Version November 2024
Dosage guidance:
Dosing: Individualize glucocorticoid dosing and use the minimum effective dose/duration. Evidence to support an optimal dose and duration is lacking for most indications; recommendations provided are general guidelines only.
Clinical considerations: HPA-axis suppression is likely in any adult receiving >3 mg/day (daytime dosing) or ≥0.75 mg per 24 hours (evening or night dosing) for >2 weeks or with Cushingoid appearance (Ref); do not abruptly discontinue treatment in these patients; dose tapering may be necessary (Ref).
Usual dosage range: Oral, IV, IM: 4 to 20 mg/day given in a single daily dose or in 2 to 4 divided doses; High dose: 0.4 to 0.8 mg/kg/day (usually not to exceed 40 mg/day).
Acute mountain sickness/high-altitude cerebral edema (off-label use):
Prevention, moderate- to high-risk situations (alternative agent): Note: Use in addition to gradual ascent and start the day of ascent.
Oral: 2 mg every 6 hours or 4 mg every 12 hours; may be discontinued after staying at the same elevation for 2 to 4 days or if descent is initiated. Due to adverse effects, limit duration to ≤10 days (Ref); some experts limit to ≤7 days (Ref). In situations of rapid ascent to altitudes >3,500 meters (eg, rescue or military operations), 4 mg every 6 hours may be considered (Ref).
Treatment:
Acute mountain sickness (moderate to severe): Note: Dexamethasone does not facilitate acclimatization; further ascent should be delayed until patient is asymptomatic off medication (Ref).
Oral, IM, IV: 4 mg every 6 hours, continue until 24 hours after symptoms resolve or descent completed (not longer than 7 days total) (Ref).
High-altitude cerebral edema: Oral, IM, IV: 8 mg as a single dose, followed by 4 mg every 6 hours until descent is complete and symptoms resolve (Ref).
Acute respiratory distress syndrome, moderate to severe (off-label use): Note: May consider in most patients with persistent or refractory moderate to severe acute respiratory distress syndrome who are relatively early in the disease course (within 14 days). Do not abruptly discontinue since this may cause deterioration due to inflammatory response (Ref).
IV: 20 mg once daily from days 1 to 5, then 10 mg once daily from days 6 to 10 (Ref).
Adrenal insufficiency, adrenal crisis (alternative agent): Note: Dexamethasone should only be used if hydrocortisone is unavailable. Corticosteroid therapy should be combined with adequate fluid resuscitation in patients with primary adrenal insufficiency (Ref).
IV: 4 mg every 12 hours; transition to hydrocortisone as soon as possible (Ref).
Adrenal insufficiency, primary chronic (alternative agent): Note: For use in patients who are unable to tolerate treatment with other glucocorticoids (hydrocortisone is preferred); risk of overreplacement may be higher with dexamethasone (Ref). Use in conjunction with fludrocortisone. Dose is based on prednisolone equivalency.
Chronic maintenance dosing:
Oral: Usual dosage range: 0.25 to 0.75 mg once daily (Ref).
Stress dosing:
Note: Patients who are unable to tolerate oral medication (eg, due to vomiting or diarrhea), are in active labor, or are under surgical stress may require parenteral corticosteroid therapy (preferably with hydrocortisone) to prevent adrenal crisis (Ref).
Patients with febrile illness: Oral: Double the chronic maintenance dose until recovery for fever 38°C (100.4°F) to 39°C (102.2°F) or triple the chronic maintenance dose until recovery for fever >39°C (102.2°F), then return to baseline dose within 1 to 3 days (Ref).
Minor surgical stress (eg, hernia repair, procedures with local anesthetic ): Oral: Continue chronic maintenance dose (no additional supplementation needed) (Ref); may give an additional 0.75 mg (equivalent to ~20 mg hydrocortisone) postoperatively if signs or symptoms of adrenal insufficiency are present (Ref).
Antiemetic regimens: Chemotherapy-associated nausea and vomiting, prevention (off-label use): Note: When checkpoint inhibitor therapy is administered in combination with emetogenic chemotherapy, there is no evidence to omit dexamethasone from the prophylactic antiemetic regimen (Ref).
Single-day IV chemotherapy regimens:
Highly emetogenic chemotherapy (>90% risk of emesis): Cisplatin and other highly emetogenic single agents:
Dexamethasone dose depends on specific neurokinin 1 (NK1) receptor antagonist:
Day of chemotherapy: Administer prior to chemotherapy and in combination with an NK1 receptor antagonist, a 5-HT3 receptor antagonist, and olanzapine (Ref).
In combination with aprepitant, fosaprepitant, netupitant/palonosetron (NEPA), or fosnetupitant/palonosetron: Oral, IV: 12 mg (Ref).
In combination with rolapitant: Oral, IV: 20 mg (Ref).
If NK1 receptor antagonist not used: Oral, IV: 20 mg (Ref).
Postchemotherapy days:
If aprepitant given: Oral, IV: 8 mg once daily on days 2 to 4 (Ref).
If fosaprepitant given: Oral, IV: 8 mg once on day 2, followed by 8 mg twice daily on days 3 and 4 (Ref).
If NEPA or fosnetupitant/palonosetron given: Prophylaxis with dexamethasone on subsequent days is not needed unless regimen contained cisplatin: Oral, IV: 8 mg once daily on days 2 to 4 (Ref).
If rolapitant given: Oral, IV: 8 mg twice daily on days 2 to 4 (Ref).
If NK1 receptor antagonist not used: Oral, IV: 8 mg twice daily on days 2 to 4 (Ref).
Highly emetogenic chemotherapy (>90% risk of emesis): Breast cancer regimens that include an anthracycline combined with cyclophosphamide:
Dexamethasone dose depends on specific NK1 receptor antagonist:
Day of chemotherapy: Administer prior to chemotherapy and in combination with an NK1 receptor antagonist, a 5-HT3 receptor antagonist, and olanzapine (Ref).
In combination with aprepitant, fosaprepitant, NEPA, fosnetupitant/palonosetron: Oral, IV: 12 mg (Ref).
In combination with rolapitant: Oral, IV: 20 mg (Ref).
If NK1 receptor antagonist not used: Oral, IV: 20 mg (Ref).
Postchemotherapy days: Dexamethasone use is not recommended (an alternative agent or agents is/are recommended) (Ref).
Moderately emetogenic chemotherapy (30% to 90% risk of emesis): Carboplatin-based regimens:
Dexamethasone dose depends on specific NK1 receptor antagonist (Ref):
Day of chemotherapy: Administer prior to chemotherapy and in combination with an NK1 receptor antagonist and a 5-HT3 receptor antagonist (Ref).
In combination with aprepitant, fosaprepitant, NEPA, or fosnetupitant/palonosetron: Oral, IV: 12 mg (Ref).
In combination with rolapitant: Oral, IV: 20 mg (Ref).
Postchemotherapy days: Prophylaxis is not necessary on subsequent days (Ref).
Moderately emetogenic chemotherapy (30% to 90% risk of emesis): Non-carboplatin-based regimens:
Day of chemotherapy: Administer prior to chemotherapy and in combination with a 5-HT3 receptor antagonist: Oral, IV: 8 mg (Ref).
Postchemotherapy days: Note: Consider single-agent dexamethasone on days 2 and 3 and only for regimens containing agents with known potential to induce delayed emesis (eg, oxaliplatin, cyclophosphamide, doxorubicin) (Ref).
Oral, IV: 8 mg on days 2 and 3 (Ref).
Low emetogenic risk (10% to 30% risk of emesis): Oral, IV: 4 to 8 mg administered as a single agent in a single dose prior to chemotherapy; prophylaxis is not necessary on subsequent days (Ref).
High-dose conditioning chemotherapy with hematopoietic cell or bone marrow transplant:
Day(s) of conditioning chemotherapy: Administer prior to conditioning chemotherapy and in combination with a neurokinin 1 (NK1) receptor antagonist, a 5-HT3 receptor antagonist, with or without olanzapine (Ref).
Oral, IV: 8 to 20 mg on each day of chemotherapy (Ref).
Antiemetic regimens: Postoperative nausea and vomiting, prevention (off-label use): Note: May be used alone or in combination with one or more other prophylactic interventions depending on risk factors (Ref).
IV: 4 to 10 mg once, before or after induction of anesthesia. Dose depends on risk and type of surgery (Ref).
Antiemetic regimens: Radiation therapy-associated nausea and vomiting, prevention (off-label use):
High emetogenic risk radiation therapy (total body irradiation):
Radiation day(s): Oral, IV: 4 mg once daily prior to each fraction of radiation; give in combination with a 5-HT3 receptor antagonist (Ref).
Postradiation days: Oral, IV: The appropriate duration of therapy following radiotherapy days is not well defined; American Society of Clinical Oncology (ASCO) guidelines recommend continuing dexamethasone 4 mg once on the day after each day of radiation if radiation is not planned for that day (Ref).
Moderate emetogenic risk radiation therapy (upper abdomen, craniospinal irradiation):
Radiation day(s): Oral, IV: 4 mg once daily prior to each of the first 5 fractions of radiation; give in combination with a 5-HT3 receptor antagonist (Ref).
Total body irradiation with hematopoietic cell or bone marrow transplant:
Day(s) of total body irradiation: Oral, IV: 4 mg prior to each radiation session (Ref); give in combination with a 5-HT3 receptor antagonist (Ref).
Postradiation day(s): Oral, IV: ASCO guidelines recommend continuing dexamethasone 4 mg once on the day after each day of radiation if radiation is not planned for that day (Ref).
Asthma, acute exacerbation (alternative agent) (off-label use): Note: Alternative to a longer course of other corticosteroids in mild to moderate exacerbations or in patients who do not respond promptly and completely to short-acting beta-agonists; administer within 1 hour of presentation to emergency department (Ref).
Oral: 12 to 16 mg daily for 1 to 2 days only (Ref); longer treatment at this dose may be associated with metabolic adverse effects (Ref).
Cancer-related pain, advanced cancer, adjuvant therapy (off-label use): Note: Although available data are limited and with mixed results, dexamethasone may provide clinical benefit in the management of a variety of types of pain in patients with advanced cancer (Ref). Due to the risk for potential toxicity, carefully consider the risks and benefits of glucocorticoid use for treating cancer-related pain, including the availability of other treatments, duration of treatment, other symptoms, and life expectancy.
Low-dose regimen for pain and other symptoms in the context of advanced cancer and short prognosis: Oral, IV: Initial: 0.75 to 1.5 mg once or twice daily; usual effective dose range: 1 to 2 mg IV or orally twice daily (Ref).
Higher-dose regimen for pain crisis that is poorly responsive to initial opioid therapy: Oral, IV: Initial: 8 to 10 mg once; if responsive, then may consider 4 mg twice daily or 8 mg once daily; use the lowest dose that maintains pain relief while other analgesic treatments are added, if indicated (Ref).
Cerebral (vasogenic) edema associated with brain tumor:
Moderate to severe symptoms (eg, lowered consciousness/brainstem dysfunction):
Initial: IV: 10 mg once followed by maintenance dosing (Ref).
Maintenance: IV, Oral: 4 mg every 6 hours (Ref). Note: Consider taper after 7 days of therapy; taper slowly over several weeks (Ref).
Mild symptoms: IV, Oral: 4 to 8 mg/day in 1 to 4 divided doses (Ref). Note: Consider taper after 7 days of therapy; taper slowly over several weeks (Ref).
COVID-19, hospitalized patients (off-label use):
Note: Dexamethasone is recommended for treatment of COVID-19 in hospitalized patients requiring supplemental oxygen or ventilatory support (Ref). An equivalent dose of an alternative glucocorticoid may be substituted if dexamethasone is unavailable (Ref).
IV, Oral: 6 mg once daily for up to 10 days (or until discharge if sooner) as part of an appropriate combination regimen (Ref).
Cushing syndrome, diagnosis: Note: Interpretation requires evaluation of one or more of the following: serum cortisol concentration, serum dexamethasone concentration, urinary cortisol excretion, or 17-hydroxycorticosteroid excretion; consultation with a clinical endocrinologist is recommended (Ref).
Initial testing:
Overnight 1 mg dexamethasone suppression test: Oral: 1 mg given once between 11 PM and 12 AM (Ref).
Longer low-dose dexamethasone suppression test (2 mg/day for 48 hours): Note: May be preferred in patients with depression, anxiety, obsessive-compulsive disorder, morbid obesity, alcoholism, or diabetes mellitus (Ref).
Oral: 0.5 mg every 6 hours for 48 hours for a total of 8 doses; start time varies (eg, 9 AM or 12 PM) (Ref).
Fetal lung maturation, acceleration of (maternal administration) (off-label use): Note: Generally, for patients between 24 and 34 weeks of gestation, including those with ruptured membranes or multiple gestations, who are at risk of delivering within 7 days. A single course may be appropriate in some pregnant patients beginning at 22 weeks' gestation or late preterm (between 34 0/7 weeks' and 36 6/7 weeks' gestation) who are at risk of delivering within 7 days.
IM: 6 mg every 12 hours for a total of 4 doses. May repeat course in select patients (eg, patients with pregnancies up to 34 weeks' gestation at risk for delivery within 7 days and >14 days have elapsed since initial course of antenatal corticosteroids) (Ref).
