61 Acute Liver Failure Overview

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Questions and Answers

What is a defining characteristic of acute liver failure?

Presence of fatty liver changes

Encephalopathy with deranged coagulation (correct)

Normal liver function tests

Chronic viral hepatitis

Which of the following is a common cause of acute liver failure in the UK?

Paracetamol overdose (correct)

Hemorrhagic fever virus

Wilson disease

Hepatitis A

What condition is not typically associated with acute liver failure?

Herbal medicine toxicity

Chronic hepatitis B infection (correct)

Acute fatty liver of pregnancy

Vascular causes like Budd-Chiari syndrome

Which substance is noted to potentially induce severe fatty change in the liver?

Intravenous tetracycline Signup and view all the answers

Which of the following is a vascular cause of hepatic failure?

Portal vein thrombosis Signup and view all the answers

Which symptom is NOT commonly associated with acute liver failure?

Severe headache Signup and view all the answers

What is the main characteristic of hepatorenal syndrome?

Renal impairment secondary to liver disease Signup and view all the answers

Which stage of hepatic encephalopathy involves confusion?

Stage 1 Signup and view all the answers

What term is used to describe minimal hepatic encephalopathy that affects social function?

Covert HE Signup and view all the answers

What primarily causes cerebral edema in patients with hepatic encephalopathy?

Swelling of astrocytes due to increased glutamine Signup and view all the answers

Which of the following is NOT a precipitating factor for hepatic encephalopathy?

Diabetes mellitus Signup and view all the answers

In hepatic encephalopathy, what does portosystemic shunting allow?

More ammonia to enter systemic circulation Signup and view all the answers

Which classification type of hepatic encephalopathy corresponds to acute liver failure?

Type A Signup and view all the answers

What is the significance of a low threshold for paracentesis of ascitic fluid?

It allows for early diagnosis and treatment. Signup and view all the answers

Which enzyme is considered a sensitive and specific marker for hepatocellular damage?

Alanine transaminase (ALT) Signup and view all the answers

What does an AST/ALT ratio greater than 5 typically indicate?

Extrahepatic source of AST. Signup and view all the answers

Which liver enzyme is primarily associated with obstruction to bile flow?

Alkaline phosphatase (ALP) Signup and view all the answers

What does a notable increase in alkaline phosphatase (ALP) suggest about the liver?

There may be bile flow obstruction. Signup and view all the answers

What can a normal or mildly elevated ALT suggest about chronic liver disease?

Some hepatocyte damage is present. Signup and view all the answers

What role does Gamma-glutamyl transferase (GGT) play concerning alkaline phosphatase (ALP)?

It confirms the ALP elevation is from a liver origin. Signup and view all the answers

Which conditions may lead to an AST/ALT ratio of approximately 2?

Alcohol-related damage and certain liver diseases. Signup and view all the answers

What is the most common cause of portal hypertension?

Cirrhosis Signup and view all the answers

Which treatment is primarily used in the management of variceal bleeding?

Non-selective beta blockers Signup and view all the answers

What is one of the primary causes of ascites in liver disease?

Sodium retention by kidneys Signup and view all the answers

What characterizes spontaneous bacterial peritonitis?

Infection of ascitic fluid without intra-abdominal cause Signup and view all the answers

Which of the following is NOT a classification of portal hypertension?

Pre-cirrhotic Signup and view all the answers

What consequence can arise from increased portal hypertension?

Spontaneous bacterial peritonitis Signup and view all the answers

Which procedure is typically performed to manage therapeutic ascites?

Paracentesis Signup and view all the answers

Which of the following is a potential risk associated with renal impairment when using certain medications in liver disease?

Diuretics Signup and view all the answers

Which of the following best describes the characteristics of esophageal varices?

They can lead to high mortality and recurrence rates. Signup and view all the answers

What is the role of lactulose in the context of liver diseases?

It reduces ammonia absorption and production. Signup and view all the answers

What is the primary renal complication associated with acute liver failure?

Hepatorenal syndrome Signup and view all the answers

Which stage of hepatic encephalopathy is characterized by drowsiness?

Stage 2 Signup and view all the answers

What is the effect of cerebral edema in relation to hepatic encephalopathy?

Reduction in brain perfusion Signup and view all the answers

In which classification of hepatic encephalopathy does porto-systemic shunting occur with normal liver function?

