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dexamethasone sodium phosphate

Pronunciation

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

Warning(s)

Special Alerts:

[Posted 03/31/2014] ISSUE: FDA is warning that injection of corticosteroids into the epidural space of the spine may result in rare but serious adverse events, including loss of vision, stroke, paralysis, and death. The injections are given to treat neck and back pain, and radiating pain in the arms and legs. The effectiveness and safety of epidural administration of corticosteroids have not been established, and FDA has not approved corticosteroids for this use.

FDA is requiring the addition of a Warning to the drug labels of injectable corticosteroids to describe these risks.

BACKGROUND: To raise awareness of the risks of epidural corticosteroid injections in the medical community, FDA’s Safe Use Initiative convened a panel of experts, including pain management experts to help define the techniques for such injections which would reduce preventable harm. The expert panel’s recommendations will be released when they are finalized. FDA will convene an Advisory Committee meeting of external experts in late 2014 to discuss the benefits and risks of epidural corticosteroid injections and to determine if further FDA actions are needed.

RECOMMENDATION: Patients should discuss the benefits and risks of epidural corticosteroid injections with their health care professionals, along with the benefits and risks associated with other possible treatments. See the Drug Safety Communication for a Data Summary and additional information for both patients and healthcare professionals.

Healthcare professionals and patients are encouraged to report adverse events or side effects related to the use of these products to the FDA's MedWatch Safety Information and Adverse Event Reporting Program.

For more information visit the FDA website at: and .

Introduction

Synthetic glucocorticoid; minimal mineralocorticoid activity.a b g

Uses for dexamethasone sodium phosphate

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 c

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

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 c d f

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

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

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.b

Adrenogenital Syndrome

Lifelong glucocorticoid treatment of congenital adrenogenital syndrome.a c d f

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 c d f

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

Treatment of hypercalcemia associated with sarcoidosis.b

Treatment of hypercalcemia associated with vitamin D intoxication.b

Not effective for hypercalcemia caused by hyperparathyroidism.b

Thyroiditis

Treatment of granulomatous (subacute, nonsuppurative) thyroiditis.a c d f

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 homones.b

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, dematomyositis [polymyositis], polyarteritis nodosa, vasculitis) refractory to more conservative measures.a c d f

Relieves inflammation and suppresses symptoms but not disease progression.b

Rarely indicated as maintenance therapy.b

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.a b c d f

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

Slideshow: Multiple Sclerosis: What's New in Treatment Options?

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 c d f

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 c d f

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 c d

Acute optic neuritis optimally treated with intial 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

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

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.j

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

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

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.b

For severe persistent asthma once intial 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 asthmab (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).b

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.b

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

COPD

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.

Croup

Adjunctive treatment of croup in pediatric patients.j

Decreases edema in laryngeal mucosa.j

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

Sarcoidosis

Management of symptomatic sarcoidosis.a b c d f

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

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.a

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.b

Lipid Pneumonitis

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

Pneumocystis carinii Pneumonia

Systemic adjunctive glucocorticoids decrease the likelihood of deterioration of oxygenation, respiratory failure, and/or death in moderate to severe Pneumocystis carinii pneumonia in acquired immunodeficiency syndrome (AIDS).

Prevents early deterioration in oxygenation associated with antipneumocystis therapy; initiate adjunctive glucocorticoid therapy as early as possible in moderate to severe pneumocystis pneumonia.

Not known whether patients with mild pneumocystis pneumonia (arterial oxygen pressure >70 mm Hg or arterial-alveolar gradient <35 mm Hg on room air) will have clinically important benefit with adjunctive glucocorticoid therapy.

Other glucocorticoids (e.g., oral prednisone, parenteral methylprednisolone) generally are preferred.

Loeffler’s Syndrome

Symptomatic relief of acute manifestations of symptomatic Loeffler’s syndrome not manageable by other means.a b c d f

Berylliosis

Symptomatic relief of acute manifestations of berylliosis.a b c d f

Aspiration Pneumonitis

Symptomatic relief of acute manifestations of aspiration pneumonitis.a b c d f

Anthrax

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.a b c d f

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

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.b

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

Shock

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.b

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.b

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.

