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Dexamethasone (Systemic)

Class: Adrenals
VA Class: NT200
CAS Number: 50-02-2
Brands: Dexpak

Medically reviewed by on Aug 30, 2021. Written by ASHP.


Synthetic glucocorticoid; minimal mineralocorticoid activity.

Uses for Dexamethasone (Systemic)

Treatment of a wide variety of diseases and conditions principally for glucocorticoid effects as an anti-inflammatory and immunosuppressant agent and for its effects on blood and lymphatic systems in the palliative treatment of various diseases.

Usually, inadequate alone for adrenocortical insufficiency because of minimal mineralocorticoid activity.

Adrenocortical Insufficiency

Corticosteroids are administered in physiologic dosages to replace deficient endogenous hormones in patients with adrenocortical insufficiency.

Because production of both mineralocorticoids and glucocorticoids is deficient in adrenocortical insufficiency, hydrocortisone or cortisone (in conjunction with liberal salt intake) usually is the corticosteroid of choice for replacement therapy.

If dexamethasone is used, must also administer a mineralocorticoid (fludrocortisone), particularly in infants.

In suspected or known adrenal insufficiency, parenteral therapy may be used preoperatively or during serious trauma, illness, or shock unresponsive to conventional therapy.

In shock, IV therapy in conjunction with other therapy for shock is essential; hydrocortisone is preferred, but a synthetic glucocorticoid like dexamethasone can be substituted.

Adrenogenital Syndrome

Lifelong glucocorticoid treatment of congenital adrenogenital syndrome.

In salt-losing forms, cortisone or hydrocortisone is preferred in conjunction with liberal salt intake; a mineralocorticoid may be necessary in conjunction through at least 5–7 years of age.

A glucocorticoid, usually alone, for long-term therapy after early childhood.

In hypertensive forms, do not use dexamethasone because of tendency toward overdosage and growth retardation.


Treatment of hypercalcemia associated with malignancy.

Usually ameliorates hypercalcemia associated with bone involvement in multiple myeloma.

Treatment of hypercalcemia associated with sarcoidosis.

Treatment of hypercalcemia associated with vitamin D intoxication.

Not effective for hypercalcemia caused by hyperparathyroidism.


Treatment of granulomatous (subacute, nonsuppurative) thyroiditis.

Anti-inflammatory action relieves fever, acute thyroid pain, and swelling.

May reduce orbital edema in endocrine exophthalmos (thyroid ophthalmopathy).

Usually reserved for palliative therapy in severely ill patients unresponsive to salicylates and thyroid hormones.

Rheumatic Disorders and Collagen Diseases

Short-term palliative treatment of acute episodes or exacerbations and systemic complications of rheumatic disorders (e.g., rheumatoid arthritis, juvenile arthritis, psoriatic arthritis, acute gouty arthritis, posttraumatic osteoarthritis, synovitis of osteoarthritis, epicondylitis, acute nonspecific tenosynovitis, ankylosing spondylitis, Reiter syndrome, rheumatic fever [especially with carditis]) and collagen diseases (e.g., acute rheumatic carditis, systemic lupus erythematosus, dermatomyositis [polymyositis], polyarteritis nodosa, vasculitis) refractory to more conservative measures.

Relieves inflammation and suppresses symptoms but not disease progression.

Rarely indicated as maintenance therapy.

May be used as maintenance therapy (e.g., in rheumatoid arthritis, acute gouty arthritis, systemic lupus erythematosus, acute rheumatic carditis) as part of a total treatment program in selected patients when more conservative therapies have proven ineffective.

Glucocorticoid withdrawal is extremely difficult if used for maintenance; relapse and recurrence usually occur with drug discontinuance.

Local injection can provide dramatic relief initially for articular manifestations of rheumatic disorders (e.g., rheumatoid arthritis) that involve only a few persistently inflamed joints or for inflammation of tendons or bursae; inflammation tends to recur and sometimes is more intense after drug cessation.

Local injection can prevent invalidism by facilitating movement of joints that might otherwise become immobile.

Controls acute manifestations of rheumatic carditis more rapidly than salicylates and may be life-saving; cannot prevent valvular damage and no better than salicylates for long-term treatment.

Adjunctively for severe systemic complications of Wegener’s granulomatosis, but cytotoxic therapy is the treatment of choice.

Primary treatment to control symptoms and prevent severe, often life-threatening complications in patients with dermatomyositis and polymyositis, polyarteritis nodosa, relapsing polychondritis, polymyalgia rheumatica and giant-cell (temporal) arteritis, or mixed connective tissue disease syndrome. High dosage may be required for acute situations; after a response has been obtained, drug must often be continued for long periods at low dosage.

Polymyositis associated with malignancy and childhood dermatomyositis may not respond well.

Rarely indicated in psoriatic arthritis, diffuse scleroderma (progressive systemic sclerosis), acute and subacute bursitis, or osteoarthritis; risks outweigh benefits.

In osteoarthritis, intraarticular injections may be beneficial but should be limited in number as joint damage may occur.

Dermatologic Diseases

Treatment of pemphigus and pemphigoid, bullous dermatitis herpetiformis, severe erythema multiforme (Stevens-Johnson syndrome), exfoliative dermatitis, uncontrollable eczema, cutaneous sarcoidosis, mycosis fungoides, lichen planus, severe psoriasis, and severe seborrheic dermatitis.

Usually reserved for acute exacerbations unresponsive to conservative therapy.

Early initiation of systemic glucocorticoid therapy may be life-saving in pemphigus vulgaris and pemphigoid, and high or massive doses may be required.

For control of severe or incapacitating allergic conditions (e.g., contact dermatitis, atopic dermatitis) intractable to adequate trials of conventional treatment.

Chronic skin disorders seldom an indication for systemic glucocorticoids.

Intralesional or sublesional injections occasionally indicated for localized chronic skin disorders (e.g., keloids, psoriatic plaques, alopecia areata, discoid lupus erythematosus, granuloma annulare) unresponsive to topical therapy.

Rarely indicated for psoriasis; if used, exacerbation may occur when the drug is withdrawn or dosage is decreased.

Rarely indicated for alopecia (areata, totalis, or universalis); may stimulate hair growth, but hair loss returns when the drug is discontinued.

Allergic Conditions

For control of severe or incapacitating allergic conditions intractable to adequate trials of conventional treatment and control of acute manifestations, including anaphylactic and anaphylactoid reactions, angioedema, acute noninfectious laryngeal edema, serum sickness, allergic symptoms of trichinosis, urticarial transfusion reactions, drug hypersensitivity reactions, and severe seasonal or perennial rhinitis.

Systemic therapy usually reserved for acute conditions and severe exacerbations.

For acute conditions, usually used in high dosage and with other therapies (e.g., antihistamines, sympathomimetics).

Reserve prolonged treatment of chronic allergic conditions for disabling conditions unresponsive to more conservative therapy and when risks of long-term glucocorticoid therapy are justified.

Ocular Disorders

To suppress a variety of allergic and nonpyogenic ocular inflammations.

To reduce scarring in ocular injuries.

For the treatment of severe acute and chronic allergic and inflammatory processes involving the eye and adnexa (e.g., allergic conjunctivitis, keratitis, allergic corneal marginal ulcers, herpes zoster ophthalmicus, iritis and iridocyclitis, chorioretinitis, diffuse posterior uveitis and choroiditis, anterior segment inflammation, optic neuritis, retrobulbar neuritis, sympathetic ophthalmia).

Acute optic neuritis optimally treated with initial high-dose IV therapy followed by chronic oral therapy. Can slow progression to clinically definite multiple sclerosis.