Type B Signup and view all the answers

Patients with minimal hepatic encephalopathy may experience which of the following?

Deterioration in social function Signup and view all the answers

What is the consequence of increased glutamine in the brain during hepatic encephalopathy?

Cerebral edema Signup and view all the answers

Which of the following is a common precipitating factor for hepatic encephalopathy?

Infections Signup and view all the answers

What is the relationship of portal hypertension to hepatorenal syndrome?

It leads to renal impairment Signup and view all the answers

What is a significant histological finding in acute liver failure?

Necrosis of acini involving a substantial part of the liver Signup and view all the answers

Which of the following disorders is classified under vascular causes of hepatic failure?

Budd-Chiari syndrome Signup and view all the answers

What potential effect can occur as a result of paracetamol overdose?

Acute liver failure with encephalopathy Signup and view all the answers

Hepatic encephalopathy can potentially be precipitated by which of the following?

Renal failure Signup and view all the answers

In the context of acute liver failure, which feature distinguishes viral hemorrhagic fevers from other causes?

Rapid progression and multiorgan system involvement Signup and view all the answers

What laboratory value indicates the need for treatment in cases of spontaneous bacterial peritonitis?

Ascitic fluid cell count >250 polys/mm3 Signup and view all the answers

Which of the following statements about AST and ALT levels in chronic liver disease is true?

ALT levels can be normal despite the presence of severe liver damage. Signup and view all the answers

What does an AST/ALT ratio significantly greater than 5 typically suggest?

Extrahepatic source of AST Signup and view all the answers

What is one of the main effects of sodium retention by the kidneys in liver disease?

Development of ascites and edema Signup and view all the answers

In the context of cholestasis, what is the typical role of alkaline phosphatase (ALP)?

Elevated due to leakage from hepatocytes obstructed by bile flow. Signup and view all the answers

Which intervention is commonly used for both primary and secondary prevention of variceal bleeding?

Endoscopic band ligation Signup and view all the answers

Which enzyme is used to correlate with elevated alkaline phosphatase levels to assess liver origin?

Gamma-glutamyl transferase (GGT) Signup and view all the answers

Which is a consequence of increased hydrostatic pressure due to portal hypertension?

Ascites formation Signup and view all the answers

What does a low albumin level indicate in the context of liver function tests?

Chronic liver damage Signup and view all the answers

What is a significant complication associated with esophageal varices?

High rates of mortality after bleeding episodes Signup and view all the answers

What aspect of the AST and ALT relationship is typically observed in chronic alcoholic hepatitis?

AST/ALT ratio approaching 2 suggests alcoholic pathology. Signup and view all the answers

What characterizes spontaneous bacterial peritonitis in patients with cirrhosis?

Infection of ascitic fluid without evidence of a surgical cause Signup and view all the answers

What is a characteristic feature of gamma-glutamyl transferase (GGT) in liver enzyme tests?

It can be elevated due to alcohol and drugs. Signup and view all the answers

Which therapeutic approach is least favored in the treatment of variceal bleeding due to complications?

Endoscopic sclerotherapy Signup and view all the answers

In the classification of portal hypertension, what is a post-hepatic cause?

Obstruction of venous outflow from the liver Signup and view all the answers

What distinguishes a therapeutic paracentesis from a diagnostic tap of ascitic fluid?

Performed when ascites are resistant to treatment Signup and view all the answers

What role does rifaximin play in the management of liver disease?

Reduces ammonia production and absorption Signup and view all the answers

Study Notes

Acute Liver Failure

Acute liver failure is a rare but life-threatening syndrome characterized by acute liver injury, encephalopathy (brain dysfunction), and deranged coagulation (INR > 1.5) in a patient with a previously normal liver.
Caused by hepatitis due to various factors, such as viral infections, drug overdose, toxins, and other underlying conditions.
Histologically, there is necrosis of the liver acini, involving a large portion of the liver tissue.
Severe fatty change may occur in some cases, including pregnancy, Reye syndrome, or after intravenous tetracycline administration.

