The Confusing World of Corticosteroids: A Practical Prescriber's Guide

Dr Neeraj Manikath , claude.ai

Abstract

Corticosteroids remain among the most prescribed medications in critical care and general medicine, yet their use is fraught with complexity and potential complications. This comprehensive review addresses practical challenges in corticosteroid prescribing, including dose equivalencies, withdrawal risks, tapering strategies, chronic side effect management, and stress dosing protocols. Written for postgraduate trainees in critical care and internal medicine, this guide synthesizes evidence-based recommendations with clinical pearls to optimize patient outcomes while minimizing adverse effects.

Keywords: Corticosteroids, adrenal insufficiency, HPA axis suppression, stress dosing, steroid tapering, critical care

Introduction

Corticosteroids are indispensable therapeutic agents with profound anti-inflammatory and immunosuppressive properties. Despite their ubiquity in clinical practice, prescribing corticosteroids appropriately requires nuanced understanding of pharmacokinetics, equivalency dosing, hypothalamic-pituitary-adrenal (HPA) axis physiology, and potential complications. Errors in dosing conversions, abrupt discontinuation, inadequate stress dosing, or failure to mitigate chronic side effects can lead to significant morbidity and mortality.

This review provides a practical framework for safe and effective corticosteroid prescribing in hospitalized and ambulatory patients, with emphasis on high-risk scenarios encountered in critical care settings.

1. Equivalent Dosing: Converting Between Prednisone, Methylprednisolone, and Dexamethasone

The Foundation: Understanding Potency and Duration

Corticosteroids differ significantly in glucocorticoid potency, mineralocorticoid activity, and biological half-life. These pharmacological distinctions are crucial for appropriate dosing conversions.

Table 1: Comparative Corticosteroid Properties

Agent	Equivalent Dose (mg)	Glucocorticoid Potency	Mineralocorticoid Potency	Biological Half-Life	Duration of Action
Hydrocortisone	20	1	1	8-12 hours	Short (8-12h)
Prednisone/Prednisolone	5	4	0.8	12-36 hours	Intermediate (12-36h)
Methylprednisolone	4	5	0.5	12-36 hours	Intermediate (12-36h)
Dexamethasone	0.75	25-30	0	36-72 hours	Long (36-72h)
Fludrocortisone	N/A (mineralocorticoid)	10	125	18-36 hours	N/A

Practical Conversion Formulas

Key Clinical Conversions:

Prednisone to Methylprednisolone: Multiply by 0.8
- 40 mg prednisone = 32 mg methylprednisolone
Prednisone to Dexamethasone: Divide by 6.67 (approximately 7)
- 40 mg prednisone ≈ 6 mg dexamethasone
Methylprednisolone to Dexamethasone: Divide by 5.33 (approximately 5)
- 40 mg methylprednisolone ≈ 7.5 mg dexamethasone
Hydrocortisone to Prednisone: Divide by 4
- 100 mg hydrocortisone = 25 mg prednisone

Clinical Pearls 💎

Pearl 1: The Dexamethasone Dilemma Dexamethasone's prolonged HPA axis suppression (36-54 hours) makes it unsuitable for every-other-day regimens and complicates transition to physiologic replacement. Use short-acting agents (hydrocortisone) or intermediate-acting agents (prednisone) when tapering is anticipated.

Pearl 2: Mineralocorticoid Considerations When converting from hydrocortisone (significant mineralocorticoid activity) to prednisone or dexamethasone (minimal mineralocorticoid activity), consider adding fludrocortisone 0.05-0.1 mg daily for patients with adrenal insufficiency to prevent salt-wasting and hypotension.

Pearl 3: The Methylprednisolone IV Advantage Methylprednisolone has superior bioavailability when given intravenously (88% vs. 82% for hydrocortisone) and causes less mineralocorticoid-mediated sodium retention—ideal for pulse-dose therapy in conditions like severe COPD exacerbations or acute spinal cord injury.

Oyster Alert 🦪

Oyster 1: Prednisone vs. Prednisolone Prednisone requires hepatic conversion to active prednisolone. In severe hepatic dysfunction, prednisolone should be prescribed directly, or alternative agents used. This distinction is often overlooked in cirrhotic patients.

Oyster 2: The Bioavailability Trap Oral bioavailability varies: prednisone (80%), methylprednisolone (90%), dexamethasone (80%). When converting from IV to PO, some clinicians erroneously increase doses. The conversions in Table 1 already account for bioavailability differences for standard preparations.

