Acute liver failure

(Definition,Etiology & Management)

DR. PANKAJ INGALE

MD DNB (Gastroenterology)
Amravati Institute Of Gastroentrology
Definition
Acute liver failure(ALF) intially defined as
onset of hepatic encephalopathy (HE) within 8
weeks of development of clinical jaundice in
the absence of preexisting liver disease

Trey C, Davidson CS; Prog liver ds,1970;3:282-98

Lancet1993:342:252-3
Definition
O’grady proposed classification depending on interval b/w jaundice
& encephalopathy
Hyperacute <1 week
Acute 1-4 wk
Subacute 5-12 wk
Tandon et al defined SAHF as distinct entity as persistence of
acute hepatitis with:
Progressive Liver Dysfunction
Ascites AND /OR Encephalopathy at 5th to 24th wks(1-6 mo)
after onset of symptoms
Absence of pre-existing liver disease

Lancet1993:342:273-5
IASL 1999
AASLD Consensus Definition for ALF

The most widely accepted definition of ALF

includes Acute liver injury with evidence of
coagulation abnormality, usually
an International Normalized Ratio (INR) 1.5,
and
any degree of mental alteration in a
patient without preexisting cirrhosis and with
an illness of <26 weeks’ duration.

Trey C, Davidson CS., 1970

AASLD 2011
Etiology as per Country
Etiology
 ALF etiology (Indian Series)

Etiology Arora et al Bendre et al Poddar et al VBapu et al Samanta et al

(1996),n- (1999),n-36 (2002), n-67 (2001),n-37 (2007),n-35
40,Delhi Pune Chandigarh Chennai Kolkata

Viral 28 (70%) 22 (61.1%) 63 (94%) 35 (95%) 30 (86%)

HAV 4 (10%) 12 (33.3%) 34 (54%) 17 (47%) 9 (26%)
HEV 6 (15%) 1 (2.7%) 17 (27%) 2 (4.7%) 7 (20%)
HBV 6 (15%) 3 (8.5%) 5 (8.0%) 3 (8%) 6 (17%)
Multiple 12 (29.7%) 6 (16.6%) 7 (11%) 16%(A+E) 8 (23%)
HAV+HE 9 4 7 4.7%(A+B)
V
Drugs 3 (7.5%) 2 (5.5%) - - -
others 4 (10%) 4 (8.5%) 0 - -
Unknown 5 (12.5%) 8 (22.2%) 4 (6%) - -
Management
Q1 Does the Patient have ALF?

Q2 Is there specific therapy to treat the

underlying cause of ALF and promote recovery?

Q3 To anticipate and prevent complications HE,

cerebral edema, sepsis, GI bleed, RF, MOF?

Q4 Should the Patient be listed for liver

transplantation?
Q1 Does the patient have acute liver
failure?
All patients who do not have known liver disease and who
fulfill AASLD definition.

Are there any D/D :treatable conditions

Typhoid
Malaria
Dengue fever
Alcoholic Hepatitis
Clinical evaluation
History:
Onset of jaundice, HE, complications
Exposure to contacts with jaundice, BT, drug intake,
F/H of jaundice
H/o developmental delay ,seizures
Examination:
Liver span ,Assessment of grade of HE, features of
raised ICT
Splenomegaly, ascites, peripheral stigmata of CLD
Nutritional status,bruises,petechiae
KF Ring
Grades of Encephalopathy

Conn H, Lieberthal M.
Laboratory tests

General: CBC, Electrolytes , KFT, Ca,P, Ammonia (arterial if possible)

X ray chest , USG abdomen , ABG (when required)
Blood culture, urine culture

Liver specific tests-LFT, PT

Diagnostic tests
1. Serologies for HAV ,HBV, HEV.
2. EBV IgM, CMV IgM
3. AI markers
4. S.ceruloplasmin
5. Toxicology screen: urine toxic screen,
s.acetaminophen level
6. Metabolic workup

Clin Liver Dis 10 (2006) 149– 168

 Q2 Is there Cause of ALF to need
Specific treatment ?

Acetaminophen toxicity-N-acetyl Cysteine (NAC)

Amanita /Mushroom poisoning –Penicillin G +NAC
Herpes Simplex –Acyclovir 30mg/kg
Cytomegalovirus - Ganciclovir
EBV- Steroids, Acyclovir
Autoimmune Hepatits –Steroids(Methyl prednisolone)
Wilson disease- Chelators +/-
Acute Hepatitis B - Antivirals
General management
Nursing in quiet enviroment

Avoidance of stimulation and pain

Prevention of hypoglycemia(<45 mg/dl).

