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 hormones.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 initial high-dose IV therapy followed by chronic oral therapy.b Can slow progression to clinically definite multiple sclerosis.b

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

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

Asthma

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

Maintenance therapy with low doses of an orally inhaled corticosteroid is preferred treatment for adults and children with mild persistent 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 switched to an equivalent regimen of an oral glucocorticoid.

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

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

Neoplastic Diseases

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

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
Furosemide
Granisetron HCl
Lidocaine HCl
Meropenem
Mitomycin
Nafcillin sodium
Palonosetron HCI
Prochlorperazine edisylate
Ranitidine HCl
Verapamil HCl
Incompatible
Daunorubicin HCl
Diphenhydramine HCl with lorazepam and metoclopramide HCl
Variable
Amikacin sulfate
Ondansetron HCl

Y-Site CompatibilityHID

Compatible
Acetaminophen
Acyclovir sodium
Allopurinol sodium
Amifostine
Amikacin sulfate
Amphotericin B cholesteryl sulfate complex
Amsacrine
Anidulafungin
Aztreonam
Bivalirudin
Ceftaroline fosamil
Cisatracurium besylate
Cladribine
Dexmedetomidine HCl
Docetaxel
Doripenem
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
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
Tacrolimus
Telavancin HCl
Teniposide
Theophylline
Thiotepa
Vinorelbine tartrate
Zidovudine
Incompatible
Ciprofloxacin
Fenoldopam mesylate
Idarubicin HCl
Methotrexate sodium
Midazolam HCl
Topotecan HCl

Dexamethasone Sodium Phosphate, a synthetic adrenocortical steroid, is a white or slightly yellow, crystalline powder. It is freely soluble in water and is exceedingly hygroscopic. The molecular weight is 516.41. It is designated chemically as 9-fluoro-11β,17-dihydroxy-16α-methyl-21-(phosphonooxy)pregna-1,4-diene-3,20-dione disodium salt. The empirical formula is C22H28FNa2O8P and the structural formula is:

Dexamethasone Sodium Phosphate injection, USP is a sterile solution of Dexamethasone Sodium Phosphate, and is supplied in 4 mg/ mL and 10 mg /mL.

Dexamethasone Sodium Phosphate injection, USP 4 mg/mL is a sterile solution for intravenous, intramuscular, intra-articular, intralesional and soft tissue administration. Each mL contains:

Active: Dexamethasone Sodium Phosphate 4.4 mg (equivalent to dexamethasone phosphate 4 mg). Preservatives: Methylparaben 1.5 mg; Propylparaben 0.2 mg. Inactives: Edetate Disodium 0.11 mg; Sodium Citrate Anhydrous 10 mg; Citric Acid and/or Sodium Hydroxide q.s to adjust pH 7.0 to 8.5 and Water for Injection q.s to 1 mL.

Dexamethasone Sodium Phosphate injection, USP 10 mg/mL is a sterile solution for intravenous or intramuscular use only. Each mL contains:

Actives: Dexamethasone Sodium Phosphate 11 mg (equivalent to dexamethasone phosphate 10 mg). Preservatives: Methylparaben 1.5 mg; Propylparaben 0.2 mg. Inactives: Edetate Disodium 0.11 mg; Sodium Citrate Anhydrous 10 mg; Citric Acid and/or Sodium Hydroxide q.s to adjust pH 7.0 to 8.5 and Water for Injection q.s to 1 mL.

Dexamethasone Sodium Phosphate injection has a rapid onset but short duration of action when compared with less soluble preparations. Because of this, it is suitable for the treatment of acute disorders responsive to adrenocortical steroid therapy.

Naturally occurring glucocorticoids (hydrocortisone and cortisone), which also have salt-retaining properties, are used as replacement therapy in adrenocortical deficiency states. Their synthetic analogs, including dexamethasone, are primarily used for their potent anti-inflammatory effects in disorders of many organ systems.

Glucocorticoids cause profound and varied metabolic effects. In addition, they modify the body's immune responses to diverse stimuli.

At equipotent anti-inflammatory doses, dexamethasone almost completely lacks the sodium-retaining property of hydrocortisone and closely related derivatives of hydrocortisone.

A. By intravenous or intramuscular injection when oral therapy is not feasible:

1. Endocrine disorders:

Primary or secondary adrenocortical insufficiency (hydrocortisone or cortisone is the drug of choice; synthetic analogs may be used in conjunction with mineralocorticoids where applicable; in infancy, mineralocorticoid supplementation is of particular importance).

Acute adrenocortical insufficiency (hydrocortisone or cortisone is the drug of choice; mineralocorticoid supplementation may be necessary, particularly when synthetic analogs are used).

Preoperatively, and in the event of serious trauma or illness, in patients with known adrenal insufficiency or when adrenocortical reserve is doubtful.

Shock unresponsive to conventional therapy if adrenocortical insufficiency exists or is suspected.

Congenital adrenal hyperplasia.

Nonsuppurative thyroiditis.

Hypercalcemia associated with cancer.