Clinical Hack 🔧

Quick Mental Math for Dexamethasone: Divide prednisone dose by 7 for rapid approximation. For example, 60 mg prednisone ≈ 8-9 mg dexamethasone. This "divide by 7" rule works reasonably well in most clinical scenarios and is easier to remember than 6.67.

2. The Perils of Sudden Withdrawal: HPA Axis Suppression and Adrenal Insufficiency

Understanding HPA Axis Physiology

The HPA axis represents a delicate neuroendocrine feedback system. Exogenous glucocorticoids suppress corticotropin-releasing hormone (CRH) and adrenocorticotropic hormone (ACTH) secretion, leading to adrenal atrophy. Recovery of the HPA axis after cessation of exogenous steroids can take 6-12 months or longer.

Risk Factors for HPA Axis Suppression

High-Risk Scenarios:

Duration: >3 weeks of supraphysiologic doses (>5 mg/day prednisone equivalent)
Dose: Any dose >20 mg/day prednisone for >2 weeks
Timing: Evening dosing (disrupts circadian cortisol rhythm more than morning dosing)
Potency: Long-acting agents (dexamethasone) suppress HPA axis more profoundly
Route: Topical, inhaled, or intra-articular steroids can cause HPA suppression with prolonged use

Clinical Manifestations of Acute Adrenal Insufficiency

Acute adrenal crisis is a life-threatening emergency with mortality up to 6% even with treatment:

Classic Presentation:

Hypotension refractory to fluids and vasopressors
Fever, altered mental status
Nausea, vomiting, abdominal pain
Hyponatremia, hyperkalemia (in primary adrenal insufficiency)
Hypoglycemia
Eosinophilia

Atypical Presentations in the ICU:

Unexplained hypotension after routine procedures
Prolonged vasopressor dependence in septic shock
"Failure to wean" from mechanical ventilation
Hypoglycemia in non-diabetic patients

Diagnosis and Management

Diagnostic Approach:

Random cortisol level: <3 μg/dL strongly suggests adrenal insufficiency; >15 μg/dL makes it unlikely
ACTH stimulation test: Can be performed but should NOT delay treatment
Threshold for empiric treatment should be LOW in suspected cases

Acute Management Protocol:

Hydrocortisone 100 mg IV bolus immediately (do NOT wait for test results)
Aggressive fluid resuscitation: 1-2L normal saline bolus
Continued hydrocortisone: 50-100 mg IV every 6-8 hours or 200 mg/24h continuous infusion
Identify and treat precipitating factors: Infection, trauma, surgery, rapid steroid taper
Transition to oral therapy: Once stable, switch to oral hydrocortisone 15-25 mg/day in divided doses

Clinical Pearls 💎

Pearl 4: The "Cushingoid" Patient Can Still Have Adrenal Insufficiency Physical signs of Cushing's syndrome (moon facies, striae, buffalo hump) indicate chronic steroid exposure but do NOT exclude HPA axis suppression. These patients are at HIGH risk for adrenal crisis if steroids are abruptly discontinued.

Pearl 5: Infection as a Trigger In patients on chronic steroids, any acute illness (infection, trauma, surgery) can precipitate adrenal crisis. Maintain high index of suspicion in chronic steroid users with unexplained shock.

Pearl 6: The Dexamethasone Diagnostic Window If adrenal insufficiency is suspected but diagnosis uncertain, give dexamethasone 4 mg IV (does NOT interfere with cortisol assay) while performing ACTH stimulation test. This provides glucocorticoid coverage without compromising diagnostic accuracy.

Oyster Alert 🦪

Oyster 3: Secondary vs. Primary Adrenal Insufficiency Steroid-induced HPA suppression causes SECONDARY adrenal insufficiency (low ACTH). Unlike primary adrenal insufficiency (Addison's disease), mineralocorticoid function is preserved via the renin-angiotensin system. Therefore, hyperkalemia is UNCOMMON. Hyponatremia may still occur via vasopressin-mediated mechanisms.

Oyster 4: Inhaled Steroids Are Not Innocent High-dose inhaled corticosteroids (>1000 μg/day fluticasone equivalent) can suppress the HPA axis, especially in children and when combined with oral steroids. Consider HPA suppression even in patients not on oral steroids.