Immune thrombocytopenia (initial therapy): Note: Goal of therapy is to provide a safe platelet count to prevent clinically important bleeding rather than normalization of the platelet count (Ref).
Oral, IV: 40 mg once daily for 4 days and then stop (no taper); may be repeated up to 3 times if inadequate response (Ref). For severe bleeding with thrombocytopenia, give in combination with other therapies (Ref).
Iodinated contrast media allergic-like reaction, prevention (alternative agent): Note: Generally for patients with a prior allergic-like or unknown-type iodinated contrast reaction who will be receiving another iodinated contrast agent. Nonurgent premedication with an oral corticosteroid (eg, prednisone) is generally preferred when contrast administration is scheduled to begin in ≥12 hours; however, consider an urgent (accelerated) regimen with an IV corticosteroid for those requiring contrast in <12 hours. Efficacy of premedication regimens starting <4 to 5 hours before the use of contrast has not been demonstrated (Ref).
Urgent (accelerated) regimen: IV: 7.5 mg every 4 hours until contrast medium administration in combination with diphenhydramine (Ref).
Meningitis (bacterial), prevention of neurologic complications (off-label use): Note: Administer first dose of dexamethasone shortly before or at the same time as the first dose of antibacterials. If antibacterials have already been administered, do not administer dexamethasone. In patients with pneumococcal meningitis who receive dexamethasone, some experts recommend adding rifampin to the standard initial antibacterial regimen or adding rifampin if susceptibility tests, once available, show intermediate susceptibility (MIC ≥2 mcg/mL) to ceftriaxone and cefotaxime (Ref).
Developed world (suspected or confirmed pneumococcal meningitis): IV: 0.15 mg/kg/dose or 10 mg every 6 hours for 4 days; discontinue if culture data reveal non-pneumococcal etiology (Ref).
Developing world (strongly suspected or confirmed bacterial meningitis): IV: 0.4 mg/kg/dose every 12 hours for 4 days; discontinue if culture data reveal non-pneumococcal etiology; not recommended in regions with high rates of HIV infection and/or malnutrition or in cases of delayed clinical presentation (Ref).
Multiple myeloma : Note: Multiple dexamethasone-containing regimens are available. Refer to literature/guidelines for additional details. For many regimens, dexamethasone is continued until disease progression or unacceptable toxicity. Dexamethasone total weekly dose may be split over 2 days when combination therapies are administered on successive days (refer to protocol) (Ref).
Frail patients (eg, >75 years of age, BMI <18.5 kg/m2, poorly controlled diabetes, corticosteroid intolerance) : When administered weekly, dexamethasone is usually reduced to 20 mg once weekly for frail patients (Ref). May consider lower initial dexamethasone doses (8 to 20 mg once weekly) in patients >75 years of age or those with comorbidities, with subsequent titration based on response/tolerance (Ref).
Combination regimens that do not include a monoclonal antibody:
Oral:
40 mg once weekly on days 1, 8, 15, and 22 every 28 days in combination with lenalidomide (Ref), pomalidomide (Ref), ixazomib and lenalidomide (Ref), ixazomib and lenalidomide for 18 cycles (Ref), carfilzomib and lenalidomide (Ref), or bortezomib and lenalidomide (Ref) or 40 mg once weekly on days 1, 8, 15, and 22 every 28 days in cycles 1 to 9, and then 40 mg once weekly on days 1, 8, and 15 every 28 days beginning at cycle 10 (in combination with carfilzomib) (Ref).
or
20 mg on days 1, 8, 15, and 22 every 28 days (in combination with lenalidomide) for 9 cycles, followed by lenalidomide maintenance (Ref) or 20 mg on days 1, 2, 4, 5, 8, 9, 11, and 12 every 21 days (in combination with bortezomib and lenalidomide) for 8 cycles (induction), followed by 40 mg on days 1, 8, 15, and 22 every 28 days (in combination with lenalidomide) for maintenance (Ref) or 20 mg on days 1, 2, 8, 9, 15, 16, 22, and 23 every 28 days (in combination with carfilzomib) (Ref) or 20 mg on days 1 and 3 of each week (in combination with selinexor) (Ref) or 20 mg on days 1, 2, 8, 9, 15, 16, 22, 23, 29, and 30 every 35 days (in combination with selinexor and bortezomib) (Ref).
or
40 mg once daily on days 1 to 4 and 9 to 12 every 28 days in combination with bortezomib and lenalidomide for 6 cycles followed by transplant (Ref) or 40 mg once daily on days 1 to 4, 9 to 12, and 17 to 20 every 28 days in combination with bortezomib and doxorubicin for 3 cycles as induction (Ref). Note: Some experts reserve this dosing (for 1 cycle, followed by 40 mg once weekly thereafter) for patients with an aggressive disease presentation or acute renal failure from light chain cast nephropathy (Ref).
Combination regimens that include a monoclonal antibody:
Oral, IV:
40 mg weekly in combination with daratumumab and pomalidomide (Ref) or daratumumab/hyaluronidase and pomalidomide (Ref) or daratumumab and lenalidomide (Ref) or daratumumab/hyaluronidase and lenalidomide (Ref) or daratumumab and carfilzomib (Ref) or isatuximab and pomalidomide (Ref) or 20 mg once daily on days 1, 2, 4, 5, 8, 9, 11, and 12 every 21 days in combination with daratumumab and bortezomib (Ref) or 20 mg once daily on days 1, 2, 8, 9, 15, 16, 22, and 23 every 28 days in combination with isatuximab and carfilzomib (Ref). Note: In some studies, the dexamethasone dose is split over 2 days (20 mg before daratumumab and 20 mg the day after daratumumab infusion).
or
40 mg weekly, except on days elotuzumab is administered (administer dexamethasone 28 mg orally [8 mg orally in patients >75 years of age] plus 8 mg IV prior to elotuzumab) in combination with elotuzumab and pomalidomide (Ref) or elotuzumab and lenalidomide (Ref).
Neoplastic epidural spinal cord compression, symptomatic: Note: As an adjunct to definitive treatment (radiotherapy or surgery), particularly in patients with neurologic deficits (Ref).
IV (initial dose): 10 or 16 mg followed by oral dosing (Ref).
Oral (after IV dose): 16 mg/day (usually given in 2 to 4 divided doses). Once definitive treatment is underway, taper gradually over 1 to 2 weeks until discontinuation (Ref).
Tuberculosis, CNS: Note: In general, glucocorticoids are indicated for patients with established or suspected tuberculous meningitis, regardless of HIV status (Ref).
IV: Initial dose: 0.3 to 0.4 mg/kg/day for 2 weeks, then 0.2 mg/kg/day for week 3, then 0.1 mg/kg/day for week 4, followed by oral therapy (Ref).
Oral: Starting week 5 of treatment: 4 mg/day, then taper by 1 mg of the daily dose each week for 4 weeks; total combined IV/oral therapy duration: ~8 weeks (Ref); for patients with HIV, continue for 12 weeks (Ref).
Waldenström macroglobulinemia:
DRC regimen: IV: 20 mg on day 1 of a 21-day treatment cycle (in combination with rituximab and cyclophosphamide) for 6 cycles (Ref).
BDR regimen: IV: 40 mg on days 1, 4, 8, and 11 of a 21-day treatment cycle (in combination with bortezomib and rituximab) for 4 cycles, followed by a 12-week rest, then an additional 4 cycles (as an 84-day treatment cycle) for a total of 8 cycles (Ref) or 40 mg on days 1, 8, 15, and 22 of a 35-day treatment cycle during cycles 2 and 5 (in combination with bortezomib and rituximab) for a total of 5 cycles of therapy, with a total of 8 dexamethasone doses (Ref).
CaRD regimen: IV: 20 mg on days 1, 2, 8, and 9 of a 21-day treatment cycle (in combination with carfilzomib and rituximab) for 6 induction cycles, followed 8 weeks later by maintenance therapy of 20 mg on days 1 and 2 every 8 weeks (in combination with carfilzomib and rituximab) for 8 cycles (Ref).
Dosage adjustment for concomitant therapy: Significant drug interactions exist, requiring dose/frequency adjustment or avoidance. Consult drug interactions database for more information.
The renal dosing recommendations are based upon the best available evidence and clinical expertise. Senior Editorial Team: Bruce Mueller, PharmD, FCCP, FASN, FNKF; Jason A. Roberts, PhD, BPharm (Hons), B App Sc, FSHP, FISAC; Michael Heung, MD, MS.
Note: The pharmacokinetics and pharmacodynamics of corticosteroids in kidney impairment are not well understood (Ref). Dexamethasone half-life is decreased in patients with severe kidney impairment (Ref), potentially due to decreased protein binding (Ref); however, the clinical implications of these findings are unclear.
Oral, parenteral:
Altered kidney function: No dosage adjustment necessary for any degree of kidney dysfunction (Ref).
Hemodialysis, intermittent (thrice weekly): No supplemental dose or dosage adjustment necessary (Ref).
Peritoneal dialysis: No dosage adjustment necessary (Ref).
CRRT: No dosage adjustment necessary (Ref).
PIRRT (eg, sustained, low-efficiency diafiltration): No dosage adjustment necessary (Ref).
There are no dosage adjustments provided in the manufacturer’s labeling.
The recommendations for dosing in patients with obesity are based upon the best available evidence and clinical expertise. Senior Editorial Team: Jeffrey F. Barletta, PharmD, FCCM; Manjunath P. Pai, PharmD, FCP; Jason A. Roberts, PhD, BPharm (Hons), B App Sc, FSHP, FISAC.
Class 1, 2 and 3 obesity (BMI ≥30 kg/m2):
Oral, IV, IM:
Non–weight-based dosing: No dosage adjustment necessary (Ref). Refer to adult dosing for indication-specific doses.
Weight-based dosing: Use ideal body weight to avoid overdosing and subsequent toxicity (Ref). Refer to adult dosing for indication-specific doses.
Rationale for recommendations: Corticosteroids are lipophilic compounds; however, the reported pharmacokinetic variability due to obesity is limited and inconsistent. Two small studies evaluated pharmacokinetic changes with oral dexamethasone in patients with obesity. One study reported lower AUC in patients with obesity compared to patients with normal weight (Ref), while another study reported a positive correlation between actual body weight and AUC (Ref). Weight-based dosing using actual body weight could lead to supratherapeutic levels (Ref).
Refer to adult dosing. Use cautiously in the elderly at the lowest possible dose.
(For additional information see "Dexamethasone (systemic): Pediatric drug information")
COVID-19, treatment: Very limited data available:
Note: Safety and effectiveness of dexamethasone or other corticosteroids for COVID-19 treatment have not been sufficiently evaluated in pediatric patients; use is extrapolated from adult patients; use caution. Reserve use for hospitalized patients who require high-flow oxygen, noninvasive ventilation, invasive mechanical ventilation, or extracorporeal membrane oxygenation (ECMO); not routinely recommended for pediatric patients requiring low levels of oxygen support (ie, nasal canula only). Use in profoundly immunocompromised pediatric patients should be considered only on a case-by-case basis as it has not been evaluated and may be harmful. Pediatric patients with COVID-19 should be enrolled in clinical trials whenever possible (Ref).
Infants, Children, and Adolescents: IV, Oral: 0.15 to 0.3 mg/kg/dose once daily for up to 10 days; maximum dose: 6 mg/dose (Ref). Note: An equivalent dose of an alternative glucocorticoid may be substituted if dexamethasone is unavailable (Ref).
Acute mountain sickness (AMS) (moderate)/high-altitude cerebral edema (HACE), treatment: Limited data available: Note: Dexamethasone does not facilitate acclimatization; further ascent should be delayed until patient is asymptomatic off medication (Ref).
Infants, Children, and Adolescents: Oral, IM, IV: 0.15 mg/kg/dose every 6 hours; maximum dose: 4 mg/dose (Ref).
Airway edema or extubation: Limited data available: Infants, Children, and Adolescents: Oral, IM, IV: 0.5 mg/kg/dose (maximum dose: 10 mg/dose) administered 6 to 12 hours prior to extubation then every 6 hours for 6 doses (total dexamethasone dose: 3 mg/kg) (Ref).
Anti-inflammatory: Infants, Children, and Adolescents: Oral, IM, IV: Initial dose range: 0.02 to 0.3 mg/kg/day or 0.6 to 9 mg/m2/day in divided doses every 6 to 12 hours; dose depends upon condition being treated and response of patient; dosage for infants and children should be based on disease severity and patient response; usual adult initial daily dose range: 0.75 to 9 mg/day.
Asthma exacerbation: Limited data available: Infants, Children, and Adolescents: Oral, IM, IV: 0.6 mg/kg once daily as a single dose or once daily for 2 days; maximum dose: 16 mg/dose (Ref); single dose regimens as low as 0.3 mg/kg/dose and as high as 1.7 mg/kg/dose have also been reported (Ref). Note: Duration >2 days is not recommended due to increased risk of metabolic effects (Ref).
