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Decadron Phosphate Injection (Merck)

  • Description
  • Chemical Structure
  • Clinical Pharmacology
  • Indications and Usage
  • Contraindications
  • Warnings
  • Precautions
  • Adverse Reactions
  • Overdosage
  • Dosage and Administration
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    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-11(beta), 17-dihydroxy-16(alpha)-methyl-21-(phosphonooxy)pregna-1, 4-diene-3, 20-dione disodium salt. The empirical formula is C 22 H 28 FNa 2 O 8 P and the structural formula is:

    DECADRON * Phosphate (Dexamethasone Sodium Phosphate) injection is a sterile solution (pH 7.0 to 8.5) of dexamethasone sodium phosphate, sealed under nitrogen, and is supplied in two concentrations: 4 mg/mL and 24 mg/mL. The 24 mg/mL concentration offers the advantage of less volume in indications where high doses of corticosteroids by the intravenous route are needed.

    Each milliliter of DECADRON Phosphate injection, 4 mg/ mL, contains dexamethasone sodium phosphate equivalent to 4 mg dexamethasone phosphate or 3.33 mg dexamethasone. Inactive ingredients per mL: 8 mg creatinine, 10 mg sodium citrate, sodium hydroxide to adjust pH, and Water for Injection q.s., with 1 mg sodium bisulfite, 1.5 mg methylparaben, and 0.2 mg propylparaben added as preservatives.

    Each milliliter of DECADRON Phosphate injection, 24 mg/ mL, contains dexamethasone sodium phosphate equivalent to 24 mg dexamethasone phosphate or 20 mg dexamethasone. Inactive ingredients per mL: 8 mg creatinine, 10 mg sodium citrate, 0.5 mg disodium edetate, sodium hydroxide to adjust pH, and Water for Injection q.s., with 1 mg sodium bisulfite, 1.5 mg methylparaben, and 0.2 mg propylparaben added as preservatives.

    *Registered trademark of Merck & CO., INC.


    DECADRON 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.


    1. 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
        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
        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
        Diffuse posterior uveitis and choroiditis
        Optic neuritis
        Sympathetic ophthalmia
        Anterior segment inflammation
        Allergic conjunctivitis
        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
        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 (I.V. only; I.M. 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
        Tuberculous 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.
    2. 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
      Acute nonspecific tenosynovitis
      Post-traumatic osteoarthritis.
    3. By intralesional injection:
      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).


    Systemic fungal infections. (See WARNINGS regarding amphotericin B.)

    Hypersensitivity to any component of this product, including sulfites (see WARNINGS ).


    Because rare instances of anaphylactoid reactions have occurred in patients receiving parenteral corticosteroid therapy, appropriate precautionary measures should be taken prior to administration, especially when the patient has a history of allergy to any drug. Anaphylactoid and hypersensitivity reactions have been reported for Injection DECADRON Phosphate (see ADVERSE REACTIONS ).

    Injection DECADRON Phosphate contains sodium bisulfite, a sulfite that may cause allergic-type reactions including anaphylactic symptoms and life-threatening or less severe asthmatic episodes in certain susceptible people. The overall prevalence of sulfite sensitivity in the general population is unknown and probably low. Sulfite sensitivity is seen more frequently in asthmatic than in nonasthmatic people.

    Corticosteroids may exacerbate systemic fungal infections and therefore should not be used in the presence of such infections unless they are needed to control drug reactions due to amphotericin B. Moreover, there have been cases reported in which concomitant use of amphotericin B and hydrocortisone was followed by cardiac enlargement and congestive failure.

    In patients on corticosteroid therapy subjected to any unusual stress, increased dosage of rapidly acting corticosteroids before, during, and after the stressful situation is indicated.

    Drug-induced secondary adrenocortical insufficiency may result from too rapid withdrawal of corticosteroids and may be minimized by gradual reduction of dosage. This type of relative insufficiency may persist for months after discontinuation of therapy; therefore, in any situation of stress occurring during that period, hormone therapy should be reinstituted. If the patient is receiving steroids already, dosage may have to be increased. Since mineralocorticoid secretion may be impaired, salt and/or a mineralocorticoid should be administered concurrently. (See PRECAUTIONS .)

    Corticosteroids may mask some signs of infection, and new infections may appear during their use. There may be decreased resistance and inability to localize infection when corticosteroids are used. Moreover, corticosteroids may affect the nitroblue-tetrazolium test for bacterial infection and produce false negative results.

    In cerebral malaria, a double-blind trial has shown that the use of corticosteroids is associated with prolongation of coma and a higher incidence of pneumonia and gastrointestinal bleeding.