Clinical Hack 🔧

The "Steroid Passport" System: Implement a standardized alert in the electronic medical record for all patients receiving >20 mg prednisone equivalent for >2 weeks. Include automatic alerts for stress-dosing protocols during hospitalizations, procedures, or illness. Consider providing patients with a "steroid card" documenting their regimen.

3. Tapering Strategies: When and How to Taper Safely

When to Taper vs. Abrupt Discontinuation

Safe for Abrupt Discontinuation:

<3 weeks of therapy at any dose
Any duration of physiologic replacement dosing (≤5 mg prednisone daily)
Alternate-day short-acting regimens of <10 days

Requires Tapering:

3 weeks of supraphysiologic dosing
Any duration if Cushingoid features present
Uncertain duration or patient non-adherent to previous courses

Evidence-Based Tapering Approaches

Multiple tapering strategies exist, but no single approach has been proven superior. The key principles are: gradual dose reduction, monitoring for adrenal insufficiency, and individualization.

Standard Tapering Protocol:

Initial Phase (Rapid Taper): If >40 mg/day prednisone, reduce by 5-10 mg weekly until reaching 20 mg/day
Intermediate Phase (Moderate Taper): From 20 mg to 10 mg, reduce by 2.5-5 mg weekly
Final Phase (Slow Taper): Below 10 mg/day (approaching physiologic doses):
- Reduce by 1 mg every 2-4 weeks OR
- Reduce by 2.5 mg every 2-4 weeks until 5 mg daily
Physiologic Replacement Phase: At 5 mg/day, some clinicians:
- Continue 5 mg daily for 4-8 weeks to allow HPA axis recovery, then discontinue OR
- Taper to 2.5 mg for 2-4 weeks, then discontinue OR
- Perform ACTH stimulation testing before complete cessation

Alternative: Hybrid Approach

Transition to hydrocortisone 15-20 mg/day (mimics physiologic cortisol secretion) given as 10 mg AM, 5 mg afternoon
Continue for 1-2 months, then taper hydrocortisone by 2.5 mg every 2 weeks
This approach may facilitate HPA axis recovery by allowing physiologic diurnal variation

Disease-Specific Considerations

Autoimmune Conditions:

Monitor disease activity markers (ESR, CRP, disease-specific symptoms)
Be prepared to slow taper or increase dose temporarily if flare occurs
Consider steroid-sparing immunosuppressive agents early

Severe Asthma/COPD:

Optimize inhaled corticosteroids and bronchodilators before tapering systemic steroids
Monitor FEV1 and symptoms closely
Consider slower taper in frequent exacerbators

Polymyalgia Rheumatica/Giant Cell Arteritis:

Classic prolonged taper (12-24 months typical)
Initial dose 40-60 mg prednisone; reduce by 10 mg every 2 weeks to 20 mg
Then 2.5 mg every 2-4 weeks with close symptom monitoring
ESR/CRP surveillance for disease recurrence

Monitoring During Tapering

Clinical Assessment:

Fatigue, weakness, anorexia, weight loss (adrenal insufficiency symptoms)
Disease-specific symptoms (joint pain, shortness of breath, rash, etc.)
Vital signs: postural hypotension suggests adrenal insufficiency

Laboratory Monitoring:

Morning cortisol level (drawn before AM steroid dose) when reaching 5 mg prednisone or equivalent
- 10 μg/dL: HPA axis recovery likely adequate
- 3-10 μg/dL: Indeterminate; may need stimulation test or continued slow taper
- <3 μg/dL: HPA axis suppressed; continue replacement
ACTH stimulation test (if available and indicated): Peak cortisol >18-20 μg/dL indicates adequate adrenal reserve

Clinical Pearls 💎

Pearl 7: The Morning Cortisol Timing Trick When checking morning cortisol to assess HPA axis recovery, draw labs at 8 AM BEFORE the morning steroid dose (ideally after holding steroids for 24 hours). Cortisol levels peak physiologically at 8 AM; levels at other times are less interpretable.

Pearl 8: Symptoms Lag Behind Labs Patients may experience fatigue and malaise during tapering even with adequate cortisol levels. This may represent a "steroid withdrawal syndrome" (distinct from adrenal insufficiency). Consider slower taper, patient education, and symptomatic support, but don't abandon the taper without evidence of true adrenal insufficiency.