Causes of Acute Liver Failure

Viral infections: Hepatitis A, hepatitis B, cytomegalovirus, hemorrhagic fever viruses
Drugs: Paracetamol, antibiotics, antidepressants, salicylate (Reye syndrome), NSAIDs, herbal medicines
Toxins: Organic solvents, mushroom toxins
Pregnancy: Acute fatty liver of pregnancy, HELLP syndrome
Vascular causes: Budd-Chiari syndrome, portal vein thrombosis
Alpha-1 antitrypsin deficiency
Wilson disease
Malignancy and extensive metastases
Heatstroke

Clinical Features of Acute Liver Failure

Jaundice
Hepatic encephalopathy
Fever, vomiting, low blood pressure, and low blood glucose
Cerebral edema occurs in 80% of patients.
Impaired gluconeogenesis (glucose production by the liver)
Kidney injury: Hepatorenal syndrome and acute tubular necrosis.

Hepatorenal Syndrome

Renal impairment secondary to liver disease.
Haemodynamic changes due to portal hypertension reduce renal perfusion, often associated with ascites.
Diagnosis of exclusion: other kidney pathologies should be ruled out.
Poor prognosis

Hepatic Encephalopathy

A spectrum of neuro-psychiatric abnormalities seen in liver dysfunction and/or portosystemic shunting (abnormal blood flow bypassing the liver).
Functional disturbance of the brain, potentially reversible.
In severe cases, it can be associated with cerebral edema and cerebral hypoperfusion.

Classification of Hepatic Encephalopathy Types

Type A: Acute liver failure.
Type B: Porto-systemic shunting with a normal liver.
Type C: Cirrhosis (decompensated cirrhosis).
Episodic: May be recurrent, with or without persistent HE.

Stages of Hepatic Encephalopathy

Stage 1: Confusion
Stage 2: Drowsiness
Stage 3: Somnolence
Stage 4: Coma

Minimal HE

May be detected through psychometric testing.
Can affect social function, work life, behavior, and driving ability.
Minimal HE and Stage 1 HE are considered covert HE, while Stages 2 to 4 are considered overt HE.

Pathogenesis of Hepatic Encephalopathy

Reduced detoxification in the liver.
Portosystemic shunting allows more ammonia to enter the systemic circulation, bypassing the liver.
Detoxification of ammonia occurs primarily in skeletal muscle and kidney, converted to glutamate, rather than urea as in the liver.
Astrocytes in the brain also detoxify ammonia through glutamine synthetase.
Increased glutamine in the brain draws more water into astrocytes, leading to swelling and cerebral edema, causing increased intracranial pressure.

Management of Hepatic Encephalopathy

Identify and correct precipitating factors:
- Infections.
- Bleeding and other causes of hypoperfusion.
- Dehydration due to diuretics.
- Drugs (sedatives such as opiates, alcohol).
Reduce Ammonia Production and Absorption:
- Lactulose (oral or enema): Gut acidification
- Non-absorbable antibiotics (e.g. rifaximin): To reduce urease-producing bacteria
- Fluids: Dehydration reduces toxin clearance.
- Stop diuretic therapy.

Portal Hypertension

Classified by the level or site of origin of the portal hypertension.
Cirrhosis is the most common cause.
Pathogenesis in cirrhosis:
- Initiated by increased resistance to portal blood flow.
- Augmented by increased portal blood flow.

Classification of Portal Hypertension Causes

Pre-hepatic: Portal vein thrombosis
Hepatic:
- Cirrhosis: Most common cause.
- Non-cirrhotic: Portal tract fibrosis due to schistosomiasis.
Post-hepatic: Obstruction of venous outflow from the liver (rare).

Consequences of Portal Hypertension

Porto-systemic collaterals:
- Extrahepatic portal vein and systemic venous circulations anastomose (connect).
- Varices: Esophageal and gastric varices (high risk of bleeding).
- Rectal: Dilated veins in the rectum
- Periumbilical: Dilated abdominal wall veins ("caput medusae")
Shunting of portal venous blood: Reduced liver function.
Haemodynamic alterations:
- Ascites and hepatorenal syndrome.
Splenomegaly (congestive): Secondary hypersplenism (overactive spleen destroying blood cells).

Esophageal and Gastric Varices

About 30% of patients with esophageal varices will experience bleeding.
High mortality rate due to bleeding and high recurrence rate.
Heavy alcohol users are at higher risk.