    Corticosteroids may activate latent amebiasis. Therefore, it is recommended that latent or active amebiasis be ruled out before initiating corticosteroid therapy in any patient who has spent time in the tropics or any patient with unexplained diarrhea.

    Prolonged use of corticosteroids may produce posterior subcapsular cataracts, glaucoma with possible damage to the optic nerves, and may enhance the establishment of secondary ocular infections due to fungi or viruses.

    Usage in pregnancy.  Since adequate human reproduction studies have not been done with corticosteroids, use of these drugs in pregnancy or in women of childbearing potential requires that the anticipated benefits be weighed against the possible hazards to the mother and embryo or fetus. Infants born of mothers who have received substantial doses of corticosteroids during pregnancy should be carefully observed for signs of hypoadrenalism.

    Corticosteroids appear in breast milk and could suppress growth, interfere with endogenous corticosteroid production, or cause other unwanted effects. Mothers taking pharmacologic doses of corticosteroids should be advised not to nurse.

    Average and large doses of cortisone or hydrocortisone can cause elevation of blood pressure, salt and water retention, and increased excretion of potassium. These effects are less likely to occur with the synthetic derivatives except when used in large doses. Dietary salt restriction and potassium supplementation may be necessary. All corticosteroids increase calcium excretion.

    Administration of live virus vaccines, including smallpox, is contraindicated in individuals receiving immunosuppressive doses of corticosteroids. If inactivated viral or bacterial vaccines are administered to individuals receiving immunosuppressive doses of corticosteroids, the expected serum antibody response may not be obtained. However, immunization procedures may be undertaken in patients who are receiving corticosteroids as replacement therapy, e.g., for Addison's disease.

    Patients who are on drugs which suppress the immune system are more susceptible to infections than healthy individuals. Chickenpox and measles, for example, can have a more serious or even fatal course in non-immune patients on corticosteroids. In such patients who have not had these diseases, particular care should be taken to avoid exposure. The risk of developing a disseminated infection varies among individuals and can be related to the dose, route and duration of corticosteroid administration as well as to the underlying disease. If exposed to chickenpox, prophylaxis with varicella zoster immune globulin (VZIG) may be indicated. If chickenpox develops, treatment with antiviral agents may be considered. If exposed to measles, prophylaxis with immune globulin (IG) may be indicated. (See the respective package inserts for VZIG and IG for complete prescribing information.)

    Similarly, corticosteroids should be used with great care in patients with known or suspected Strongyloides (threadworm) infestation. In such patients, corticosteroid-induced immunosuppression may lead to Strongyloides hyperinfection and dissemination with widespread larval migration, often accompanied by severe enterocolitis and potentially fatal gram-negative septicemia.

    The use of DECADRON Phosphate injection in active tuberculosis should be restricted to those cases of fulminating or disseminated tuberculosis in which the corticosteroid is used for the management of the disease in conjunction with an appropriate antituberculous regimen.

    If corticosteroids are indicated in patients with latent tuberculosis or tuberculin reactivity, close observation is necessary as reactivation of the disease may occur. During prolonged corticosteroid therapy, these patients should receive chemoprophylaxis.

    Literature reports suggest an apparent association between use of corticosteroids and left ventricular free wall rupture after a recent myocardial infarction; therefore, therapy with corticosteroids should be used with great caution in these patients.


    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.

    Co-administration of thalidomide with DECADRON Phosphate injection should be employed cautiously, as toxic epidermal necrolysis has been reported with concomitant use.

    Aspirin should be used cautiously 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 to prevent peptic ulcer.

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

    Cytochrome P450 3A4 (CYP 3A4) enzyme inducers, such as phenytoin, barbiturates (e.g., phenobarbital), carbamazepine, and rifampin may enhance the metabolic clearance of corticosteroids resulting in decreased blood levels and lessened physiologic activity, thus requiring an increase in corticosteroid dosage.

    Dexamethasone is metabolized by CYP 3A4. Concomitant administration of dexamethasone with inducers of CYP 3A4 (as listed above) has the potential to result in decreased plasma concentrations of dexamethasone. In addition, concomitant administration of dexamethasone with known inhibitors of CYP 3A4 (e.g., ketoconazole, macrolide antibiotics such as erythromycin) has the potential to result in increased plasma concentrations of dexamethasone. Effects of other drugs on the metabolism of dexamethasone may interfere with dexamethasone suppression tests, which should be interpreted with caution during administration of such drugs.