Pearl 9: The Alternate-Day Strategy For chronic steroid-dependent conditions, consider alternate-day therapy with short-acting agents (prednisone, prednisolone) once daily dose is <15 mg. Give entire dose on alternate mornings. This minimizes HPA suppression while maintaining therapeutic effect for some conditions. Does NOT work with long-acting dexamethasone.

Oyster Alert 🦪

Oyster 5: The "Stuck at 5 mg" Phenomenon Many patients and physicians get "stuck" at 5 mg prednisone for years due to fear of adrenal crisis or symptom recurrence. However, 5 mg prednisone is still supraphysiologic (physiologic production = 15-25 mg hydrocortisone ≈ 4 mg prednisone), leading to cumulative steroid toxicity. Don't abandon the taper—but go slowly below 5 mg.

Oyster 6: Over-reliance on Cortisol Levels A low morning cortisol during taper doesn't always require stopping the taper or increasing the dose. If patient is asymptomatic and not facing physiologic stress, many clinicians continue slow taper with close monitoring. The ultimate goal is discontinuation.

Clinical Hack 🔧

Microdose Tapering for Difficult Cases: For patients who repeatedly fail conventional tapers, consider 0.5-1 mg reductions every 4-6 weeks. Use liquid prednisone formulations or compound customized doses. Though slower, this ultra-gradual approach has high success rates in steroid-dependent patients.

4. Managing Chronic Side Effects: Osteoporosis, Hyperglycemia, and Cataracts

Chronic corticosteroid therapy causes predictable, dose-dependent, cumulative adverse effects. Preventive strategies must be implemented early and monitored throughout treatment.

Glucocorticoid-Induced Osteoporosis (GIOP)

GIOP is the most common cause of secondary osteoporosis. Fracture risk increases within 3-6 months of initiating therapy, even before significant bone density decline.

Pathophysiology:

Decreased osteoblast function and increased osteoclast activity
Impaired intestinal calcium absorption and increased renal calcium excretion
Suppressed sex hormone production
Direct myopathic effects leading to falls

Prevention and Treatment Guidelines:

All Patients on ≥2.5 mg Prednisone Daily for ≥3 Months:

Calcium supplementation: 1200-1500 mg/day (dietary + supplemental)
Vitamin D: 800-1000 IU daily (target 25-OH vitamin D >30 ng/mL)
Lifestyle modifications: Weight-bearing exercise, smoking cessation, fall prevention
FRAX score calculation: Assess 10-year fracture risk

High-Risk Patients Requiring Bisphosphonate Therapy:

Postmenopausal women or men >50 years on ≥7.5 mg prednisone equivalent daily
Any patient with prior fragility fracture
T-score ≤-2.5 at spine or hip
T-score -1.0 to -2.5 with FRAX 10-year major osteoporotic fracture risk >20% or hip fracture risk >3%

Preferred Agents:

Alendronate 70 mg weekly or risedronate 35 mg weekly (first-line)
Zoledronic acid 5 mg IV annually (if poor oral tolerance or adherence)
Denosumab 60 mg SC every 6 months (if contraindications to bisphosphonates)
Teriparatide (PTH 1-34) (for severe osteoporosis or multiple fractures; anabolic agent)

Monitoring:

Baseline DXA scan before or within 6 months of starting chronic steroids
Repeat DXA every 1-2 years (more frequently if high risk or declining BMD)
Annual vertebral fracture assessment (VFA) or lateral spine X-rays in high-risk patients

Steroid-Induced Hyperglycemia and Diabetes

Corticosteroids cause insulin resistance and increase hepatic gluconeogenesis. Hyperglycemia pattern is typically characterized by post-prandial elevation with relatively preserved fasting glucose initially.

Risk Stratification:

Highest risk: Pre-existing diabetes, prediabetes, obesity, family history
Dose-dependent: Risk increases significantly at >20 mg/day prednisone equivalent
Time-dependent: Hyperglycemia typically emerges within days of starting therapy

Screening and Monitoring:

Pre-treatment: Hemoglobin A1c and fasting glucose in all patients
During therapy:
- Non-diabetics on high-dose steroids: Check fasting glucose or random glucose 1-2 times weekly initially
- Known diabetics: Intensify glucose monitoring; expect insulin requirement increases of 50-200%
- Consider continuous glucose monitoring (CGM) in high-risk inpatients

Management Strategies:

Inpatient Hyperglycemia:

Insulin therapy is FIRST-LINE for significant steroid-induced hyperglycemia
- NPH insulin pattern matches prednisone-induced hyperglycemia (afternoon peak)
- Typical regimen: NPH 0.1-0.2 units/kg with breakfast (for AM prednisone)
- Add rapid-acting insulin for meal coverage as needed
- For dexamethasone (long-acting): Consider basal insulin (glargine/degludec) or split NPH dosing
Adjust insulin doses proactively with steroid dose changes (increase insulin proportionally)

Outpatient Management:

Metformin: Continue if already prescribed; limited efficacy as monotherapy for SIDM
DPP-4 inhibitors: Moderate efficacy; well-tolerated
GLP-1 agonists: Increasingly used; address both hyperglycemia and weight gain
Insulin: Often necessary for adequate control; educate patients on temporary need
Target HbA1c: <8% reasonable for most patients on chronic steroids (balance control vs. hypoglycemia risk)

Special Consideration: "Steroid Diabetes" Resolution Steroid-induced hyperglycemia typically resolves or improves significantly after steroid discontinuation. Anticipate reducing or stopping diabetes medications during steroid taper. Monitor for hypoglycemia.

Ocular Complications: Cataracts and Glaucoma

Posterior Subcapsular Cataracts (PSC):

Occur in 10-30% of patients on chronic steroids (dose and duration-dependent)
Risk increases significantly with >10 mg/day prednisone for >1 year
May be irreversible even after steroid cessation
Screening: Annual ophthalmologic examination for patients on chronic steroids

Steroid-Induced Glaucoma:

Elevated intraocular pressure in 30-40% of patients (genetic susceptibility)
Can occur with topical, inhaled, or systemic steroids
Usually reversible with steroid discontinuation but may cause permanent vision loss if undetected
Screening: Baseline and periodic intraocular pressure measurements

Prevention: No effective prevention for cataracts; early detection is key. For glaucoma, consider prophylactic IOP-lowering drops in high-risk patients or those on long-term therapy.

Other Important Chronic Side Effects

Cardiovascular:

Hypertension (monitor BP at every visit; treat per guidelines)
Dyslipidemia (screen lipids; consider statin therapy)
Increased cardiovascular events (minimize dose and duration)

Infection Risk:

Screen for latent TB before starting long-term therapy (>1 month of ≥15 mg/day)
Pneumocystis jirovecii pneumonia (PCP) prophylaxis if ≥20 mg prednisone for >1 month + other immunosuppression
Consider strongyloides screening in endemic areas

Psychiatric:

Insomnia, mood changes, psychosis (5-10% of patients)
Dose-related; risk highest with >40 mg/day prednisone
Usually resolves with dose reduction; may require antipsychotics for severe cases

Dermatologic:

Skin thinning, easy bruising, striae, poor wound healing
No effective prevention; minimize trauma

Gastrointestinal:

Controversial association with PUD (may be confounded by NSAID use)
PPI generally NOT required unless concurrent NSAIDs or PUD history

Clinical Pearls 💎

Pearl 10: Bisphosphonates Should Be Preventive, Not Reactive Unlike postmenopausal osteoporosis where treatment is often initiated after bone loss occurs, GIOP prevention with bisphosphonates should start early—ideally when initiating chronic steroids in high-risk patients. Fracture risk increases BEFORE significant BMD decline.

Pearl 11: The Steroid-Hyperglycemia Pattern Prednisone taken in the morning causes afternoon and evening hyperglycemia with relative sparing of fasting glucose. Tailor insulin regimens accordingly (NPH with breakfast works well). Dexamethasone causes more prolonged, sustained hyperglycemia.

Pearl 12: GLP-1 Agonists as Dual-Purpose Agents GLP-1 receptor agonists (semaglutide, dulaglutide) address two major steroid side effects: hyperglycemia AND weight gain. Consider in appropriate patients on long-term steroids, particularly those with obesity or metabolic syndrome.

Oyster Alert 🦪

Oyster 7: The PPI Overuse Problem Routine PPI prophylaxis in patients on steroids alone (without NSAIDs) lacks evidence and contributes to polypharmacy. PPIs themselves have risks (C. difficile infection, fractures, micronutrient deficiencies). Reserve for patients with concurrent NSAID use or PUD history.

Oyster 8: The "My Patient Needs Calcium and Vitamin D" Illusion Calcium and vitamin D alone are INSUFFICIENT to prevent GIOP in high-risk patients. They are necessary but not sufficient. Many clinicians stop at calcium/vitamin D supplementation without prescribing indicated bisphosphonate therapy, leaving patients unprotected.