Management of Esophageal and Gastric Varices

Primary prevention:
- Screening to identify and treat moderate to severe varices before the first bleed.
- Endoscopic band ligation and/or non-selective beta-blockers.
Secondary prevention:
- Treatment to prevent recurrent bleeding.
- Endoscopic band ligation and/or non-selective beta-blockers.
Variceal bleed:
- Resuscitation, medications to reduce portal blood flow.
- Prevention and treatment of complications (aspiration pneumonia, infections, HE).
- Endoscopic treatment of varices by band ligation.
- Endoscopic sclerotherapy is not favored due to complications.
- If the above fail: Placement of TIPS (Transjugular intrahepatic portosystemic shunt) or surgery.

Ascites in Liver Disease

Causes:
- Sodium retention by the kidneys: Increases the volume of extracellular fluid.
- Increased hydrostatic pressure due to portal hypertension.
- Lower oncotic pressure (fluid retention) due to low albumin.
Clinical Presentation:
- Abdominal distension.
- Shifting or flank dullness on percussion (sound of organs being tapped, dullness shifts when the patient changes positions).

Causes of Ascites

Cirrhosis: Most common cause, more than 80%.
Malignancy: Ovarian cancer is classic, but GI cancers can also cause it.
Rare Causes:
- Non-cirrhotic portal hypertension.
- Heart failure, pancreatitis, tuberculosis.

Management of Ascites

Paracentesis: Tap of ascites fluid:
- Diagnostic tap: Cell count, microbiology (blood culture bottles), albumin, cytology.
- Therapeutic tap: For diuretic-resistant ascites in cirrhosis.
General Management:
- Sodium restriction.
- Diuretics (spironolactone).
- Avoid NSAIDs (risk of acute renal failure and hyponatremia, reduces the effect of diuretics).
- High index of suspicion for infection (low threshold for paracentesis).
- Diuretic-resistant: Refractory ascites.

Spontaneous Bacterial Peritonitis (SBP)

Infection of ascites fluid without a surgically treatable intra-abdominal cause.
Associated with cirrhosis, commonly caused by E. coli and Klebsiella.
Early diagnosis and prompt treatment improve outcomes.
Subtle or silent presentation.
Clinical Suspicion:
- Fever, abdominal pain/tenderness, altered mental state.
Treatment:
- Treat if ascites fluid cell count >250 polys/mm3.
Antibiotic prophylaxis: Recommended for high-risk patients (e.g., previous SBP or bleed).

Liver Blood Tests

Related to liver cell (hepatocellular) damage:
- Transaminases (ALT, AST).
Related to obstruction to bile flow (cholestasis):
- Alkaline phosphatase (ALP), Gamma-glutamyl transferase (GGT).
- Bilirubin.
Related to liver function:
- Bilirubin: Abnormality is not liver or biliary tract specific.
- Albumin: Long half-life, indicates chronic damage.
- Coagulation function (PT/INR): Clotting factors have short half-lives, a better indicator of acute damage.

### Hepatocellular Damage: Liver Enzymes

Alanine transaminase (ALT):
- Sensitive and specific marker for hepatocellular damage.
Aspartate transaminase (AST):
- Less specific, found in muscle, myocardium, and kidney.
- Both enzymes leak from damaged hepatocytes.
AST/ALT Ratio:
- Usually approximately 2:1 in healthy individuals.
- Can be informative in diagnosing different causes of liver damage.
- 5 indicates an extrahepatic source of AST.

Obstructive (Cholestatic) Liver Enzymes

Alkaline phosphatase (ALP):
- Located on the hepatocyte border of bile canaliculi.
- Elevated levels indicate obstruction to bile flow.
- Also found in bone and placenta.
Gamma-glutamyl transferase (GGT):
- Very sensitive but not specific.
- Helps identify liver-specific elevation of ALP.
- Induced by alcohol and drugs.

Acute Liver Failure

Acute liver failure is a rare but life-threatening syndrome characterized by acute liver injury, encephalopathy, and deranged coagulation (INR > 1.5) in a patient with a previously normal liver.
Most common causes of acute liver failure: viral hepatitis and paracetamol overdose.
The causes vary across the world, for example, paracetamol overdose is common in the UK.
Histologically, acute liver failure is characterized by necrosis of acini involving a substantial part of the liver.
Severe fatty change can be observed in some cases, such as in pregnancy, Reye syndrome, or after intravenous tetracycline.

