dexamethasone sodium phosphate

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

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}

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 asthma^b (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 syndrome^{a 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 dos