Drug class: Adrenals

Medically reviewed by Drugs.com on Apr 10, 2024. Written by ASHP.

Introduction

Synthetic glucocorticoid; minimal mineralocorticoid activity.^{a b g}

Uses for Dexamethasone

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.^{a b}

Usually, inadequate alone for adrenocortical insufficiency because of minimal mineralocorticoid activity.^{a b}

Adrenocortical Insufficiency

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

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.^{a b d}

If dexamethasone is used, must also administer a mineralocorticoid (fludrocortisone), particularly in infants.^{a b d}

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

Adrenogenital Syndrome

Lifelong glucocorticoid treatment of congenital adrenogenital syndrome.^{a d}

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.^b

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

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

Hypercalcemia

Treatment of hypercalcemia associated with malignancy.^{a b d}

Usually ameliorates hypercalcemia associated with bone involvement in multiple myeloma.^b

Treatment of hypercalcemia associated with sarcoidosis^{† [off-label]}.^b

Treatment of hypercalcemia associated with vitamin D intoxication^{† [off-label]}.^b

Not effective for hypercalcemia caused by hyperparathyroidism^{† [off-label]}.^b

Thyroiditis

Treatment of granulomatous (subacute, nonsuppurative) thyroiditis.^{a d}

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

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

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

Rheumatic Disorders and Collagen Diseases

Short-term adjunctive 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^{† [off-label]}, rheumatic fever^{† [off-label]} [especially with carditis]) and collagen diseases (e.g., acute rheumatic carditis, systemic lupus erythematosus, dermatomyositis^† [polymyositis], polyarteritis nodosa^†, vasculitis^†) refractory to more conservative measures.^{a d}

Relieves inflammation and suppresses symptoms but not disease progression.^b

Rarely indicated as maintenance therapy.^b

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;^b inflammation tends to recur and sometimes is more intense after drug cessation.^b

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

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.^b

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

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^†.^b 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.^b

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

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

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

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.^{a d}

Usually reserved for acute exacerbations unresponsive to conservative therapy.^b

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

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

Chronic skin disorders seldom an indication for systemic glucocorticoids.^b

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.^b

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

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

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.^{a b d}

Systemic therapy usually reserved for acute conditions and severe exacerbations.^b

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

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.^b

Ocular Disorders

To suppress a variety of allergic and nonpyogenic ocular inflammations.^b

To reduce scarring in ocular injuries^†.^b

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).^{a d}

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

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

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

Asthma

Corticosteroids are used as adjunctive treatment of acute asthma exacerbations^† and for maintenance treatment of persistent asthma^†.^{b 774}

Systemic glucocorticoids (usually prednisone, prednisolone, and dexamethasone) are used for treatment of moderate to severe acute exacerbations of asthma; speeds resolution of airflow obstruction and reduces rate of relapse.⁷⁷⁴

COPD

The Global Initiative for Chronic Obstructive Lung Disease (GOLD) guideline states that oral glucocorticoids play a role in the acute management of COPD exacerbations, but have no role in the chronic daily treatment of COPD because of the lack of benefit and high rate of systemic complications.⁵⁶⁴

Croup

Adjunctive treatment of croup^† in pediatric patients.^{j k}

Decreases laryngeal mucosa edema through its anti-inflammatory effects.^j

Evidence from randomized controlled studies have shown that corticosteroids (e.g., dexamethasone, budesonide) reduce need for hospitalization, shorten duration of hospitalization, and reduce need for subsequent interventions (e.g., epinephrine).^{j k}

Sarcoidosis

Management of symptomatic sarcoidosis.^{a b d}

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

Tuberculosis

Treatment of fulminating or disseminated pulmonary tuberculosis when used concurrently with appropriate antituberculous therapy.^a

Treatment of tuberculous meningitis with subarachnoid block or impending block when used with appropriate antituberculous therapy..^a

Lipid Pneumonitis

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

Coronavirus Disease 2019 (COVID-19)

Adjunctive therapy in the treatment of serious complications from COVID-19^†.^{1004 1005 1006 1007 1013}

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).¹⁰⁰⁵ NIH panel recommends against use of dexamethasone in nonhospitalized adults and hospitalized adults who do not require supplemental oxygen.¹⁰⁰⁵ 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.¹⁰⁰⁵ 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-19.¹⁰⁰⁵ 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).¹⁰⁰⁵ Consult the most recent NIH COVID-19 treatment guidelines for additional information on use of corticosteroids in patients with COVID-19.¹⁰⁰⁵