Causes of Acute Hepatic Failure

Viral causes: hepatitis A, hepatitis B, cytomegalovirus, hemorrhagic fever virus
Drugs: paracetamol, antibiotics, antidepressants, salicylate (Reye syndrome), NSAIDs, herbal medicines
Toxins: organic solvents, mushroom toxin
Hepatic failure in pregnancy: acute fatty liver of pregnancy, HELLP syndrome
Vascular causes: Budd-Chiari syndrome, portal vein thrombosis
Alpha-1 antitrypsin deficiency
Wilson disease
Malignancy: extensive metastases
Heatstroke

Clinical Features of Acute Liver Failure

Jaundice
Hepatic encephalopathy
Fever, vomiting, low blood pressure, low blood glucose
Cerebral edema in 80% of patients
Impaired gluconeogenesis
Kidney injury: hepatorenal syndrome
Acute tubular necrosis

Hepatorenal Syndrome

Renal impairment secondary to liver disease
This happens due to haemodynamic effects of portal hypertension, which reduce renal perfusion.
It is typically associated with ascites and is a diagnosis of exclusion, meaning other kidney pathologies need to be ruled out.
Poor prognosis.

Hepatic Encephalopathy

Spectrum of neuro-psychiatric abnormalities seen in liver dysfunction and/or porto-systemic shunting
Represents a functional disturbance of the brain, potentially reversible
Severe cases can be associated with cerebral edema and cerebral hypoperfusion
Classification:
- Type A: acute liver failure
- Type B: porto-systemic shunting with normal liver
- Type C: cirrhosis (= decompensation)
- Episodic (may be recurrent) HE +/- persistent HE

Stages of Hepatic Encephalopathy

Stage 1: confusion
Stage 2: drowsiness
Stage 3: somnolence
Stage 4: coma

Psychometric Testing for Covert HE

Minimal HE can be detected using psychometric testing.
Minimal HE can affect social function, work life, behaviour, and fitness to drive.
Minimal HE + Stage 1 HE = covert HE.
Stages 2 to 4 HE = overt HE.

Hepatic Encephalopathy: Pathogenesis

Reduced detoxification in the liver
Portosystemic shunting allows more ammonia to enter the systemic circulation, bypassing the liver
Detoxification of ammonia occurs in skeletal muscle and kidney, converted to glutamate (NOT urea as in the liver).
Astrocytes in the brain also detoxify ammonia via glutamine synthetase.
This increases glutamine in the brain, which draws more water into the astrocytes. This leads to swelling of astrocytes, cerebral edema, and intracranial hypertension.

Hepatic Encephalopathy: Treatment

Identify and correct precipitating factors:
- Infection
- Bleeding, other causes of hypoperfusion
- Dehydration (diuretics)
- Drugs (sedatives, e.g. opiates, alcohol).
Reduce ammonia production and absorption:
- Lactulose (oral or enema): gut acidification
- Non-absorbable antibiotic (e.g. rifaximin): reduce urease-producing bacteria
- Fluids (dehydration decreases toxin clearance)
- Stop diuretic therapy

Portal Hypertension

Classified by level/site of origin of portal hypertension.
The most common cause is cirrhosis.
Pathogenesis in cirrhosis:
- Initiated: increased resistance to portal blood flow.
- Augmented: increased portal blood flow.
Classification of causes of portal hypertension:
- Pre-hepatic: portal vein thrombosis
- Hepatic:
  - Cirrhosis
  - Non-cirrhotic (e.g., portal tract fibrosis due to schistosomiasis)
- Post-hepatic: obstruction of venous outflow from the liver (rare)

Consequences of Portal Hypertension

Porto-systemic collaterals:
- Extrahepatic anastomoses:
  - Varices (esophageal and gastric, risk of bleed)
  - Rectal, periumbilical (caput medusae)
Shunting of portal venous blood (reduced liver function).
Haemodynamic alterations:
- Ascites and hepatorenal syndrome.
Splenomegaly (congestive)
- Secondary hypersplenism.

Oesophageal and Gastric Varices

30% of patients with oesophageal varices will experience a bleed.
High mortality rates due to bleeding.
High rate of recurrence.
Heavy alcohol users are at higher risk.
Important to remember: not all upper GI bleeds are varices.

