When to Initiate Corticosteroids in Sepsis
Consider initiating low-dose corticosteroids (hydrocortisone 200 mg/day) in patients with septic shock who require vasopressors despite adequate fluid resuscitation, particularly those with high SOFA scores and evidence of multiorgan dysfunction. 1
Primary Indication: Septic Shock with Vasopressor Dependence
The key trigger for corticosteroid initiation is septic shock requiring vasopressors to maintain adequate perfusion pressure despite fluid resuscitation. 2, 1 This represents the population with the strongest evidence for potential mortality benefit, though the recommendation remains weak due to modest effect size (approximately 2% absolute mortality reduction). 2
Specific Clinical Criteria:
- Infection with SOFA score ≥2 (defining sepsis) 2
- Vasopressor requirement to maintain mean arterial pressure despite adequate fluid repletion 2, 1
- Elevated serum lactate despite fluid resuscitation 2
Patient Selection: Who Benefits Most
Patients at highest risk of death derive the greatest absolute mortality benefit from corticosteroids. 2 This includes:
- Escalating vasopressor requirements (not just stable low-dose pressors) 1, 3
- High SOFA scores indicating severe multiorgan dysfunction 2, 1
- Refractory shock despite standard resuscitation 2, 1
- Primary lung infections as the sepsis source 3
When NOT to Initiate Corticosteroids
Do not routinely use corticosteroids in sepsis without shock, as there is no evidence of benefit and potential for harm. 1 Patients with infection and organ dysfunction (SOFA ≥2) who maintain adequate blood pressure without vasopressors should not receive corticosteroids for sepsis treatment.
Practical Implementation
Dosing Strategy:
Use hydrocortisone 200-300 mg/day for 5-7 days (long course, low-dose strategy). 1, 4, 5 This regimen showed mortality benefit, whereas short-term high-dose therapy (up to 42g for 1-2 days) was ineffective or harmful. 4
Timing:
Initiate corticosteroids immediately after recognizing vasopressor-dependent septic shock. 5 Do not delay for corticotropin testing, as the benefit appears consistent regardless of adrenal insufficiency status. 2
Route of Administration:
Administer intravenously during the acute phase. 5 There is no clear advantage to continuous infusion over intermittent boluses for reducing hyperglycemia. 3
Evidence Quality and Clinical Nuance
The recommendation is weak because the mortality benefit is modest (2% absolute reduction), the confidence interval crosses the line of no difference, and trial results show inconsistency. 2 Both using and not using corticosteroids are reasonable management options. 2
The decision should incorporate patient values: 2, 1
- Patients prioritizing mortality reduction over quality of life concerns would likely choose corticosteroids
- Patients prioritizing functional independence and quality of life may reasonably decline, given the risk of neuromuscular weakness
Expected Benefits Beyond Mortality
Corticosteroids consistently accelerate shock reversal (increased proportion by day 7: RR 1.31) 6 and may reduce:
- ICU length of stay by approximately 2 days 2, 6
- Hospital length of stay 6
- SOFA score by day 7 (mean difference -1.53) 6
- Duration of mechanical ventilation 3
Important Adverse Effects to Monitor
Corticosteroids increase the risk of: 2, 6
- Hyperglycemia (RR 1.26) - monitor glucose closely and treat aggressively
- Hypernatremia (RR 1.64) - monitor electrolytes
- Potential neuromuscular weakness - though evidence is low quality and may be underestimated 2
Corticosteroids do NOT increase: 6
- Gastrointestinal bleeding (RR 1.24, not significant)
- Superinfection rates (RR 1.02)
Common Pitfalls to Avoid
- Do not use high-dose, short-course regimens (these are ineffective or harmful) 4
- Do not delay initiation waiting for corticotropin stimulation test results 5
- Do not routinely taper - there is no advantage to tapering for preventing rebound hypotension 3
- Do not withhold in patients without documented adrenal insufficiency - the benefit appears independent of baseline cortisol response 2