Clinical Hack 🔧

Steroid Side Effect Bundle Order Set: Create a standardized order set for chronic steroid prescriptions that automatically includes:

Calcium 1200 mg + Vitamin D 800 IU daily
PPI only if concurrent NSAID or PUD history
Bisphosphonate prescription pending DXA results (for high-risk patients)
Ophthalmology referral for annual eye exam
Glucose monitoring orders
Patient education handout on steroid side effects and warning signs

This "bundle" approach dramatically improves adherence to preventive care guidelines.

5. Stress Dosing for the Hospitalized Patient on Chronic Steroids

Physiologic Principles

Normal adrenal cortisol production is 15-25 mg/day (cortisol equivalent). During physiologic stress (surgery, infection, trauma), cortisol production increases 2-10 fold (up to 200-300 mg/day cortisol equivalent in severe stress). Patients with HPA axis suppression cannot mount this response, risking cardiovascular collapse.

Risk Stratification for HPA Axis Suppression

High Risk (Assume HPA Suppression):

Current use of ≥20 mg/day prednisone for ≥3 weeks
Cushingoid features (regardless of dose or duration)
Any supraphysiologic dose (>5 mg prednisone) for >3 months
Stopped steroids within past 12 months (after prolonged use)

Intermediate Risk (Consider Testing or Empiric Coverage):

10-20 mg/day prednisone for 2-3 weeks
Lower doses for >3 months without Cushingoid features
Multiple short courses in past year

Low Risk (HPA Axis Likely Intact):

<10 mg/day prednisone for <3 weeks
Physiologic replacement doses only (≤5 mg/day)
Stopped steroids >12 months ago (after short-term use)

Stress Dosing Protocols by Stress Level

Minor Stress (e.g., Dental Procedures, Simple Diagnostic Tests):

Continue usual dose; no additional coverage needed
Examples: Dental cleaning, endoscopy without sedation, minor dermatologic procedures

Moderate Stress (e.g., Moderate Surgery, Severe Illness):

Protocol: Hydrocortisone 50 mg IV before procedure, then 25 mg IV q8h for 24-48 hours
Alternative: Continue home dose + supplemental hydrocortisone 50 mg IV/PO on day of stress
Examples: Colonoscopy with sedation, pneumonia, cholecystectomy, joint arthroplasty, severe cellulitis

Major Stress (e.g., Major Surgery, Critical Illness, Septic Shock):

Protocol: Hydrocortisone 100 mg IV bolus, then 50 mg IV q6-8h or 200 mg/24h continuous infusion
Taper over 2-3 days as stress resolves: 100 mg → 50 mg → 25 mg q8h → home dose
Examples: Cardiac surgery, major abdominal surgery, septic shock, ARDS, severe trauma, ICU admission with hemodynamic instability

Practical Implementation

Preoperative Assessment:

Identify all patients on steroids (including recent discontinuation)
Stratify risk of HPA suppression
Coordinate with surgery and anesthesia teams
Order stress-dose hydrocortisone to be available immediately

Intraoperative/Procedure:

Administer hydrocortisone before induction (ideally 30-60 minutes prior)
Continue intraoperative dosing per protocol
Monitor blood pressure closely; unexplained hypotension may indicate inadequate dosing

Postoperative/Post-Event:

Continue stress dosing for 24-48 hours (moderate stress) or until hemodynamically stable (major stress)
Taper back to home regimen over 1-3 days
Do NOT abruptly stop stress dosing and return to physiologic doses

Special Populations and Scenarios

Septic Shock:

Consider "low-dose hydrocortisone" for refractory septic shock: 200 mg/24h continuous infusion or 50 mg IV q6h
This is BOTH stress-dose coverage AND adjunctive sepsis treatment
Continue for 3-7 days, then taper gradually

Trauma and Burns:

Assume HPA axis suppression in chronic steroid users with major trauma
Use high-dose stress coverage (hydrocortisone 100 mg q8h or 300 mg/24h infusion)
Prolonged coverage may be necessary (days to weeks)

Unrecognized Adrenal Insufficiency:

If unexplained shock in any patient (steroid use unknown), consider empiric hydrocortisone 100 mg IV
"When in doubt, treat" — risk-benefit strongly favors treatment
Send cortisol and ACTH levels BEFORE first dose (but don't delay treatment)

