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Bedside Snapshot
  • Core Use: High-potency, long-acting glucocorticoid with strong anti-inflammatory and anti-edema effects; minimal mineralocorticoid activity
  • Common Applications: Cerebral edema from brain tumors/metastases, airway edema (post-extubation, croup, anaphylaxis adjunct), ARDS/COVID-19 pneumonia, antiemetic adjunct
  • Half-Life: Biologic half-life ~36–72 hours; once-daily dosing often sufficient
  • Key Advantage: Strong glucocorticoid effect without significant sodium/water retention (preferred for cerebral edema and neuro cases)
  • Key Danger: Hyperglycemia, infection risk, myopathy, delirium, and adrenal suppression with prolonged use; HPA-axis suppression more pronounced than with hydrocortisone
  • Special Note: Short courses relatively safe; prolonged/repeated high doses require careful risk-benefit assessment
Brand & Generic Names
  • Generic Name: Dexamethasone
  • Brand Names: Decadron, Ozurdex (ophthalmic), many generics
Medication Class

Long-acting systemic glucocorticoid; minimal mineralocorticoid activity

Pharmacology

Mechanism of Action:

  • Synthetic glucocorticoid that diffuses into cells and binds cytosolic glucocorticoid receptors; the complex translocates to the nucleus and alters transcription of numerous genes
  • Downregulates pro-inflammatory cytokines (e.g., IL-1, IL-6, TNF-α), adhesion molecules, and COX-2, while upregulating anti-inflammatory mediators
  • Stabilizes lysosomal and cellular membranes, reduces capillary permeability, and decreases leukocyte migration into inflamed tissues, limiting edema and tissue damage
  • Minimal mineralocorticoid activity means little direct effect on sodium retention or potassium excretion compared with hydrocortisone or fludrocortisone
  • In cerebral edema from tumors or metastases, decreases vasogenic edema by reducing capillary permeability in tumor-associated vasculature, thereby lowering intracranial pressure over hours–days

Pharmacokinetics:

  • Routes: IV, IM, PO; oral bioavailability is high (~80–90%), allowing easy IV↔PO transitions when gut is functional
  • Onset: Anti-inflammatory effect begins within several hours; for airway edema (e.g., croup, post-extubation), clinical improvement often seen within 4–8 hours
  • Distribution: Widely distributed, including CNS; highly protein bound; crosses placenta and enters breast milk
  • Metabolism: Predominantly hepatic (CYP3A4) to inactive metabolites
  • Elimination: Metabolites primarily renal; elimination half-life ~3–5 hours, but biologic half-life is long (36–72 hours), reflecting prolonged genomic effects
  • Steroid Potency Equivalence: 0.75 mg dexamethasone ≈ 5 mg prednisone ≈ 20 mg hydrocortisone
Indications
  • Cerebral edema due to brain tumors and metastatic lesions; occasionally used as adjunct in bacterial meningitis (selected cases, e.g., pneumococcal meningitis when given early)
  • Airway edema: croup, post-extubation stridor, anaphylaxis adjunct (after epinephrine), upper airway trauma/inflammation where airway compromise is a concern
  • ARDS and severe COVID-19 pneumonia: systemic anti-inflammatory effect to blunt lung injury and improve outcomes in selected patients
  • Adjunct antiemetic for chemotherapy-induced nausea and vomiting and in some ED migraine regimens to reduce recurrence
  • Perioperative steroid coverage in chronic steroid users (often used when longer effect is desired or per institutional preference)
Dosing & Administration

Available Forms:

  • Injectable solution: commonly 4 mg/mL or 10 mg/mL vials or prefilled syringes for IV/IM use
  • Oral tablets: 0.5 mg, 0.75 mg, 1 mg, 1.5 mg, 2 mg, 4 mg, 6 mg (varies by manufacturer)
  • Oral solution: e.g., 0.5–1 mg/mL concentrations (check local formularies)
  • Specialty formulations (e.g., intra-articular, ophthalmic implants) exist but are less relevant to ED/ICU bedside use

