ACUTE LIVER FAILURE

✓ Medically ReviewedDISEASEID: MDBT0116🚨 TRIAGE: EMERGENCYICD-10: K72.00

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Definition

CLINICAL DEFINITION

Acute liver failure is sudden loss of liver function without prior cirrhosis (long term scarring). It needs coagulopathy (poor clotting with high INR) plus encephalopathy (brain change with confusion). Jaundice (yellow skin from bile pigment) is usual with very high injury enzymes. Illness builds over days to weeks in a previously healthy liver.

IN PLAIN ENGLISH

Liver cleans blood. It can fail fast. Blood stops clotting well. Waste harms brain. It needs emergency care.

COMMON MISCONCEPTION / WHAT IT DOES NOT MEAN

Acute liver failure is not chronic failure with known cirrhosis (long scarring). It is not simple hepatitis (liver inflammation) with normal thinking. It is not blocked bile ducts (bile tube block) with yellow skin alone. It is not poor clotting alone from other causes without brain change. Prior belly fluid or vein bleeding points to chronic disease.

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Word Breakdown

liver failure

=liver (filter organ) and failure (loss of function)

Literal Meaning: sudden loss of liver function

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Abbreviations

ALF=Acute liver failure - sudden loss of liver function

INR=International normalised ratio - clotting measure from blood test

ICU=Intensive care unit - hospital unit for very sick patients

NAC=N-acetylcysteine - antidote that restores liver protection

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Synonyms & Variants

Fulminant hepatic failure›Acute hepatic failure›Fulminant liver failure›

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Category-Specific Context

Acute liver failure is a Disease because it is a syndrome (linked failure pattern) with causes and course. It is not a Symptom (patient complaint) or lab change alone. It reflects massive liver cell loss with body-wide effects. Care targets cause, complications and urgent transplant review. It sits under liver failure with encephalopathy as its defining mark.

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Clinical Context & Usage

CLINICAL SETTINGS

Emergency DepartmentIntensive Care UnitLiver Transplant CentreAcute Medical UnitObstetric Unit for Pregnancy Causes

USAGE & DOCUMENTATION NOTES

Use acute liver failure only when poor clotting and brain change coexist without prior cirrhosis. Record time from jaundice (yellow skin) to confusion to define subtype. State suspected cause with transplant candidacy (suitability for new liver). Avoid use for hepatitis with normal mental state.

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Primary Causes & Pathophysiology

PATHOPHYSIOLOGY

Massive cell death rapidly cuts protein and clotting factor making. Poor clearing raises ammonia (brain toxin) and injures nerve cells. Systemic inflammation (body-wide immune activation) with poor flow harms many organs. Low sugar from lost control plus acid buildup worsens injury. Brain swelling can raise skull pressure and threaten life.

PRIMARY CAUSES

Paracetamol overdose (painkiller excess)

Toxic byproduct depletes protection and kills liver cells across zones

Hepatitis B with acute flare (liver virus surge)

Immune attack plus direct viral injury destroys large liver volumes in days

Autoimmune hepatitis flare (mistaken immune attack)

Misdirected immunity causes rapid widespread cell death with loss of function

Ischaemic injury from shock (poor blood flow)

Severe low flow starves central cells of oxygen and causes rapid death

Wilson crisis with copper release (inherited metal overload)

Sudden copper surge breaks red cells and kills liver cells at once

Budd-Chiari with vein block (liver vein clot)

Blocked outflow congests the liver and causes pressure-driven cell death

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Drug-Induced Causes

💊 Paracetamol including staggered overdose ↗

Mechanism: Toxic metabolite depletes glutathione (protective molecule) causing cell necrosis (cell death)

→ Stop drug at once, give N-acetylcysteine promptly with urgent transplant referral

💊 Isoniazid ↗

Mechanism: Toxic intermediates from idiosyncratic metabolism (unpredictable breakdown) injure liver cells

→ Stop drug at once with close monitoring and transplant centre input

💊 Valproate ↗

Mechanism: Mitochondrial injury (energy factory damage) impairs fat handling with small-droplet failure

→ Stop drug with supportive ICU care and metabolic specialist input

💊 Amanita mushrooms with amatoxin (wild fungus poison) ↗

Mechanism: Toxin blocks protein making and kills liver and gut cells

→ Stop exposure, give supportive care with poison centre and transplant input

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Epidemiology

Prevalence:Acute liver failure is uncommon in general practice. It forms few admissions among liver disorders at referral centres. Paracetamol injury dominates in some regions while viral causes dominate elsewhere. Overall burden stays low beside chronic liver disease.

Age Group:All ages can be affected from infancy to old age. Young adults are often affected by paracetamol excess and acute viral infection. Pregnancy-related failure affects young women in late gestation (late pregnancy). Wilson disease typically presents in children and young adults.

Geographic Distribution:Acute liver failure occurs worldwide in all regions. Cause mix varies by setting and local context. Paracetamol injury clusters where access is easy. Viral and toxin patterns follow local spread and foraging habits.