Gastroprotective measures with PPI/H2 blockers

Prevention of sepsis using broad spectrum antibiotics

General management
adequate fluid resuscitation

- parenteral vitamin K
- N-acetylcysteine,
- within 15 hours
- transplant-free survival was significantly better in
patients with grade 1 to 2 encephalopathy
- glucocorticoid therapy – no benefit

Crit Care Med 2007 Vol. 35, No. 11

Seminars in liver disease 2008 Vol 28.
Q3 Management of Complications
Cerebral oedema
Hepatic encephalopathy
Sepsis
Coagulopathy
Circulatory dysfunction
Metabolic dearrangements
Renal failure

Leading causes of death are: Cerebral edema & Sepsis

Cerebral edema
Seen in around 80% of patients dying from ALF.

Cerebral edema and ICH - related to severity of

encephalopathy

The risk of edema increases to

25% to 35% grade III, and
65% to 75% grade IV coma.

Crit Care Med 2007 Vol. 35, No. 11

Cerebral edema
In absence of ICP monitoring -
clinical signs frequently monitored,
Hypertension, bradycardia and irregular respiration

Pupillary dilatation or signs of decerebration are

typically evident only late in the course.

It occurs more commonly in hyper acute liver failure

(70%) than ALF (55%).

Walker’s pediatric Gastrointestinal Disease

Grade I/II Encephalopathy
Consider transfer to liver transplant facility and
listing for transplantation
Brain CT: rule out other causes of decreased mental
status;
Antibiotics: treatment of infection required;
prophylaxis possibly helpful
Lactulose, possibly helpful
Sedation is to be avoided,
unmanageable agitation :short-acting benzodiazepines
Grade III/IV Encephalopathy
Intubate trachea (may require sedation)
Elevate head of bed
ICP monitoring device
Immediate treatment of seizures required
Mannitol: severe elevation of ICP or clinical signs of
herniation
Hypertonic saline : serum sodium to 145-155 mmol/L
Hyperventilation: effects short-lived
non-depolarizing neuro-muscular blocking cis-atracurium
preferable , do not cause muscle contraction
Does the Patient require placement of a
device to monitor intracranial pressure?

Role is Controversial .
Useful role : In pt waiting for transplant,&
Pt on vasopressors with deep HE to
maintain CPP.

Risk: Intracranial bleed in 10 -20 % of pt ,

No controlled trials showing survival benefit .
Does the patient require placement of a
device to monitor intracranial pressure?

Not recommended in patients with

HE stages I/II
Clinical evidence of Diencephalic herniation and/or
intractable arterial hypotension, in whom death is
imminent.

Aim of ICP monitoring is ICP< 20-25 mmhg.

CPP(MAP-ICP) >50 mm hg
Epidural safer than subdural / subarachnoid
catheters,but measurements are less precise.
General measures for raised ICT
Head end elevated to 30 degrees in neutral position

Minimize Chest physiotherapy and endotracheal

suctioning .

Maintain Euthermia (36.5–37.5°C) .

Fever should be treated aggressively .

Shivering, should be treated with increased

sedation .
Treatment for raised ICT
Treatment options include:
Mannitol,
Hypertonic saline,
Hyperventilation,
Barbiturates,
Hypothermia
Treatment for raised ICT:
Mannitol
First line treatment.
Dose:0.5– 1 g/kg bolus ,
Onset of action 15 min ,DOA-3-8 hrs
Administered when ICP >25 mm Hg
Repeated 6 hrly if ICP > 25 mm Hg and S.osmolality <
320 mOsm/l
In pt without ICP catheter,clinical signs helpful.

Prophylactic administration of mannitol is not

recommended

Crit Care Med 2007 Vol. 35, No. 11 2503

Treatment for raised ICT:
Hypertonic saline

When administered prophylactically to ALF patients with

HE:
1. as a constant infusion (30%, 5–20 mL/hr)
2. to achieve a serum sodium of 145 mmol/L to 155
mmol/L.

Induction and maintenance of hypernatremia can

reduce the incidence and severity of ICH in patients
presenting with ALF.