2. Rheumatic Disorders:

As adjunctive therapy for short-term administration (to tide the patient over an acute episode or exacerbation) in:

Post-traumatic osteoarthritis.

Synovitis of osteoarthritis.

Rheumatoid arthritis, including juvenile rheumatoid arthritis (selected cases may require low-dose maintenance therapy).

Acute and subacute bursitis.

Epicondylitis.

Acute nonspecific tenosynovitis.

Acute gouty arthritis.

Psoriatic arthritis.

Ankylosing spondylitis.

3. Collagen Diseases:

During an exacerbation or as maintenance therapy in selected cases of:

Systemic lupus erythematosus.

Acute rheumatic carditis.

4. Dermatologic Diseases:

Pemphigus.

Severe erythema multiforme. (Stevens-Johnson Syndrome)

Exfoliative dermatitis.

Bullous dermatitis herpetiformis.

Severe seborrheic dermatitis.

Severe psoriasis.

Mycosis fungoides.

5. Allergic States:

Control of severe or incapacitating allergic conditions intractable to adequate trials of conventional treatment in:

Bronchial asthma.

Contact dermatitis.

Atopic dermatitis.

Serum sickness.

Seasonal or perennial allergic rhinitis.

Drug hypersensitivity reactions.

Urticarial transfusion reactions.

Acute noninfectious laryngeal edema (epinephrine is the drug of first choice).

6. Ophthalmic Diseases:

Severe acute and chronic allergic and inflammatory processes involving the eye, such as:

Herpes zoster ophthalmicus.

Iritis, iridocyclitis.

Chorioretinitis.

Diffuse posterior uveitis and choroiditis.

Optic neuritis.

Sympathetic ophthalmia.

Anterior segment inflammation.

Allergic conjunctivitis.

Keratitis.

Allergic corneal marginal ulcers.

7. Gastrointestinal Diseases:

To tide the patient over a critical period of the disease in:

Ulcerative colitis (systemic therapy).

Regional enteritis (systemic therapy).

8. Respiratory Diseases:

Symptomatic sarcoidosis.

Berylliosis.

Fulminating or disseminated pulmonary tuberculosis when used concurrently with appropriate antituberculous chemotherapy.

Loeffler's syndrome not manageable by other means.

Aspiration pneumonitis.

9. Hematologic Disorders:

Acquired (autoimmune) hemolytic anemia.

Idiopathic thrombocytopenic purpura in adults (IV only; IM administration is contraindicated).

Secondary thrombocytopenia in adults.

Erythroblastopenia (RBC anemia).

Congenital (erythroid) hypoplastic anemia.

10. Neoplastic Diseases:

For palliative management of:

Leukemias and lymphomas in adults.

Acute leukemia of childhood.

11. Edematous States:

To induce diuresis or remission of proteinuria in the nephrotic syndrome, without uremia, of the idiopathic type or that due to lupus erythematosus.

12. Miscellaneous:

 Tuberculosis meningitis with subarachnoid block or impending block when used concurrently   with appropriate antituberculous chemotherapy.

 Trichinosis with neurologic or myocardial involvement.

13.  Diagnostic testing of adrenocortical hyperfunction.

14.  Cerebral Edema associated with primary or metastatic brain tumor, craniotomy, or head injury. Use in cerebral edema is not a substitute for careful neurosurgical evaluation and definitive management such as neurosurgery or other specific therapy.

B. By intra-articular or soft tissue injection:

As adjunctive therapy for short-term administration (to tide the patient over an acute episode or exacerbation) in:

Synovitis of osteoarthritis.

Rheumatoid arthritis.

Acute and subacute bursitis.

Acute gouty arthritis.

Epicondylitis.

Acute nonspecific tenosynovitis.

Post-traumatic osteoarthritis.

C. By intralesional injection:

Keloids.

Localized hypertrophic, infiltrated, inflammatory lesions of: lichen planus, psoriatic plaques, granuloma annulare, and lichen simplex chronicus (neurodermatitis).

Discoid lupus erythematosus.

Necrobiosis lipoidica diabeticorum.

Alopecia areata.

May also be useful in cystic tumors of an aponeurosis or tendon (ganglia).

This product, like many other steroid formulations, is sensitive to heat. Therefore, it should not be autoclaved when it is desirable to sterilize the exterior of the vial.

Following prolonged therapy, withdrawal of corticosteroids may result in symptoms of the corticosteroid withdrawal syndrome including fever, myalgia, arthralgia, and malaise. This may occur in patients even without evidence of adrenal insufficiency.

There is an enhanced effect of corticosteroids in patients with hypothyroidism and in those with cirrhosis.

Corticosteroids should be used cautiously in patients with ocular herpes simplex for fear of corneal perforation.

The lowest possible dose of corticosteroid should be used to control the condition under treatment, and when reduction in dosage is possible, the reduction must be gradual.

Psychic derangements may appear when corticosteroids are used, ranging from euphoria, insomnia, mood swings, personality changes, and severe depression to frank psychotic manifestations. Also, existing emotional instability or psychotic tendencies may be aggravated by corticosteroids.

