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Betamethasone (Systemic)

Class: Adrenals
ATC Class: H02AB01
VA Class: HS051
CAS Number: 378-44-9
Brands: Celestone, Celestone Soluspan

Medically reviewed by on Dec 27, 2021. Written by ASHP.


Synthetic glucocorticoid; minimal mineralocorticoid activity.

Uses for Betamethasone (Systemic)

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.

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

Adrenocortical Insufficiency

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

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.

If betamethasone is used, must also administer a mineralocorticoid (fludrocortisone), particularly in infants.

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

In shock unresponsive to conventional therapy, IV therapy in conjunction with other therapy for shock is essential; hydrocortisone is preferred, but a synthetic glucocorticoid like betamethasone can be substituted.

Adrenogenital Syndrome

Lifelong glucocorticoid treatment of congenital adrenogenital syndrome.

In salt-losing forms, cortisone or hydrocortisone is preferred in conjunction with liberal salt intake; addition of a mineralocorticoid may be necessary through at least 5–7 years of age.

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

In hypertensive forms, a short-acting glucocorticoid with minimal mineralocorticoid activity (e.g., methylprednisolone, prednisone) is preferred; avoid long-acting glucocorticoids (e.g., dexamethasone, betamethasone) because of tendency toward overdosage and growth retardation.


Treatment of hypercalcemia associated with malignancy.

Usually ameliorates hypercalcemia associated with bone involvement in multiple myeloma.

Treatment of hypercalcemia associated with sarcoidosis.

Treatment of hypercalcemia associated with vitamin D intoxication.

Not effective for hypercalcemia caused by hyperparathyroidism.


Treatment of granulomatous (subacute, nonsuppurative) thyroiditis.

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

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

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

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, acute and subacute bursitis, epicondylitis, acute nonspecific tenosynovitis, peritendinitis, ankylosing spondylitis, Reiter syndrome, rheumatic fever [especially with carditis]) and collagen diseases (e.g., acute rheumatic carditis, systemic lupus erythematosus, polyarteritis nodosa, vasculitis) refractory to more conservative measures.

Reduces the size of cystic tumors of an aponeurosis, tendon, or ganglia.

Relieves inflammation and suppresses symptoms but not disease progression.

Rarely indicated as maintenance therapy.

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.

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

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

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

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.

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

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. 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.

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

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

In osteoarthritis, intra-articular injections may be beneficial but should be limited in number as joint damage may occur.

Dermatologic Diseases

Treatment of pemphigus and pemphigoid, bullous dermatitis herpetiformis, severe erythema multiforme (Stevens-Johnson syndrome), exfoliative dermatitis, lichen planus, uncontrollable eczema, cutaneous sarcoidosis, mycosis fungoides, severe psoriasis, and severe seborrheic dermatitis.

Usually reserved for acute exacerbations unresponsive to conservative therapy.

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

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

Chronic skin disorders seldom an indication for systemic glucocorticoids.

Intralesional or sublesional injections occasionally indicated for localized chronic skin disorders (e.g., keloids, psoriatic plaques, alopecia areata, discoid lupus erythematosus, necrobiosis lipoidica diabeticorum, granuloma annulare) unresponsive to topical therapy.

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

Rarely indicated systemically for alopecia (areata, totalis, or universalis). May stimulate hair growth, but hair loss returns when the drug is discontinued.

Allergic Conditions

For control of severe or incapacitating allergic conditions intractable to adequate trials of conventional treatment and control of acute manifestations, including acute noninfectious laryngeal edema, serum sickness, allergic symptoms of trichinosis, urticarial transfusion reactions, drug hypersensitivity reactions, and severe seasonal or perennial rhinitis.

Systemic therapy usually reserved for acute conditions and severe exacerbations.

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

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.

Ocular Disorders

To suppress a variety of allergic and nonpyogenic ocular inflammations.

To reduce scarring in ocular injuries.

For the treatment of severe acute and chronic allergic and inflammatory processes involving the eye that are intractable to adequate trials of conventional treatment (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, sympathetic ophthalmia).

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

Glucocorticoids used systemically in stubborn cases of anterior segment eye disease and when deeper ocular structures are involved.