Hepatology 2004; 39:464–470

Hyperventilation
Hyperventilation to PaCO2 of 25-30 mmHg

restores cerebrovascular autoregulation

resulting in vasoconstriction and reduction of ICP

Refractory ICT
Barbiturate coma, induced by
1. Pentobarbital (3–5 mg/kg intravenous loading bolus
followed by 1-3 mg/kg/hr,
2. Thiopental (5–10 mg/kg loading bolus followed by 3–5
mg/kg per hr)

Indomethacin (25 mg infused intravenously over 1

min) also has been shown to acutely decrease ICP
and increase CPP by causing cerebral
vasoconstriction
Refractory ICT
Induced moderate hypothermia (32– 33°C)

AASLD have used as a Bridge to OLT in patients with

osmotherapy-refractory intracranial hypertension .

Increase the risk of cardiovascular instability and/or

infection/bleeding .

Further strategies :
1. Therapeutic hepatectomy
2. Bioartificial LA devices.

Gastroenterology 2004; 127:1338–1346

Role of EEG
Recommended for the following indications:
grade III or IV hepatic encephalopathy;
sudden unexplained deterioration in neurologic
examination;
Myoclonus
To titrate therapy when barbiturate coma is used
Seizure activity to be treated with phenytoin

Crit Care Med 2007 Vol. 35, No. 11 2503

Role of Phenytoin in ALF
Subclinical seizure activity is missed in gr 3 & 4 HE.

Controlled Trial in 42 ALF pt ,20 received phenytoin,22

controls.

Prophylactic use of phenytoin did not prevent

cerebral edema, seizures or need for mechanical
ventilation, and did not improve survival

HEPATOLOGY 2000;32:536-541
N-Acetyl Cysteine
improve liver blood flow and function in patients with
septic shock
It acts by replenishing glutathione that detoxifies
the metabolite, N-acetyl-pbenzo-quinoneimine.
In addition, excess NAC also provides substrates for
hepatic ATP synthesis, thus supporting mitochondrial
energy metabolism.
improve systemic hemodynamics and tissue oxygen
delivery and consumption.
NAC in Non-Acetaminophen induced
ALF in children

Retrospective study,in children ,NAC was administered as a

continuous infusion (100 mg/kg/24 hours) until INR 1.4,
death, or liver transplantation (LT).
Liver Transpl 14:25-30, 2008
NAC in Non-Acetaminophen induced
ALF in children

NAC was associated

with a shorter length of
hospital stay,
higher incidence of
native liver recovery
without transplantation,
and
better survival after
transplantation.

Liver Transpl 14:25-30, 2008

NAC in Non-Acetaminophen induced
ALF
Prospective, randomized,
double blind placebo-controlled
trial
Significantly improved NAC I-II significantly better
transplant free survival at 3 transplant free survival
weeks and 1 year in NAC than all others
treated patients for non
acetaminophen ALF
Benefit only those in early
coma grades .
Advanced coma grades showed
no benefit from NAC

Lee at al GASTROENTEROLOGY
2009;137:856–864
NAC in Non-Acetaminophen induced
ALF
47 adult ALF pt compared to 44 controls (historical)
in centre without facility for liver transplant.

A total of 34 (37.36%) patients survived.

Of which 22 were (47%) in group 1 (NAC group) and
12 (27%) in group 2 (controls) (P = 0.05). 

On multivariable regression analysis, patients not

given NAC was independent predictor of mortality.

Hepatol Int. 2009 Aug 29.

Sepsis in ALF
Sites of sepsis in ALF Predominant bacterial
pathogens are:
21.6 15.7
S.aureus, CONS, E.coli.
E.coli
11.8
fungal : yeasts,
candida,rarely aspergillus,
Seen mainly in 2 nd week
75% by S. aureus after admission.
51

blood iv cannulae
chest urinary tract

Seminars in liver diseases ,2002

Sepsis in ALF
Empirical antibiotic 3rd gen Cephalosporins in most
centres.
If iv line sepsis then vancomycin.
Avoid aminoglycosides.
Empirical antifungal therapy
In a combined study, comparison of frequency of
developing infections b/w prophylactic antibiotic
(35%) vs none grp ( 58%)

J Hepatol. 1992;14:280–285.
HEPATIC ENCEPHALOPATHY-
Treatment

Strategies to lower ammonia

production/absorption
Nutritional management
Protein restriction -Protein administered at
(0.5–1.0 g/kg per day) .