Bacterial meningitis (Haemophilus influenzae type b): Limited data available:
Infants >6 weeks and Children: IV: 0.15 mg/kg/dose every 6 hours for the first 2 to 4 days of antibiotic treatment; start dexamethasone 10 to 20 minutes before or with the first dose of antibiotic; if antibiotics have already been administered, dexamethasone use has not been shown to improve patient outcome and is not recommended (Ref). Note: For pneumococcal meningitis, efficacy results are variable and use is controversial; risk and benefits should be considered prior to use (Ref).
Cerebral edema: Limited data available: Note: Dose, route, and duration may vary due to underlying cause of edema; tapering may be required. Infants, Children, and Adolescents: Oral, IM, IV: Loading dose: 1 to 2 mg/kg/dose as a single dose; maintenance: 1 to 2 mg/kg/day in divided doses every 4 to 6 hours; maximum daily dose: 16 mg/day (Ref).
Chemotherapy-induced nausea and vomiting, prevention: Reported regimens variable; optimal dose not established (Ref). Refer to individual protocols and emetogenic potential:
Infants, Children, and Adolescents:
POGO recommendations (Ref): Note: Reduce dose by 50% if administered concomitantly with aprepitant:
Highly/severely emetogenic chemotherapy: Oral, IV: 6 mg/m2/dose every 6 hours.
Moderately emetogenic chemotherapy: Oral, IV:
BSA ≤0.6 m2: 2 mg every 12 hours.
BSA >0.6 m2: 4 mg every 12 hours.
Alternate dosing: Highly/severely emetogenic chemotherapy: IV: Usual: 10 mg/m2/dose once daily on days of chemotherapy; some patients may require every 12-hour dosing; usual range: 8 to 14 mg/m2/dose (Ref).
Congenital adrenal hyperplasia, maintenance: Adolescents (fully grown): Oral: 0.25 to 0.5 mg once daily; use of a liquid dosage form may be preferable to allow for better dose titration (Ref). Note: For younger patients who are still growing, hydrocortisone or fludrocortisone are preferred.
Croup (laryngotracheobronchitis): Limited data available; dosing regimens variable:
Infants and Children: Oral, IM, IV: 0.6 mg/kg once; reported maximum dose highly variable; usual maximum dose: 16 mg/dose (Ref); in trials, maximum doses of 10 to 20 mg/dose have been reported with similar efficacy findings for mild to moderate croup. The majority of reported experience in infants are those ≥3 months of age; data available in <3 months of age is very limited (Ref). In one evaluation of 22 children >2 years of age, a maximum dose of 12 mg/dose (at 0.6 mg/kg/dose) did not decrease endogenous glucocorticoid levels (Ref). A single oral dose of 0.15 mg/kg has also been shown effective in infants ≥3 months and children with mild to moderate croup (Ref).
Dosage adjustment for concomitant therapy: Significant drug interactions exist, requiring dose/frequency adjustment or avoidance. Consult drug interactions database for more information.
Infants, Children, and Adolescents: IM, IV, Oral:
Kidney impairment: There are no dosage adjustments provided in the manufacturer's labeling; use with caution.
Hemodialysis or peritoneal dialysis: Based on adult data, supplemental dose is not necessary (Ref).
Infants, Children, and Adolescents: There are no dosage adjustments provided in the manufacturer's labeling.
Adrenal suppression (tertiary adrenal insufficiency) may occur with glucocorticoids, including dexamethasone, and results from inadequate stimulation of the adrenal glands (Ref). Glucocorticoid-induced adrenal insufficiency usually resolves with discontinuation of dexamethasone, but symptoms may persist for 6 to 12 months (Ref). Adrenal insufficiency may lead to adrenal crisis, a life-threatening emergency that may present like a hypotensive shock state (Ref).
Mechanism: Dose- and time-related; occurs due to lack of or diminished cortisol production by the adrenal gland (Ref). Exogenous glucocorticoids produce a similar negative feedback mechanism as endogenous cortisol, causing a subsequent decrease in adrenocorticotrophic hormone (ACTH) secretion; thus, cortisol production is suppressed resulting in adrenal atrophy and subsequent insufficiency (ie, hypothalamic-pituitary-adrenal-axis [HPA-axis] suppression) (Ref). In times of stress (eg, critical illness, trauma, surgery), the body requires stress doses in patients taking dexamethasone chronically (Ref). Primary adrenal insufficiency can be caused by dexamethasone alone (without fludrocortisone) because of its lack of mineralocorticoid activity (Ref).
Onset: Varied; acute (minutes after administration) and/or chronic (2 to 20 hours to days) (Ref). Chronic dexamethasone use does not allow for the HPA axis to recover quickly (Ref).
Risk factors:
• High doses for prolonged periods: Although some patients may become HPA suppressed with lower doses or briefer exposure, some experts consider HPA axis-suppression likely in any adult receiving a dose comparable to prednisone >20 mg/day (daytime dosing) or a dose comparable to prednisone ≥5 mg per 24 hours (evening or night dosing) for >3 weeks or with cushingoid appearance (Ref)
• Potency of glucocorticoids (Ref); dexamethasone is the most potent glucocorticoid for suppressing the HPA axis (Ref).
• Abrupt withdrawal (Ref)
• Concurrent interacting medications (eg, carbamazepine, St John's wort, mitotane, rifampicin, itraconazole, diltiazem, thyroid replacement therapy) (Ref)
• History of previous adrenal crisis (Ref)
• Use of glucocorticoid therapy delivered by various routes of administration (oral and inhaled greater risk than topical or intra-articular) (Ref)
Glucocorticoids, including dexamethasone, may cause a myriad of CNS and psychiatric/behavioral adverse reactions (Ref). Patients may develop apathy or depression. More commonly, patients develop excitatory psychiatric disturbances (including agitation, anxiety, distractibility, fear, hypomania, insomnia, irritability, lethargy, labile mood, mania, pressured speech, restlessness, and tearfulness) (Ref). Exact incidences are unclear but range from 1.8% to 57% (Ref). Severe psychiatric effects have been reported in 6% of adults receiving high-dose regimens, while depression or mania have been reported in 36% (Ref). Discontinuation or dose reductions generally resolve symptoms over days to weeks (Ref).
Mechanism: Dose-related; not clearly established. Dexamethasone and other glucocorticoids may alter feedback on the hypothalamic-pituitary-adrenal axis, which may lead to mood changes (Ref). Glucocorticoids may induce glutamate release, which may be responsible for neuronal toxicity (Ref). Exogenous glucocorticoids may also impact GABAergic steroids (Ref).
Onset: Varied; most cases occur early in treatment (within the first 5 days), average of 11.5 days. The majority develop within 6 weeks of initiation (Ref).
Risk factors:
• Higher doses (comparable to ≥80 mg prednisone) (Ref)
Possible additional risk factors:
• Age >30 years (Ref)
• Females (Ref)
• History of neuropsychiatric disorders (Ref)
Glucocorticoids may cause a cushingoid appearance (truncal obesity, facial adipose tissue, dorsocervical adipose tissue), which are adverse reactions related to patient's physical features (Ref). Reactions are more metabolic than weight gain, which is related to fluid retention (edema) (Ref). Iatrogenic Cushing syndrome resulting from glucocorticoid therapy increases morbidity and mortality and decreases quality of life (Ref).
Mechanism: Dose- and time-related; excess cortisol from exogenous source (dexamethasone) results in suppression of adrenocorticotrophic hormone (ACTH), commonly called iatrogenic Cushing syndrome (Ref).
Onset: Delayed; may develop within the first 2 months of dexamethasone therapy, with the risk dependent on the dose and duration of treatment (Ref).
Risk factors:
• Higher doses (Ref)
• Longer duration of use (Ref)
• Drug interactions prolonging the half-life of glucocorticoids via cytochrome P450 (Ref)
• BMI (high) (Ref)
• Daily caloric intake (>30 kcal/kg/day) (Ref)
Glucocorticoids, including dexamethasone, may cause GI effects, including peptic ulcer (with possible perforation and hemorrhage), dyspepsia, gastritis, abdominal distention, and ulcerative esophagitis (Ref). Meta-analyses suggest that glucocorticoid monotherapy carries little to no risk of peptic ulcer disease in the general population (Ref). Studies have demonstrated an increased risk of focal small bowel perforation in infants with low birth weight receiving dexamethasone (Ref).
Mechanism: Dose-related; glucocorticoids inhibit gastroprotective prostaglandin synthesis and reduce gastric mucus and bicarbonate secretion (Ref). Glucocorticoid immunosuppressive effects may prevent wound healing as well as mask GI signs and symptoms (Ref). Focal small bowel perforation is thought to be due to segmental degeneration of the muscularis externa (Ref).
Risk factors:
• Higher doses (equivalent to methylprednisolone ≥4 mg/day) (Ref)
• Concurrent aspirin or nonsteroidal anti-inflammatory drugs (NSAIDs) (Ref)
• Hospitalized (but not ambulatory) patients (Ref)
• Infants with low birth weight (Ref)
• Recent glucocorticoid users (7 to 28 days) versus remote or nonusers (Ref)
Glucocorticoids, including dexamethasone, may provoke new-onset hyperglycemia in patients without a history of diabetes and may cause an exacerbation of diabetes mellitus (Ref). Glucose levels have been noted to increase 68% above baseline (Ref). Certain patient populations (eg, transplant, cancer, chronic rheumatologic conditions) are at particular risk due to medication combinations (Ref). Resolution may occur within 24 to 36 hours after dexamethasone discontinuation (Ref).
Mechanism: Dose- and time-related; increased insulin resistance (Ref). May also interfere with insulin signaling by direct effects on the insulin receptor and the glucose transporter and may promote gluconeogenesis via liver stimulation (Ref).
Onset: Rapid; 4 hours (Ref). Rapid onset of steroid-induced hyperglycemia occurred within 2 days after initiation of glucocorticoids with a peak in the late afternoon following daily dosing in the morning (Ref).
Risk factors:
• Dose and type of glucocorticoid (Ref)
• Duration of use (Ref)
• Divided versus once-daily dosing (Ref)
• IV and oral routes of administration (Ref)
• Older age (Ref)
• Males (Ref)
• BMI >25 kg/m2 (Ref)
• African American or Hispanic (Ref)
• eGFR <40 mL/minute/1.73 m2 (Ref)
• HbA1c ≥6% (Ref)
• History of gestational diabetes (Ref)
• Family history of diabetes mellitus (Ref)
• Concurrent use of mycophenolate mofetil and calcineurin inhibitors (Ref)
• Previous history of impaired fasting glucose or impaired glucose tolerance (Ref)
• Patients receiving palliative care (Ref)
Glucocorticoids, including dexamethasone, have immunosuppressive and anti-inflammatory effects that are reversible with discontinuation. Infection may occur after prolonged use, including Pneumocystis jirovecii pneumonia (PJP), herpes zoster, tuberculosis, and other more common bacterial infections (Ref).
Mechanism: Dose- and time-related; related to pharmacologic action (ie, multiple activities on cell macrophage production and differentiation, inhibition of T-cell activation, and effects on dendritic cells) (Ref).
Onset: Varied; in one study, the median duration of glucocorticoid use prior to PJP diagnosis was 12 weeks but also occurred earlier or later in some cases (Ref).
Risk factors:
• Higher dose and longer duration of glucocorticoid (Ref); however, may also increase risk at lower doses (eg, ≤5 mg/day of prednisone or equivalent) (Ref).
• Immunocompromised state (Ref)
• Concurrent medications (immunosuppressive) (Ref)
• Rheumatoid arthritis (Ref)
• Interstitial lung disease (Ref)
• Older adults (Ref)
• Male (Ref)
• Low performance status (Ref)
Glucocorticoid (including dexamethasone)-induced neuromuscular and skeletal effects can take the form of various pathologies in patients ranging from osteoporosis and vertebral compression fracture to myopathy to osteonecrosis in adult and pediatric patients (Ref). Glucocorticoid use is the most common cause of secondary osteoporosis; may be underrecognized and undertreated due to underestimation of risk in this patient population (Ref). Vertebral fractures are the most common glucocorticoid-related fracture (Ref). Myopathies can also occur secondary to direct skeletal muscle catabolism (Ref). Acute steroid myopathy is rare (Ref).
Mechanism: Dose- and time-related; glucocorticoids have direct/indirect effects on bone remodeling with osteoblast recruitment decreasing and apoptosis increasing (Ref). Myopathies or myasthenia result from reductions in protein synthesis and protein catabolism, which can manifest as proximal muscle weakness and atrophy in the upper and lower extremities (Ref).
Onset: Delayed; vertebral fracture risk is increased within 3 months of initiation and peaks at 12 months (Ref).