For treatment of patients with nonsevere COVID-19, WHO Guideline Development Group suggests not using systemic corticosteroids, regardless of hospitalization status;¹⁰⁰⁶ however, if clinical condition of such patients worsens, systemic corticosteroids are recommended.¹⁰⁰⁶ 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.¹⁰⁰⁶ 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).¹⁰⁰⁶ Consult the most recent WHO COVID-19 treatment guidelines for additional information.¹⁰⁰⁶

Loeffler’s Syndrome

Symptomatic relief of acute manifestations of symptomatic Loeffler’s syndrome not manageable by other means.^{a b d}

Berylliosis

Symptomatic relief of acute manifestations of berylliosis.^{a b d}

Aspiration Pneumonitis

Symptomatic relief of acute manifestations of aspiration pneumonitis.^{a b d}

Anthrax

Has been used as an adjunct to anti-infective therapy in the treatment of anthrax^†; evidence of effect based on small observational studies.^{611 612} Some clinicians recommend that adjunctive corticosteroids be considered in patients with extensive edema especially of the head or neck, suspected bacterial meningitis, or vasopressor-resistant shock.^{611 612 613}

Antenatal Use in Preterm Labor

Short-course IM therapy in selected women with preterm labor to accelerate fetal maturation^† (e.g., lungs, cerebral blood vessels), including women with preterm premature rupture of membranes, preeclampsia, or third-trimester hemorrhage.^{530 531 532 535 539 540 541}

Antenatal corticosteroid administration has resulted in significantly lower severity and frequency of respiratory distress syndrome in neonates.⁷⁵⁵

Betamethasone and dexamethasone are the most widely studied corticosteroids for this use.⁷⁵⁵

Combined effects on multiple organ maturation reduces neonatal morbidity and mortality.⁷⁵⁵

Hematologic Disorders

Management of acquired (autoimmune) hemolytic anemia, idiopathic thrombocytopenic purpura (ITP), secondary thrombocytopenia, erythroblastopenia, or congenital (erythroid) hypoplastic anemia.^{a b d}

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

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

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

Shock

Corticosteroids have been used in the treatment of shock.^{409 410 411 412 413 414 415 418}

The Surviving Sepsis Campaign guidelines suggest the use of IV corticosteroids for adults with septic shock and an ongoing requirement for vasopressor therapy; however, optimal dose, timing of initiation, and duration remain uncertain.⁴¹⁶

Dexamethasone sodium phosphate injection is indicated for the treatment of shock unresponsive to conventional therapy if adrenocortical insufficiency exists or is suspected.^{d e}

GI Diseases

Short-term palliative therapy for acute exacerbations and systemic complications of ulcerative colitis, regional enteritis, and celiac disease^†.^{a b d}

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

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.^b

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

Crohn’s Disease

Oral corticosteroids may be used for short-term treatment of moderate to severely active Crohn’s disease^†.⁴³¹

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).^{a b d}

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.^b

Cancer Chemotherapy-induced Nausea and Vomiting

Prevention of nausea and vomiting associated with emetogenic cancer chemotherapy^†.^{100 101 102 103 104 129 130 131 769}

Corticosteroids have been shown to be safe and effective when used as monotherapy for low emetogenic chemotherapy or as a component of combination antiemetic regimens with moderate and highly emetogenic chemotherapy; most clinical experience to date has been with dexamethasone.^{495 496 497 498 499 500 501 502 503 504 505 506 507 508 510 511 512 526 527 528 769}

The American Society of Clinical Oncology (ASCO) guidelines recommend that adults treated with cisplatin and other high-emetic-risk single agents be offered a 4-drug combination of an neurokinin-1 (NK1) receptor antagonist, a serotonin (5-HT3) receptor antagonist, dexamethasone, and olanzapine on day 1; dexamethasone and olanzapine should be continued on days 2 to 4.⁷⁶⁹ Adults treated with an anthracycline combined with cyclophosphamide should be offered a 4-drug combination of an NK1 receptor antagonist, a 5-HT3 receptor antagonist, dexamethasone, and olanzapine on day 1; olanzapine should be continued on days 2 to 4.⁷⁶⁹

In patients receiving moderate-emetic risk antineoplastic agents, ASCO recommends that adults treated with carboplatin area under the curve (AUC) ≥4 mg/mL/min should be offered a 3-drug combination of an NK1 receptor antagonist, a 5-HT3 receptor antagonist, and dexamethasone on day 1.⁷⁶⁹ Adults treated with moderate-emetic-risk antineoplastic agents (excluding carboplatin AUC ≥4 mg/mL/min) should be offered a 2-drug combination of a 5-HT3 receptor antagonist and dexamethasone on day 1.⁷⁶⁹ Adults treated with cyclophosphamide, doxorubicin, oxaliplatin, and other moderate-emetic-risk antineoplastic agents known to cause delayed nausea and vomiting may be offered dexamethasone on days 2 to 3.⁷⁶⁹