Medications to counteract ammonia’s effect on

brain cell function

Devices to compensate for liver dysfunction

Non-absorbable disaccharides

Lower colonic pH favoring formation of non-

absorbable NH4 ions.
Preferential growth of non-urease producing bacteria.
Cathartic action.
Increased consumption of NH3 by gut flora.
Non-absorbable disaccharides

Lactulose:
Dose 1-2 ml/kg/dose in 3- 4 doses
Goal is 2-3 stools/day, pH<6
SE: abdominal cramping, diarrhea, flatulence

Lactitol: similar efficacy.

lactulose - small increase in survival time,
no difference in severity of
encephalopathy or in overall outcome

J Hepatol 2002;36:33A
L-Ornithine L-Aspartate

Activates carbamyl
phosphate synthetase

Activates ornithine carbamyl

transferase

Stimulates glutamine synthesis

Substrate for ureagenesis

Urea cycle
L-Ornithine L-Aspartate in ALF

Placebo controlled blinded study in 201 ALF pt. showed:

There was no significant reduction in mortality,HE
grade,survival time, seizures with LOLA treatment

There was significant decrease in ammonia levels in

both groups with time (P < .001)

Hence LOLA infusion did not lower the ammonia or

improved survival in ALF.

Gastroenterology. 2009 Jun;136(7):2159-68

Oral Antibiotics

Antibiotics reduce urease producing bacteria

Neomycin:
no benefit over placebo
associated with ototoxicity and nephrotoxity.
Rifaximin
Oral antibiotic, poorly absorbed rifamycin derivative
Minimal absorption (<0.4%).
Broad spectrum activity against enteric bacteria
No significant drug interactions/dose adjustment in hepatic or
renal dysfunction.
Bleeding
uncommon (10%)
capillary-type, usually from mucosal sites
Both quantitative and qualitative platelet dysfunction.
platelet transfusions are not generally recommended
in the absence of spontaneous bleeding or prior to
invasive procedures.
Before invasive procedures /clinically significant
bleeding, aim to improve P/C 50,000/mm3

J Hepatol 2005; 42:365–370

Coagulopathy

In minority Vitamin K deficiency may contribute to

the coagulopathy .

Prophylactic FFP to improve coagulopathy not

recommended

J Hepatol 2005; 42:365–370

Coagulopathy

rFVIIa in circumstances :
1. Where FFP fail to correct INR
2. Already volume overloaded pt., before invasive
procedures with a high risk of bleeding

Dose-80 ug/kg
Procedure should be performed within 30–60 mins,
though the effect persists for >2 hrs
Risk : thrombotic complications .
Plasma exchange is the last option.

Liver Transpl 2005; 11:872–874

Gastroenterology
Circulatory dysfunction
resuscitated with normal saline first, and changed to
half-normal saline containing 75 mEq/L sodium
bicarbonate if acidotic
Crystalloid solutions should contain dextrose to
prevent hypoglycemia
Inotropes required in order to maintain a MAP of at
least 75 mmHg or a CPP of 60-80mmHg
Norepinephrine preferred, than dopamine.
Relative adrenal insufficiency :hydrocortisone may
improve the vasopressor response .
Renal failure
Incidence of ARF is 10-15% in ALF.

Maintain adequate hemodynamics, avoid nephrotoxic

agents such as aminoglycosides and NSAID, prompt
identification and treatment of infection.

Insufficient data to recommend specific criteria to

start or discontinue renal replacement therapy (RRT).

Intermittent hemodialysis tolerated poorly.

Therefore, AASLD prefer continuous RRT

Mechanical ventilation
Indications
Respiratory failure (hypoxemia, hypercapnia),
Airway protection in the setting of advanced HE(stage III/IV),
Imminent ICP monitor placement.

Generally, tidal volume and plateau pressure should be limited (6

mL/kg predicted body weight and 30 cm H2O, respectively) in
pt. with established ALI.

Low tidal volumes also may decrease the risk of progression to

ARDS.