Oral to IV Conversion During NPO Status:

If patient NPO: Convert home oral dose to IV equivalent (use Table 1)
Example: Home dose prednisone 10 mg PO daily → hydrocortisone 40 mg IV daily (given as 20 mg IV q12h or 10 mg IV q6h) + stress-dose supplementation as indicated

Clinical Pearls 💎

Pearl 13: Don't Forget the Dexamethasone Caveat If adrenal insufficiency suspected, dexamethasone 4 mg IV can be given BEFORE diagnostic testing (ACTH stimulation) without interfering with cortisol assay (dexamethasone doesn't cross-react with cortisol immunoassay). Switch to hydrocortisone after testing.

Pearl 14: The "Double Coverage" Myth Some clinicians worry about giving stress-dose steroids to patients already on chronic steroids, fearing toxicity. However, even patients on 60 mg prednisone daily require ADDITIONAL hydrocortisone during major stress because:

The HPA axis is suppressed and cannot respond to stress
Stress cortisol requirements (200-300 mg) exceed chronic oral doses
Short-term high-dose steroids (2-3 days) rarely cause significant harm

Pearl 15: The Taper After Stress After major stress, don't abruptly return to chronic maintenance dose. Taper stress-dose steroids over 2-3 days (e.g., 100 mg q8h → 50 mg q8h → 25 mg q8h → resume home dose) to mimic physiologic cortisol recovery and prevent rebound hypotension.

Oyster Alert 🦪

Oyster 9: Inhaled/Topical Steroid Users Need Stress Dosing Too High-dose inhaled corticosteroids (>1000 μg/day fluticasone or equivalent) or potent topical steroids (especially clobetasol on large surface areas) can suppress the HPA axis. Don't dismiss the need for stress dosing in these patients—obtain detailed medication history including all steroid formulations.

Oyster 10: The Etomidate Problem Etomidate, commonly used for rapid sequence intubation, inhibits 11β-hydroxylase and causes temporary adrenal insufficiency lasting 24-48 hours. In patients with pre-existing HPA suppression, a single dose of etomidate can precipitate profound adrenal crisis. Consider alternative induction agents (ketamine, propofol) or provide stress-dose steroids.

Clinical Hack 🔧

The "Rule of 100s" for Stress Dosing: For quick bedside decision-making:

Moderate stress: ~100 mg hydrocortisone total per day (e.g., 50 mg IV × 1, then 25 mg q8h)
Major stress: ~100 mg hydrocortisone every 8 hours (or 300 mg/24h infusion)
Duration: 100 mg protocol for 2-3 days, then taper

This oversimplified rule works for most clinical scenarios and is easy to remember under pressure.

Conclusion

Corticosteroids remain powerful therapeutic tools, but their use demands meticulous attention to dosing equivalencies, withdrawal risks, chronic complications, and stress-dosing requirements. Key principles for safe prescribing include:

Master the conversions: Understanding glucocorticoid potency differences prevents dosing errors during transitions between agents
Respect the HPA axis: Assume suppression after 3 weeks of supraphysiologic doses; taper gradually and monitor for adrenal insufficiency
Prevent before you treat: Implement osteoporosis prevention, glucose monitoring, and ophthalmologic surveillance from the outset of chronic therapy
Stress dose liberally: When in doubt, provide stress-dose coverage for hospitalized patients with risk factors for HPA suppression
Individualize therapy: Cookie-cutter approaches fail; tailor dosing, tapering, and monitoring to each patient's unique circumstances

As prescribers, our goal is to harness the anti-inflammatory power of corticosteroids while vigilantly mitigating their substantial risks. By integrating these practical strategies into clinical practice, we can optimize outcomes for patients requiring these indispensable yet challenging medications.

Key Take-Home Points for Critical Care Practitioners

✓ Equivalency conversions must account for both potency and duration of action; dexamethasone's prolonged half-life complicates tapering

✓ HPA axis suppression can occur with >3 weeks of >5 mg/day prednisone; assume suppression in any patient with Cushingoid features

✓ Acute adrenal crisis is life-threatening; maintain low threshold for empiric hydrocortisone 100 mg IV in unexplained shock

✓ Tapering should be gradual, especially below 10 mg/day prednisone; ultra-slow tapers (0.5-1 mg reductions) succeed where conventional tapers fail

✓ Osteoporosis prevention with bisphosphonates should be PROACTIVE in high-risk patients, not reactive after fractures occur