Systemically (IM or orally) for control of severe or incapacitating allergic bronchial asthma intractable to adequate trials of conventional treatment recommended by the manufacturer. However, experts do not recommend IM administration of betamethasone for treatment of asthma.

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


Management of symptomatic sarcoidosis.

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

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.

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; used in the treatment of tuberculous meningitis with subarachnoid block or impending block concurrently with appropriate antituberculous chemotherapy.

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.

Loeffler’s Syndrome

Symptomatic relief of acute manifestations of symptomatic Loeffler’s syndrome not manageable by other means.


Symptomatic relief of acute manifestations of berylliosis.

Aspiration Pneumonitis

Symptomatic relief of acute manifestations of aspiration pneumonitis.

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 premature rupture of membranes, preeclampsia, or third-trimester hemorrhage.

Combined effects on multiple organ maturation reduces neonatal mortality; beneficial effects extend to a broad range of gestational ages (i.e., 24–34 weeks).

Efficacy and safety of antenatal glucocorticoid therapy before 24 weeks or after 34 weeks of gestation have not been established.

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.

Reduces the incidence and/or severity of neonatal respiratory distress syndrome (RDS) and neonatal mortality as indicated by a reduction in requirements for neonatal ventilatory support or surfactant therapy; beneficial effects are additive with those of surfactant.

Can improve neonatal circulatory stability and reduce the incidence 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.

Use 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.

Hematologic Disorders

Management of acquired (autoimmune) hemolytic anemia, idiopathic thrombocytopenic purpura (ITP), secondary thrombocytopenia, erythroblastopenia, or congenital (erythroid) hypoplastic anemia.

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

Glucocorticoids, immune globulin IV (IGIV), or splenectomy are first-line therapies for moderate to severe ITP, depending on the extent of bleeding involved.

GI Diseases

Short-term palliative therapy for acute exacerbations and systemic complications of ulcerative colitis, regional enteritis (Crohn’s disease), or celiac disease.

Use with caution if there is a probability of impending perforation, abscess, or other pyogenic infection.

Rarely indicated for maintenance therapy in chronic GI diseases (ulcerative colitis, celiac disease) since therapy does not prevent relapses and may produce severe adverse reactions with long-term administration.

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

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

Parenteral glucocorticoids recommended for patients with severe fulminant Crohn’s disease. Once patients respond to parenteral therapy, gradually switch to an equivalent regimen of an oral glucocorticoid.

Some experts state that glucocorticoids should not be used for the management of mildly to moderately active Crohn’s disease because of the high incidence of adverse effects. Reserve use for patients with moderately to severely active disease.

Should not be used for maintenance therapy of chronic GI diseases (e.g., ulcerative colitis, Crohn’s disease) because they usually do not prevent relapses, and the drugs may produce severe adverse effects with long-term administration.

Has 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).

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.

Alone or as a component of various combination chemotherapeutic regimens for palliative treatment of advanced, symptomatic (i.e., painful) hormone-refractory prostate cancer.

Low Back Pain

Has been used epidurally (alone or combined with a local anesthetic and/or an opiate analgesic) for symptomatic relief of low back pain.

Although use remains controversial and convincing evidence of efficacy is lacking, most experts consider such therapy an option for short-term relief of acute, subacute, or chronic radicular pain in patients with low back pain and radiculopathy associated with disk disease or herniation or spinal stenosis. Use when more conservative therapies (e.g., rest, analgesics, physical therapy) fail and as a means of potentially avoiding surgery. (See Nervous System Effects under Cautions.)

Limited evidence suggests that therapeutic facet joint and intradiscal glucocorticoid injections are minimally effective or ineffective in the treatment of low back pain, although facet joint injections may be useful in some patients with facet arthropathy. Inclusion of a glucocorticoid in trigger point injections does not appear to be beneficial.

Sacroiliac joint injections performed using fluoroscopic guidance may provide temporary pain relief in some patients when the principal source of spinal pain is the sacroiliac joint.

Oral glucocorticoids have been used; however, they do not appear to be effective and evidence supporting such use is lacking.

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.

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


Treatment of trichinosis with neurologic or myocardial involvement.

Nephrotic Syndrome and Lupus Nephritis

Treatment of idiopathic nephrotic syndrome without uremia.

Can induce diuresis and remission of proteinuria in nephrotic syndrome.

Treatment of lupus nephritis.