In general,the lowest level of PEEP that achieves adequate

oxygenation should be applied.
Q3 Should the Patient be listed for
liver transplantation?
Unlikely to survive without transplant
Indeterminate ALF
Idiosyncratic drug rx
Autoimmune hepatitis
Spontaneous recovery
Acetaminophen toxicity
Hepatitis A
Ischemic hepatitis
Herpes infection
Unlikely to benefit from transplant

Mitochondrial disease
HCC
Potentially Helpful Indicators* of
Poor Prognosis in Patients With ALF
Transplant criteria-King’s college
Acetaminophen-induced ALF:
Arterial pH <7.3 (following
adequate volume
resuscitation) irrespective of
coma grade
OR all of following
1.PT> 100 seconds (INR > 6.5)
2.serum creatinine >300 mol/L
(3.4 mg/ dL)
3. grade III/IV coma
Non-acetaminophen-
induced ALF:
PT> 100 seconds irrespective
of coma grade
OR
Any three of the following,
irrespective of coma grade:
Drug toxicity, indeterminate
cause of ALF
Age <10 years or> 40 years
Jaundice to coma interval >7
days
PT >50 seconds (INR> 3.5)
Serum bilirubin> 300 mol/L
(17.5 mg/dL)
Q4 Should the patient be listed for
liver transplantation?
Relative and Absolute contraindications to
transplantation include
Uncontrolled infection or sepsis,
Active or recent malignancy,
Uncontrolled intracranial hypertension
Severe intracranial hemorrhage,
Progressive or end-stage extra-hepatic disease or
systemic disease that will not corrected by liver
transplantation
Liver transplant
spontaneous survival in ALF patients improved from
10% to 20% to about 40
transplantation has coincided with further
improvement in overall survival rates to over 60%
listed as a UNOS status 1A

Living donor liver transplantation (LDLT)

Auxiliary liver transplant

HEPATOLOGY, April 2008

Extracorporeal systems
Temporarily take over the function of the liver,
Artificial Support:These sorbent-based systems,
The molecular absorbents recirculation system
(MARS)
Prometheus albumin dialysis
Bioartificial devices
HepatAssist
extracorporeal liver support device
modular extracorporeal liver support system
bioartificial liver support system
Amsterdam Medical Center bioartificial liver
A recent meta-analysis, considering all forms of
devices together, demonstrated no efficacy for
bioartificial liver devices for the treatment of ALF
HEPATOCYTE TRANSPLANTATION
Hepatocyte transplantation involves injection of
donor hepatocytes into the liver or
spleen.120 Donor hepatocytes then integrate into the
local tissues with the potential to
restore hepatic functions in a patient with ALF.
Wilson ALF - Management

Identified etiology in 5% of ALF patients worldwide.

Life-threatening without liver transplantation.
Initial non specific symptoms f/b rapidly increasing
jaundice ,anemia, encephalopathy, renal failure.
Diagnostic issues
Management issues – Chelation vs transplant
Wilson ALF -Diagnosis
Low Cp level less reliable in ALF setting.
KF ring + in 50% pt ,not possible in critically ill.
Liver bx and urine Cu ,difficult to procure & interpret
in ALF setting.
Rapidly increasing bilirubin ,Coombs neg hemolytic
anemia.
A high bilirubin (mg/dL) to alkaline phosphatase
(IU/L) ratio (>2.0) is a rapid, reliable (albeit indirect)
indicator ofWilson disease

Pediatr Crit Care Med. 2003 Jul;4(3):338-43

HEPATOLOGY, October 2008.
Wilson ALF - Management
Nazer index – prognostic score, >=11 ,poor survival

The sensitivity and specificity of the Nazer

scoring system was 87% and 90%, with a positive
predictive value of 72%.

Gut, 1986, 27, 1377-1381

Wilson ALF - Management
Modified new Wilson Index score

 93% sensitive, 98% specific, and positive predictive

value of 93%.
All children with a score > 11 died without transplant.
All who responded to medical treatment had a
score < 6.
Liver Transplantation, Vol 11, No 4 (April), 2005: pp 441-448
Treatment to acutely lower serum copper and to limit
further hemolysis should include
albumin dialysis,
continuous hemofiltration,
plasmapheresis,or
plasma exchange.
Initiation of treatment with penicillamine is ? in ALF
as there is a risk of hypersensitivity
promptly considered for liver transplantation
AIH
Fulminant presentation of AIH rare.
May be First presentation or as relapse on non
compliance of treatment.
Diagnosis:
Positive AI markers with negative workup for others.
Higher ASL/ALT levels, elevated IgG levels
Histology more frequently cetrilobular zone 3
necrosis with plasmacytic infiltration and bile duct
injury.
This may transform to classic pattern of interface
hepatitis as disease evolves.

Czaja, Seminar in liver disease 2009

AIH management
MELD score useful in identifying pt ,who are likely to
fail to corticosteroid therapy ,require transplant.
MELD>= 12 at presentation ,specificity 68%, sensitivity
97% for treatment failure.
Important dictum : to limit corticosteroid therapy to 2
weeks or less and to heed implications of MELD.
In a pt on corticosteroids :
Resolution /non worsening of LFT,PT –indicates to
continue steroid & defer transplant.
On contrast progressive hyperbilirubinemia during tt &
multiacinar necrosis on bx –justifies liver transplant .