Risk factors:
Drug-related risks:
• Cumulative dose of glucocorticoids prednisone >5 g or equivalent (Ref)
• Children receiving ≥4 courses of glucocorticoids (Ref)
• Prednisone ≥2.5 mg to 7.5 mg daily or equivalent for ≥3 months (Ref)
• Myopathy may occur at prednisone doses ≥10 mg daily or equivalent, with higher doses potentiating more of a rapid onset (Ref)
• Fluorinated glucocorticoid preparations (eg, dexamethasone, betamethasone, triamcinolone) have a higher risk of myopathies (Ref)
General fracture risks:
• Age >55 years (Ref)
• BMI <18.5 kg/m2 (Ref)
• Bone mineral T score below -1.5 (Ref)
• Endocrine disorders (eg, hypogonadism, hyper- or hypoparathyroidism) (Ref)
• Excess alcohol use (>2 units/day) (Ref)
• Females (Ref)
• History of falls (Ref)
• Malabsorption (Ref)
• Menopause and duration of menopause (Ref)
• White race (Ref)
• Patients with cancer (Ref)
• Previous fracture (Ref)
• Smoking (Ref)
• Underlying inflammatory condition in all ages (eg, inflammatory bowel disease, rheumatoid arthritis) (Ref)
Glucocorticoid (including dexamethasone)-induced ocular effects may include increased intraocular pressure (IOP), glaucoma (open-angle), and subcapsular posterior cataract in adult and pediatric patients (Ref). Cataracts may persist after discontinuation of glucocorticoid therapy (Ref).
Mechanism: Dose- and time-related; Glucocorticoids can induce cataracts by covalently bonding to lens proteins, causing destabilization of the protein structure, and oxidative changes leading to cataracts formation (Ref). There are various proposed mechanisms of IOP contributing to glaucoma, including accumulation of polymerized glycosaminoglycans in the trabecular meshwork, producing edema and increasing outflow resistance (Ref). Another mechanism may include inhibition of phagocytic endothelial cells, leading to accumulation of aqueous debris (Ref). Glucocorticoids can also alter the trabecular meshwork causing an increase in nuclear size and DNA content (Ref). In addition, they can decrease the synthesis of prostaglandins which regulate the aqueous outflow (Ref).
Onset: Delayed; cataracts may occur at least 1 year after initiation of chronic glucocorticoid therapy (Ref). IOP may occur at 4 years or more after initiation (Ref).
Risk factors:
• Dose (Ref)
• Topical > Systemic (Ref)
• Duration of use in all ages (Ref)
• Family history of open-angle glaucoma (Ref)
• Type I diabetes mellitus (Ref)
• High myopia (Ref)
• Pseudophakia (Ref)
• Prior vitrectomies (Ref)
• Connective tissue disease and sex (eg, rheumatoid arthritis in males) (Ref)
• Older patients or age <6 years (Ref)
• Genetics (Ref)
• Angle recessive glaucoma (Ref)
The following adverse drug reactions and incidences are derived from product labeling unless otherwise specified. Some reactions listed are based on reports for other agents in this same pharmacologic class and may not be specifically reported for dexamethasone.
Frequency not defined:
Cardiovascular: Bradycardia, cardiac arrhythmia, cardiomegaly, circulatory shock, edema, embolism (fat), heart failure (in susceptible patients), hypertension, myocardial rupture (after recent myocardial infarction), syncope, tachycardia, thromboembolism, thrombophlebitis, vasculitis
Dermatologic: Acne vulgaris, allergic dermatitis, alopecia, atrophic striae, diaphoresis, ecchymoses, erythema of skin, facial erythema, fragile skin, hyperpigmentation, hypertrichosis, hypopigmentation, inadvertent suppression of skin test reaction, perianal skin irritation (itching, burning, tingling; following rapid IV injection; more common in females, with higher doses; sudden onset with resolution in <1 minute) (Allan 1986; Neff 2002; Perron 2003; Singh 2011), skin atrophy, skin rash, subcutaneous atrophy, urticaria, xeroderma
Endocrine & metabolic: Decreased serum potassium, fluid retention, growth suppression (children), hirsutism, hypokalemic alkalosis, menstrual disease, negative nitrogen balance (due to protein catabolism), sodium retention, weight gain
Gastrointestinal: Hiccups, increased appetite, nausea, pancreatitis, pruritus ani (following IV injection)
Genitourinary: Defective spermatogenesis (increased or decreased), glycosuria
Hematologic & oncologic: Kaposi sarcoma (Goedert 2002), petechia
Hepatic: Hepatomegaly, increased serum transaminases
Hypersensitivity: Anaphylaxis, angioedema, nonimmune anaphylaxis
Infection: Sterile abscess
Local: Postinjection flare (intra-articular use)
Nervous system: Amyotrophy, emotional lability, euphoria, headache, increased intracranial pressure, intracranial hypertension (idiopathic; usually following discontinuation), malaise, myasthenia, neuritis, neuropathy, paresthesia, personality changes, seizure, vertigo
Neuromuscular & skeletal: Charcot arthropathy, rupture of tendon
Ophthalmic: Exophthalmos
Respiratory: Pulmonary edema
Miscellaneous: Wound healing impairment
Postmarketing:
Cardiovascular: Hypertrophic cardiomyopathy (premature infants) (Kale 2015)
Endocrine & metabolic: Adrenal suppression (tertiary) (Dineen 2019), Cushing syndrome (iatrogenic) (Hopkins 2005), cushingoid appearance (Hopkins 2005), exacerbation of diabetes mellitus (Tamez-Pérez 2015), hyperglycemia (Tamez-Pérez 2015), impaired glucose tolerance (Tamez-Pérez 2015), moon face (Hopkins 2005), redistribution of body fat (Hopkins 2005)
Gastrointestinal: Abdominal distention (Liu 2013), intestinal perforation (Gordon 1999, Gordon 2001), peptic ulcer (with possible perforation and hemorrhage) (Liu 2013), ulcerative esophagitis (Liu 2013)
Hematologic & oncologic: Tumor lysis syndrome (Chanimov 2006)
Infection: Infection (Youssef 2016)
Nervous system: Apathy (Ciriaco 2013, Warrington 2006), depression (Ciriaco 2013, Warrington 2006), psychiatric disturbance (including agitation, anxiety, distractibility, euphoria, fear, hypomania, insomnia, irritability, labile mood, lethargy, pressured speech, restlessness, tearfulness) (Ciriaco 2013, Warrington 2006)
Neuromuscular & skeletal: Bone fracture (Buckley 2018), myopathy (Liu 2013), osteonecrosis (femoral and humoral heads) (Liu 2013), osteoporosis (Buckley 2018), steroid myopathy (Haran 2018), vertebral compression fracture (Buckley 2018)
Ophthalmic: Glaucoma (Phulke 2017), increased intraocular pressure (Phulke 2017), subcapsular posterior cataract (Urban 1986)
Hypersensitivity to dexamethasone or any component of the formulation; systemic fungal infections.
Canadian labeling: Additional contraindications (not in US labeling):
Injection: Bacteremia; gastric and duodenal ulcers; glaucoma; Cushing syndrome; certain viral infections (ie, varicella, herpes genitalis); administration to live virus vaccines.
Oral: Gastric and duodenal ulcers; infection with tropical worms; active or suspected ocular or periocular infections; advanced glaucoma in patients with cup to disk ratios >0.8; systemic infection unless specific anti-infective therapy is employed.
Concerns related to adverse effects:
• Adrenal suppression: May cause hypercortisolism or suppression of hypothalamic-pituitary-adrenal axis, particularly in younger children.
• Anaphylactoid reactions: Rare cases of anaphylactoid reactions have been observed in patients receiving corticosteroids.
• Kaposi sarcoma: Prolonged treatment with corticosteroids has been associated with the development of Kaposi sarcoma; if noted, discontinuation of therapy should be considered.
Disease-related concerns:
• Adrenal insufficiency: Dexamethasone does not provide any mineralocorticoid activity in adrenal insufficiency (may be employed as a single dose while cortisol assays are performed). Hydrocortisone is the preferred treatment of chronic primary adrenal insufficiency and adrenal crisis (ES [Bornstein 2016]).
• Cardiovascular disease: Use with caution in patients with heart failure and/or hypertension; use has been associated with fluid retention, electrolyte disturbances, and hypertension. Monitor BP. Use with caution following acute myocardial infarction; corticosteroids have been associated with myocardial rupture.
• GI disease: Use with caution in patients with GI diseases (diverticulitis, fresh intestinal anastomoses, active or latent peptic ulcer, ulcerative colitis, abscess, or other pyogenic infection) due to GI perforation risk. Signs of GI perforation may be masked in patients receiving corticosteroid therapy.
• Head injury: Increased mortality was observed in patients receiving high-dose IV methylprednisolone. High-dose corticosteroids should not be used for the management of head injury (BTF [Carney 2016]).
• Hepatic impairment: Use with caution in patients with hepatic impairment, including cirrhosis; long-term use has been associated with fluid retention.
• Hepatitis B: Reactivation may occur; consider consultation with health care provider experienced with hepatitis B in patients who show evidence of hepatitis B infection.
• Myasthenia gravis: Use may cause transient worsening of myasthenia gravis (MG) (eg, within first 2 weeks of treatment); monitor for worsening MG (AAN [Narayanaswami 2021]).
• Ocular disease: Use with caution in patients with a history of ocular herpes simplex; corneal perforation has occurred; do not use in active ocular herpes simplex. Not recommended for the treatment of optic neuritis; may increase frequency of new episodes.
• Pheochromocytoma: Pheochromocytoma crisis (may be fatal) has been reported after administration of systemic corticosteroids. Consider the risk of pheochromocytoma crisis in patients with suspected or confirmed pheochromocytoma.
• Renal impairment: Use with caution in patients with renal impairment; fluid retention may occur.
• Seizure disorders: Use corticosteroids with caution in patients with a history of seizure disorder; seizures have been reported with adrenal crisis.
• Systemic sclerosis: Use with caution in patients with systemic sclerosis; an increase in scleroderma renal crisis incidence has been observed with corticosteroid use. Monitor BP and renal function in patients with systemic sclerosis treated with corticosteroids (EULAR [Kowal-Bielecka 2017]).
• Thyroid disease: Changes in thyroid status may necessitate dosage adjustments; metabolic clearance of corticosteroids increases in hyperthyroid patients and decreases in hypothyroid patients.
Concurrent drug therapy issues:
• Immunizations: Avoid administration of live or live attenuated vaccines in patients receiving immunosuppressive doses of corticosteroids. Non-live or inactivated vaccines may be administered, although the response cannot be predicted.
Special populations:
• Older adult: Use with caution in elderly patients with the smallest possible effective dose for the shortest duration.
• Pediatric: May affect growth velocity; growth should be routinely monitored in pediatric patients.
Dosage form specific issues:
• Benzyl alcohol and derivatives: Some dosage forms may contain sodium benzoate/benzoic acid; benzoic acid (benzoate) is a metabolite of benzyl alcohol; large amounts of benzyl alcohol (≥99 mg/kg/day) have been associated with a potentially fatal toxicity (“gasping syndrome”) in neonates; the “gasping syndrome” consists of metabolic acidosis, respiratory distress, gasping respirations, CNS dysfunction (including convulsions, intracranial hemorrhage), hypotension, and cardiovascular collapse (AAP ["Inactive" 1997]; CDC 1982); some data suggests that benzoate displaces bilirubin from protein binding sites (Ahlfors 2001); avoid or use dosage forms containing benzyl alcohol derivative with caution in neonates. See manufacturer's labeling.
• Propylene glycol: Some dosage forms may contain propylene glycol; large amounts are potentially toxic and have been associated hyperosmolality, lactic acidosis, seizures, and respiratory depression; use caution (AAP ["Inactive" 1997]; Zar 2007).
• Sulfite: Some products may contain sodium sulfite, a sulfite that may cause allergic-type reactions including anaphylaxis and life-threatening or less severe asthmatic episodes in susceptible patients.
Other warnings/precautions:
• Discontinuation of therapy: Withdraw therapy with gradual tapering of dose.
• Epidural injection: Corticosteroids are not approved for epidural injection. Serious neurologic events (eg, spinal cord infarction, paraplegia, quadriplegia, cortical blindness, stroke), some resulting in death, have been reported with epidural injection of corticosteroids, with and without use of fluoroscopy.
• Intra-articular injection: May produce systemic as well as local effects. Appropriate examination of any joint fluid present is necessary to exclude a septic process. Avoid injection into an infected site. Do not inject into unstable joints. Patients should not overuse joints in which symptomatic benefit has been obtained as long as the inflammatory process remains active. Frequent intra-articular injection may result in damage to joint tissues.
• Stress: Patients may require higher doses when subject to stress (ie, trauma, surgery, severe infection).
In premature neonates, the use of high-dose dexamethasone (approximately >0.5 mg/kg/day) for the prevention or treatment of bronchopulmonary dysplasia has been associated with adverse neurodevelopmental outcomes, including higher rates of cerebral palsy without additional clinical benefit over lower doses; current data do not support use of high doses; further studies are needed (Watterberg 2010).
Some dosage forms may contain propylene glycol; in neonates, large amounts of propylene glycol delivered orally, intravenously (eg, >3,000 mg/day), or topically have been associated with potentially fatal toxicities, which can include metabolic acidosis, seizures, renal failure, and CNS depression; toxicities have also been reported in children and adults, including hyperosmolality, lactic acidosis, seizures, and respiratory depression; use caution (AAP 1997; Shehab 2009).