Less severe allergic and inflammatory allergic conditions of the eye are treated with topical (to the eye) corticosteroids.

Systemically in stubborn cases of anterior segment eye disease and when deeper ocular structures are involved.


Adjunctively for moderate to severe exacerbations of asthma and for maintenance in persistent asthma.

Systemically (oral or IV) for treatment of moderate to severe acute exacerbations of asthma (oral prednisone usually preferred); speeds resolution of airflow obstruction and reduces rate of relapse.

Because onset of effects is delayed, do not use alone for emergency treatment.

Early systemic glucocorticoid therapy particularly important for asthma exacerbations in infants and children.

In hospital management of an acute asthma exacerbation, systemic adjunctive glucocorticoids if response to oral inhalation therapy is not immediate, if oral corticosteroids were used as self-medication prior to hospitalization, or if the episode is severe.

For severe persistent asthma once initial control is achieved, high dosages of inhaled corticosteroids are preferable to oral glucocorticoids for maintenance because inhaled corticosteroids have fewer systemic effects.

Maintenance therapy with low doses of an orally inhaled corticosteroid is preferred treatment for adults and children with mild persistent asthma (i.e., patients with daytime symptoms of asthma more than twice weekly but less than once daily, and nocturnal symptoms of asthma more than twice per month).

Orally as an adjunct to other therapy to speed resolution of all but the mildest exacerbations of asthma when response to a short-acting inhaled β2-agonist is not prompt or sustained after 1 hour or in those who have a history of severe exacerbations.

Oral glucocorticoids with minimal mineralocorticoid activity and relatively short half-life (e.g., prednisone, prednisolone, methylprednisolone) are preferred.


For severe exacerbations of COPD, a short (e.g., 1–2 weeks) course of oral glucocorticoids can be added to existing therapy.

Effects of glucocorticoids in stable COPD are much less dramatic than in asthma, and role of glucocorticoids in the management of stable COPD is limited to very specific indications.


Adjunctive treatment of croup in pediatric patients.

Decreases edema in laryngeal mucosa.

Reduces need for hospitalization, shorter duration of hospitalization, and reduces need for subsequent interventions (e.g., epinephrine).


Management of symptomatic sarcoidosis.

Systemic glucocorticoids are indicated for hypercalcemia; ocular, CNS, glandular, myocardial, or severe pulmonary involvement; or severe skin lesions unresponsive to intralesional injections of glucocorticoids.

Advanced Pulmonary and Extrapulmonary Tuberculosis

Systemically as adjunctive therapy with effective antimycobacterial agents (e.g., streptomycin, isoniazid) to suppress manifestations related to the host’s inflammatory response to the bacillus (Mycobacterium tuberculosis) and ameliorate complications in severe pulmonary or extrapulmonary tuberculosis.

Adjunctive glucocorticoid therapy may enhance short-term resolution of disease manifestations (e.g., clinical and radiographic abnormalities) in advanced pulmonary tuberculosis and also may reduce mortality associated with certain forms of extrapulmonary disease (e.g., meningitis, pericarditis).

Systemic adjunctive glucocorticoids may reduce sequelae (e.g., intellectual impairment) and/or improve survival in moderate to severe tuberculous meningitis.

Systemic adjunctive glucocorticoid therapy rapidly reduces the size of pericardial effusions and the need for drainage procedures and decreases mortality (probably through control of hemodynamically threatening effusion) in acute tuberculous pericarditis.

Hastens the resolution of pain, dyspnea, and fever associated with tuberculous pleurisy.

Lipid Pneumonitis

Promotes the breakdown or dissolution of pulmonary lesions and eliminates sputum lipids in lipid pneumonitis.

Coronavirus Disease 2019 (COVID-19)

Adjunctive therapy in the treatment of serious complications from COVID-19.

NIH COVID-19 Treatment Guidelines Panel recommends use of dexamethasone in hospitalized adults with COVID-19 who require supplemental oxygen or are receiving mechanical ventilation or extracorporeal membrane oxygenation (ECMO). NIH panel recommends against use of dexamethasone in nonhospitalized adults and hospitalized adults who do not require supplemental oxygen. Data regarding potential adverse effects in COVID-19 patients, efficacy in combination with other treatments (e.g., remdesivir, tocilizumab, baricitinib), and efficacy in other patient populations (e.g., pediatric patients, pregnant women) not available to date. Although concomitant use of dexamethasone and remdesivir not rigorously studied to date, NIH panel states there is a theoretical rationale for using dexamethasone plus remdesivir in patients with rapidly progressing COVID-19. Although it is not known whether other corticosteroids have a similar benefit as dexamethasone, if dexamethasone not available, NIH panel recommends using alternative corticosteroids (e.g., hydrocortisone, methylprednisolone, prednisone). Consult the most recent NIH COVID-19 treatment guidelines for additional information on use of corticosteroids in patients with COVID-19.

For treatment of patients with nonsevere COVID-19, WHO Guideline Development Group suggests not using systemic corticosteroids, regardless of hospitalization status; however, if clinical condition of such patients worsens, systemic corticosteroids are recommended. WHO strongly recommends use of systemic corticosteroids over no systemic corticosteroid therapy for treatment of patients with severe and/or critical COVID-19, regardless of hospitalization status. WHO recommends against discontinuing systemic corticosteroids in patients with nonsevere COVID-19 who are receiving systemic corticosteroids for chronic conditions (e.g., COPD, autoimmune diseases). Consult the most recent WHO COVID-19 treatment guidelines for additional information.

Loeffler’s Syndrome

Symptomatic relief of acute manifestations of symptomatic Loeffler’s syndrome not manageable by other means.


Symptomatic relief of acute manifestations of berylliosis.

Aspiration Pneumonitis

Symptomatic relief of acute manifestations of aspiration pneumonitis.


Adjunct to anti-infective therapy in the treatment of anthrax in an attempt to ameliorate toxin-mediated effects associated with Bacillus anthracis infections.

For cutaneous anthrax if there are signs of systemic involvement or extensive edema involving the neck and thoracic region, anthrax meningitis, and inhalational anthrax that occurs as the result of exposure to anthrax spores in the context of biologic warfare or bioterrorism if extensive edema, respiratory compromise, or meningitis is present.

Antenatal Use in Preterm Labor

Short-course IM therapy in selected women with preterm labor to hasten fetal maturation (e.g., lungs, cerebral blood vessels), including women with preterm premature rupture of membranes, preeclampsia, or third-trimester hemorrhage.

Reduces the incidence and/or severity of neonatal respiratory distress syndrome (RDS) as indicated by a reduction in requirements for neonatal ventilatory support or surfactant therapy; beneficial effects are additive with those of surfactant.

Combined effects on multiple organ maturation reduces neonatal mortality; beneficial effects extend to a broad range of gestational ages (i.e., 24–34 weeks).

Can improve neonatal circulatory stability and reduce the incidence or severity of intraventricular hemorrhage.

Maternal use of tocolytic agents in conjunction with glucocorticoids may delay delivery in preterm labor long enough for the fetus to derive benefit from glucocorticoid-induced accelerated fetal maturation.

Additive effect with postnatal prophylactic lung surfactant therapy in reducing the incidence of RDS and neonatal mortality. In addition, antenatal glucocorticoids can reduce the incidence and/or severity of intraventricular hemorrhage, which surfactant therapy alone does not appear to benefit.

Conflicting data concerning the effects on the incidence of necrotizing colitis, bronchopulmonary dysplasia, and patent ductus arteriosus in neonates.

Efficacy and safety of antenatal glucocorticoid therapy before 24 weeks or after 34 weeks of gestation have not been established.