ASCO recommends that adults treated with low-emetic-risk antineoplastic agents should be offered a single dose of a 5-HT3 receptor antagonist or a single 8-mg dose of dexamethasone before antineoplastic treatment.⁷⁶⁹

Cerebral Edema

To decrease cerebral edema associated with brain tumors and neurosurgery (e.g., craniotomy).^{a b d}

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

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

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

Bacterial Meningitis

Has been used for short-term adjunctive therapy (i.e., IV dexamethasone for the first 2–4 days of anti-infective therapy) of bacterial meningitis^†.^{127 128 132 136}

In a Cochrane review, corticosteroids were found to reduce hearing loss and neurological sequelae, but did not improve overall mortality.¹³² The benefits were limited to high-income countries; there was no beneficial effect of corticosteroid therapy in low-income countries.¹³²

Multiple Sclerosis

Corticosteroids (e.g., dexamethasone, methylprednisolone) have been used in the treatment of multiple sclerosis^†, but are no longer used as disease-modifying agents because of serious adverse effects associated with chronic administration and the development of more effective disease-modifying drugs..^{574 575} However, corticosteroids may improve symptoms during an acute exacerbation.^{574 575}

Organ Transplants

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

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

Trichinosis

Treatment of trichinosis with neurologic or myocardial involvement.^{a d}

Nephrotic Syndrome and Lupus Nephritis

Treatment of idiopathic nephrotic syndrome without uremia.^{a d}

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

Treatment of lupus nephritis.^{a b d}

Diagnostic Uses

Diagnosis (dexamethasone suppression test; DST) of adrenocortical hyperfunction (e.g., Cushing’s syndrome, adrenal hyperplasia, adrenal adenoma).^{a b d}

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.^b

Has been used to aid in the diagnosis of major depression; however, considerable controversy currently exists regarding the clinical utility of the test.^{398 424 425}

Dexamethasone Dosage and Administration

General

Route of administration and dosage depend on the condition being treated and the patient response.^{a b d e}

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.^b This regimen provides relief of symptoms while minimizing adrenal suppression, protein catabolism, and other adverse effects.^b

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

• 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).^b

• 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.^b

Discontinuance of Therapy

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

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

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

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

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

• 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.^b

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

• 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.^b 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.^b

• 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).^{a b} Administer an initially high dose on the first day of therapy, and then withdraw therapy by tapering the dose over several days.^{a b}

Administration

Administer dexamethasone orally.^a

Administer dexamethasone sodium phosphate by IV injection or infusion, or IM injection.^{a d e} Dexamethasone sodium phosphate 4-mg/mL injection also may be administered locally by intra-articular, intralesional, intrasynovial, or soft-tissue injection.^d The 10-mg/mL injection is for IV or IM use only.^e

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

Oral Administration

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

Dilution

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

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

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

Consume the liquid or food containing dexamethasone immediately.^a

IV Administration

Administer dexamethasone sodium phosphate by IV injection or infusion.^d

Dilution

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

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

Use within 24 hours.^d

IM Administration

Administer dexamethasone sodium phosphate by IM injection.^d

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

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

Dosage

Available as dexamethasone and dexamethasone sodium phosphate.^{a d e} Dosage of dexamethasone sodium phosphate is expressed in terms of dexamethasone phosphate.^{d e}

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.^{b d}

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

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.^b

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

Massive dosages may be required for the treatment of shock.^{b e}

Pediatric Patients

Usual Dosage

Oral

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

IV or IM

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

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

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

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

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

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

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

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

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.^g

Bacterial Meningitis†

IV

Infants and children: 0.15 mg/kg 4 times daily for the first 2–4 days of anti-infective therapy has been administered.^{110 112 113 114 115 116 119 127 128 136}

Alternatively, 0.4 mg/kg every 12 hours for the first 2–4 days of anti-infective therapy has been administered.¹²⁷

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.¹⁰⁰⁵ If dexamethasone not available, may consider equivalent dosages of alternative corticosteroids.¹⁰⁰⁵ Consult most recent NIH COVID-19 treatment guidelines for additional information on use of corticosteroids in pediatric patients with COVID-19.¹⁰⁰⁵

