What is the role of steroids in acute liver failure?

Role of Steroids in Acute Liver Failure

Corticosteroids should NOT be used to control elevated intracranial pressure in patients with acute liver failure, but they may be considered in specific scenarios such as refractory shock requiring high-dose vasopressors or autoimmune hepatitis-related acute liver failure. 1

General Approach to Steroids in Acute Liver Failure

Acute liver failure (ALF) is a life-threatening condition requiring prompt management. The role of steroids varies significantly depending on the underlying etiology:

When Steroids Are NOT Recommended:

1. Management of Intracranial Hypertension

   • The AASLD Practice Guidance explicitly states that corticosteroids should not be used to control elevated intracranial pressure in patients with acute liver failure 1
   • This recommendation is based on level I evidence (highest quality)

2. Non-autoimmune, Non-shock Related ALF

   • No evidence supports routine use of steroids in viral, drug-induced, or other forms of ALF

When Steroids ARE Recommended:

1. Refractory Shock in Critically Ill Patients with Cirrhosis

   • Consider hydrocortisone 50 mg IV every 6 hours or 200-mg infusion for 7 days or until ICU discharge 1
   • Indicated for treatment of refractory shock requiring high-dose vasopressors
   • Based on the ADRENAL and APROCCHSS trials showing earlier shock reversal and potential mortality benefit

2. Autoimmune Hepatitis (AIH) Presenting as ALF

   • Standard first-line treatment is prednisolone (0.5-1 mg/kg/day) alone or in combination with azathioprine 2
   • Early treatment is crucial - most effective when initiated within 2 weeks of symptom onset 3

Specific Scenarios and Recommendations

Alcoholic Hepatitis

• Corticosteroids significantly reduce mortality in patients with a Discriminant Function ≥32 or hepatic encephalopathy 1
• Early identification of non-responders is important (Lille score >0.45 after 7 days predicts poor response)
• Consider stopping steroids in null responders (Lille score >0.56) 1
• Caution: Heightened risks of sepsis and gastrointestinal hemorrhage

Autoimmune Hepatitis with Acute Presentation

• Prednisolone 0.5-1 mg/kg/day is recommended even in severe presentations 1, 2
• For severe acute AIH presentations with INR ≥1.5:
  • Consider high-dose IV corticosteroids (≥1 mg/kg) at earliest opportunity 1
  • Prophylactic antibiotics may be justified due to infection risk
  • If no improvement in serum bilirubin, MELD-Na or UKELD within seven days, consider liver transplantation 1

Relative Adrenal Insufficiency in Cirrhosis

• Present in up to 49% of patients with acute decompensation of cirrhosis 1
• Associated with significantly higher 90-day mortality (26% vs. 10%)
• Consider screening for adrenal insufficiency or empiric trial of hydrocortisone in refractory shock 1

Prognostic Factors for Steroid Response

Patients most likely to benefit from steroids in acute liver injury include:

• Those with ALT levels ≥30× the upper limit of normal 3
• Coma grade <4 and MELD scores <35 3
• Illness duration ≤2 weeks 3
• Autoimmune etiology with no evidence of cirrhosis 2

Cautions and Monitoring

• Risk of Infection: Monitor closely for bacterial and fungal infections
• Contraindications: Exercise caution in patients with:
  • Active infections (relative contraindication)
  • Gastrointestinal bleeding
  • Hepatorenal syndrome
• Monitoring: Regular assessment of:
  • Liver function tests
  • Signs of infection
  • Blood glucose
  • Electrolytes

Key Pitfalls to Avoid

1. Inappropriate Use: Using steroids for intracranial hypertension in ALF is contraindicated
2. Delayed Recognition of Non-response: Failure to identify non-responders within 7 days
3. Infection Risk: Failure to monitor for or prophylactically treat infections
4. Rare Paradoxical Reaction: In rare cases, corticosteroids themselves can cause drug-induced liver injury 4

Remember that while steroids may be beneficial in specific scenarios of acute liver failure, they are not universally recommended and their use should be guided by the underlying etiology and clinical presentation.