Antenatal glucocorticoids to reduce infant morbidity and mortality in women with preterm premature rupture of membranes is somewhat controversial, since the magnitude of neonatal benefit on RDS appears to be less and the risk of neonatal infection greater than those in women with intact membranes.

Postnatal Use for Bronchopulmonary Dysplasia

Has been used for prevention or treatment of bronchopulmonary dysplasia in very low-birth-weight infants (i.e., <1.5 kg) who require mechanical ventilation. However, the AAP states that routine use of systemic glucocorticoids in such patients is not recommended.

May provide short-term pulmonary benefits but does not reduce mortality and is associated with an increased risk of serious adverse effects (e.g., hyperglycemia, hypertension, GI bleeding or intestinal perforation, hypertrophic obstructive cardiomyopathy, poor weight gain, poor growth of head circumference) and long-term sequelae (e.g., neurodevelopmental delay, cerebral palsy, impaired cognitive function, and stunted growth at or before school age).

Hematologic Disorders

Management of acquired (autoimmune) hemolytic anemia, idiopathic thrombocytopenic purpura (ITP), secondary thrombocytopenia, erythroblastopenia, or congenital (erythroid) hypoplastic anemia.

High or even massive dosages decrease bleeding tendencies and normalize blood counts; does not affect the course or duration of hematologic disorders.

Glucocorticoids, immune globulin IV (IGIV), or splenectomy are first-line therapies for moderate to severe ITP, depending on the extent of bleeding involved.

May not affect or prevent renal complications in Henoch-Schoenlein purpura.

Insufficient evidence of effectiveness in aplastic anemia in children, but widely used.


Although IV glucocorticoids may be life-saving in shock secondary to adrenocortical insufficiency (see Adrenocortical Insufficiency under Uses), the value of the drugs in the treatment of shock resulting from other causes is controversial.

Management of shock should be based on specific treatment of the primary cause and secondary abnormalities, and glucocorticoids, if used, should be regarded only as adjunctive supportive treatment.

Value in adjunctive treatment of septic shock is particularly controversial. Conflicting evidence regarding effects of high-dose regimens on morbidity and mortality in septic shock.


To reduce the pain, fever, and inflammation of pericarditis, including that associated with MI.

Glucocorticoids can provide effective symptomatic relief, but aspirin considered the treatment of choice for postmyocardial infarction pericarditis because of greater evidence establishing benefit.

Important to distinguish between pain caused by pericarditis and that caused by ischemia since management will differ.

Consider possibility that cardiac rupture may account for recurrent pain since use of glucocorticoids may be a risk factor in its development.

Glucocorticoids may cause thinning of developing scar and myocardial rupture.

Management of tuberculous pericarditis. (See Advanced Pulmonary and Extrapulmonary Tuberculosis under Uses.)

GI Diseases

Short-term palliative therapy for acute exacerbations and systemic complications of ulcerative colitis, regional enteritis, and celiac disease.

Do not use if a probability of impending perforation, abscess, or other pyogenic infection.

Rarely indicated for maintenance therapy in chronic GI diseases (e.g., ulcerative colitis, celiac disease) since does not prevent relapses and may produce severe adverse reactions with long-term administration.

Occasionally, low dosages, in conjunction with other supportive therapy, may be useful for disease unresponsive to the usual therapy indicated for chronic conditions.

Crohn’s Disease

Management of mildly to moderately active and moderately to severely active Crohn’s disease.

Some experts state that conventional glucocorticoids should not be used for the management of mildly to moderately active disease, because of the high incidence of adverse effects and therefore, their use should be reserved for patients with moderately to severely active disease.

Parenteral glucocorticoids recommended for patients with severe fulminant Crohn’s disease. Once patients respond to parenteral therapy, they should gradually be switched to an equivalent regimen of an oral glucocorticoid.

Glucocorticoids should not be used for maintenance therapy of Crohn’s disease, because they usually do not prevent relapses and the drugs may produce severe adverse reactions with long-term administration.

Glucocorticoids been used in the management of moderately to severely active Crohn’s disease and in mild esophageal or gastroduodenal Crohn’s disease in pediatric patients.

Neoplastic Diseases

Alone or as a component of various chemotherapeutic regimens in the palliative treatment of neoplastic diseases of the lymphatic system (e.g., leukemias and lymphomas in adults and acute leukemias in children).

Treatment of breast cancer; glucocorticoids alone not as effective as other agents (e.g., cytotoxic agents, hormones, antiestrogens) and should be reserved for unresponsive disease.

Glucocorticoids alone or as a component of various combination chemotherapeutic regimens for palliative treatment of advanced, symptomatic (i.e., painful) hormone-refractory prostate cancer.

Cancer Chemotherapy-induced Nausea and Vomiting

Prevention of nausea and vomiting associated with emetogenic cancer chemotherapy.

Addition of dexamethasone to monotherapy with a selective 5-HT3 antagonist (e.g., granisetron, ondansetron) or a substituted benzamide (e.g., metoclopramide) increases antiemetic efficacy; combined therapy may be useful for nausea and vomiting refractory to monotherapy.

Cerebral Edema

To decrease cerebral edema associated with brain tumors and neurosurgery (e.g., craniotomy).

Cerebral edema associated with pseudotumor cerebri may also benefit, but efficacy of glucocorticoids is controversial and remains to be established.

Edema resulting from brain abscesses is less responsive than that resulting from brain tumors.

Pharmacologic management of cerebral edema is not a substitute for careful neurosurgical evaluation and definitive management such as neurosurgery or other specific therapy.

Head Injury

Efficacy of glucocorticoid therapy is not established; such therapy can be detrimental and is associated with a substantial increase in risk of death. Use in improving outcomes or reducing intracranial pressure in patients with head injury not recommended.

Cerebral Malaria

Glucocorticoids are not effective and can have detrimental effects in the management of cerebral malaria caused by Plasmodium falciparum; no longer recommended for this condition.

Bacterial Meningitis

Short-term adjunctive therapy (i.e., IV dexamethasone for the first 2–4 days of anti-infective therapy) of bacterial meningitis.

To benefit CSF abnormalities involving prostaglandin, lactate, glucose, and protein concentrations and to decrease neurologic manifestations and sequelae (e.g., development of hearing loss).

AAP currently recommends that adjunctive therapy with IV dexamethasone for bacterial meningitis be considered on an individualized basis in infants and children ≥6 weeks of age after weighing the relative risks and benefits.

Multiple Sclerosis

Glucocorticoids are drugs of choice for the management of acute relapses of multiple sclerosis.

Anti-inflammatory and immunomodulating effects accelerate neurologic recovery by restoring the blood-brain barrier, reducing edema, and possibly improving axonal conduction.

Shortens the duration of relapse and accelerates recovery; remains to be established whether the overall degree of recovery improves or the long-term course is altered.

Myasthenia Gravis

Management of myasthenia gravis, usually when there is an inadequate response to anticholinesterase therapy.

Parenterally for the treatment of myasthenic crisis.

Organ Transplants

In massive dosage, used concomitantly with other immunosuppressive drugs to prevent rejection of transplanted organs.

Incidence of secondary infections is high with immunosuppressive drugs; limit to clinicians experienced in their use.


Treatment of trichinosis with neurologic or myocardial involvement.

Nephrotic Syndrome and Lupus Nephritis

Treatment of idiopathic nephrotic syndrome without uremia.

Can induce diuresis and remission of proteinuria in nephrotic syndrome secondary to primary renal disease, especially when there is minimal renal histologic change.

Treatment of lupus nephritis.

Diagnostic Uses

Diagnosis (dexamethasone suppression test; DST) of adrenocortical hyperfunction (e.g., Cushing’s syndrome, adrenal hyperplasia, adrenal adenoma).

