Acute fulminant hepatic failure for the undergraduate

1. Acute (Fulminant)
Liver Failure
PROF. DR. MOHAMED-NAGUIB WIFI
PROFESSOR OF MEDICINE AND
HAPATOGASTROENTEROLOGY
CAIRO UNIVERSITY

2. Definition
• Hepatic failure with
• Encephalopathy/
Coagulopathy/ ± other system
affection
• Developing in less than 8
weeks after the onset of
jaundice (+↑↑↑ transaminases)
• In a patient without pre-
existing liver disease.
Acute
Fulminant

3. What If?
• Less than 1 week
•  Hyper-acute
• More than 8 weeks
•  Sub-acute
• Less Severe
•  Sub-fulminant
• Pre-existing Liver Disease
•  Acute on top of Chronic (AoCL)

5. INH
Valproate
Autoimmune
Reye Syndrome
Sepsis

7. • Acute Fatty Liver of Pregnancy
• A rare and serious condition.
• Abnormal fatty acid metabolites produced by the fetus enter the circulation and overcome maternal
hepatic mitochondrial oxidation system.
• Presents in the last trimester with fulminant hepatitis.
• Immediate delivery may save both baby and mother.
• Reye Syndrome
• It presents by acute encephalopathy in children
• Inhibition of β-oxidation and uncoupling of oxidation phosphorylation in hepatic mitochondria
leading to diffuse microvesicular fatty infiltration.
• Aspirin ingestion and viral infections have been implicated as precipitating agents.
• Mortality is about 50% due to cerebral edema.
What Is?

8. Pathophysiology
•Poorly understood.
•Direct Cytotoxic Effect &/or Hyperimmune Response
 Massive Hepatocyte destruction
•Factors contributing:
• Impaired hepatocyte regeneration
• Altered parenchymal perfusion
• Endotoxemia
• Decreased hepatic reticuloendothelial function

10. Investigations
1- Liver Function Tests:
• Bilirubin: ↑↑↑ (assess prognosis)
• ALT/AST: ↑↑↑ initially  later ↓ due to extensive cell loss
• PT/ PC: ↑↑↑
• Albumin: initially NORMAL  later on start to ↑↑↑ (after 3 Wks if pt. survive)
2- Other Labs: KFTs / CBC / Electrolytes / Glucose, …etc
3- Liver Imaging: Normal
4- EEG: EEG changes (WHY??)
5- Investigations of the Cause: viral markers, toxicology screen, ...etc

11. Adverse Prognosis
• Age over 40years or less than 10years
• Complications: coagulopathy and encephalopathy
• Cause: HAV is better than HBV, paracetamol
overdose is better than other DILI. Worst prognosis
 liver failure of unidentified etiology.
• Onset: The long duration (>7days) (J to En).

12. Prognosis
Several prognostic scores had been used to predict mortality and assess
the prognosis especially in the era of liver transplantation.

14. Treatment of fulminant hepatic failure
which is an emergency situation is mainly
supportive in hope of spontaneous
regeneration of the hepatocytes (ideally in
liver transplant center)
Treatment

15. 1. Hospitalization
2. Treatment of the cause:
If possible to avoid further progression of the condition.
3. Treatment of precipitating factors:
Infections, hypokalemia.
4. Treatment of hepatic encephalopathy.
Treatment

16. 5. Correction of complications:
Cerebral edema, hypoglycemia, infection, renal,
respiratory or circulatory failure.
6. Liver transplantation:
The one-year survival after transplantation is 60%.
Survival without transplantation is below 10%.
Treatment