Adult Dosing (Systemic):

Indication / Scenario Typical Dose Route / Frequency Notes
Cerebral edema from brain tumors/metastases 10 mg IV bolus Then 4 mg IV/PO q6h Adjust per neuro-onc/neurosurg; taper over days–weeks as symptoms/ICP improve
Bacterial meningitis (e.g., pneumococcal; timing critical) 10 mg IV q6h for 4 days First dose ideally given before or with first antibiotic dose; follow ID/neuro guidelines
ARDS / severe COVID-19 pneumonia 6 mg IV/PO once daily up to 10 days Other ARDS protocols use 20 mg x 5 days then 10 mg x 5 days; follow institutional policy
Post-extubation airway edema / stridor 4–10 mg IV q6–12h for 24–48h Evidence mixed; often used empirically with racemic Epi and supportive care
Croup (adult/peds framing) 0.15–0.6 mg/kg (max 10 mg) PO/IV/IM once Single dose often sufficient; pediatrics dosing per local guideline
Severe asthma/COPD exacerbation 10–16 mg IV/PO daily Approx equivalent to 40–60 mg prednisone; typically 5–7 days total
Antiemetic adjunct (chemo, ED migraine) 4–10 mg IV once Often part of multi-drug antiemetic regimen
Stress-dose coverage for chronic steroid user 4–10 mg IV q6–12h initially Exact regimen depends on prior steroid exposure and procedure severity

Additional Dosing Notes:

  • For cerebral edema, higher initial doses (e.g., 10–20 mg IV) and q6h regimens may be used in severe cases; once symptoms stabilize, taper as quickly as clinically feasible to limit complications
  • In ARDS/COVID regimens, fixed daily dosing (e.g., 6 mg) is common; avoid abrupt discontinuation after prolonged high-dose steroids—taper may be needed in long courses
  • In chronic steroid users, consider total glucocorticoid exposure from all sources; dexamethasone is quite potent, so small doses can be equivalent to large prednisone/hydrocortisone doses
Contraindications

Absolute/Major Contraindications:

  • Serious hypersensitivity reaction to dexamethasone or formulation components
  • Systemic fungal infections when used as monotherapy without appropriate antifungal coverage

Major Precautions:

  • Active infection or sepsis: steroids may mask fever and leukocytosis; use when there is a clear indication and follow sepsis guidelines
  • Poorly controlled diabetes or DKA/HHS risk: dexamethasone can significantly increase blood glucose; insulin often needs escalation
  • History of peptic ulcer disease or GI bleeding: steroids increase risk when combined with NSAIDs, antiplatelets, or anticoagulants; consider GI prophylaxis
  • Psychiatric history (e.g., bipolar disorder, psychosis): steroids can worsen mood instability and precipitate steroid psychosis
  • Osteoporosis, myopathy, or frailty: prolonged high-dose therapy increases risk of fractures and ICU-acquired weakness
  • Chronic use (>2–3 weeks) at moderate–high doses leads to HPA-axis suppression; abrupt discontinuation may precipitate adrenal crisis
HPA-Axis Suppression: Chronic use at moderate to high doses can suppress the hypothalamic-pituitary-adrenal axis. Abrupt discontinuation may precipitate adrenal crisis. Taper appropriately after prolonged courses.
Adverse Effects

Common (Short- to Moderate-Term):

  • Hyperglycemia and increased insulin requirements
  • Leukocytosis (neutrophil demargination), which can confuse sepsis workup
  • Insomnia, agitation, and mood changes
  • Mild fluid retention and hypertension (less than with hydrocortisone)
  • Gastric irritation, dyspepsia

Serious / Long-Term:

  • Steroid psychosis, severe mood disturbance, suicidality
  • GI bleeding or perforation, especially with NSAIDs or severe stress gastritis
  • Opportunistic infections and reactivation of latent infections (e.g., TB, strongyloides)
  • Myopathy and ICU-acquired weakness, especially when combined with neuromuscular blockade
  • Osteoporosis, osteonecrosis (e.g., femoral head) with chronic use
  • Adrenal suppression with risk of adrenal crisis upon sudden withdrawal
Special Populations

Elderly Patients:

  • Higher risk of adverse effects including hyperglycemia, confusion, and myopathy
  • Consider lower doses and closer monitoring

Renal Impairment:

  • No specific dose adjustment required, but monitor for fluid retention and electrolyte disturbances

Hepatic Impairment:

  • Use with caution; metabolism is hepatic, but no specific dosing guidelines exist

Pregnancy:

  • Category C: Crosses placenta; use only if benefit justifies potential fetal risk
  • May increase risk of cleft palate with first-trimester use
  • Monitor for maternal hyperglycemia and adrenal suppression in neonate

Lactation:

  • Enters breast milk; high doses may suppress infant growth and interfere with endogenous corticosteroid production
  • Consider risk-benefit for breastfeeding during therapy
Monitoring

Clinical Monitoring:

  • Blood glucose trends and insulin requirements, especially in diabetics and critically ill patients
  • Vital signs and infection markers (fever pattern, WBC, cultures) to detect masked or worsening infection
  • Mental status for delirium, agitation, or steroid psychosis
  • Electrolytes and fluid balance in patients with heart failure, renal disease, or on high-dose/prolonged therapy

Long-Term Monitoring:

  • In prolonged courses, assess for proximal muscle weakness
  • Consider adrenal suppression testing if tapering after long exposure
Clinical Pearls
Hydrocortisone vs. Dexamethasone: Hydrocortisone = shorter-acting with mineralocorticoid effect (better for adrenal crisis/septic shock). Dexamethasone = long-acting, purely glucocorticoid (better for cerebral edema, ARDS regimens).
Cerebral Edema Response: Symptom improvement (headache, nausea, focal deficits) often tracks with ICP reduction. If no clinical response, reassess diagnosis and imaging.
COVID/ARDS Use: Dexamethasone is not a rescue therapy for refractory hypoxemia; benefits are more about modulating lung inflammation over days than immediate oxygenation changes.
Duration and Taper: Short 'burst' courses (e.g., 1–3 doses for airway edema) usually don't require taper, but longer or high-dose regimens do. Be deliberate with duration and taper strategy.
Documentation: Document indication, planned duration, and taper strategy early—many patients otherwise stay on steroids longer than necessary in the ICU/floor handoff chain.
Potency Reminder: Dexamethasone is highly potent. 0.75 mg dexamethasone ≈ 5 mg prednisone ≈ 20 mg hydrocortisone. Small doses pack a big punch.
References
  • 1. Lexicomp. (2024). Dexamethasone: Drug information. Wolters Kluwer.
  • 2. The RECOVERY Collaborative Group. (2021). Dexamethasone in hospitalized patients with Covid-19. New England Journal of Medicine, 384(8), 693–704. https://doi.org/10.1056/NEJMoa2021436
  • 3. Farkas, J. (2023). Steroids in the ICU. EMCrit Project / IBCC. https://emcrit.org/ibcc/steroids/
  • 4. Keh, D., Trips, E., Marx, G., et al. (2016). Effect of hydrocortisone on development of shock among patients with severe sepsis: The HYPRESS randomized clinical trial. JAMA, 316(17), 1775–1785. https://doi.org/10.1001/jama.2016.14799
  • 5. Roberts, R. J., Welch, E. K., Devlin, J. W., et al. (2017). Corticosteroids for sepsis and septic shock. Cochrane Database of Systematic Reviews, 12, CD002243. https://doi.org/10.1002/14651858.CD002243.pub3
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