Croup†

IM

Single dose of 0.6 mg/kg.^j

Adults

Usual Dosage

Oral

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

IV or IM

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

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

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

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

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

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

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

Ganglia: 1–2 mg repeated as needed.^g

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.^g

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.^{a g}

Tuberculosis Meningitis

IM

Initially, an IM dosage of 8–12 mg daily tapered over 6–8 weeks.^{137 139}

No additional benefit from higher dosages but may be associated with more frequent adverse effects.^{137 139}

Antenatal Use in Preterm Labor†

IM

6 mg every 12 hours for 4 doses in preterm labor that begins at 24–34 weeks gestation.⁷⁵⁵

A single course is recommended.⁷⁵⁵

Shock

IV

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.^{d g}

Alternatively, 20 mg by IV injection initially followed by continuous IV infusion of 3 mg/kg per 24 hours.^{d g}

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

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.^{a d}

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.^{a d g}

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

Bacterial Meningitis†

IV

0.15 mg/kg 4 times daily for the first 2–4 days of anti-infective therapy has been administered.^{110 112 113 114 115 116 119 127 128 136}

Alternatively, 0.4 mg/kg every 12 hours for the first 2–4 days of anti-infective therapy has been administered.¹²⁷

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.^{1004 1005} WHO Guidelines Development Group recommends 6 mg once daily for 7–10 days.¹⁰⁰⁶ Consult most recent NIH and WHO COVID-19 treatment guidelines for additional information on use of corticosteroids in patients with COVID-19.¹⁰⁰⁵

Diagnostic Uses

Cushing’s Syndrome

Oral

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

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

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.^a

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.^g

To distinguish Cushing’s syndrome due to pituitary ACTH excess from Cushing’s syndrome due to other causes, 2 mg orally every 6 hours for 48 hours.^{a g}

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

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

Cautions for Dexamethasone

Contraindications

• Known hypersensitivity to dexamethasone or any component of the product.^{a b}

• Systemic fungal infections.^a

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

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

Warnings/Precautions

Warnings

Nervous System Effects

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

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

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.^{1000 1001 1002 1003}

FDA states efficacy and safety of epidural glucocorticoid administration not established; not FDA-labeled for this use.^{1000 1001}

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.^b

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.^{b d}

Withdraw dexamethasone very gradually following long-term therapy with pharmacologic dosages.^b

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

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.^b Since mineralocorticoid secretion may be impaired, sodium chloride and/or a mineralocorticoid should also be administered.^b

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

Immunosuppression

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

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

Increased Susceptibility to Infection

Corticosteroids increase susceptibility to and mask symptoms of infection.^a

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; reactivation of latent infections may occur.^a

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

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

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

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.^a

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

Prolonged use of systemic corticosteroids in patients with COVID-19^† may increase risk of reactivation of latent infections (e.g., HBV, herpesvirus, strongyloidiasis, tuberculosis).^{1005 1015 1016} Risk of reactivation of latent infections following a 10-day course of dexamethasone (6 mg once daily) not well established.¹⁰⁰⁵ 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.^{1005 1015 1016}

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

Do not use for cerebral malaria.^a

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

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

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.^b These adverse effects may be especially serious in geriatric or debilitated patients.^b 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).^{a a}

Osteoporosis and related fractures are one of the most serious adverse effects of long-term glucocorticoid therapy.⁵⁷² The American College of Rheumatology (ACR) has published guidelines on prevention and treatment of glucocorticoid-induced osteoporosis.⁵⁷² Recommendations are made according to a patient's risk of fracture.⁵⁷²

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.^d Risk is increased with high-dose dexamethasone for prolonged periods.^b Edema and CHF (in susceptible patients) may occur.^{b d}

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

Increased calcium excretion and possible hypocalcemia.^b

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.^{b 553}

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

Cortical blindness has occurred following epidural glucocorticoid injection.^{1001 1002 1003}

Do not use in patients with active ocular herpes simplex infections for fear of corneal perforation.^{b d}

Endocrine and Metabolic Effects

Administration over a prolonged period may produce various endocrine disorders including hypercorticism (cushingoid state) and amenorrhea or other menstrual difficulties.^b 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.^b If glucocorticoid therapy is required in patients with diabetes mellitus, changes in insulin or oral antidiabetic agent dosage or diet may be necessary.^b

