is a catabolic state

Negative nitrogen balance

Immunodeficiency

Enteral nutrition when possible

Hi-cal

Avoid free water and hypo-osmolarity

TPN when:

Specific contraindication for enteral feeds


Seizure prophylaxis and surveillance

Seizure Prophylaxis and Surveillance

Nonconvulsive seizure activity is common

Prophylactic antiepileptics not recommended

EEG when:

Grade II/IV encephalopathy

Sudden neuro deterioration

Myoclonus

To titrate use of barbiturates

Tx.

Phenytoin

Propofol, midaz, barbiturates


Cvs dysfunction

CVS Dysfunction

Correct hypovolaemia before starting vasopressors

Pressors needed for hypotension and low CPP

Norad is first line, can give high dose dopamine

Adrenaline may compromise HBF

Vasopressin not recommended because directly causes cerebral vasodilation and high ICPs

Medium doses of steroid may improve pressor response


Mx of cerebral oedema and intracranial hypertension

Mx. of Cerebral Oedema and Intracranial Hypertension

Raised ICP due to cerebral oedema is one of major causes of M&M

CTB for Grade III/IV

To rule out anything else, i.e. bleed

ICP monitor

Grade III/IV encephalopathy

To optimize CPP

Not routine


Raised icp

Raised ICP

Aim for

ICP<25mmHg

CPP 50-80

General recommendations

Keep it quiet , minimize chest physio and ETT suctioning, head at 30o

Don’t treat spontaneous hyperventilation, keep PaCO2 35-40mmHg, treat fever aggressively with physical measures


Raised icp1

Raised ICP

Specific management

Manitol: first line therapy

Hypertonic Saline

Induced hypothermia

Barbiturate coma

Indomethacin: 25mg IV over 1min.


Mechanical ventilation

Mechanical Ventilation

When to intubate:

Respiratory failure

Airway protection in advanced encephalopathy

Agitation

Imminent ICP monitor placement


Mechanical ventilation1

Mechanical Ventilation

Pts. w/ALF often develop ALI/ARDS

Follow ARDSNet protocol

Avoid high PEEP

Use the minimum needed


Acute liver failure

CRRT

Indicated for:

Renal failure

Fluid overload

Metabolic derangements

Need to create space for IV colloids, i.e. FFP

CRRT preferred over IRRT

HD instability common


Acute liver failure

CRRT

Use citrate over heparin

Monitor ionized calcium

Use bicarb buffer over lactate or citrate buffer

Liver won’t be able to convert them to HCO3-

Avoid hyponatraemia

May exacerbate cerebral oedema


Liver transplant

Liver Transplant

  • Orthotopic liver transplant is the definitive treatment for patients who meet the criteria

    • or·tho·top·ic (ôrth-tpk)adj.In the normal or usual position

  • 1 yr. and 5 yr . survival of patients undergoing OLT for ALF is about 20% lower than elective cases for cirrhotic patients

  • Auxiliary liver transplantation is and alternative


Liver transplant1

Liver Transplant

  • Absolute contraindications

    • Overwhelming sepsis

    • Refractory hypotension

    • AIDS

    • Uncontrolled raised ICP with likely permanent damange


Hepatic assist devices

Hepatic assist devices

  • MARS: molecular absorption and recirculation system

    • Adaptation of haemodialysis

    • Blood is dialysed against 20% albumin

      • Shown to improve encephalopathy, renal function and haemodynamic parameters

    • The efficacy of this technique has not yet been studied


So what have we learned

So, what have we learned?


Thank you

Thank you!


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