Excipient information presented when available (limited, particularly for generics); consult specific product labeling. [DSC] = Discontinued product
Concentrate, Oral:
dexAMETHasone Intensol: 1 mg/mL (30 mL) [contains alcohol, usp; unflavored flavor]
Elixir, Oral:
Generic: 0.5 mg/5 mL (237 mL)
Kit, Injection, as sodium phosphate:
ReadySharp dexAMETHasone: 10 mg/mL [DSC] [contains benzyl alcohol, sodium sulfite]
TopiDex: 10 mg/mL [contains benzyl alcohol]
Kit, Injection, as sodium phosphate [preservative free]:
Active Injection D: 10 mg/mL [DSC]
DoubleDex: 10 mg/mL
MAS Care-Pak: 10 mg/mL
Solution, Oral:
Generic: 0.5 mg/5 mL (240 mL, 500 mL)
Solution, Injection, as sodium phosphate:
Generic: 4 mg/mL (1 mL); 20 mg/5 mL (5 mL); 120 mg/30 mL (30 mL); 10 mg/mL (1 mL); 100 mg/10 mL (10 mL)
Solution, Injection, as sodium phosphate [preservative free]:
Generic: 10 mg/mL (1 mL)
Solution Prefilled Syringe, Injection, as sodium phosphate [preservative free]:
Generic: 4 mg/mL (1 mL); 10 mg/mL (1 mL)
Tablet, Oral:
Decadron: 0.5 mg [DSC] [scored; contains fd&c yellow #5 (tartrazine), quinoline yellow (d&c yellow #10)]
Decadron: 0.75 mg [DSC] [scored; contains fd&c blue #1 (brilliant blue), quinoline yellow (d&c yellow #10)]
Decadron: 4 mg [DSC], 6 mg [DSC] [scored]
Hemady: 20 mg [contains corn starch]
Generic: 0.5 mg, 0.75 mg, 1 mg, 1.5 mg, 2 mg, 4 mg, 6 mg
Tablet Therapy Pack, Oral:
Dexabliss: 1.5 MG (39) (39 ea)
DexPak 10 Day: 1.5 mg (35 ea [DSC]) [contains fd&c red #40(allura red ac)aluminum lake]
DexPak 13 Day: 1.5 mg (51 ea [DSC]) [contains fd&c red #40(allura red ac)aluminum lake]
DexPak 6 Day: 1.5 mg (21 ea [DSC]) [contains fd&c red #40(allura red ac)aluminum lake]
Dxevo 11-Day: 1.5 mg (39 ea [DSC])
Dxevo 11-Day: 1.5 mg (39 ea [DSC]) [scored]
HiDex 6-Day: 1.5 mg (21 ea) [scored; contains fd&c red #40 (allura red ac dye)]
TaperDex 12-Day: 1.5 mg (49 ea) [contains fd&c red #40 (allura red ac dye)]
TaperDex 6-Day: 1.5 mg (21 ea) [scored; contains fd&c red #40 (allura red ac dye)]
TaperDex 6-Day: 1.5 mg (21 ea) [scored; contains fd&c red #40(allura red ac)aluminum lake]
TaperDex 7-Day: 1.5 mg (27 ea) [scored; contains fd&c red #40 (allura red ac dye)]
ZCORT 7-Day: 1.5 mg (25 ea [DSC]) [scored]
Generic: 1.5 mg (21 ea, 35 ea, 51 ea)
May be product dependent
Concentrate (dexAMETHasone Intensol Oral)
1 mg/mL (per mL): $1.07
Elixir (dexAMETHasone Oral)
0.5 mg/5 mL (per mL): $0.11 - $1.77
Kit (DoubleDex Injection)
10 mg/mL (per each): $598.00
Kit (MAS Care-Pak Injection)
10 mg/mL (per each): $605.00
Solution (dexAMETHasone Oral)
0.5 mg/5 mL (per mL): $0.27
Solution (dexAMETHasone Sod Phosphate PF Injection)
10 mg/mL (per mL): $2.10 - $9.00
Solution (dexAMETHasone Sodium Phosphate Injection)
4 mg/mL (per mL): $0.93 - $3.46
10 mg/mL (per mL): $1.49 - $1.72
20 mg/5 mL (per mL): $0.21 - $1.66
100 mg/10 mL (per mL): $0.48 - $1.86
120 mg/30 mL (per mL): $0.39 - $1.63
Solution Prefilled Syringe (dexAMETHasone Sodium Phosphate Injection)
4 mg/mL (per mL): $3.47
Tablet Therapy Pack (dexAMETHasone Oral)
1.5MG (21) (per each): $8.06 - $8.54
1.5MG (35) (per each): $8.55
1.5MG (51) (per each): $8.54
Tablet Therapy Pack (HiDex 6-Day Oral)
1.5MG (21) (per each): $33.29
Tablet Therapy Pack (TaperDex 12-Day Oral)
1.5MG (49) (per each): $5.68
Tablet Therapy Pack (TaperDex 6-Day Oral)
1.5 mg (per each): $10.80
1.5MG (21) (per each): $10.80
Tablet Therapy Pack (TaperDex 7-Day Oral)
1.5MG (27) (per each): $8.66
Tablets (dexAMETHasone Oral)
0.5 mg (per each): $0.14 - $0.21
0.75 mg (per each): $0.25 - $0.27
1 mg (per each): $0.30 - $0.37
1.5 mg (per each): $0.48 - $15.95
2 mg (per each): $0.55 - $0.74
4 mg (per each): $1.19 - $1.25
6 mg (per each): $1.78 - $1.90
Tablets (Hemady Oral)
20 mg (per each): $32.88
Disclaimer: A representative AWP (Average Wholesale Price) price or price range is provided as reference price only. A range is provided when more than one manufacturer's AWP price is available and uses the low and high price reported by the manufacturers to determine the range. The pricing data should be used for benchmarking purposes only, and as such should not be used alone to set or adjudicate any prices for reimbursement or purchasing functions or considered to be an exact price for a single product and/or manufacturer. Medi-Span expressly disclaims all warranties of any kind or nature, whether express or implied, and assumes no liability with respect to accuracy of price or price range data published in its solutions. In no event shall Medi-Span be liable for special, indirect, incidental, or consequential damages arising from use of price or price range data. Pricing data is updated monthly.
Excipient information presented when available (limited, particularly for generics); consult specific product labeling.
Elixir, Oral:
Generic: 0.5 mg/5 mL (100 ea, 100 mL)
Solution, Injection, as sodium phosphate:
Generic: 4 mg/mL (5 mL); 10 mg/mL (1 mL, 10 mL)
Tablet, Oral:
Generic: 0.5 mg, 0.75 mg, 2 mg, 4 mg
Oral: Administer with meals to help prevent GI upset. If appropriate, may administer antacids between meals to help prevent peptic ulcers.
Oral concentrate: Use only the calibrated dropper provided. Draw dose into dropper; squeeze dropper contents into a liquid or semi-solid food (water, juice, soda or soda-like beverage, applesauce, pudding). Gently stir for a few seconds. Administer the entire mixture immediately. Do not store for future use.
IV: May administer 4 mg/mL or 10 mg/mL concentration undiluted over ≥1 minute (Ref) or infuse by IVPB over 5 to 30 minutes (Ref). Rapid administration of dexamethasone may be associated with perineal irritation (especially with higher doses); consider further dilution and slower administration by IVPB to avoid perineal irritation (Ref).
IM: Administer 4 mg/mL or 10 mg/mL concentration by deep IM injection.
Intra-articular or soft tissue injection: Note: Dexamethasone sodium phosphate (a short-acting solution) is the only formulation available for intra-articular or soft tissue injections in the United States or Canada. Other glucocorticoids, such as triamcinolone acetonide or methylprednisolone acetate, are used more commonly for intra-articular or soft tissue injection (Ref). Refer to product-specific labeling for further details.
Intra-articular: Administer into affected joint.
Soft tissue: Administer into affected tissue.
Intralesional injection: Note: Dexamethasone sodium phosphate (a short-acting solution) is the only formulation available for intralesional injections in the United States or Canada. Another glucocorticoid, triamcinolone acetonide, is used more commonly for intralesional injection (Ref). Refer to product-specific labeling for further details.
Intralesional: Administer into affected area.
Oral: May administer with food or milk to decrease GI adverse effects.
Parenteral: Use preservative-free dosage forms in neonates.
IM: May administer 4 mg/mL or 10 mg/mL undiluted.
IV: May administer as undiluted solution (4 mg/mL or 10 mg/mL) slow IV push, usually over 1 to 4 minutes; rapid administration is associated with perineal discomfort (burning, tingling) (Ref); may consider further dilution of high doses and administration by IV intermittent infusion over 15 to 30 minutes (Ref).
Oral, IV, or IM injection: Anti-inflammatory or immunosuppressant agent in the treatment of a variety of diseases, including those of allergic, hematologic (eg, immune thrombocytopenia), dermatologic, neoplastic (leukemias, lymphomas, and multiple myeloma), rheumatic, autoimmune, nervous system, renal, and respiratory origin; primary or secondary adrenocorticoid deficiency (not first line); management of shock, cerebral edema, and as a diagnostic agent.
Intra-articular or soft tissue injection: As adjunctive therapy for short-term administration in synovitis of osteoarthritis, rheumatoid arthritis, acute and subacute bursitis, acute gouty arthritis, epicondylitis, acute nonspecific tenosynovitis, and posttraumatic osteoarthritis.
Intralesional injection: Keloids; localized hypertrophic, infiltrated, inflammatory lesions of lichen planus, psoriatic plaques, granuloma annulare, and lichen simplex chronicus (neurodermatitis); discoid lupus erythematosus; necrobiosis lipoidica diabeticorum; alopecia areata; cystic tumors of an aponeurosis or tendon (ganglia).
Acute mountain sickness/high-altitude cerebral edema; Acute respiratory distress syndrome, moderate to severe; Antiemetic regimens: Chemotherapy-associated nausea and vomiting, prevention; Antiemetic regimens: Postoperative nausea and vomiting, prevention; Antiemetic regimens: Radiation therapy-associated nausea and vomiting, prevention; Asthma, acute exacerbation; Cancer-related cachexia; Cancer-related pain, advanced cancer, adjuvant therapy; COVID-19, hospitalized patients; Fetal lung maturation, acceleration of; Meningitis (bacterial), prevention of neurologic complications; Migraine, recurrence prevention
DexAMETHasone may be confused with desoximetasone, dexmedeTOMIDine, dextroamphetamine
Decadron may be confused with Percodan
Dexamethasone is identified in the Screening Tool of Older Person's Prescriptions (STOPP) criteria as a potentially inappropriate medication in older adults (≥65 years of age) as long-term monotherapy (>3 months) for rheumatoid arthritis or osteoarthritis treatment (unless as periodic intra-articular use). In addition, some disease states of concern include heart failure, peptic ulcer disease, erosive esophagitis, and chronic obstructive pulmonary disease (inhaled therapies preferred) (O’Mahony 2023).
Substrate of CYP3A4 (major), P-glycoprotein/ABCB1 (minor); Note: Assignment of Major/Minor substrate status based on clinically relevant drug interaction potential; Induces CYP3A4 (weak)
Note: Interacting drugs may not be individually listed below if they are part of a group interaction (eg, individual drugs within “CYP3A4 Inducers [Strong]” are NOT listed). For a complete list of drug interactions by individual drug name and detailed management recommendations, use the drug interactions program by clicking on the “Launch drug interactions program” link above.