Inhibits pituitary corticotropin (ACTH) release and decreases output of endogenous corticosteroids when given in an amount that does not itself appreciably affect levels of urinary 17-hydroxycorticosteroids.

Diagnosis (DST) of mental depression; however, considerable controversy currently exists regarding the clinical utility of the test.

Sensitivity of DST in depression is relatively modest (about 40–50%), and a positive test result (nonsuppression) does not appear to reliably predict response to antidepressant therapy and a negative test result (suppression) is not an indication for withholding antidepressant therapy.

Dexamethasone (Systemic) Dosage and Administration


Route of administration and dosage depend on the condition being treated and the patient response.

Alternate-day Therapy

  • Alternate-day therapy in which a single dose is administered every other morning is the dosage regimen of choice for long-term oral glucocorticoid treatment of most conditions. This regimen provides relief of symptoms while minimizing adrenal suppression, protein catabolism, and other adverse effects.

  • Because dexamethasone’s HPA-axis suppression persists for 2.75 days, alternate-day regimens are not appropriate.

  • If alternate-day therapy is preferred, only use a “short-acting” glucocorticoid that suppresses the HPA axis <1.5 days after a single oral dose (e.g., prednisone, prednisolone, methylprednisolone).

  • Some conditions (e.g., rheumatoid arthritis, ulcerative colitis) require daily glucocorticoid therapy because symptoms of the underlying disease cannot be controlled by alternate-day therapy.

Discontinuance of Therapy

  • A steroid withdrawal syndrome consisting of lethargy, fever, myalgia can develop following abrupt discontinuance. Symptoms often occur without evidence of adrenal insufficiency (while plasma glucocorticoid concentrations were still high but were falling rapidly).

  • If used for only brief periods (a few days) in emergency situations, may reduce and discontinue dosage quite rapidly.

  • Very gradually withdraw systemic glucocorticoids until recovery of HPA-axis function occurs following long-term therapy with pharmacologic dosages. (See Adrenocortical Insufficiency under Warnings.)

  • Exercise caution when transferring from systemic glucocorticoid to oral or nasal inhalation corticosteroid therapy.

  • Many methods of slow withdrawal or “tapering” have been described.

  • In one suggested regimen, decrease by 0.375–0.75 mg every 3–7 days of until the physiologic dose (0.75 mg) is reached.

  • Other recommendations state that decrements usually should not exceed 0.375 mg every 1–2 weeks.

  • When a physiologic dosage has been reached, single 20-mg oral morning doses of hydrocortisone can be substituted for whatever glucocorticoid the patient has been receiving. After 2–4 weeks, may decrease hydrocortisone dosage by 2.5 mg every week until a single morning dosage of 10 mg daily is reached.

  • For certain acute allergic conditions (e.g., contact dermatitis such as poison ivy) or acute exacerbations of chronic allergic conditions, glucocorticoids may be administered short term (e.g., for 6 days). Administer an initially high dose on the first day of therapy, and then withdraw therapy by tapering the dose over several days.


Administer dexamethasone orally; administer dexamethasone sodium phosphate by IV injection or infusion, or IM injection.

Administer dexamethasone sodium phosphate for local effect by intra-articular, intralesional, intrasynovial, or soft-tissue injection.

Generally reserve IM or IV therapy for patients who are not able to take the drug orally or for use in an emergency situation. If an adequate clinical response does not occur after a reasonable period, discontinue the injection and transfer the patient to other therapy.

Oral Administration

Administer dexamethasone orally as tablets, solution, or concentrate solution.


May dilute the oral concentrate in juice or other flavored liquid diluent or in semisolid food (e.g., applesauce) prior to administration.

Use only the calibrated dropper provided by the manufacturer. Draw into the dropper the amount of concentrate solution prescribed.

Squeeze the dropper contents into a liquid or semi-solid food. Stir the liquid or food gently for a few seconds.

Consume the liquid or food containing dexamethasone immediately.

IV Administration

Administer dexamethasone sodium phosphate by IV injection or infusion.

For solution and drug compatibility information, see Compatibility under Stability.


When dexamethasone sodium phosphate is administered by IV infusion, the drug can be added to dextrose or sodium chloride injections.

Solutions used for IV administration for further dilution of the injection should be preservative free when used in neonates, especially premature neonates.

Use within 24 hours.

IM Administration

Administer dexamethasone sodium phosphate by IM injection.

Although rapidly absorbed from IM injection sites, consider the slower rate of absorption compared to IV administration.

Do not administer IM for conditions prone to bleeding (e.g., idiopathic thrombocytopenic purpura [ITP]).


Available as dexamethasone and dexamethasone sodium phosphate. Dosage of dexamethasone sodium phosphate is expressed in terms of dexamethasone phosphate.

After a satisfactory response is obtained, decrease dosage in small decrements to the lowest level that maintains an adequate clinical response, and discontinue the drug as soon as possible.

Monitor patients continually for signs that indicate dosage adjustment is necessary, such as remissions or exacerbations of the disease and stress (surgery, infection, trauma).

High dosages may be required for acute situations of certain rheumatic disorders and collagen diseases; after a response has been obtained, drug often must be continued for long periods at low dosage.

High or massive dosages may be required in the treatment of pemphigus, exfoliative dermatitis, bullous dermatitis herpetiformis, severe erythema multiforme, or mycosis fungoides. Early initiation of systemic glucocorticoid therapy may be life-saving in pemphigus vulgaris. Reduce dosage gradually to the lowest effective level, but discontinuance may not be possible.

Massive dosages may be required for the treatment of shock.

Pediatric Patients

Base pediatric dosage on severity of the disease and patient response rather than on strict adherence to dosage indicated by age, body weight, or body surface area.

Usual Dosage

0.024–0.34 mg/kg daily or 0.66–10 mg/m2 daily, administered in 4 divided doses.

IV or IM

6–40 µg/kg or 0.235–1.25 mg/m2 IM or IV 1 or 2 times daily.

Intra-articular, Intrasynovial, Intralesional, or Soft-tissue Injection

Dosage varies depending on location, size, and degree of inflammation.

Adolescents: 0.2–6 mg, repeated at 3-day to 3-week intervals if necessary.

Large joints (e.g., knee), Adolescents: 2–4 mg every 2–3 weeks as needed.

Smaller joints, Adolescents: 0.8–1 mg repeated every 2–3 weeks as needed.

Bursae, Adolescents: 2–3 mg every 3–5 days as needed.

Ganglia, Adolescents: 1–2 mg repeated as needed.

Soft tissues, Adolescents: 0.4–6 mg repeated as needed; 0.4–1 mg for tendon sheath inflammation and 2–6 mg for soft-tissue infiltration.

Bacterial Meningitis†

Infants and children: 0.15 mg/kg 4 times daily for the first 2–4 days of anti-infective therapy.

Alternatively, 0.4 mg/kg every 12 hours for the first 2–4 days of anti-infective therapy.

Coronavirus Disease 2019 (COVID-19)†
IV or Oral

NIH COVID-19 Treatment Guidelines Panel recommends 0.15 mg/kg (maximum 6 mg) once daily for up to 10 days. If dexamethasone not available, may consider equivalent dosages of alternative corticosteroids. Consult most recent NIH COVID-19 treatment guidelines for additional information on use of corticosteroids in pediatric patients with COVID-19.


Single dose of 0.6 mg/kg.


Usual Dosage

Usually, 0.75–6 mg daily, depending on disease being treated, and usually divided into 2–4 doses.

IV or IM

Usually, 0.5–24 mg daily, depending on the condition being treated and patient response.