Oesophageal and Gastric Varices: Prevention and Management

Primary prevention: screen to identify and treat moderate to severe varices before the first bleed.
- Endoscopic band ligation and/or non-selective beta blockers.
Secondary prevention: treat to prevent recurrent bleeding.
- Endoscopic band ligation and/or non-selective beta blockers.
Variceal bleed:
- Resuscitate, drugs to reduce portal blood flow.
- Prevent/treat complications: aspiration, infection, HE.
- Endoscopic treatment of varices by band ligation.
- Endoscopic sclerotherapy is not favoured due to complications.
- If the above measures fail: placement of TIPS or surgery.

Ascites in Liver Disease

Sodium retention by the kidneys increases the volume of extracellular fluid, leading to ascites and edema.
Increased hydrostatic pressure due to portal hypertension.
Lower oncotic pressure due to low albumin.
Clinical features:
- Abdominal distension.
- Shifting dullness on percussion.

Ascites

Cirrhosis: most common cause (>80%)
Other causes:
- Malignancy (ovarian cancer classic, but also GI cancers)
- Rare: non-cirrhotic portal hypertension
- Rare: heart failure, pancreatitis, TB

Ascites: Management

Paracentesis: tap ascites fluid.
- Diagnostic tap: do cell count, microbiology, albumin, cytology.
- Therapeutic tap: diuretic-resistant ascites in cirrhosis.
Sodium restriction and diuretics (spironolactone).
Avoid NSAIDs: risk of acute renal failure and hyponatremia, lowers the effect of diuretics.
High index of suspicion for infection: low threshold for paracentesis.
Diuretic-resistant = refractory ascites.

Spontaneous Bacterial Peritonitis

Infection of ascites fluid without evidence of a surgically treatable intra-abdominal cause.
Infection associated with cirrhosis (E.coli, Klebsiella).
Early diagnosis and prompt treatment improve outcomes.
Subtle/silent presentation.
Low threshold for paracentesis of ascites fluid.
Suspect: fever, abdominal pain/tenderness, altered mental state.
Treat if ascites fluid cell count >250 polys/mm3.
Antibiotic prophylaxis for high-risk patients (e.g., previous SBP or bleed).

Liver Blood Tests

Related to liver cell (hepatocellular) damage:
- Transaminases (ALT, AST)
Related to obstruction to bile flow (cholestasis):
- Alkaline phosphatase (ALP), Gamma-glutamyl transferase (GGT)
- Bilirubin
Related to liver function:
- Bilirubin (abnormality is not liver or biliary tract specific).
- Albumin (long half-life, indicator of chronic damage).
- Coagulation function (PT/INR) (clotting factors have short half-life - better indicator of acute damage).

Hepatocellular Damage: Liver Enzymes

Alanine transaminase (ALT): sensitive and specific marker for hepatocellular damage.
Aspartate transaminase (AST): less specific, also found in muscle, myocardium, kidney.
Both ALT and AST leak from damaged hepatocytes.
The level of rise in these enzymes is poorly correlated with severity or prognosis.
Very high levels in acute hepatocellular damage.
May be only mildly elevated or normal despite chronic liver disease.

AST/ALT Ratio

The ratio of AST to ALT produced by hepatocytes is approximately 2.5:1. AST is removed from serum by the liver sinusoidal cells twice as quickly, so resulting serum levels are basically equal in healthy individuals.
However, in conditions with chronic, constant hepatocyte damage (e.g., alcoholic hepatitis, hepatocellular carcinoma), the ratio is closer to 1.
During early-stage acute liver damage (e.g. viral hepatitis), the serum levels of AST and ALT reflect levels closer to background in hepatocytes.
An AST/ALT ratio >5 indicates an extrahepatic source of AST.

Obstructive (Cholestatic) Liver Enzymes

Alkaline phosphatase (ALP):
- Situated on the hepatocyte border of bile canaliculi.
- Hepatocytes react to obstruction of bile flow by leaking ALP.
- Other sources: bone, placenta.
Gamma-glutamyl transferase (GGT):
- Very sensitive but not specific.
- Good for correlating with elevated alkaline phosphatase to demonstrate that ALP is of liver origin.
- Also induced by alcohol and drugs.

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Explore the critical aspects of acute liver failure, a life-threatening condition characterized by severe liver injury and brain dysfunction. This quiz covers its causes, including viral infections, drug overdose, and toxins, as well as major histological changes. Test your knowledge on this important medical syndrome and its implications.