Aspirin should be used with caution in conjunction with corticosteroids in hypoprothrombinemia.

Steroids should be used with caution in nonspecific ulcerative colitis, if there is a probability of impending perforation, abscess, or other pyogenic infection, also in diverticulitis, fresh intestinal anastomoses, active or latent peptic ulcer, renal insufficiency, hypertension, osteoporosis, and myasthenia gravis. Signs of peritoneal irritation following gastrointestinal perforation in patients receiving large doses of corticosteroids may be minimal or absent. Fat embolism has been reported as a possible complication of hypercortisonism.

When large doses are given, some authorities advise that antacids be administered between meals to help prevent peptic ulcer.

Growth and development of infants and children on prolonged corticosteroid therapy should be carefully followed.

Steroids may increase or decrease motility and number of spermatozoa in some patients.

Phenytoin, phenobarbital, ephedrine, and rifampin may enhance the metabolic clearance of corticosteroids, resulting in decreased blood levels and lessened physiologic activity, thus requiring adjustment in corticosteroid dosage. These interactions may interfere with dexamethasone suppression tests which should be interpreted with caution during administration of these drugs.

False negative results in the dexamethasone suppression test (DST) in patients being treated with indomethacin have been reported. Thus, results of the DST should be interpreted with caution in these patients.

The prothrombin time should be checked frequently in patients who are receiving corticosteroids and coumarin anticoagulants at the same time because of reports that corticosteroids have altered the response to these anticoagulants. Studies have shown that the usual effect produced by adding corticosteroids is inhibition of response to coumarins, although there have been some conflicting reports of potentiation not substantiated by studies.

When corticosteroids are administered concomitantly with potassium depleting diuretics, patients should be observed closely for development of hypokalemia.

Intra-articular injection of a corticosteroid may produce systemic as well as local effects.

Appropriate examination of any joint fluid present is necessary to exclude a septic process.

A marked increase in pain accompanied by local swelling, further restriction of joint motion, fever, and malaise is suggestive of septic arthritis. If this complication occurs and the diagnosis of sepsis is confirmed, appropriate antimicrobial therapy should be instituted.

Injection of a steroid into an infected site is to be avoided.

Corticosteroids should not be injected into unstable joints.

Patients should be impressed strongly with the importance of not overusing joints in which symptomatic benefit has been obtained as long as the inflammatory process remains active.

Frequent intra-articular injection may result in damage to joint tissues.

The slower rate of absorption by intramuscular administration should be recognized.

Information for Patients

Susceptible patients who are on immunosuppressant doses of corticosteroids should be warned to avoid exposure to chickenpox or measles. Patients should also be advised that if they are exposed, medical advice should be sought without delay.

Reports of acute toxicity and/or death following overdosage of glucocorticoids are rare. In the event of overdosage, no specific antidote is available; treatment is supportive and symptomatic.

The oral LD50 of dexamethasone in female mice was 6.5 g/kg. The intravenous LD50 of Dexamethasone Sodium Phosphate in female mice was 794 mg/kg.

Dexamethasone Sodium Phosphate injection, USP 4 mg/mL is for-intravenous, intramuscular, intra-articular, intralesional and soft tissue administration available as follows:

NDC Number	Fill volume	Pack size
67457-423-12	1 mL Single-Dose Vial	25’s
67457-422-54	5 mL Multi-Dose Vial	25’s
67457-421-30	30 mL Multi-Dose Vial	25’s

Dexamethasone Sodium Phosphate injection, USP 10 mg/mL is for intravenous and intramuscular injection only available as follows:

NDC Number	Fill volume	Pack size
67457-420-10	10 mL Multi-Dose Vial	10’s

Store at 20° to 25°C (68° to 77°F). [See USP Controlled Room Temperature.]

Protect from light.

Sensitive to heat. Do not autoclave. Protect from freezing.

REFERENCES

1. Cavanagh, D.; Singh, K. B.: Endotoxin shock in pregnancy and abortion, in: "Corticosteroids in the Treatment of Shock," Schumer, W.; Nyhus, L. M., Editors, Urbana, University of Illinois Press, 1970, pp. 86–96. 2. Dietzman, R. H.; Ersek, R. A.; Bloch, J. M.; Lilleher, R. C.: High-output, low-resistance gram-negative septic shock in man, Angiology 20: 691–700, Dec. 1969. 3. Frank, E.: Clinical observations in shock and management (in: Shields, T. F., ed.: Symposium on current concepts and management of shocks), J. Maine Med. Ass. 59: 195 – 200, Oct. 1968. 4. Oaks, W. W.; Cohen, H. E.: Endotoxin shock in the geriatric patient, Geriat. 22: 120–130, Mar. 1967. 5. Schumer, W.; Nyhus, L. M.: Corticosteroid effect on biochemical parameters of human oligemic shock, Arch. Surg. 100: 405–408, Apr. 1970.

Manufactured for:

Mylan Institutional LLC

Rockford, IL 61103 U.S.A.

Made in India

DECEMBER 2015