Carpal Tunnel Syndrome

Local injection into the tissue near the carpal tunnel has been used in a limited number of patients to relieve symptoms (e.g., pain, edema, sensory deficit) of carpal tunnel syndrome.

Betamethasone (Systemic) Dosage and Administration


  • Route of administration and dosage depend on the condition being treated and the patient response.

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. Provides relief of symptoms while minimizing adrenal suppression, protein catabolism, and other adverse effects.

  • Because betamethasone’s HPA-axis suppression persists for 3.25 days, alternate-day regimens are not appropriate.

  • 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).

  • 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.

Discontinuance of Therapy

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

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

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

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

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

  • In one suggested regimen, decrease by 0.3–0.6 mg every 3–7 days until the physiologic dose (0.6 mg) is reached.

  • Other recommendations state that decrements usually should not exceed 0.3 mg every 1–2 weeks.

  • When a physiologic dosage has been reached, single 20-mg oral morning doses of hydrocortisone can be substituted. 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.


Administer orally or by IM injection. Do not administer IV.

Administer locally by intra-articular, intralesional, soft tissue, or epidural injection.

Intrathecal administration associated with neurotoxicity.

Oral Administration

Administer betamethasone orally as a solution.

IM Administration

Administer betamethasone sodium phosphate and betamethasone acetate by IM injection. Generally reserve IM therapy for patients who are not able to take oral glucocorticoids.

Intra-articular, Intralesional, and Soft-tissue Administration

Administer betamethasone sodium phosphate and betamethasone acetate by intra-articular, intralesional (intradermal, not sub-Q), or soft-tissue injection.

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

For intra-articular injections, use a 20- to 24-gauge needle; verify needle placement (aspirate a few drops of synovial fluid) prior to drug administration with a second syringe.

Avoid intra-articular injection into a previously infected joint. Prior to intra-articular administration, examine the joint fluid to exclude septic arthritis. Symptoms of septic arthritis include local swelling, further restriction of joint motion, fever, or malaise. If septic arthritis is confirmed, institute appropriate antimicrobial therapy.

Do not inject drug into unstable joints.

For management of tenosynovitis and tendinitis, inject into affected tendon sheaths rather than into tendons.

For dermatologic conditions, use a tuberculin syringe with a 25-gauge, ½-inch needle for intralesional administration.

For disorders of the foot (bursitis, tenosynovitis, acute gouty arthritis), use a tuberculin syringe with a 25-gauge, 3/4-inch needle for intra-articular or soft-tissue administration.

May mix injection with a local anesthetic (e.g., 1–2% lidocaine hydrochloride) using formulations that do not contain parabens or phenol. Do not mix with diluents or local anesthetics containing preservatives (e.g., parabens, phenol) because flocculation of suspension may result. (See Compatibility under Stability.)

Epidural Administration†

Long-acting injectable suspension has been administered by epidural injection, although safety of epidural injections using preserved formulations is controversial and epidural administration of these formulations is not recommended by the manufacturer. Limited evidence suggests that large particles in glucocorticoid suspensions may cause embolic vascular occlusion following inadvertent intra-arterial injection. (See Nervous System Effects under Cautions.)

Inject into the epidural space near the site where the nerve roots pass before entering the intervertebral foramen.

Epidural injections may be performed by caudal, interlaminar, or transforaminal approaches; the transforaminal approach requires the smallest injection volume and appears to be the most specific and possibly most effective route.

Because of the potential for complications related to improper needle placement or drug administration, many experts state that epidural injections should be performed by an experienced clinician using fluoroscopic guidance and contrast control to ensure that the needle is correctly positioned and that the injection is not performed intravascularly, intrathecally, or into tissues other than the epidural space. However, serious adverse neurologic effects have been reported even with fluoroscopic guidance. (See Nervous System Effects under Cautions.)

Optimal technique, dosage, timing of initial injection, injection frequency, and maximum number of injections remain to be established.


Available as betamethasone and as a fixed combination of betamethasone sodium phosphate and betamethasone acetate. Dosage of betamethasone sodium phosphate is expressed in terms of betamethasone. Each mL of the fixed-combination injectable suspension contains 3 mg of betamethasone (as betamethasone sodium phosphate) and 3 mg of betamethasone acetate.

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 gradually as soon as possible.