Red Flags & Triage ★

TRIAGE LEVEL

🚨 EMERGENCY

DO NOT MISS — LIFE-THREATENING PRESENTATIONS

Paracetamol overdose needing antidote
Wilson crisis needing transplant workup
Budd-Chiari with outflow block
Fatty liver of pregnancy needing urgent delivery
Mushroom poisoning needing poison input

URGENT EVALUATION TRIGGERS

New confusion or coma with jaundice
Rising INR with bleeding
Low sugar or acid buildup with liver injury
Low pressure with multi-organ decline
Unequal pupils or coma suggesting brain shift

Contraindications & Precautions

CONTRAINDICATIONS

Do not use liver-injuring drugs including excess paracetamol in suspected failure
Do not use sedatives that mask brain change and slow breathing
Do not correct clotting with plasma alone without bleeding or procedure
Do not delay referral when transplant criteria may be met

SPECIAL PRECAUTIONS

Watch for brain swelling with frequent nerve checks
Monitor sugar with salts and acid balance closely
Use infection surveillance (regular germ checks) because fever may be absent
Handle bleeding risk with care during invasive procedures
Transfer early to a transplant centre before deep coma

Complications

DOWNSTREAM CLINICAL COMPLICATIONS

Cerebral oedema with brain shift and herniation (brain squeeze)
Coagulopathy with bleeding plus low pressure from vessel widening
Acute kidney injury with acid buildup and low sugar
Infection from weak defence with multi-organ failure
Death without timely support or transplant

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Confused With (LASA & DDx) ★

LEXICAL (LASA) — SIMILAR NAMES

Acute liver injury

Shares wording but means abnormal labs without brain change, while failure needs brain change with clotting loss

Chronic liver failure

Shares jaundice and fluid but occurs with known cirrhosis and prior episodes

Alcoholic hepatitis

Shares jaundice and poor clotting but usually follows chronic alcohol use without rapid brain failure

CLINICAL DIFFERENTIAL DIAGNOSES (DDx)

Severe acute hepatitis

Key Distinguishing Feature: Clear thinking despite high enzymes without brain change

Decompensated cirrhosis

Key Distinguishing Feature: Known chronic disease with prior fluid or vein bleeding

Ischaemic hepatitis with shock

Key Distinguishing Feature: Very high enzymes after low pressure with fast recovery after flow returns

Sepsis with coagulopathy

Key Distinguishing Feature: Dominant infection with shock and modest pigment rise plus clear source

Acute fatty liver of pregnancy

Key Distinguishing Feature: Late pregnancy with nausea, high uric acid (waste marker) and quick recovery after delivery

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Clinical Pearls

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Check paracetamol level in every case and start N-acetylcysteine (protective antidote) early when overdose is possible. Do not wait for levels when risk is high.

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Do not correct INR (clotting number) with plasma alone without bleeding or procedure. Correction hides prognosis and adds fluid load.

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Assess brain change often with simple orientation checks. Early worsening should trigger ICU escalation at once.

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Search for Wilson disease (copper overload) in young patients with red cell breakdown and low alkaline phosphatase (liver enzyme pattern). Speed transplant referral when suspected.

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Prevent infection with hand hygiene and line care plus low threshold cultures. Fever may be absent from weak defence.

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Example Usage & SOAP

CLINICAL SENTENCE

""24-year-old with jaundice and confusion has acute liver failure needing transplant review.""

IN A SOAP NOTE

S: 24-year-old with 2 days nausea, vomiting and confusion, no known liver disease. O: Temp 38.0C, BP 92/58, HR 118, RR 24, SpO2 94 percent on air, yellow skin, disoriented with flap, labs show high pigment with poor clotting. A: Acute liver failure with brain change and poor clotting. P: Resuscitate with fluids and support, give antidote, correct sugar and salts, urgent transfer to transplant ICU.

DIFFERENTIAL DIAGNOSIS CONTEXT

Jaundice with poor clotting plus confusion favours acute liver failure over hepatitis alone. Known scarring with fluid favours chronic decline. Clear thinking despite high enzymes favours acute hepatitis. Fever with shock and modest pigment favours sepsis. Late pregnancy with liver injury favours fatty liver of pregnancy. Check mental state with clotting and liver history.

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Classifications & Scoring

STAGING SCALE

O Grady time-based classification

Stages by jaundice to brain-change interval as hyperacute, acute and subacute. Guides cause thinking and transplant timing.

SCORING TOOL

King College Criteria

Prognostic rules using INR, bilirubin, time course and brain grade to list for transplant.

SCORING TOOL

Model for End-stage Liver Disease (MELD)

Score from bilirubin, INR, creatinine (kidney marker) and dialysis need to rank liver urgency.

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Prognosis

SHORT-TERM OUTCOME

Short term risk is high without urgent ICU care. Coma with bleeding and multi-organ shutdown can arrive in days. Early transplant improves survival for selected patients. Late referral with advanced brain swelling worsens outcome.

LONG-TERM PROGNOSIS

Long term outlook follows cause and transplant need. Paracetamol survivors often regain normal liver work without lasting harm. Other causes more often need transplant with lifelong anti-rejection drugs. Transplant recipients need lifelong follow-up for rejection and infection.

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References & Coding

ICD-10 DIAGNOSTIC CODE

K72.00

LITERATURE CITATIONS & GUIDELINES

[1]WHO ICD-10 K72.0 Acute and subacute hepatic failure

[2]AASLD Guidance on acute liver failure

[3]EASL Clinical Practice Guidelines on liver failure

[4]Harrison's Principles of Internal Medicine liver disorders

MEDICAL DISCLAIMER — This content is intended for educational purposes and qualified healthcare professionals only. Always refer to current clinical diagnostic criteria, institutional protocols, and official guidelines. Medobo is not responsible for clinical decisions made based on this content.