    Dexamethasone is a moderate inducer of CYP 3A4. Co-administration of dexamethasone with other drugs that are metabolized by CYP 3A4 (e.g., indinavir, erythromycin) may increase their clearance, resulting in decreased plasma concentrations.

    In post-marketing experience, there have been reports of both increases and decreases in phenytoin levels with dexamethasone co-administration, leading to alterations in seizure control.

    Although ketoconazole may increase dexamethasone plasma concentrations through inhibition of CYP 3A4, ketoconazole alone can inhibit adrenal corticosteroid synthesis and may cause adrenal insufficiency during corticosteroid withdrawal (see WARNINGS ).

    Ephedrine may enhance the metabolic clearance of corticosteroids, resulting in decreased blood levels and lessened physiologic activity, thus requiring an increase in corticosteroid dosage.

    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.

    Pediatric Use

    Growth and development of pediatric patients on prolonged corticosteroid therapy should be carefully followed.


    Fluid and electrolyte disturbances

    Sodium retention

    Fluid retention

    Congestive heart failure in susceptible patients

    Potassium loss

    Hypokalemic alkalosis



    Muscle weakness

    Steroid myopathy

    Loss of muscle mass


    Vertebral compression fractures

    Aseptic necrosis of femoral and humeral heads

    Pathologic fracture of long bones

    Tendon rupture


    Peptic ulcer with possible subsequent perforation and hemorrhage

    Perforation of the small and large bowel, particularly in patients with inflammatory bowel disease


    Abdominal distention

    Ulcerative esophagitis


    Impaired wound healing

    Thin fragile skin

    Petechiae and ecchymoses


    Increased sweating

    May suppress reactions to skin tests

    Burning or tingling, especially in the perineal area (after I.V. injection)

    Other cutaneous reactions, such as allergic dermatitis, urticaria, angioneurotic edema



    Increased intracranial pressure with papilledema (pseudotumor cerebri) usually after treatment



    Psychic disturbances

    Cerebral palsy in preterm infants


    Menstrual irregularities

    Development of cushingoid state

    Suppression of growth in pediatric patients

    Secondary adrenocortical and pituitary unresponsiveness, particularly in times of stress, as in trauma, surgery, or illness

    Decreased carbohydrate tolerance

    Manifestations of latent diabetes mellitus


    Increased requirements for insulin or oral hypoglycemic agents in diabetics



    Posterior subcapsular cataracts

    Increased intraocular pressure



    Retinopathy of prematurity


    Negative nitrogen balance due to protein catabolism


    Myocardial rupture following recent myocardial infarction (see WARNINGS )

    Hypertrophic cardiomyopathy in low birth weight infants


    Anaphylactoid or hypersensitivity reactions


    Weight gain

    Increased appetite




    The following additional adverse reactions are related to parenteral corticosteroid therapy:

    Rare instances of blindness associated with intralesional therapy around the face and head

    Hyperpigmentation or hypopigmentation

    Subcutaneous and cutaneous atrophy

    Sterile abscess

    Postinjection flare (following intra-articular use)

    Charcot-like arthropathy


    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.

    Significant lethality was observed in female mice at single oral doses of 3630 mg/m 2 (1210 mg/kg) and single intravenous doses of 2382 mg/m 2 (794 mg/kg).


    DECADRON Phosphate injection, 4 mg/mL-- For intravenous, intramuscular, intra-articular, intralesional, and soft tissue injection.

    DECADRON Phosphate injection, 24 mg/mL-- For intravenous injection only.

    DECADRON Phosphate injection can be given directly from the vial, or it can be added to Sodium Chloride Injection or Dextrose Injection and administered by intravenous drip.

    Solutions used for intravenous administration or further dilution of this product should be preservative-free when used in the neonate, especially the premature infant.

    When it is mixed with an infusion solution, sterile precautions should be observed. Since infusion solutions generally do not contain preservatives, mixtures should be used within 24 hours.

    Parenteral drug products should be inspected visually for particulate matter and discoloration prior to administration, whenever solution and container permit.


    Intravenous and Intramuscular Injection

    The initial dosage of DECADRON Phosphate injection varies from 0.5 to 9 mg a day depending on the disease being treated. In less severe diseases doses lower than 0.5 mg may suffice, while in severe diseases doses higher than 9 mg may be required.

    The initial dosage should be maintained or adjusted until the patient's response is satisfactory. If a satisfactory clinical response does not occur after a reasonable period of time, discontinue DECADRON Phosphate injection and transfer the patient to other therapy.