Intra-articular, Intrasynovial, Intralesional, or Soft-tissue Injection

Dosage varies depending on location, size, and degree of inflammation.

0.2–6 mg, repeated at 3-day to 3-week intervals if necessary.

Large joints (e.g., knee): 2–4 mg every 2–3 weeks as needed.

Smaller joints: 0.8–1 mg repeated every 2–3 weeks as needed.

Bursae: 2–3 mg every 3–5 days as needed.

Ganglia: 1–2 mg repeated as needed.

Soft tissues: 0.4–6 mg repeated as needed; 0.4–1 mg for tendon sheath inflammation and 2–6 mg for soft-tissue infiltration.

Allergic Conditions
IM then Oral

For acute self-limited allergic conditions or acute exacerbations of chronic allergic disorders, initially 4–8 mg IM on the first day; 3 mg orally in 2 divided doses on the second and third days; 1.5 mg orally in 2 divided doses on the fourth day; and a single oral daily dose of 0.75 mg on the fifth and sixth days; then discontinue the drug.

Tuberculosis Meningitis

Initially, an IM dosage of 8–12 mg daily tapered over 6–8 weeks.

No additional benefit from higher dosages but may be associated with more frequent adverse effects.

Antenatal Use in Preterm Labor†

6 mg every 12 hours or 4 mg every 8 hours, for 2 days in preterm labor that begins at 24–34 weeks gestation.

Beneficial effects on fetal maturation are greatest >24 hours after initiating therapy and extend up to at least 7 days.

A single course for all pregnant women between 24–34 weeks’ gestation who are at risk of preterm delivery within 7 days; do not routinely repeat antenatal courses of antenatal glucocorticoids since risks and benefits remain to be fully elucidated.

Attempt antenatal administration of even a partial course unless immediate delivery is anticipated since some benefit is likely.


Life-threatening shock: Massive doses such as 1–6 mg/kg as a single IV injection or a 40-mg IV injection repeated every 2–6 hours if needed.

Alternatively, 20 mg by IV injection initially followed by continuous IV infusion of 3 mg/kg per 24 hours.

Continue high-dose therapy only until the patient’s condition has stabilized and usually not beyond 48–72 hours.

Cancer Chemotherapy-induced Nausea and Vomiting†

Usually, 10–20 mg IV before administration of the chemotherapy.

Additional IV or oral doses (usually lower than the initial dose) may be needed for 24–72 hours.

Cerebral Edema
IV then IM or Oral

Initially, 10 mg IV, then 4 mg IM every 6 hours for 2–4 days, then taper over 5–7 days.

IM or IV or Oral

In patients with recurrent or inoperable brain tumors, maintenance dosage of 2 mg IM, IV, or orally 2 or 3 times daily.

When possible, replace IM with oral therapy 1–3 mg 3 times daily.

Bacterial Meningitis†

0.15 mg/kg 4 times daily for the first 2–4 days of anti-infective therapy.

Alternatively, 0.4 mg/kg every 12 hours for the first 2–4 days of anti-infective therapy.

Coronavirus Disease 2019 (COVID-19)†
IV or Oral

NIH COVID-19 Treatment Guidelines Panel recommends 6 mg once daily for up to 10 days or until hospital discharge, whichever comes first. WHO Guidelines Development Group recommends 6 mg once daily for 7–10 days. Consult most recent NIH and WHO COVID-19 treatment guidelines for additional information on use of corticosteroids in patients with COVID-19.

Diagnostic Uses
Cushing’s Syndrome

Initially, 0.5 mg every 6 hours for 48 hours after baseline 24-hour urinary 17-hydroxycorticosteroid (17-OHCS) concentrations are determined.

During the second 24 hours of administration, collect the urine and analyze for 17-OHCS.

Alternatively, after a baseline plasma cortisol determination, administer 1-mg orally at 11 p.m., and determine plasma cortisol concentrations at 8 a.m. the following morning.

Plasma cortisol and urinary output of 17-OHCS are depressed following administration in healthy individuals but remain at basal levels in patients with Cushing’s syndrome.

To distinguish adrenal tumor from adrenal hyperplasia, 2 mg orally every 6 hours for 48 hours.

During the second 24 hours of administration, collect the urine and analyze for 17-OHCS.

In adrenal hyperplasia, urinary 17-OHCS levels are decreased and remain at basal levels in patients with adrenocortical tumors.


If used for dexamethasone suppression test (DST) for depression, 1 mg at 11 p.m.

Following day, obtain venous blood samples at 8 a.m., 4 p.m. and 11 p.m.; usually, only at 11 p.m. for outpatients.

Depending on assay used, a serum cortisol concentration >4.5–5 µg/dL for any blood sample is abnormal and represents a positive test.

Cautions for Dexamethasone (Systemic)


  • Known hypersensitivity to dexamethasone, any ingredient in the respective formulation, or any other corticosteroid.

  • Systemic fungal infections unless needed to control drug reactions due to amphotericin B.

  • Concurrent administration of live virus vaccines in patients receiving immunosuppressive doses of corticosteroids.

  • IM administration for conditions prone to bleeding (e.g., idiopathic thrombocytopenic purpura [ITP]).



Nervous System Effects

May precipitate mental disturbances ranging from euphoria, insomnia, mood swings, depression and anxiety, and personality changes to frank psychoses. Use may aggravate emotional instability or psychotic tendencies.

Use with caution in patients with myasthenia gravis receiving anticholinesterase therapy.

Serious, potentially permanent, and sometimes fatal adverse neurologic events (e.g., spinal cord infarction, paraplegia, quadriplegia, cortical blindness, stroke, seizures, nerve injury, brain edema) reported rarely, often within minutes to 48 hours following epidural glucocorticoid injection given either with or without fluoroscopic guidance.

FDA states efficacy and safety of epidural glucocorticoid administration not established; not FDA-labeled for this use. (See Advice to Patients.)

Adrenocortical Insufficiency

When given in supraphysiologic doses for prolonged periods, glucocorticoids may cause decreased secretion of endogenous corticosteroids by suppressing pituitary release of corticotropin (secondary adrenocortical insufficiency).

The degree and duration of adrenocortical insufficiency is highly variable among patients and depends on the dose, frequency and time of administration, and duration of glucocorticoid therapy.

Acute adrenal insufficiency (even death) may occur if the drugs are withdrawn abruptly or if patients are transferred from systemic glucocorticoid therapy to local (e.g., inhalation) therapy.

Withdraw dexamethasone very gradually following long-term therapy with pharmacologic dosages. (See Discontinuance of Therapy under Dosage and Administration: General.)

Adrenal suppression may persist up to 12 months in patients who receive large dosages for prolonged periods.

Until recovery occurs, signs and symptoms of adrenal insufficiency may develop if subjected to stress (e.g., infection, surgery, trauma) and replacement therapy may be required. Since mineralocorticoid secretion may be impaired, sodium chloride and/or a mineralocorticoid should also be administered.

If the disease flares up during withdrawal, dosage may need to be increased and followed by a more gradual withdrawal.


Increased susceptibility to infections secondary to glucocorticoid-induced immunosuppression. Certain infections (e.g., varicella [chickenpox], measles) can have a more serious or even fatal outcome in such patients. (See Increased Susceptibility to Infection under Warnings.)

Administration of live virus vaccines, including smallpox, is contraindicated in patients receiving immunosuppressive dosages of glucocorticoids. If inactivated viral or bacterial vaccines are administered to such patients, the expected serum antibody response may not be obtained. May undertake immunization procedures in patients receiving glucocorticoids as replacement therapy (e.g., Addison’s disease).