✓ Steroid-induced hyperglycemia requires insulin therapy; NPH insulin matches prednisone's afternoon peak

✓ Stress dosing saves lives: moderate stress needs ~100 mg/day hydrocortisone; major stress needs ~300 mg/day

✓ When uncertain about adrenal sufficiency in a critically ill patient, give hydrocortisone first, ask questions later

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Appendix: Quick Reference Tables

Table 2: Rapid Steroid Conversion Calculator

If patient is on:	To convert to:	Multiply by:
Prednisone	Hydrocortisone	4
Prednisone	Methylprednisolone	0.8
Prednisone	Dexamethasone	0.15 (÷7)
Methylprednisolone	Prednisone	1.25
Methylprednisolone	Hydrocortisone	5
Methylprednisolone	Dexamethasone	0.19 (÷5)
Dexamethasone	Prednisone	6.7 (×7)
Dexamethasone	Methylprednisolone	5.3 (×5)
Dexamethasone	Hydrocortisone	26.7
Hydrocortisone	Prednisone	0.25 (÷4)

Table 3: Taper Protocol Summary

Starting Dose (Prednisone Equivalent)	Reduction Schedule	Monitoring
>40 mg/day	Reduce 5-10 mg weekly	Symptoms, disease activity
20-40 mg/day	Reduce 5 mg every 1-2 weeks	Symptoms, disease activity
10-20 mg/day	Reduce 2.5 mg every 2 weeks	Symptoms, disease activity
5-10 mg/day	Reduce 1-2.5 mg every 2-4 weeks	Symptoms, AM cortisol at 5 mg
<5 mg/day	Reduce 1 mg every 4 weeks OR switch to hydrocortisone taper	AM cortisol, ACTH stim test if available

Table 4: Stress Dosing at a Glance

Stress Level	Examples	Hydrocortisone Dose	Duration
Minor	Dental cleaning, routine labs, minor infections	Continue home dose	N/A
Moderate	Colonoscopy, pneumonia, cholecystectomy, COVID-19	50 mg IV before, then 25 mg IV q8h	24-48 hours
Major	Cardiac surgery, septic shock, major trauma, ARDS	100 mg IV bolus, then 50 mg q6-8h or 200 mg/24h infusion	Until stable, then taper over 2-3 days

Table 5: Side Effect Monitoring Checklist

Side Effect	Baseline	Follow-up	Intervention Threshold
Osteoporosis	DXA scan, FRAX score	DXA every 1-2 years	T-score ≤-2.5 or high FRAX → bisphosphonate
Hyperglycemia	HbA1c, fasting glucose	Weekly glucose checks initially	Fasting >126 mg/dL or random >200 mg/dL → treatment
Hypertension	BP measurement	Every visit	>140/90 mmHg → antihypertensive
Cataracts	Ophthalmology exam	Annual eye exam	Visual symptoms → surgical evaluation
Glaucoma	IOP measurement	Annual or as needed	IOP >21 mmHg → ophthalmology referral
Infection	TB screening (PPD/IGRA)	Clinical vigilance	Fever, symptoms → aggressive workup
Psychiatric	Mental health history	Every visit	Severe symptoms → psychiatry, dose reduction

Abbreviations

ACTH = Adrenocorticotropic hormone
ARDS = Acute respiratory distress syndrome
BMD = Bone mineral density
COPD = Chronic obstructive pulmonary disease
CRH = Corticotropin-releasing hormone
DXA = Dual-energy X-ray absorptiometry
FRAX = Fracture Risk Assessment Tool
GIOP = Glucocorticoid-induced osteoporosis
GLP-1 = Glucagon-like peptide-1
HPA = Hypothalamic-pituitary-adrenal
IOP = Intraocular pressure
IV = Intravenous
NPH = Neutral protamine Hagedorn (insulin)
PCP = Pneumocystis jirovecii pneumonia
PO = Per os (oral)
PPI = Proton pump inhibitor
PSC = Posterior subcapsular cataract
PUD = Peptic ulcer disease
TB = Tuberculosis
VFA = Vertebral fracture assessment

Disclosure: The author reports no conflicts of interest.

Author Contributions: This review was prepared as an educational resource for postgraduate medical trainees in critical care medicine.

Acknowledgments: The author thanks the critical care and endocrinology communities for their ongoing contributions to evidence-based corticosteroid management.

Thursday, October 2, 2025