If a satisfactory response is not obtained, discontinue betamethasone and substitute other appropriate therapy.

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

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.

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


Usual Dosage

Initially, 0.6–7.2 mg, depending on the disease and disease severity.


Initially, 0.5–9 mg daily (0.08–1.5 mL of the suspension), depending on disease being treated. Extremely high parenteral dosage may be justified in life-threatening situations.

Rheumatic Disorders and Collagen Diseases
Bursitis, Tenosynovitis, Peritendinitis
Intralesional, Intrasynovial, or Soft-tissue Injection

Acute bursitis of subdeltoid, subacromial, olecranon, or prepatellar bursae: 6 mg (i.e., 3 mg of betamethasone as the sodium phosphate and 3 mg of betamethasone acetate in 1 mL of suspension) into the bursa as a single dose.

Recurrent acute bursitis or acute exacerbations of chronic bursitis of subdeltoid, subacromial, olecranon, or prepatellar bursae: 6 mg into bursa; repeated doses may be required. Reduce dosage for chronic bursitis once acute condition is controlled.

Bursae under heloma durum or molle: 1.5–3 mg (0.25–0.5 mL) repeated every 3 days to 1 week.

Bursae over hallus rigidus or digiti quinti varus: 3 mg (0.5 mL) repeated every 3 days to 1 week.

Tenosynovitis, periostitis of cuboid bone: 3 mg (0.5 mL) repeated every 3 days to 1 week.

Tenosynovitis or tendinitis: 6 mg for 3 or 4 injections at intervals of 1–2 weeks.

Ganglions of joint capsules and tendon sheaths: 3 mg (0.5 mL) directly into ganglion cysts.

Acute Gouty Arthritis
Intra-articular or Soft-tissue Injection

Foot: 3–6 mg (0.5–1 mL) repeated every 3 days to 1 week.

Rheumatoid Arthritis and Osteoarthritis
Intra-articular Injection

Varies depending on location, size, and degree of inflammation.

Very large joints (e.g., hip): 6–12 mg (1–2 mL of the suspension).

Large joints (e.g. knee, ankle, shoulder): 6 mg (1 mL of the suspension).

Medium joints (e.g., elbow, wrist): 3–6 mg (0.5–1 mL of the suspension).

Smaller joints (e.g., hand, chest): 1.5–3 mg (0.25–0.5 mL of the suspension).

Dermatologic Diseases
Intralesional Injection

1.2 mg/cm2 (0.2 mL) injected intradermally; do not exceed a total dosage of 6 mg/week.

Antenatal Use in Preterm Labor†

12 mg once daily for 2 days in preterm labor that begins at 24–34 weeks’ gestation.

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 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.

Prescribing Limits


Dermatologic Diseases
Intralesional Injection

Maximum total dosage of 6 mg/week.

Cautions for Betamethasone (Systemic)


  • Systemic fungal infections.

  • Concurrent administration of live virus or live, attenuated vaccines in patients receiving immunosuppressive dosages of glucocorticoids. (See Immunosuppression under Cautions.)

  • Epidural administration in patients with local or systemic infection; individuals with bleeding disorders or receiving concurrent anticoagulant therapy (e.g., warfarin, heparin, antiplatelet agents); patients with known hypersensitivity to local anesthetic agents, contrast agents, or glucocorticoids; and patients who experienced complications with prior glucocorticoid injections.



Nervous System Effects

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

Use with caution in patients with myasthenia gravis.

Aseptic meningitis, arachnoiditis, exacerbation of pain, spinal cord trauma, subdural injection, intracranial air injection, increased intracranial pressure, nerve injury, seizures, bladder or bowel dysfunction, paraparesis or paralysis, sensory disturbances, and brain damage reported following epidural and/or intrathecal glucocorticoid injection. Unclear whether these effects involved improper needle placement or were related to administration of the drug and/or preservatives.

Serious, potentially permanent, and sometimes fatal adverse neurologic events (e.g., spinal cord infarction, paraplegia, quadriplegia, cortical blindness, stroke, seizures, nerve injury, brain edema) reported rarely, often within minutes to 48 hours following epidural glucocorticoid injection given either with or without fluoroscopic guidance.

FDA states efficacy and safety of epidural glucocorticoid administration not established; not FDA-labeled for this use. (See Advice to Patients.)