Pericarditis

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

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.a b c d f n o

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

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

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 swiched 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).a b c d f

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

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.100 101 102 103 104 129 130 131

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).a b c d f

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 c d f

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.b

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 manifesations and sequelae (e.g., development of hearing loss).b

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.127

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.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 c d f

Nephrotic Syndrome and Lupus Nephritis

Treatment of idiopathic nephrotic syndrome without uremia.a c d f f

Can induce diuresis and remission of proteinuria in nephrotic syndromea b c d f secondary to primary renal disease, especially when there is minimal renal histologic change.b

Treatment of lupus nephritis.a b c d

Diagnostic Uses

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

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

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 sodium phosphate Dosage and Administration

General

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

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 f

  • 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; administer dexamethasone sodium phosphate by IV injection or infusion, or IM injection.a c d f

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

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

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

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. Dosage of dexamethasone sodium phosphate is expressed in terms of dexamethasone phosphate.d

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

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.c

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 mcg/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.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.127

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

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.

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

Cancer Chemotherapy-induced Nausea and Vomiting
Prevention
IV

Usually, 10–20 mg IV before administration of the chemotherapy.100 101 102 103 104

Additional IV or oral doses (usually lower than the initial dose) may be needed for 24–72 hours.101 102 103 104

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.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.127

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.f 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.f

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

Depression
Oral

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 mcg/dL for any blood sample is abnormal and represents a positive test.

Cautions for dexamethasone sodium phosphate

Contraindications

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

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

  • 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

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 (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.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 f

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 immunosupression.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

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

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.b

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.

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

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

Can reactivate tuberculosis.f 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).

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.b

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.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

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

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.

GU Effects

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

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

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

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

Pregnancy

Category C.d

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.c d

Pediatric Use

With long-term use, may delay growth and maturation in children and adolescents.b c Monitor carefully the growth and development of pediatric patients receiving prolonged corticosteroid therapy.a c d Titrate dosage to the lowest effective level.b 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.b

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 consistently ingest either through diet or supplementation adequate calcium and vitamin D.

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 (See Warnings/Precautions under Cautions.)

Interactions for dexamethasone sodium phosphate

Induces and is metabolized by CYP3A4.c

Drugs Affecting Hepatic Microsomal Enzymes

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

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

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

Specific Drugs

Drug

Interaction

Comments

Anticoagulants, oral

Conflicting reports of alterations in the anticoagulant responsec

Monitor prothrombin time frequentlyc

Antidiabetic therapy

Increased blood glucose concentrations in diabetes mellitus

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

Barbiturates

Decreased blood concentrations of dexamethasonec

Increase dosage of dexamethasonec

Carbamazepine

Decreased blood concentrations of dexamethasonec

Increase dosage of dexamethasonec

Diuretics, potassium-depleting

Enhance the potassium-wasting effects of glucocorticoidsb

Monitor for development of hypokalemiac

Ephedrine

Decreased blood concentrations of dexamethasonec

May interfere with dexamethasone suppression testsd

Increase dosage of dexamethasonec

Interpret results of the test with cautiond

Indinavir

Decreased plasma concentrations of indinavirc

Indomethacin

False-negative results in the dexamethasone suppression testc

Interpret results of the test with cautiond

Ketoconazole

Increased plasma dexamethasone concentrationsc

Inhibits adrenal corticosteroid synthesis, causing adrenal insufficiency during corticosteroid withdrawalc

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

Macrolide antibiotics

Increased plasma dexamethasone concentrationsc

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

NSAIAs

Increases the risk of GI ulcerationb

Decreased serum salicylate concentrationsb When corticosteroids are discontinued, serum salicylate concentration may increase, possibly resulting in salicylate intoxicationb

Use concurrently with cautionb

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

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

Use aspirin and corticosteroids with caution in hypoprothrombinemiad

Phenytoin

Decreased blood concentrations of dexamethasonec

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

Increase dosage of dexamethasonec

Rifampin

Decreased blood concentrations of dexamethasonec d

May interfere with dexamethasone suppression testsd

Increase dosage of dexamethasonec

Interpret results of the test with cautiond

Vaccines and Toxoids

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

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

Can aggravate neurologic reactions to some vaccines (supraphysiologic dosages)b

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

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

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

dexamethasone sodium phosphate 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.c