    After a favorable initial response, the proper maintenance dosage should be determined by decreasing the initial dosage in small amounts to the lowest dosage that maintains an adequate clinical response.

    Patients should be observed closely for signs that might require dosage adjustment, including changes in clinical status resulting from remissions or exacerbations of the disease, individual drug responsiveness, and the effect of stress (e.g., surgery, infection, trauma). During stress it may be necessary to increase dosage temporarily.

    If the drug is to be stopped after more than a few days of treatment, it usually should be withdrawn gradually.

    When the intravenous route of administration is used, dosage usually should be the same as the oral dosage. In certain overwhelming, acute, life-threatening situations, however, administration in dosages exceeding the usual dosages may be justified and may be in multiples of the oral dosages. The slower rate of absorption by intramuscular administration should be recognized.


    There is a tendency in current medical practice to use high (pharmacologic) doses of corticosteroids for the treatment of unresponsive shock. The following dosages of DECADRON phosphate injection have been suggested by various authors:

    Author ** Dosage
    Cavanagh 1 3 mg/kg of body weight per 24 hours by constant intravenous infusion after an initial intravenous injection of 20 mg
    Dietzman 2 2 to 6 mg/kg of body weight as a single intravenous injection
    Frank 3 40 mg initially followed by repeat intravenous injection every 4 to 6 hours while shock persists
    Oaks 4 40 mg initially followed by repeat intravenous injection every 2 to 6 hours while shock persists
    Schumer 5 1 mg/kg of body weight as a single intravenous injection

    Administration of high dose corticosteroid therapy should be continued only until the patient's condition has stabilized and usually not longer than 48 to 72 hours.

    Although adverse reactions associated with high dose, short term corticosteroid therapy are uncommon, peptic ulceration may occur.

    **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.; Lillehei, 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 shock), 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.

    Cerebral Edema

    DECADRON Phosphate injection is generally administered initially in a dosage of 10 mg intravenously followed by 4 mg every six hours intramuscularly until the symptoms of cerebral edema subside. Response is usually noted within 12 to 24 hours and dosage may be reduced after two to four days and gradually discontinued over a period of five to seven days. For palliative management of patients with recurrent or inoperable brain tumors, maintenance therapy with two mg two or three times a day may be effective.

    Acute Allergic Disorders

    In acute, self-limited allergic disorders or acute exacerbations of chronic allergic disorders, the following dosage schedule combining parenteral and oral therapy is suggested:

    DECADRON Phosphate injection, 4 mg/mL: first day, 1 or 2 mL (4 or 8 mg), intramuscularly.

    DECADRON (Dexamethasone) tablets, 0.75 mg: second and third days, 4 tablets in two divided doses each day; fourth day, 2 tablets in two divided doses; fifth and sixth days, 1 tablet each day; seventh day, no treatment; eighth day, follow-up visit.

    This schedule is designed to ensure adequate therapy during acute episodes, while minimizing the risk of overdosage in chronic cases.

    Intra-articular, Intralesional, and Soft Tissue Injection

    Intra-articular, intralesional, and soft tissue injections are generally employed when the affected joints or areas are limited to one or two sites. Dosage and frequency of injection varies depending on the condition and the site of injection. The usual dose is from 0.2 to 6 mg. The frequency usually ranges from once every three to five days to once every two to three weeks. Frequent intra-articular injection may result in damage to joint tissues.

    Some of the usual single doses are:

    Site of Injection
    Amount of
    Large Joints
        (e.g., Knee)
    2 to 4
    Small Joints
        (e.g., Interphal-
         angeal, Temporo-

    0.8 to 1


    2 to 3
    Tendon Sheaths
    0.4 to 1
    Soft Tissue
    2 to 6
    1 to 2

    DECADRON Phosphate injection is particularly recommended for use in conjunction with one of the less soluble, longer-acting steroids for intra-articular and soft tissue injection.


    No 7628X--Injection DECADRON Phosphate, 4 mg per mL, is a clear, colorless solution, and is available in 5 mL and 25 mL vials as follows:

    NDC 0006-7628-03, 5 mL vial

    NDC 0006-7628-25, 25 mL vial.


    No. 7646--Injection DECADRON Phosphate, 24 mg per mL, is a clear, colorless to light yellow solution and is available in 5 mL vials as follows:

    NDC 0006-7646-03, 5 mL vial.


    Store at 25°C (77°F), excursions permitted to 15-30°C (59-86°F) [See USP Controlled Room Temperature].

    Sensitive to heat. Do not autoclave.

    Protect from freezing.

    Protect from light. Store container in carton until contents have been used.

    9051534    Issued November 2001

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