Increased Susceptibility to Infection

Glucocorticoids, especially in large doses, increase susceptibility to and mask symptoms of infection.

Infections with any pathogen, including viral, bacterial, fungal, protozoan, or helminthic infections in any organ system, may be associated with glucocorticoids alone or in combination with other immunosuppressive agents.

Infections may be mild, but they can be severe or fatal, and localized infections may disseminate.

Do not use, except in life-threatening situations, in patients with viral infections or bacterial infections not controlled by anti-infectives.

Some infections (e.g., varicella [chickenpox], measles) can have a more serious or even fatal outcome, particularly in children.

Children and any adult who are not likely to have been exposed to varicella or measles should avoid exposure to these infections while receiving glucocorticoids.

If exposure to varicella or measles occurs in susceptible patients, treat appropriately (e.g., VZIG, IG, acyclovir).

Fatal outcome (e.g., in those developing hemorrhagic varicella) may not always be avoided even if appropriate therapy is initiated aggressively.

Immunosuppression may result in activation of latent infection or exacerbation of intercurrent infections (e.g., those caused by Candida, Mycobacterium, Toxoplasma, Strongyloides, Pneumocystis, Cryptococcus, Nocardia, Ameba). Use with great care in patients with known or suspected Strongyloides (threadworm) infection. Immunosuppression may lead to Strongyloides hyperinfection and dissemination with widespread larval migration, often accompanied by severe enterocolitis and potentially fatal gram-negative septicemia.

Prolonged use of systemic corticosteroids in patients with COVID-19 may increase risk of reactivation of latent infections (e.g., HBV, herpesvirus, strongyloidiasis, tuberculosis). Risk of reactivation of latent infections following a 10-day course of dexamethasone (6 mg once daily) not well established. When initiating dexamethasone in patients with COVID-19, consider appropriate screening and treatment to reduce the risk of Strongyloides hyperinfection in those at high risk (e.g., patients from tropical, subtropical, or warm, temperate regions or those engaged in agricultural activities) and reduce the risk of fulminant reactivation of HBV.

May exacerbate fungal infections and should not be used in the presence of such infection unless needed to control drug reactions to amphotericin B.

Not effective and can have detrimental effects (prolongation of coma, higher incidence of pneumonia and GI bleeding) in the management of cerebral malaria.

Can reactivate tuberculosis. Include chemoprophylaxis in patients with a history of active tuberculosis undergoing prolonged glucocorticoid therapy. Observe closely for evidence of reactivation. Restrict use in active tuberculosis to those with fulminating or disseminated tuberculosis in which glucocorticoids are used in conjunction with appropriate chemoprophylaxis.

Can reactivate latent amebiasis. Exclude possible amebiasis in any patient who has been in the tropics or who has unexplained diarrhea prior to initiating therapy.

Musculoskeletal Effects

Muscle wasting, muscle pain or weakness, delayed wound healing, and atrophy of the protein matrix of the bone resulting in osteoporosis, vertebral compression fractures, aseptic necrosis of femoral or humeral heads, or pathologic fractures of long bones are manifestations of protein catabolism that may occur during prolonged therapy with glucocorticoids. These adverse effects may be especially serious in geriatric or debilitated patients. A high-protein diet may help to prevent adverse effects associated with protein catabolism.

An acute, generalized myopathy can occur with the use of high doses of glucocorticoids, particularly in patients with disorders of neuromuscular transmission (e.g., myasthenia gravis) or in patients receiving concomitant therapy with neuromuscular blocking agents (e.g., pancuronium).

Tendon rupture, particularly of the Achilles tendon.

Osteoporosis and related fractures are one of the most serious adverse effects of long-term glucocorticoid therapy.

To minimize the risk of glucocorticoid-induced bone loss, the smallest possible effective dosage and duration should be used. Topical and inhaled preparations should be used whenever possible.

Before initiating glucocorticoid therapy in postmenopausal women, consider that they are especially prone to osteoporosis.

Withdraw glucocorticoids if osteoporosis develops, unless their use is life-saving.

Glucocorticoid-induced bone loss can be both prevented and treated. Baseline measurement of bone mass density (BMD) at the lumbar spine and/or hip should be obtained when initiating long-term (e.g., exceeding 6 months) glucocorticoid therapy and appropriate preventive therapy should be initiated. Longitudinal measurements may be repeated as often as every 6 months to detect possible bone loss. Less frequent (e.g., annually) follow-up probably is sufficient in patients who are receiving therapy to prevent bone loss.

Skeletal wasting is most rapid during the initial 6 months of therapy, and trabecular bone is affected to a greater degree than is cortical bone.

Calcium and vitamin D supplementation, bisphosphonate (e.g., alendronate, risedronate), and a weight-bearing exercise program that maintains muscle mass are suitable first-line therapies aimed at reducing the risk of adverse bone effects.

Calcitonin may be considered as second-line therapy for patients who refuse or do not tolerate bisphosphonate therapy or in whom the drugs are contraindicated.

Fluid and Electrolyte Disturbances

Sodium retention with resultant edema, potassium loss, and elevation of BP may occur but is less common with dexamethasone than with average or large doses of cortisone or hydrocortisone. Risk is increased with high-dose dexamethasone for prolonged periods. Edema and CHF (in susceptible patients) may occur.

Dietary salt restriction is advisable and potassium supplementation may be necessary.

Increased calcium excretion and possible hypocalcemia.

Ocular Effects

Prolonged use may result in posterior subcapsular and nuclear cataracts (particularly in children), exophthalmos, and/or increased IOP which may result in glaucoma or may occasionally damage the optic nerve.

May enhance the establishment of secondary fungal and viral infections of the eye.

Cortical blindness has occurred following epidural glucocorticoid injection.

Do not use in patients with active ocular herpes simplex infections for fear of corneal perforation.

Endocrine and Metabolic Effects

Administration over a prolonged period may produce various endocrine disorders including hypercorticism (cushingoid state) and amenorrhea or other menstrual difficulties. Corticosteroids have also been reported to increase or decrease motility and number of sperm in some men.

May decrease glucose tolerance, produce hyperglycemia, and aggravate or precipitate diabetes mellitus, especially in patients predisposed to diabetes mellitus. If glucocorticoid therapy is required in patients with diabetes mellitus, changes in insulin or oral antidiabetic agent dosage or diet may be necessary.

Exaggerated response to the glucocorticoids in hypothyroidism.

Cardiovascular Effects

Use with extreme caution in recent MI since an association between use of glucocorticoids and left ventricular free-wall rupture has been suggested.

Sensitivity Reactions

Anaphylactic and hypersensitivity reactions reported.

General Precautions


Prior to initiation of long-term glucocorticoid therapy, perform baseline ECGs, blood pressures, chest and spinal radiographs, glucose tolerance tests, and evaluations of HPA-axis function on all patients.

Perform upper GI radiographs in patients predisposed to GI disorders, including those with known or suspected peptic ulcer disease.

During long-term therapy, perform periodic height, weight, chest and spinal radiographs, hematopoietic, electrolyte, glucose tolerance, and ocular and blood pressure evaluations.

GU Effects

Increased or decreased motility and number of sperm in some men.

GI Effects

Corticosteroids should be used with caution in patients with diverticulitis, nonspecific ulcerative colitis (if there is a probability of impending perforation, abscess, or other pyogenic infection), or those with recent intestinal anastomoses.

Use with caution in patients with active or latent peptic ulcer. Manifestations of peritoneal irritation following GI perforation may be minimal or absent in patients receiving corticosteroids. Suggest concurrent administration of antacids between meals to prevent peptic ulcer formation in patients receiving high dosages of corticosteroids.