Stability

Storage

Oral

Tablets

15–30°C.f

Solution Concentrate

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

Parenteral

Solution for Injection

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

Compatibility

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

Parenteral

Solution CompatibilityHID

Compatible

Dextrose 5% in water

Sodium chloride 0.9%

Drug Compatibility
Admixture CompatibilityHID

Compatible

Aminophylline

Bleomycin sulfate

Cimetidine HCl

Furosemide

Granisetron HCl

Lidocaine HCl

Meropenem

Mitomycin

Nafcillin sodium

Oxycodone HCI

Palonosetron HCI

Prochlorperazine edisylate

Ranitidine HCl

Verapamil HCl

Incompatible

Daunorubicin HCl

Diphenhydramine HCl with lorazepam and metoclopramide HCl

Metaraminol bitartrate

Vancomycin HCl

Variable

Amikacin sulfate

Ondansetron HCl

Y-Site CompatibilityHID

Compatible

Acyclovir sodium

Allopurinol sodium

Amifostine

Amikacin sulfate

Amphotericin B cholesteryl sulfate complex

Amsacrine

Aztreonam

Bivalirudin

Cefepime HCl

Cisplatin

Cladribine

Cyclophosphamide

Cytarabine

Dexmedetomidine HCl

Docetaxel

Doxorubicin HCl

Doxorubicin HCl liposome injection

Etoposide phosphate

Famotidine

Fentanyl citrate

Filgrastim

Fluconazole

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

Lansoprazole

Levofloxacin

Linezolid

Lorazepam

Melphalan HCl

Meperidine HCl

Meropenem

Methadone HCl

Milrinone lactate

Morphine sulfate

Ondansetron HCl

Oxaliplatin

Paclitaxel

Pemetrexed disodium

Piperacillin sodium–tazobactam sodium

Potassium chloride

Propofol

Remifentanil HCl

Sargramostim

Sodium bicarbonate

Sufentanil citrate

Tacrolimus

Teniposide

Theophylline

Thiotepa

Vinorelbine tartrate

Vitamin B complex with C

Zidovudine

Incompatible

Ciprofloxacin

Fenoldopam mesylate

Idarubicin HCl

Midazolam HCl

Topotecan HCl

Variable

Methotrexate sodium

Actions

  • Principally an anti-inflammatory or immunosuppressant agent.g

  • Exhibits potent anti-inflammatory activity and minimal mineralocorticoid properties.a b c f

  • 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).

  • 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.

  • 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.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.

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

Dexamethasone

Routes

Dosage Forms

Strengths

Brand Names

Manufacturer

Oral

Elixir

0.5 mg/5 mL*

Dexamethasone Elixir (with alcohol 5%)

Actavis

Solution

0.5 mg/5 mL

Dexamethasone Oral Solution

Roxane

Solution, concentrate

0.5 mg/0.5 mL

Dexamethasone Intensol (with alcohol 30%)

Roxane

Tablets

0.25 mg*

0.5 mg*

Dexamethasone Tablets

Roxane

0.75 mg*

Dexamethasone Tablets

Roxane

1 mg

Dexamethasone Tablets

Roxane

1.5 mg*

Dexpak

ECR

Dexamethasone Tablets

Roxane

2 mg

Dexamethasone Tablets

Roxane

4 mg*

Dexamethasone Tablets

Roxane

6 mg*

Dexamethasone Tablets

Roxane

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

Dexamethasone Acetate

Routes

Dosage Forms

Strengths

Brand Names

Manufacturer

Parenteral

Injectable suspension

8 mg (of dexamethasone) per mL*

Decaject-L.A. (with benzyl alcohol and sodium bisulfite)

Merz

Dexone L.A. (with benzyl alcohol and sodium bisulfite)

Keene

Solurex L.A. (with benzyl alcohol and sodium bisulfite)

Hyrex

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

Dexamethasone Sodium Phosphate

Routes

Dosage Forms

Strengths

Brand Names

Manufacturer

Parenteral

Injection, for IM or IV use

4 mg (of dexamethasone phosphate) per mL*

Decaject (with parabens and sodium bisulfite)

Merz

Dexamethasone Sodium Phosphate Injection

Baxter

Solurex (with parabens and sodium bisulfite)

Hyrex

10 mg (of dexamethasone phosphate) per mL*

Dexamethasone Sodium Phosphate Injection

Baxter, Sicor

Comparative Pricing

This pricing information is subject to change at the sole discretion of DS Pharmacy. This pricing information was updated 05/2014. Actual costs to patients will vary depending on the use of specific retail or mail-order locations and health insurance copays.

Dexamethasone 0.5MG/5ML Elixir (MORTON GROVE PHARMACEUTICALS): 120/$49.99 or 360/$115.97

Dexamethasone 0.5MG Tablets (ROXANE): 30/$12.99 or 60/$14.46

Dexamethasone 0.75MG Tablets (ROXANE): 30/$13.99 or 60/$17.97

Dexamethasone 1MG Tablets (ROXANE): 30/$19.99 or 60/$28.98

Dexamethasone 1.5MG Tablets (ROXANE): 30/$12.99 or 60/$16.98

Dexamethasone 2MG Tablets (ROXANE): 30/$21.99 or 90/$47.97

Dexamethasone 4MG Tablets (ROXANE): 90/$21.99 or 180/$32.97

Dexamethasone 6MG Tablets (ROXANE): 30/$22.99 or 60/$35.97

AHFS DI Essentials. © Copyright, 2004-2014, Selected Revisions August 1, 2007. American Society of Health-System Pharmacists, Inc., 7272 Wisconsin Avenue, Bethesda, Maryland 20814.