Abrocitinib: Corticosteroids (Systemic) may enhance the immunosuppressive effect of Abrocitinib. Management: The use of abrocitinib in combination with other immunosuppressants is not recommended. Doses equivalent to more than 2 mg/kg or 20 mg/day of prednisone (for persons over 10 kg) administered for 2 or more weeks are considered immunosuppressive. Risk D: Consider therapy modification
Acetylcholinesterase Inhibitors: Corticosteroids (Systemic) may enhance the adverse/toxic effect of Acetylcholinesterase Inhibitors. Increased muscular weakness may occur. Risk C: Monitor therapy
Aldesleukin: Corticosteroids (Systemic) may diminish the therapeutic effect of Aldesleukin. Risk X: Avoid combination
Amphotericin B: Corticosteroids (Systemic) may enhance the hypokalemic effect of Amphotericin B. Risk C: Monitor therapy
Androgens: Corticosteroids (Systemic) may enhance the fluid-retaining effect of Androgens. Risk C: Monitor therapy
Antacids: May decrease the bioavailability of Corticosteroids (Oral). Management: Consider separating doses by 2 or more hours. Budesonide enteric coated tablets could dissolve prematurely if given with drugs that lower gastric acid, with unknown impact on budesonide therapeutic effects. Risk D: Consider therapy modification
Antidiabetic Agents: Hyperglycemia-Associated Agents may diminish the therapeutic effect of Antidiabetic Agents. Risk C: Monitor therapy
Antithymocyte Globulin (Equine): Corticosteroids (Systemic) may enhance the adverse/toxic effect of Antithymocyte Globulin (Equine). Specifically, these effects may be unmasked if the dose of systemic corticosteroid is reduced. Corticosteroids (Systemic) may enhance the immunosuppressive effect of Antithymocyte Globulin (Equine). Specifically, infections may occur with greater severity and/or atypical presentations. Risk C: Monitor therapy
Aprepitant: May increase the serum concentration of DexAMETHasone (Systemic). Management: Reduce dexamethasone dose 50% with aprepitant. Aprepitant labeling incorporates this recommendation into the dose provided for dexamethasone; further reduction is not necessary. No dose adjustment may be needed with single, low-dose aprepitant for PONV. Risk D: Consider therapy modification
Atogepant: CYP3A4 Inducers (Weak) may decrease the serum concentration of Atogepant. Management: For treatment of episodic migraine, the recommended dose of atogepant is 30 mg once daily or 60 mg once daily when combined with CYP3A4 inducers. When used for treatment of chronic migraine, use of atogepant with CYP3A4 inducers should be avoided. Risk D: Consider therapy modification
Baricitinib: Corticosteroids (Systemic) may enhance the immunosuppressive effect of Baricitinib. Management: The use of baricitinib in combination with potent immunosuppressants is not recommended. Doses equivalent to more than 2 mg/kg or 20 mg/day of prednisone (for persons over 10 kg) administered for 2 or more weeks are considered immunosuppressive. Risk D: Consider therapy modification
BCG Products: Corticosteroids (Systemic) may enhance the adverse/toxic effect of BCG Products. Specifically, the risk of vaccine-associated infection may be increased. Corticosteroids (Systemic) may diminish the therapeutic effect of BCG Products. Risk X: Avoid combination
Bile Acid Sequestrants: May decrease the absorption of Corticosteroids (Oral). Risk C: Monitor therapy
Brincidofovir: Corticosteroids (Systemic) may diminish the therapeutic effect of Brincidofovir. Risk C: Monitor therapy
Brivudine: May enhance the adverse/toxic effect of Corticosteroids (Systemic). Risk X: Avoid combination
Calcitriol (Systemic): Corticosteroids (Systemic) may diminish the therapeutic effect of Calcitriol (Systemic). Risk C: Monitor therapy
CAR-T Cell Immunotherapy: Corticosteroids (Systemic) may enhance the adverse/toxic effect of CAR-T Cell Immunotherapy. Specifically, the severity and duration of neurologic toxicities may be increased. Corticosteroids (Systemic) may diminish the therapeutic effect of CAR-T Cell Immunotherapy. Management: Avoid use of corticosteroids as premedication before treatment with CAR-T cell immunotherapy agents. Corticosteroids are indicated and may be required for treatment of toxicities such as cytokine release syndrome or neurologic toxicity. Risk D: Consider therapy modification
Caspofungin: Inducers of Drug Clearance may decrease the serum concentration of Caspofungin. Management: Consider using an increased caspofungin dose of 70 mg daily in adults (or 70 mg/m2, up to a maximum of 70 mg, daily in pediatric patients) when coadministered with known inducers of drug clearance. Risk D: Consider therapy modification
Chikungunya Vaccine (Live): Corticosteroids (Systemic) may enhance the adverse/toxic effect of Chikungunya Vaccine (Live). Specifically, the risk of vaccine-associated infection may be increased. Corticosteroids (Systemic) may diminish the therapeutic effect of Chikungunya Vaccine (Live). Risk X: Avoid combination
Cladribine: Corticosteroids (Systemic) may enhance the immunosuppressive effect of Cladribine. Risk X: Avoid combination
Clofazimine: May increase the serum concentration of CYP3A4 Substrates (High risk with Inhibitors). Risk C: Monitor therapy
CloZAPine: CYP3A4 Inducers (Weak) may decrease the serum concentration of CloZAPine. Risk C: Monitor therapy
Cobicistat: May increase the serum concentration of DexAMETHasone (Systemic). DexAMETHasone (Systemic) may decrease the serum concentration of Cobicistat. Management: Consider an alternative corticosteroid. Monitor patients receiving this combination closely for evidence of diminished response to the antiviral regimen as well as increased dexamethasone effects and toxicities. Risk D: Consider therapy modification
Coccidioides immitis Skin Test: Corticosteroids (Systemic) may diminish the diagnostic effect of Coccidioides immitis Skin Test. Management: Consider discontinuing systemic corticosteroids (dosed at 2 mg/kg or 20 mg/day of prednisone (for persons over 10 kg) administered for 2 or more weeks) several weeks prior to coccidioides immitis skin antigen testing. Risk D: Consider therapy modification
Corticorelin: Corticosteroids (Systemic) may diminish the therapeutic effect of Corticorelin. Specifically, the plasma ACTH response to corticorelin may be blunted by recent or current corticosteroid therapy. Risk C: Monitor therapy
Cosyntropin: Corticosteroids (Systemic) may diminish the diagnostic effect of Cosyntropin. Risk C: Monitor therapy
COVID-19 Vaccine (Adenovirus Vector): Corticosteroids (Systemic) may diminish the therapeutic effect of COVID-19 Vaccine (Adenovirus Vector). Management: Administer a 2nd dose using an mRNA COVID-19 vaccine (at least 4 weeks after the primary vaccine dose) and a bivalent booster dose (at least 2 months after the additional mRNA dose or any other boosters) Risk D: Consider therapy modification
COVID-19 Vaccine (Inactivated Virus): Corticosteroids (Systemic) may diminish the therapeutic effect of COVID-19 Vaccine (Inactivated Virus). Risk C: Monitor therapy
COVID-19 Vaccine (mRNA): Corticosteroids (Systemic) may diminish the therapeutic effect of COVID-19 Vaccine (mRNA). Management: Give a 3-dose primary series for all patients aged 6 months and older taking immunosuppressive medications or therapies. Booster doses are recommended for certain age groups. See CDC guidance for details. Risk D: Consider therapy modification
COVID-19 Vaccine (Subunit): Corticosteroids (Systemic) may diminish the therapeutic effect of COVID-19 Vaccine (Subunit). Risk C: Monitor therapy
COVID-19 Vaccine (Virus-like Particles): Corticosteroids (Systemic) may diminish the therapeutic effect of COVID-19 Vaccine (Virus-like Particles). Risk C: Monitor therapy
CYP3A4 Inducers (Moderate): May decrease the serum concentration of DexAMETHasone (Systemic). Risk C: Monitor therapy
CYP3A4 Inducers (Strong): May decrease the serum concentration of DexAMETHasone (Systemic). Management: Avoid coadministration of dexamethasone and strong CYP3A4 inducers. If concomitant use cannot be avoided, consider dexamethasone dose increases. Risk D: Consider therapy modification
CYP3A4 Inhibitors (Moderate): May increase the serum concentration of DexAMETHasone (Systemic). Risk C: Monitor therapy
CYP3A4 Inhibitors (Strong): May increase the serum concentration of DexAMETHasone (Systemic). Risk C: Monitor therapy
Daclatasvir: DexAMETHasone (Systemic) may decrease the serum concentration of Daclatasvir. Risk X: Avoid combination
Deferasirox: Corticosteroids (Systemic) may enhance the adverse/toxic effect of Deferasirox. Specifically, the risk for GI ulceration/irritation or GI bleeding may be increased. Risk C: Monitor therapy
Delavirdine: DexAMETHasone (Systemic) may decrease the serum concentration of Delavirdine. Risk C: Monitor therapy
Dengue Tetravalent Vaccine (Live): Corticosteroids (Systemic) may enhance the adverse/toxic effect of Dengue Tetravalent Vaccine (Live). Specifically, the risk of vaccine associated infection may be increased. Corticosteroids (Systemic) may diminish the therapeutic effect of Dengue Tetravalent Vaccine (Live). Risk X: Avoid combination
Denosumab: May enhance the immunosuppressive effect of Corticosteroids (Systemic). Management: Consider the risk of serious infections versus the potential benefits of coadministration of denosumab and systemic corticosteroids. If combined, monitor patients for signs/symptoms of serious infections. Risk D: Consider therapy modification
Desirudin: Corticosteroids (Systemic) may enhance the anticoagulant effect of Desirudin. More specifically, corticosteroids may increase hemorrhagic risk during desirudin treatment. Management: Discontinue treatment with systemic corticosteroids prior to desirudin initiation. If concomitant use cannot be avoided, monitor patients receiving these combinations closely for clinical and laboratory evidence of excessive anticoagulation. Risk D: Consider therapy modification
Desmopressin: Corticosteroids (Systemic) may enhance the hyponatremic effect of Desmopressin. Risk X: Avoid combination
Deucravacitinib: May enhance the immunosuppressive effect of Corticosteroids (Systemic). Management: The use of deucravacitinib in combination with potent immunosuppressants is not recommended. Doses equivalent to more than 2 mg/kg or 20 mg/day of prednisone (for persons over 10 kg) administered for 2 or more weeks are considered immunosuppressive. Risk D: Consider therapy modification
Dinutuximab Beta: Corticosteroids (Systemic) may enhance the immunosuppressive effect of Dinutuximab Beta. Management: Corticosteroids are not recommended for 2 weeks prior to dinutuximab beta, during therapy and for 1 week after treatment. Doses equivalent to over 2 mg/kg or 20 mg/day of prednisone (persons over 10 kg) for 2 or more weeks are considered immunosuppressive Risk D: Consider therapy modification
Disulfiram: May enhance the adverse/toxic effect of Products Containing Ethanol. Management: Do not use disulfiram with dosage forms that contain ethanol. Risk X: Avoid combination
Elvitegravir: DexAMETHasone (Systemic) may decrease the serum concentration of Elvitegravir. Management: Consider using an alternative corticosteroid. Monitor patients receiving these agents in combination for diminished antiviral response. Risk D: Consider therapy modification
EPHEDrine (Systemic): May decrease the serum concentration of DexAMETHasone (Systemic). Risk C: Monitor therapy
Estrogen Derivatives: May increase the serum concentration of Corticosteroids (Systemic). Risk C: Monitor therapy
Etrasimod: Corticosteroids (Systemic) may enhance the immunosuppressive effect of Etrasimod. Risk C: Monitor therapy
Fexinidazole: May increase the serum concentration of CYP3A4 Substrates (High risk with Inhibitors). Risk X: Avoid combination
Filgotinib: Corticosteroids (Systemic) may enhance the immunosuppressive effect of Filgotinib. Management: Coadministration of filgotinib with systemic corticosteroids at doses equivalent to greater than 2 mg/kg or 20 mg/day of prednisone (for persons over 10 kg) administered for 2 or more weeks is not recommended. Risk D: Consider therapy modification
Fosamprenavir: DexAMETHasone (Systemic) may decrease the serum concentration of Fosamprenavir. Fosamprenavir may increase the serum concentration of DexAMETHasone (Systemic). Risk C: Monitor therapy
Fosaprepitant: May increase the serum concentration of DexAMETHasone (Systemic). Management: Reduce the dexamethasone dose 50% when coadministered with aprepitant. Aprepitant prescribing information incorporates this recommendation into the dose provided for dexamethasone; further reduction is not necessary. Risk D: Consider therapy modification
Fosnetupitant: May increase the serum concentration of DexAMETHasone (Systemic). Management: Decrease dexamethasone doses to 12 mg on day 1, and if needed based on the emetic potential of the regimen, 8 mg daily on days 2 to 4 of chemotherapy when administered with fosnetupitant. Risk D: Consider therapy modification
Fosphenytoin: May decrease the serum concentration of DexAMETHasone (Systemic). DexAMETHasone (Systemic) may decrease the serum concentration of Fosphenytoin. DexAMETHasone (Systemic) may increase the serum concentration of Fosphenytoin. Management: Consider dexamethasone dose increases when combined with fosphenytoin and monitor closely for reduced steroid efficacy. Monitor phenytoin levels closely, both increased and decreased phenytoin levels have been reported. Risk D: Consider therapy modification
Fusidic Acid (Systemic): May increase the serum concentration of CYP3A4 Substrates (High risk with Inhibitors). Management: Consider avoiding this combination if possible. If required, monitor patients closely for increased adverse effects of the CYP3A4 substrate. Risk D: Consider therapy modification
Gallium Ga 68 Dotatate: Corticosteroids (Systemic) may diminish the diagnostic effect of Gallium Ga 68 Dotatate. Risk C: Monitor therapy
Growth Hormone Analogs: Corticosteroids (Systemic) may diminish the therapeutic effect of Growth Hormone Analogs. Growth Hormone Analogs may decrease serum concentrations of the active metabolite(s) of Corticosteroids (Systemic). Risk C: Monitor therapy