Antenatal Risks in Preterm Labor

Short-term adverse effects of antenatal administration include transient neonatal and maternal adrenal suppression and increased risk of infection. No long-term sequelae were noted in children up to 12 years of age who had been exposed to short-term antenatal glucocorticoids.

Specific Populations


Category C.


Glucocorticoids are distributed into milk and could suppress growth, interfere with endogenous glucocorticoid production, or cause other adverse effects in nursing infants. Discontinue nursing (in mothers taking pharmacologic doses) because of potential risk to nursing infants.

Pediatric Use

The effects of glucocorticoids on the pathophysiology and course of diseases considered to be similar in adults and children. Evidence of safety and efficacy of corticosteroids in pediatric patients is based on treatment of nephrotic syndrome (in patients >2 years of age) and aggressive leukemias and lymphomas (in patients >1 month of age). Evidence of safety and efficacy in other pediatric indications (e.g., severe asthma and wheezing) is based on controlled trials in adults.

Adverse effects in pediatric patients are similar to those in adults. As in adults, perform periodic evaluations of height, weight, IOP, and BP. Children, like adults, also should undergo clinical evaluation for the presence of infection, psychosocial disturbances, thromboembolism, peptic ulcers, cataracts, and osteoporosis.

With long-term use, may delay growth and maturation in children and adolescents. Monitor carefully the growth and development of pediatric patients receiving prolonged corticosteroid therapy. Titrate dosage to the lowest effective level. Alternate-day therapy with glucocorticoids that cause shorter HPA-axis suppression than does dexamethasone (e.g., prednisone, prednisolone, methylprednisolone) may minimize growth suppression and should be instituted if growth suppression occurs.

Glucocorticoid-induced osteoporosis and associated fractures are common in children and adolescents receiving long-term systemic therapy. In addition, may prevent achievement of peak bone mass during adolescence by inhibiting bone formation. Methods for monitoring bone mineralization (e.g., dual-energy x-ray absorptiometry [DXA]) in children and adolescents are similar to those in adults.

Ensure children and adolescents receiving glucocorticoids consistently ingest adequate calcium and vitamin D, either through diet or supplementation.

Safety and efficacy of dexamethasone for COVID-19 treatment not fully evaluated in pediatric patients. Use caution when extrapolating recommendations for adults with COVID-19 to patients <18 years of age. The NIH COVID-19 Treatment Guidelines Panel recommends use of dexamethasone (see Pediatric Patients under Dosage, in Dosage and Administration) for hospitalized pediatric patients with COVID-19 who are receiving high-flow oxygen, noninvasive ventilation, invasive mechanical ventilation, or ECMO; dexamethasone not routinely recommended for pediatric patients who require only low levels of oxygen support (i.e., nasal cannula only). If dexamethasone not available, the NIH panel states that alternative corticosteroids (e.g., hydrocortisone, methylprednisolone, prednisone) may be considered. Use of corticosteroids for treatment of severe COVID-19 in pediatric patients who are profoundly immunocompromised not evaluated to date and may be harmful; therefore, the NIH panel states consider such use only on a case-by-case basis. IV corticosteroids have been used as first-line therapy in pediatric patients with multisystem inflammatory syndrome in children (MIS-C); however, the NIH panel recommends consultation with a multidisciplinary team when considering and managing immunomodulating therapy for children with this condition. Optimal choice and combination of immunomodulating therapies for children with MIS-C not definitely established. Consult the most recent NIH COVID-19 treatment guidelines for additional information on use of corticosteroids in pediatric patients with COVID-19.

Geriatric Use

With prolonged therapy, muscle wasting, muscle pain or weakness, delayed wound healing, and atrophy of the protein matrix of the bone resulting in osteoporosis, vertebral compression fractures, aseptic necrosis of femoral or humeral heads, or pathologic fractures of long bones may occur. May be especially serious in geriatric or debilitated patients.

Before initiating glucocorticoid therapy in postmenopausal women, consider that such women are especially prone to osteoporosis.

Use with caution in patients with osteoporosis.

Hepatic Impairment

Patients with cirrhosis show an exaggerated response to glucocorticoids.

Renal Impairment

Use with caution.

Common Adverse Effects

Associated with long-term therapy: bone loss, cataracts, indigestion, muscle weakness, back pain, bruising, oral candidiasis. (See Warnings/Precautions under Cautions.)

Interactions for Dexamethasone (Systemic)

Induces and is metabolized by CYP3A4.

Drugs Affecting Hepatic Microsomal Enzymes

Inhibitors of CYP3A4: potential pharmacokinetic interaction (increased plasma dexamethasone concentrations).

Inducers of CYP3A4: potential pharmacokinetic interaction (decreased plasma dexamethasone concentrations).

Substrates of CYP3A4: potential pharmacokinetic interaction (decreased plasma substrate concentrations).

Specific Drugs




Anticoagulants, oral

Conflicting reports of alterations in the anticoagulant response

Monitor prothrombin time frequently

Antidiabetic therapy

Increased blood glucose concentrations in diabetes mellitus

May require dosage adjustment of concurrent insulin and/or oral hypoglycemic agents


Decreased blood concentrations of dexamethasone

Increase dosage of dexamethasone


Decreased blood concentrations of dexamethasone

Increase dosage of dexamethasone

Diuretics, potassium-depleting

Enhance the potassium-wasting effects of glucocorticoids

Monitor for development of hypokalemia


Decreased blood concentrations of dexamethasone

May interfere with dexamethasone suppression tests

Increase dosage of dexamethasone

Interpret results of the test with caution


Decreased plasma concentrations of indinavir


False-negative results in the dexamethasone suppression test

Interpret results of the test with caution


Increased plasma dexamethasone concentrations

Inhibits adrenal corticosteroid synthesis, causing adrenal insufficiency during corticosteroid withdrawal

May need a reduction in dosage of dexamethasone to avoid potential adverse effects

Macrolide antibiotics

Increased plasma dexamethasone concentrations

May need a reduction in dosage of dexamethasone to avoid potential adverse effects


Increases the risk of GI ulceration

Decreased serum salicylate concentrations When corticosteroids are discontinued, serum salicylate concentration may increase, possibly resulting in salicylate intoxication

Use concurrently with caution

Observe patients receiving both drugs closely for adverse effects of either drug

May be necessary to increase salicylate dosage when corticosteroids are administered concurrently or decrease salicylate dosage when corticosteroids are discontinued

Use aspirin and corticosteroids with caution in hypoprothrombinemia


Decreased blood concentrations of dexamethasone

Conflicting reports of increased and decreased blood phenytoin concentrations leading to alterations in seizure control

Increase dosage of dexamethasone


Decreased blood concentrations of dexamethasone

May interfere with dexamethasone suppression tests

Increase dosage of dexamethasone

Interpret results of the test with caution

Vaccines and Toxoids

May cause a diminished response to toxoids and live or inactivated vaccines

May potentiate replication of some organisms contained in live, attenuated vaccines

Can aggravate neurologic reactions to some vaccines (supraphysiologic dosages)

Defer generally routine administration of vaccines or toxoids until corticosteroid therapy is discontinued

May need serologic testing to ensure adequate antibody response for immunization Additional doses of the vaccine or toxoid may be necessary

May undertake immunization procedures in patients receiving nonimmunosuppressive doses of glucocorticoids or in patients receiving glucocorticoids as replacement therapy (e.g., Addison’s disease)

Dexamethasone (Systemic) Pharmacokinetics



Systemic absorption occurs more slowly following IM injection compared with IV administration.


In the treatment of cerebral edema with IV then IM injection, response is usually noted within 12–24 hours.