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

References

Only references cited for selected revisions after 1984 are available electronically.

100. Cassileth PA, Lusk EJ, Torri S et al. Antiemetic efficacy of dexamethasone therapy in patients receiving cancer chemotherapy. Arch Intern Med. 1983; 143:1347-9. [IDIS 172420] [PubMed 6347109]

101. Markman M, Sheidler V, Ettinger DS et al. Antiemetic efficacy of dexamethasone: randomized, double-blind, crossover study with prochlorperazine in patients receiving cancer chemotherapy. N Engl J Med. 1984; 311:549-52. [IDIS 189083] [PubMed 6379459]

102. Cassileth PA, Lusk EJ, Torri S et al. Antiemetic efficacy of high-dose dexamethasone in induction therapy in acute nonlymphocytic leukemia. Ann Intern Med. 1984; 100:701-2. [IDIS 184373] [PubMed 6712035]

103. Aapro MS, Alberts DS. High-dose dexamethasone for prevention of cis-platin-induced vomiting. Cancer Chemother Pharmacol. 1981; 7:11-4. [PubMed 6122510]

104. Aapro MS, Alberts DS. Dexamethasone as an antiemetic in patients treated with cisplatin. N Engl J Med. 1981; 305:520. [IDIS 136602] [PubMed 7195983]

105. Alhashimi MM, Krasnow SH, Johnston-Early A et al. Risks in antiemesis using dexamethasone. Ann Intern Med. 1984; 101:281.

106. Powell BL, Craig JB. Risks in antiemesis using dexamethasone. Ann Intern Med. 1984; 101:281.

107. Grunwald HW, Rosner F. Dexamethasone as an antiemetic during cancer chemotherapy. Ann Intern Med. 1984; 101:398. [IDIS 190164] [PubMed 6465707]

108. Tyson LB, Gralla RJ, Clark RA et al. Combination antiemetic trials with metoclopramide. Proc Am Soc Clin Oncol. 1983; 2:91.

109. Bruera ED, Roca E, Cedaro L et al. Improved control of chemotherapy-induced emesis by the addition of dexamethasone to metoclopramide in patients resistant to metoclopramide. Cancer Treat Rep. 1983; 67:381-3. [IDIS 171263] [PubMed 6342770]

110. Lebel MH, Freij BJ, Syrogiannopoulos GA et al. Dexamethasone therapy for bacterial meningitis: results of two double-blind, placebo-controlled trials. N Engl J Med. 1988; 319:964-71. [IDIS 246361] [PubMed 3047581]

111. Smith AL. Neurologic sequelae of meningitis. N Engl J Med. 1988; 319:1012-4. [IDIS 246362] [PubMed 3419468]

112. Lebel MH, Hoyt MJ, Waagner DC et al. Magnetic resonance imaging and dexamethasone therapy for bacterial meningitis. Am J Dis Child. 1989; 143:301-6. [IDIS 252153] [PubMed 2644815]

113. McCracken GH Jr, Lebel MH. Dexamethasone therapy for bacterial meningitis in infants and children. Am J Dis Child. 1989; 143:287-9. [IDIS 252151] [PubMed 2644814]

114. Anon. Dexamethasone for bacterial meningitis in children. Med Lett Drugs Ther. 1989; 31:6-7. [PubMed 2911250]

115. American Academy of Pediatrics Committee on Infectious Diseases. Dexamethasone therapy for bacterial meningitis in infants and children. Pediatrics. 1990; 86:130-3. [IDIS 271617] [PubMed 2193301]

116. Mustafa MM, Ramilo O, Sáez-Llorens X et al. Cerebrospinal fluid prostaglandins, interleukin 1 β, and tumor necrosis factor in bacterial meningitis: clinical and laboratory correlations in placebo-treated and dexamethasone-treated patients. Am J Dis Child. 1990; 144:883-7. [IDIS 270056] [PubMed 2116086]

117. Kaplan SL. Dexamethasone for children with bacterial meningitis: should it be routine therapy? Am J Dis Child. 1989; 143:290-2. Editorial.

118. Havens PL, Kelly KJ, Hoffman GM et al. Dexamethasone therapy for bacterial meningitis. N Engl J Med. 1989; 320:464.

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