Hormonal Contraceptives: CYP3A4 Inducers (Weak) may decrease the serum concentration of Hormonal Contraceptives. Management: Advise patients to use an alternative method of contraception or a back-up method during coadministration, and to continue back-up contraception for 28 days after discontinuing a weak CYP3A4 inducer to ensure contraceptive reliability. Risk D: Consider therapy modification
Hyaluronidase: Corticosteroids (Systemic) may diminish the therapeutic effect of Hyaluronidase. Management: Patients receiving corticosteroids (particularly at larger doses) may not experience the desired clinical response to standard doses of hyaluronidase. Larger doses of hyaluronidase may be required. Risk D: Consider therapy modification
Imatinib: DexAMETHasone (Systemic) may decrease the serum concentration of Imatinib. Management: Avoid concurrent use of imatinib with dexamethasone when possible. If such a combination must be used, increase imatinib dose by at least 50% and monitor clinical response closely. Risk D: Consider therapy modification
Immune Checkpoint Inhibitors (Anti-PD-1, -PD-L1, and -CTLA4 Therapies): Corticosteroids (Systemic) may diminish the therapeutic effect of Immune Checkpoint Inhibitors (Anti-PD-1, -PD-L1, and -CTLA4 Therapies). Management: Carefully consider the need for corticosteroids, at doses of a prednisone-equivalent of 10 mg or more per day, during the initiation of immune checkpoint inhibitor therapy. Use of corticosteroids to treat immune related adverse events is still recommended Risk D: Consider therapy modification
Indium 111 Capromab Pendetide: Corticosteroids (Systemic) may diminish the diagnostic effect of Indium 111 Capromab Pendetide. Risk X: Avoid combination
Inebilizumab: Corticosteroids (Systemic) may enhance the immunosuppressive effect of Inebilizumab. Risk C: Monitor therapy
Influenza Virus Vaccines: Corticosteroids (Systemic) may diminish the therapeutic effect of Influenza Virus Vaccines. Management: Administer influenza vaccines at least 2 weeks prior to initiation of systemic corticosteroids at immunosuppressive doses. Influenza vaccines administered less than 14 days prior to or during such therapy should be repeated 3 months after therapy. Risk D: Consider therapy modification
Isoniazid: Corticosteroids (Systemic) may decrease the serum concentration of Isoniazid. Risk C: Monitor therapy
Lapatinib: DexAMETHasone (Systemic) may decrease the serum concentration of Lapatinib. Management: If therapy overlap cannot be avoided, consider titrating lapatinib gradually from 1,250 mg/day up to 4,500 mg/day (HER2 positive metastatic breast cancer) or 1,500 mg/day up to 5,500 mg/day (hormone receptor/HER2 positive breast cancer) as tolerated. Risk X: Avoid combination
Leflunomide: Corticosteroids (Systemic) may enhance the immunosuppressive effect of Leflunomide. Management: Increase the frequency of chronic monitoring of platelet, white blood cell count, and hemoglobin or hematocrit to monthly, instead of every 6 to 8 weeks, if leflunomide is coadministered with immunosuppressive agents, such as systemic corticosteroids. Risk D: Consider therapy modification
Lenalidomide: DexAMETHasone (Systemic) may enhance the thrombogenic effect of Lenalidomide. Management: Due to the increased risk of venous and arterial thromboembolism associated with this combination, thromboprophylaxis is recommended, and the choice of regimen should be based on an assessment of the patient's underlying risks. Risk D: Consider therapy modification
Licorice: May increase the serum concentration of Corticosteroids (Systemic). Risk C: Monitor therapy
Loop Diuretics: Corticosteroids (Systemic) may enhance the hypokalemic effect of Loop Diuretics. Risk C: Monitor therapy
Lopinavir: DexAMETHasone (Systemic) may decrease the serum concentration of Lopinavir. Management: Consider alternative corticosteroids for coadministration with lopinavir/ritonavir due to the potential for dexamethasone to decrease lopinavir/ritonavir efficacy and result in the development of resistance. Risk D: Consider therapy modification
Lutetium Lu 177 Dotatate: Corticosteroids (Systemic) may diminish the therapeutic effect of Lutetium Lu 177 Dotatate. Management: Avoid repeated use of high-doses of corticosteroids during treatment with lutetium Lu 177 dotatate. Use of corticosteroids is still permitted for the treatment of neuroendocrine hormonal crisis. The effects of lower corticosteroid doses is unknown. Risk D: Consider therapy modification
Macimorelin: Corticosteroids (Systemic) may diminish the diagnostic effect of Macimorelin. Risk X: Avoid combination
Methotrimeprazine: Products Containing Ethanol may enhance the adverse/toxic effect of Methotrimeprazine. Specifically, a disulfiram-like reaction may occur and CNS depressant effects may be increased. Management: Avoid products containing alcohol in patients treated with methotrimeprazine. Risk X: Avoid combination
MetyraPONE: Corticosteroids (Systemic) may diminish the diagnostic effect of MetyraPONE. Management: Consider alternatives to the use of the metyrapone test in patients taking systemic corticosteroids. Risk D: Consider therapy modification
Mifamurtide: Corticosteroids (Systemic) may diminish the therapeutic effect of Mifamurtide. Risk X: Avoid combination
MiFEPRIStone: May diminish the therapeutic effect of Corticosteroids (Systemic). MiFEPRIStone may increase the serum concentration of Corticosteroids (Systemic). Management: Avoid mifepristone in patients who require long-term corticosteroid treatment of serious illnesses or conditions (eg, for immunosuppression following transplantation). Corticosteroid effects may be reduced by mifepristone treatment. Risk X: Avoid combination
Mumps- Rubella- or Varicella-Containing Live Vaccines: Corticosteroids (Systemic) may enhance the adverse/toxic effect of Mumps- Rubella- or Varicella-Containing Live Vaccines. Specifically, the risk of vaccine-associated infection may be increased. Corticosteroids (Systemic) may diminish the therapeutic effect of Mumps- Rubella- or Varicella-Containing Live Vaccines. Risk X: Avoid combination
Nadofaragene Firadenovec: Corticosteroids (Systemic) may enhance the adverse/toxic effect of Nadofaragene Firadenovec. Specifically, the risk of disseminated adenovirus infection may be increased. Risk X: Avoid combination
Natalizumab: Corticosteroids (Systemic) may enhance the immunosuppressive effect of Natalizumab. Risk X: Avoid combination
Netupitant: May increase the serum concentration of DexAMETHasone (Systemic). Management: Decrease dexamethasone doses to 12 mg on day 1, and if needed based on the emetic potential of the regimen, 8 mg daily on days 2 to 4 of chemotherapy when administered with netupitant. Risk D: Consider therapy modification
Neuromuscular-Blocking Agents (Nondepolarizing): May enhance the adverse neuromuscular effect of Corticosteroids (Systemic). Increased muscle weakness, possibly progressing to polyneuropathies and myopathies, may occur. Management: If concomitant therapy is required, use the lowest dose for the shortest duration to limit the risk of myopathy or neuropathy. Monitor for new onset or worsening muscle weakness, reduction or loss of deep tendon reflexes, and peripheral sensory decriments Risk D: Consider therapy modification
Nicorandil: Corticosteroids (Systemic) may enhance the adverse/toxic effect of Nicorandil. Gastrointestinal perforation has been reported in association with this combination. Risk C: Monitor therapy
NiMODipine: CYP3A4 Inducers (Weak) may decrease the serum concentration of NiMODipine. Risk C: Monitor therapy
Nirmatrelvir and Ritonavir: May increase the serum concentration of DexAMETHasone (Systemic). Risk C: Monitor therapy
Nonsteroidal Anti-Inflammatory Agents (COX-2 Selective): Corticosteroids (Systemic) may enhance the adverse/toxic effect of Nonsteroidal Anti-Inflammatory Agents (COX-2 Selective). Risk C: Monitor therapy
Nonsteroidal Anti-Inflammatory Agents (Nonselective): Corticosteroids (Systemic) may enhance the adverse/toxic effect of Nonsteroidal Anti-Inflammatory Agents (Nonselective). Risk C: Monitor therapy
Nonsteroidal Anti-Inflammatory Agents (Topical): May enhance the adverse/toxic effect of Corticosteroids (Systemic). Specifically, the risk of gastrointestinal bleeding, ulceration, and perforation may be increased. Risk C: Monitor therapy
Ocrelizumab: Corticosteroids (Systemic) may enhance the immunosuppressive effect of Ocrelizumab. Risk C: Monitor therapy
Ofatumumab: Corticosteroids (Systemic) may enhance the immunosuppressive effect of Ofatumumab. Risk C: Monitor therapy
Ornidazole: May enhance the adverse/toxic effect of Products Containing Ethanol. Specifically, a disulfiram-like reaction may occur. Risk X: Avoid combination
Ozanimod: Corticosteroids (Systemic) may enhance the immunosuppressive effect of Ozanimod. Risk C: Monitor therapy
Phenytoin: May decrease the serum concentration of DexAMETHasone (Systemic). DexAMETHasone (Systemic) may decrease the serum concentration of Phenytoin. DexAMETHasone (Systemic) may increase the serum concentration of Phenytoin. Management: Consider dexamethasone dose increases when combined with phenytoin and monitor closely for reduced steroid efficacy. Monitor phenytoin levels closely when combined with dexamethasone, both increased and decreased phenytoin levels have been reported. Risk D: Consider therapy modification
Pidotimod: Corticosteroids (Systemic) may diminish the therapeutic effect of Pidotimod. Risk C: Monitor therapy
Pimecrolimus: May enhance the immunosuppressive effect of Corticosteroids (Systemic). Risk X: Avoid combination
Pneumococcal Vaccines: Corticosteroids (Systemic) may diminish the therapeutic effect of Pneumococcal Vaccines. Risk C: Monitor therapy
Poliovirus Vaccine (Live/Trivalent/Oral): Corticosteroids (Systemic) may enhance the adverse/toxic effect of Poliovirus Vaccine (Live/Trivalent/Oral). Specifically, the risk of vaccine-associated infection may be increased. Corticosteroids (Systemic) may diminish the therapeutic effect of Poliovirus Vaccine (Live/Trivalent/Oral). Risk X: Avoid combination
Polymethylmethacrylate: Corticosteroids (Systemic) may enhance the adverse/toxic effect of Polymethylmethacrylate. Specifically, the risk for hypersensitivity or implant clearance may be increased. Management: Use caution when considering use of bovine collagen-containing implants such as the polymethylmethacrylate-based Bellafill brand implant in patients who are receiving immunosuppressants. Consider use of additional skin tests prior to administration. Risk D: Consider therapy modification
Quinolones: Corticosteroids (Systemic) may enhance the adverse/toxic effect of Quinolones. Specifically, the risk of tendonitis and tendon rupture may be increased. Risk C: Monitor therapy
Rabies Vaccine: Corticosteroids (Systemic) may diminish the therapeutic effect of Rabies Vaccine. Management: Complete rabies vaccination at least 2 weeks before initiation of immunosuppressant therapy if possible. If combined, check for rabies antibody titers, and if vaccination is for post exposure prophylaxis, administer a 5th dose of the vaccine. Risk D: Consider therapy modification
Rilpivirine: DexAMETHasone (Systemic) may decrease the serum concentration of Rilpivirine. Risk X: Avoid combination
Ritlecitinib: Corticosteroids (Systemic) may enhance the immunosuppressive effect of Ritlecitinib. Risk X: Avoid combination
Ritodrine: Corticosteroids (Systemic) may enhance the adverse/toxic effect of Ritodrine. Risk C: Monitor therapy
Ruxolitinib (Topical): Corticosteroids (Systemic) may enhance the immunosuppressive effect of Ruxolitinib (Topical). Risk X: Avoid combination
Salicylates: May enhance the adverse/toxic effect of Corticosteroids (Systemic). These specifically include gastrointestinal ulceration and bleeding. Corticosteroids (Systemic) may decrease the serum concentration of Salicylates. Withdrawal of corticosteroids may result in salicylate toxicity. Risk C: Monitor therapy
Saquinavir: DexAMETHasone (Systemic) may decrease the serum concentration of Saquinavir. Management: Consider alternatives to this combination if possible, due to the potential for decreased saquinavir/ritonavir therapeutic effect and the potential development of resistance. Risk D: Consider therapy modification
Sargramostim: Corticosteroids (Systemic) may enhance the therapeutic effect of Sargramostim. Specifically, corticosteroids may enhance the myeloproliferative effects of sargramostim. Risk C: Monitor therapy
Secnidazole: Products Containing Ethanol may enhance the adverse/toxic effect of Secnidazole. Risk X: Avoid combination
Selpercatinib: CYP3A4 Inducers (Weak) may decrease the serum concentration of Selpercatinib. Risk C: Monitor therapy
Simeprevir: DexAMETHasone (Systemic) may decrease the serum concentration of Simeprevir. Risk X: Avoid combination
Sipuleucel-T: Corticosteroids (Systemic) may diminish the therapeutic effect of Sipuleucel-T. Management: Consider reducing the dose or discontinuing immunosuppressants, such as systemic corticosteroids, prior to initiating sipuleucel-T therapy. Doses equivalent to more than 2 mg/kg or 20 mg/day of prednisone given for 2 or more weeks are immunosuppressive. Risk D: Consider therapy modification
Sirolimus (Conventional): CYP3A4 Inducers (Weak) may decrease the serum concentration of Sirolimus (Conventional). Risk C: Monitor therapy
Sirolimus (Protein Bound): CYP3A4 Inducers (Weak) may decrease the serum concentration of Sirolimus (Protein Bound). Risk C: Monitor therapy
Sodium Benzoate: Corticosteroids (Systemic) may diminish the therapeutic effect of Sodium Benzoate. Risk C: Monitor therapy
Sphingosine 1-Phosphate (S1P) Receptor Modulator: May enhance the immunosuppressive effect of Corticosteroids (Systemic). Risk C: Monitor therapy
Succinylcholine: Corticosteroids (Systemic) may enhance the neuromuscular-blocking effect of Succinylcholine. Risk C: Monitor therapy