The duration of anti-inflammatory activity of dexamethasone approximately equals the duration of HPA-axis suppression, about 2.75 days for a single 5-mg oral dose.



Most glucocorticoids are removed rapidly from the blood and distributed to muscle, liver, skin, intestines, and kidneys. Glucocorticoids appear in breast milk and the placenta.

Plasma Protein Binding

Bound weakly to transcortin.



Metabolized by CYP3A4.






Solution Concentrate

Do not store the liquid or semi-solid food containing crushed dexamethasone tablets for future use.


Solution for Injection

25°C (may be exposed to 15–30°C). Solutions of dexamethasone sodium phosphate injection are heat labile and must not be autoclaved.


For information on systemic interactions resulting from concomitant use, see Interactions.


Solution CompatibilityHID


Dextrose 5% in water

Sodium chloride 0.9%

Drug Compatibility
Admixture CompatibilityHID



Bleomycin sulfate


Granisetron HCl

Lidocaine HCl



Nafcillin sodium

Palonosetron HCI

Prochlorperazine edisylate

Ranitidine HCl

Verapamil HCl


Daunorubicin HCl

Diphenhydramine HCl with lorazepam and metoclopramide HCl


Amikacin sulfate

Ondansetron HCl

Y-Site CompatibilityHID



Acyclovir sodium

Allopurinol sodium


Amikacin sulfate

Amphotericin B cholesteryl sulfate complex





Ceftaroline fosamil

Cisatracurium besylate


Dexmedetomidine HCl



Doxorubicin HCl liposome injection

Etoposide phosphate


Fentanyl citrate



Fludarabine phosphate

Foscarnet sodium

Gallium nitrate

Gemcitabine HCl

Granisetron HCl

Heparin sodium

Heparin sodium with hydrocortisone sodium succinate

Hetastarch in lactated electrolyte injection (Hextend)

Hydromorphone HCl




Melphalan HCl

Meperidine HCl


Methadone HCl

Milrinone lactate

Morphine sulfate

Ondansetron HCl



Pemetrexed disodium

Piperacillin sodium–tazobactam sodium

Potassium chloride


Remifentanil HCl


Sodium bicarbonate


Telavancin HCl




Vinorelbine tartrate




Fenoldopam mesylate

Idarubicin HCl

Methotrexate sodium

Midazolam HCl

Topotecan HCl


  • Principally an anti-inflammatory or immunosuppressant agent.

  • Exhibits potent anti-inflammatory activity and minimal mineralocorticoid properties.

  • Decreases inflammation by stabilizing leukocyte lysosomal membranes, preventing release of destructive acid hydrolases from leukocytes, or reducing leukocyte adhesion to capillary endothelium.

  • Inhibits macrophage accumulation in inflamed areas.

  • Reduces capillary wall permeability and edema formation.

  • Antagonizes histamine activity and release of kinin from substrates.

  • Reduces fibroblast proliferation, collagen deposition, and subsequent scar tissue formation.

  • In the CSF, reduces the inflammatory response to anti-infective-liberated bacterial endotoxins and cell-wall components, including reduction of the release of cytokines (e.g., interleukin-1 beta, tumor necrosis factor).

  • Stimulates erythroid cells of bone marrow, prolongs survival time of erythrocytes and platelets, and produces neutrophilia and eosinopenia.

  • Promotes gluconeogenesis, redistribution of fat from peripheral to central areas of the body, and protein catabolism, which results in negative nitrogen balance.

  • Reduces intestinal absorption and increase renal excretion of calcium.

  • Suppresses the immune response by reducing activity and volume of the lymphatic system, producing lymphocytopenia.

  • Decreases immunoglobulin and complement concentrations and passage of immune complexes through basement membranes.

  • Depresses reactivity of tissue to antigen-antibody interactions.

  • Inhibits pituitary corticotropin (ACTH) release and decreases output of endogenous corticosteroids when given in an amount which does not itself appreciably affect levels of urinary 17-hydroxycorticosteroids.

Advice to Patients

  • In patients receiving long-term therapy, importance of not discontinuing the drug abruptly.

  • Importance of notifying a clinician of any infections, signs of infections (e.g., fever, sore throat, pain during urination, muscle aches), or injuries that develop during therapy or within 12 months after therapy is discontinued.

  • Importance of carrying identification cards listing the diseases being treated, the glucocorticoid regimen, and the name and telephone number of the clinician.

  • When surgery is required, importance of informing the attending physician, dentist, or anesthesiologist of recent (within 12 months) glucocorticoid therapy.

  • Advise patients receiving orally inhaled glucocorticoid therapy who are currently being withdrawn or who have been withdrawn from systemic therapy to immediately resume full therapeutic dosages of systemic glucocorticoids and to contact their clinician for further instructions during stressful periods (e.g., severe infection, severe asthmatic attack).

  • In immunosuppressed patients, importance of avoiding exposure to certain infections (e.g., chickenpox, measles) and of the importance of obtaining medical advice if such exposure occurs.

  • When considering epidural glucocorticoid injections for pain relief, importance of understanding potential benefits and risks of epidural injections and alternative treatments. Importance of immediately seeking emergency medical attention if unusual symptoms (e.g., loss of or changes in vision, tingling in extremities, sudden weakness or numbness affecting face or occurring unilaterally or bilaterally in arms or legs, dizziness, severe headache, seizures) occur after epidural injection.

  • Patients should carry identification cards listing the diseases for which they are being treated, the glucocorticoid they are receiving and its dosage, and the name and telephone number of their physician. Patients being transferred from systemic corticosteroid to oral inhalation therapy should carry special identification (e.g., card, bracelet) indicating the need for supplementary systemic corticosteroids during periods of stress.

  • Importance of informing clinicians of existing or contemplated concomitant therapy, including prescription and OTC drugs.

  • Importance of women informing clinicians if they are or plan to become pregnant or plan to breast-feed.

  • Importance of informing patients of other important precautionary information. (See Cautions.)


Excipients in commercially available drug preparations may have clinically important effects in some individuals; consult specific product labeling for details.

Please refer to the ASHP Drug Shortages Resource Center for information on shortages of one or more of these preparations.

* available from one or more manufacturer, distributor, and/or repackager by generic (nonproprietary) name



Dosage Forms


Brand Names




0.5 mg/5 mL*

Dexamethasone Elixir


0.5 mg/5 mL*

Dexamethasone Oral Solution

Solution, concentrate

0.5 mg/0.5 mL

Dexamethasone Intensol


0.5 mg*

Dexamethasone Tablets

0.75 mg*

Dexamethasone Tablets

1 mg*

Dexamethasone Tablets

1.5 mg*

Dexamethasone Tablets

Dexpak Taperpak (scored; available as 6-, 10-, or 13-day mnemonic pack of 21, 35, or 51 tablets, respectively)


2 mg*

Dexamethasone Tablets

4 mg*

Dexamethasone Tablets

6 mg*

Dexamethasone Tablets

* available from one or more manufacturer, distributor, and/or repackager by generic (nonproprietary) name

Dexamethasone Sodium Phosphate


Dosage Forms


Brand Names



Injection, for IM or IV use

4 mg (of dexamethasone phosphate) per mL*

Dexamethasone Sodium Phosphate Injection

10 mg (of dexamethasone phosphate) per mL*

Dexamethasone Sodium Phosphate Injection

AHFS DI Essentials™. © Copyright 2022, Selected Revisions August 30, 2021. American Society of Health-System Pharmacists, Inc., 4500 East-West Highway, Suite 900, Bethesda, Maryland 20814.

† Use is not currently included in the labeling approved by the US Food and Drug Administration.

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