Exaggerated response to the glucocorticoids in hypothyroidism.^{b d}

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.^{b d}

Sensitivity Reactions

Anaphylactic and hypersensitivity reactions reported.^{b d}

General Precautions

Monitoring

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.^b

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.^a

GU Effects

Increased or decreased motility and number of sperm in some men.^{b d}

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.^d

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

Specific Populations

Pregnancy

Corticosteroids have been shown to be teratogenic in many species when administered in clinical doses.^a No adequate and well-controlled studies in pregnant women.^a Use during pregnancy only potential benefit justifies potential risk to fetus.^a

Lactation

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

Pediatric Use

Efficacy and safety of corticosteroids in pediatric patients are based on the well-established course of effect of corticosteroids.^a Adverse effects of corticosteroids in pediatric patients are similar to those in adults.¹⁰⁷

Published studies provide evidence of efficacy and safety in pediatric patients for treatment of nephrotic syndrome (>2 years of age), and aggressive lymphomas and leukemias (>1 month of age).^a Other indications for pediatric use of corticosteroids (e.g., severe asthma) are based on adequate and well-controlled trials conducted in adults.^a

Carefully observe pediatric patients with frequent measurements of BP, weight, height, intraocular pressure, and clinical evaluation for infection, psychosocial disturbances, thromboembolism, peptic ulcers, cataracts, and osteoporosis.^a Pediatric patients who are treated with corticosteroids by any route, including systemically administered corticosteroids, may experience a decrease in growth velocity.^a

Safety and efficacy of dexamethasone for COVID-19^† treatment not fully evaluated in pediatric patients.¹⁰⁰⁵ Use caution when extrapolating recommendations for adults with COVID-19 to patients <18 years of age.¹⁰⁰⁵ The NIH COVID-19 Treatment Guidelines Panel recommends use of dexamethasone for hospitalized pediatric patients with COVID-19 who are receiving high-flow oxygen, noninvasive ventilation, invasive mechanical ventilation, or ECMO;¹⁰⁰⁵ dexamethasone not routinely recommended for pediatric patients who require only low levels of oxygen support (i.e., nasal cannula only).¹⁰⁰⁵ If dexamethasone not available, the NIH panel states that alternative corticosteroids (e.g., hydrocortisone, methylprednisolone, prednisone) may be considered.¹⁰⁰⁵ 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.¹⁰⁰⁵ 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.¹⁰⁰⁵ Optimal choice and combination of immunomodulating therapies for children with MIS-C not definitely established.¹⁰⁰⁵ Consult the most recent NIH COVID-19 treatment guidelines for additional information on use of corticosteroids in pediatric patients with COVID-19.¹⁰⁰⁵

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.^b May be especially serious in geriatric or debilitated patients.^b

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

Use with caution in patients with osteoporosis.^d

Hepatic Impairment

Patients with cirrhosis show an exaggerated response to glucocorticoids.^{b d}

Renal Impairment

Use with caution.^d

Common Adverse Effects

Associated with long-term therapy: bone loss, cataracts, indigestion, muscle weakness, back pain, bruising, oral candidiasis.^{h i}

Drug Interactions

Induces and is metabolized by CYP3A4.^a

Drugs Affecting Hepatic Microsomal Enzymes

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

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

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

Specific Drugs

Dexamethasone Pharmacokinetics

Absorption

Bioavailability

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

Onset

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

Duration

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.^b

Distribution

Extent

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

Plasma Protein Binding

Bound weakly to transcortin.^b

Elimination

Metabolism

Metabolized by CYP3A4.^a

Stability

Storage

Oral

Tablets

20–25°C.^a

Oral Solution

20–25°C.^a

Solution Concentrate

20–25°C; do not freeze.^a Discard after 90 days of opening.^a

Parenteral

Solution for Injection

20–25°C (excursions permitted to 15–30°C).^d

Actions

• Principally an anti-inflammatory or immunosuppressant agent.^g

• Exhibits potent anti-inflammatory activity and minimal mineralocorticoid properties.^{a b}

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

• Inhibits macrophage accumulation in inflamed areas.^b

• Reduces capillary wall permeability and edema formation.^b

• Antagonizes histamine activity and release of kinin from substrates.^b

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

• 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).^{a b}

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

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

• Reduces intestinal absorption and increase renal excretion of calcium.

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

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

• Depresses reactivity of tissue to antigen-antibody interactions.^b

• 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.^g

Advice to Patients

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

• 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.^b

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

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

• 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).^b

• 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.

• Importance of informing clinicians of existing or contemplated concomitant therapy, including prescription and OTC drugs.^{a b}

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

• Importance of informing patients of other important precautionary information. (See Cautions.)^{a b}

Preparations

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

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

Frequently asked questions

• Can I use expired neomycin and polymyxin b sulfates, dexamethasone ophthalmic?

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