Tacrolimus (Systemic): Corticosteroids (Systemic) may decrease the serum concentration of Tacrolimus (Systemic). Conversely, when discontinuing corticosteroid therapy, tacrolimus concentrations may increase. Risk C: Monitor therapy
Tacrolimus (Systemic): CYP3A4 Inducers (Weak) may decrease the serum concentration of Tacrolimus (Systemic). Risk C: Monitor therapy
Tacrolimus (Topical): Corticosteroids (Systemic) may enhance the immunosuppressive effect of Tacrolimus (Topical). Risk X: Avoid combination
Talimogene Laherparepvec: Corticosteroids (Systemic) may enhance the adverse/toxic effect of Talimogene Laherparepvec. Specifically, the risk of infection from the live, attenuated herpes simplex virus contained in talimogene laherparepvec may be increased. Risk X: Avoid combination
Temsirolimus: DexAMETHasone (Systemic) may decrease serum concentrations of the active metabolite(s) of Temsirolimus. Risk C: Monitor therapy
Tertomotide: Corticosteroids (Systemic) may diminish the therapeutic effect of Tertomotide. Risk X: Avoid combination
Thalidomide: DexAMETHasone (Systemic) may enhance the dermatologic adverse effect of Thalidomide. DexAMETHasone (Systemic) may enhance the thrombogenic effect of Thalidomide. Management: Consider using venous thromboembolism prophylaxis (eg, low-molecular-weight heparin or warfarin [INR 2.0 to 3.0]) in patients with multiple myeloma receiving both thalidomide and dexamethasone. Monitor for increased dermatologic adverse effects (eg, rash) Risk D: Consider therapy modification
Thiazide and Thiazide-Like Diuretics: Corticosteroids (Systemic) may enhance the hypokalemic effect of Thiazide and Thiazide-Like Diuretics. Risk C: Monitor therapy
Tofacitinib: Corticosteroids (Systemic) may enhance the immunosuppressive effect of Tofacitinib. Management: Coadministration of tofacitinib with potent immunosuppressants is not recommended. Doses equivalent to more than 2 mg/kg or 20 mg/day of prednisone (for persons over 10 kg) administered for 2 or more weeks are considered immunosuppressive. Risk D: Consider therapy modification
Typhoid Vaccine: Corticosteroids (Systemic) may enhance the adverse/toxic effect of Typhoid Vaccine. Specifically, the risk of vaccine-associated infection may be increased. Corticosteroids (Systemic) may diminish the therapeutic effect of Typhoid Vaccine. Risk X: Avoid combination
Ublituximab: Corticosteroids (Systemic) may enhance the immunosuppressive effect of Ublituximab. Risk C: Monitor therapy
Ubrogepant: CYP3A4 Inducers (Weak) may decrease the serum concentration of Ubrogepant. Management: Use an initial ubrogepant dose of 100 mg and second dose (if needed) of 100 mg when used with a weak CYP3A4 inducer. Risk D: Consider therapy modification
Upadacitinib: Corticosteroids (Systemic) may enhance the immunosuppressive effect of Upadacitinib. Management: Coadministration of upadacitinib with systemic corticosteroids at doses equivalent to greater than 2 mg/kg or 20 mg/day of prednisone (for persons over 10 kg) administered for 2 or more weeks is not recommended. Risk D: Consider therapy modification
Urea Cycle Disorder Agents: Corticosteroids (Systemic) may diminish the therapeutic effect of Urea Cycle Disorder Agents. More specifically, Corticosteroids (Systemic) may increase protein catabolism and plasma ammonia concentrations, thereby increasing the doses of Urea Cycle Disorder Agents needed to maintain these concentrations in the target range. Risk C: Monitor therapy
Vaccines (Live): Corticosteroids (Systemic) may enhance the adverse/toxic effect of Vaccines (Live). Specifically, the risk of vaccine-associated infection may be increased. Corticosteroids (Systemic) may diminish the therapeutic effect of Vaccines (Live). Management: Avoid live vaccines during and for 1 month after therapy with immunosuppressive doses of corticosteroids (equivalent to prednisone > 2 mg/kg or 20 mg/day in persons over 10 kg for at least 2 weeks). Give live vaccines 4 weeks prior to therapy if possible. Risk D: Consider therapy modification
Vaccines (Non-Live/Inactivated/Non-Replicating): Corticosteroids (Systemic) may diminish the therapeutic effect of Vaccines (Non-Live/Inactivated/Non-Replicating). Management: Administer vaccines at least 2 weeks prior to immunosuppressive corticosteroids if possible. If patients are vaccinated less than 14 days prior to or during such therapy, repeat vaccination at least 3 months after therapy if immunocompetence restored. Risk D: Consider therapy modification
Vitamin K Antagonists (eg, warfarin): Corticosteroids (Systemic) may enhance the anticoagulant effect of Vitamin K Antagonists. Risk C: Monitor therapy
Voriconazole: DexAMETHasone (Systemic) may decrease the serum concentration of Voriconazole. Risk C: Monitor therapy
Yellow Fever Vaccine: Corticosteroids (Systemic) may enhance the adverse/toxic effect of Yellow Fever Vaccine. Specifically, the risk of vaccine-associated infection may be increased. Corticosteroids (Systemic) may diminish the therapeutic effect of Yellow Fever Vaccine. Risk X: Avoid combination
The manufacturer's labeling for use of dexamethasone as part of combination therapy for multiple myeloma recommends pregnancy testing prior to use in patients who could become pregnant. Patients who may become pregnant should use effective contraception during therapy and for at least 1 month after the last dexamethasone dose. Consult individual monographs for additional information related to pregnancy testing and contraception when combination therapy is used for multiple myeloma.
Dexamethasone may alter the motility of and number of spermatozoa.
Dexamethasone crosses the placenta (Brownfoot 2013); and is partially metabolized by placental enzymes to an inactive metabolite (Murphy 2007).
Some studies have shown an association between first trimester systemic corticosteroid use and oral clefts or decreased birth weight; however, information is conflicting and may be influenced by maternal dose/indication for use (Lunghi 2010; Park-Wyllie 2000; Pradat 2003). Hypoadrenalism may occur in newborns following maternal use of corticosteroids during pregnancy; monitor.
Dexamethasone is classified as a fluorinated corticosteroid. When systemic corticosteroids are needed in pregnancy for rheumatic disorders, nonfluorinated corticosteroids (eg, prednisone) are preferred. Chronic high doses should be avoided for the treatment of maternal disease (ACR [Sammaritano 2020]).
Use of the overnight dexamethasone 1 mg suppression test for Cushing syndrome is not recommended during pregnancy due to the increased risk of false positives. In addition, dexamethasone is generally avoided for the treatment of pregnant patients with adrenal insufficiency (ES [Nieman 2008]; ESE [Luger 2021]).
Antenatal corticosteroid administration promotes fetal lung maturity and is associated with the reduction of intraventricular hemorrhage, necrotizing enterocolitis, neonatal mortality, and respiratory distress syndrome. A single course of dexamethasone is recommended for patients between 24 0/7 and 33 6/7 weeks' gestation who are at risk of delivering within 7 days. This recommendation includes those with ruptured membranes or multiple gestations. A single course of dexamethasone may be considered for patients beginning at 22 0/7 weeks' gestation who are at risk of delivering within 7 days, in consultation with the family regarding resuscitation. In addition, a single course of dexamethasone may be given to patients between 34 0/7 weeks and 36 6/7 weeks who are at risk of preterm delivery within 7 days and who have not previously received corticosteroids if induction or delivery will proceed ≥24 hours and ≤7 days; delivery should not be delayed for administration of antenatal corticosteroids. Use of concomitant tocolytics is not currently recommended and administration of late preterm corticosteroids has not been evaluated in patients with intrauterine infection, multiple gestations, pregestational diabetes, or patients who delivered previously by cesarean section at term. Multiple repeat courses are not recommended. However, in patients with pregnancies less than 34 weeks' gestation at risk for delivery within 7 days and who had a course of antenatal corticosteroids >14 days prior, a single repeat course may be considered; use of a repeat course in patients with preterm prelabor rupture of membranes is controversial (ACOG 2016; ACOG 2017; ACOG 2020; ACOG 2022a).
Dexamethasone is used off label in the management of COVID-19. In general, the treatment of COVID-19 during pregnancy is the same as in nonpregnant patients. However, because data for most therapeutic agents in pregnant patients are limited, treatment options should be evaluated as part of a shared decision-making process. Dexamethasone is recommended for hospitalized pregnant patients with COVID-19 if indicated (NIH 2023). In patients who do not require dexamethasone for fetal lung maturity, or in those who have already completed a course of dexamethasone to enhance fetal lung development, treatment recommendations are available using alternative corticosteroids which have more limited placental transfer and may provide less fetal risk. Suggested treatment algorithms are available for pregnant patients with severe or critical COVID-19 requiring corticosteroids (Saad 2020; Teelucksingh 2022). The risk of severe illness from COVID-19 infection is increased in symptomatic pregnant patients compared to nonpregnant patients (ACOG 2023). Information related to the treatment of COVID-19 during pregnancy continues to emerge; refer to current guidelines for the treatment of pregnant patients.
Some products contain alcohol, benzyl alcohol or sodium sulfite; use of preservative-free or alternative formulations in pregnancy is recommended.
Corticosteroids are present in breast milk; information specific to dexamethasone has not been located.
The manufacturer notes that when used systemically, maternal use of corticosteroids have the potential to cause adverse events in a breastfeeding infant (eg, growth suppression, interfere with endogenous corticosteroid production).
Single doses of dexamethasone are considered compatible with breastfeeding; information related to prolonged use is not available (WHO 2002). Breastfeeding can continue if dexamethasone is needed for the management of COVID-19 (NIH 2023). However, lactating patients with COVID-19 infection can transmit the virus through respiratory droplets and all precautions should be taken to avoid spreading the virus to the infant (eg, hand hygiene, mask wearing); alternatively, breast milk can be expressed and fed to the infant by someone without confirmed or suspected COVID-19 (ACOG 2023; NIH 2023). Dexamethasone is classified as a fluorinated corticosteroid. When systemic corticosteroids are needed in a lactating patient for rheumatic disorders, low doses of nonfluorinated corticosteroids (eg, prednisone) are preferred (ACR [Sammaritano 2020]).
Due to the potential for serious adverse reactions in the breastfeeding infant, some manufacturers recommend a decision be made to discontinue breastfeeding or to discontinue the drug, considering the importance of treatment to the mother. If there is concern about exposure to the infant, some guidelines recommend waiting 4 hours after the maternal dose of an oral systemic corticosteroid before breastfeeding in order to decrease potential exposure to the breastfed infant (based on a study using prednisolone) (Leachman 2006; Makol 2011; Ost 1985).
The manufacturer's labeling for use of dexamethasone as part of combination therapy for multiple myeloma recommends breastfeeding be discontinued during therapy and for 2 weeks after the last dexamethasone dose.
May be taken with meals to decrease GI upset. May need diet with increased potassium, pyridoxine, vitamin C, vitamin D, folate, calcium, and phosphorus.
Hb, occult blood loss, BP, serum potassium, blood glucose, creatine kinase (if symptoms of myopathy occur), bone mineral density; intraocular pressure with systemic use >6 weeks; consider routine eye exams with chronic use; weight and height in children; hypothalamic-pituitary-adrenal axis suppression.
Oncology patients: Evaluate pregnancy status (in patients who could become pregnant when receiving for multiple myeloma treatment). The American Society of Clinical Oncology hepatitis B virus (HBV) screening and management provisional clinical opinion (ASCO [Hwang 2020]) recommends HBV screening with hepatitis B surface antigen, hepatitis B core antibody, total Ig or IgG, and antibody to hepatitis B surface antigen prior to beginning (or at the beginning of) systemic anticancer therapy; do not delay treatment for screening/results. Detection of chronic or past HBV infection requires a risk assessment to determine antiviral prophylaxis requirements, monitoring, and follow-up.
Dexamethasone is a long-acting corticosteroid with minimal sodium-retaining potential. It decreases inflammation by suppression of neutrophil migration, decreased production of inflammatory mediators, and reversal of increased capillary permeability; suppresses normal immune response. Dexamethasone induces apoptosis in multiple myeloma cells. Dexamethasone's mechanism of antiemetic activity is unknown.
Onset of action: IV: Rapid.
Immune thrombocytopenia: Oral: Initial response: 2 to 14 days; Peak response: 4 to 28 days (Neunert 2011).
Duration: IV: Short.
Absorption: Oral: 61% to 86% (Czock 2005).
Metabolism: Hepatic.
Half-life elimination:
Extremely low birth-weight infants with BPD: 9.26 ± 3.34 hours (range: 5.85 to 16.1 hours) (Charles 1993).
Children 4 months to 16 years: 4.34 ± 4.14 hours (range: 2.33 to 9.54 hours) (Richter 1983).
Adults: Oral: 4 ± 0.9 hours (Czock 2005); IV: ~1 to 5 hours (Hochhaus 2001; Miyabo 1981; Rohdewald 1987; Tóth 1999).
Time to peak, serum: Oral: 1 to 2 hours (Czock 2005); IM: ~30 to 120 minutes (Egerman 1997; Hochhaus 2001); IV: 5 to 10 minutes (free dexamethasone) (Miyabo 1981; Rohdewald 1987).
Excretion: Urine (~10%) (Duggan 1975; Miyabo 1981).
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