Czaja Liver transpl 2007,Montano Hepatology 2007

Acetaminophen hepatotoxicity

10 gm/day (150 mg/kg). rarely when doses as low as

3-4 gm/day are taken.

Very high aminotransferase exceeding 3,500 IU/L

Activated charcoal as long as 3 to 4 hours
standard dose 1 gm/kg orally, in a slurry

NAC intravenous administration

loading dose is 150 mg/kg in 5% D over 15 minutes;
maintenance dose is 50 mg/kg given over 4 hours
followed by 100 mg/kg over 16 hours or 6
mg/kg/hr).
when to stop use of NAC, standard 72-hour period
Vs continuation until liver chemistry values have
improved.
Mushroom Poisoning Amanita
phalloides)
with a history of severe gastrointestinal symptoms
gastric lavage and activated charcoal via nasogastric
tube
Penicillin G and silibinin (silymarin) are accepted
antidotes despite a lack of controlled trials

NAC is often combined with these other therapies,

Drug Induced Liver Injury (DILI)
Idiosyncratic hepatotoxicity within the first 6
months
antibiotics, NSAID and anticonvulsants
herbal preparations, weight loss agents
discontinue all but essential medications
No specific antidotes for idiosyncratic drug
reactions;
corticosteroids are not indicated
N-acetylcysteine may be beneficial
Drugs: Idiosyncratic Liver
Injury
Isoniazid Pyrazinamide
Sulfasalazine Itraconazole
Statins Nicotinic acid Doxycycline
Propylthiouracil
Ciprofloxacin Nitrofurantoin
Disulfiram Methyldopa
Valproic acid Phenytoin Labetalol Carbamazepine
Amiodarone Dapsone Allopurinol
Methyldopa
Didanosine Ketoconazole Efavirenz Abacavir
Diclofenac
Trimethoprim-sulfamethoxazole
Rifampin-Isoniazid
Amoxicillin-clavulanate
Viral Hepatitis
Viral hepatitis A/ E/B/D
Herpes virus/ varicella zoster
Viral hepatitis A and E-supportive care
Ribavarin in HEV
Nucleos(t)ide analogues hepatitis B-associated acute
liver failure and for prevention of post-transplant
recurrence.
herpes virus or varicella zoster :acyclovir (5-10 mg/kg
IV every 8 hours) and may be considered for
transplantation .
Acute Fatty Liver of
Pregnancy/HELLP Syndrome
generally confined to the last trimester.

The triad of jaundice, coagulopathy, and low platelets.

Early recognition of these syndromes and prompt

delivery are critical in achieving good outcomes.

Recovery is typically rapid after delivery.

Acute Ischemic Injury
after cardiac arrest, any period of significant
hypovolemia/hypotension, or in the setting of severe
congestive heart failure
Aminotransferase levels will be markedly elevated as
will lactic dehydrogenase enzyme levels (indicative of
cell necrosis, not apoptosis)
improve rapidly with stabilization of the circulatory
problem.
Budd-Chiari Syndrome
Abdominal pain, ascites and striking hepatomegaly are
often present.
The diagnosis should be confirmed with hepatic
imaging studies
prognosis in this condition is poor if hepatic failure is
present
transplantation may be required as opposed to venous
decompression
Malignant Infiltration
Diagnosis should be made by imaging and biopsy, and
treatment appropriate for the underlying malignant
condition is indicated.
Transplantation is not an option for such patients.
Acute severe hepatic infiltration occurs with breast
cancer, small cell lung cancers,lymphoma, melanoma,
and myeloma.
Indeterminate Etiology
When the etiology of ALF cannot be determined
after routine evaluation, biopsy using a transjugular
approach may be helpful in diagnosing malignant
infiltration, autoimmune hepatitis, certain viral
infections and Wilson disease
Conclusions
ALF is a syndrome, not a disease, and may be
precipitated by many insults to the liver.
Etiology of ALF varies with age, metabolic causes
predominate in infancy while infections in older age
grp.
Prompt recognition & management of cerebral edema
and sepsis is required.
intensive care support after treatments for specific
etiologies
Careful attention must be paid to fluid
management,hemodynamics and metabolic parameters
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