Adrenocortical Insufficiency

When given in supraphysiologic doses for prolonged periods, glucocorticoids may cause decreased secretion of endogenous corticosteroids by suppressing pituitary release of corticotropin (secondary adrenocortical insufficiency).

The degree and duration of adrenocortical insufficiency is highly variable among patients and depends on the dose, frequency and time of administration, and duration of glucocorticoid therapy.

Acute adrenal insufficiency (even death) may occur if the drugs are withdrawn abruptly or if patients are transferred from systemic glucocorticoid therapy to local (e.g., inhalation) therapy.

Withdraw very gradually following long-term therapy with pharmacologic dosages. (See Discontinuance of Therapy under Dosage and Administration.)

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

Until recovery occurs, signs and symptoms of adrenal insufficiency may develop if subjected to stress (e.g., infection, surgery, trauma) and replacement therapy may be required. Since mineralocorticoid secretion may be impaired, sodium chloride and/or a mineralocorticoid should also be administered.

If the disease flares up during withdrawal, increase dosage and follow with a more gradual withdrawal.


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

Administration of live virus or live, attenuated vaccines, including smallpox, is contraindicated in patients receiving immunosuppressive dosages of glucocorticoids. If inactivated vaccines are administered to such patients, the expected serum antibody response may not be obtained.

Increased Susceptibility to Infection

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

Infections with any pathogen, including viral, bacterial, fungal, protozoan, or helminthic infections in any organ system, may be associated with glucocorticoids alone or in combination with other immunosuppressive agents.

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

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

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

Children and any adult who are not likely to have been exposed to varicella or measles should avoid exposure to these infections while receiving glucocorticoids.

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

Fatal outcome (e.g., in those developing hemorrhagic varicella) may not always be avoided even if appropriate therapy is initiated aggressively.

Immunosuppression may result in activation of latent infection or exacerbation of intercurrent infections (e.g., those caused by Candida, Mycobacterium, Toxoplasma, Strongyloides, Pneumocystis, Cryptococcus, Nocardia, Ameba).

Use with great care in patients with known or suspected Strongyloides (threadworm) infection. Immunosuppression may lead to Strongyloides hyperinfection and dissemination with widespread larval migration, often accompanied by severe enterocolitis and potentially fatal gram-negative septicemia.

Not effective and can have detrimental effects in the management of cerebral malaria.

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

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

Rarely, epidural abscess reported following epidural glucocorticoid injection; infectious complications (e.g., bacterial meningitis) also reported.

Musculoskeletal Effects

Muscle wasting, muscle pain or weakness, delayed wound healing, and atrophy of the protein matrix of the bone resulting in osteoporosis, vertebral compression fractures, aseptic necrosis of femoral or humeral heads, or pathologic fractures of long bones are manifestations of protein catabolism that may occur during prolonged therapy with glucocorticoids. These adverse effects may be especially serious in geriatric or debilitated patients. A high protein diet may help to prevent adverse effects associated with protein catabolism.

An acute, generalized myopathy can occur with the use of high doses of glucocorticoids, particularly in patients with disorders of neuromuscular transmission (e.g., myasthenia gravis) or in patients receiving concomitant therapy with neuromuscular blocking agents (e.g., pancuronium).

Tendon rupture, particularly of the Achilles tendon.

Osteoporosis and related fractures are one of the most serious adverse effects of long-term glucocorticoid therapy.

To minimize the risk of glucocorticoid-induced bone loss, the smallest possible effective dosage and duration should be used.

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

Withdraw glucocorticoids if osteoporosis develops, unless their use is life-saving.

Glucocorticoid-induced bone loss can be both prevented and treated. Baseline measurement of bone mineral density (BMD) at the lumbar spine and/or hip should be obtained when initiating long-term (e.g., >6 months) therapy, and appropriate preventive therapy should be initiated. Longitudinal measurements may be repeated as often as every 6 months to detect possible bone loss. Less frequent (e.g., annual) follow-up probably is sufficient in patients who are receiving therapy to prevent bone loss.

Skeletal wasting is most rapid during the initial 6 months of therapy, and trabecular bone is affected to a greater degree than is cortical bone.

Calcium and vitamin D supplementation, bisphosphonate (e.g., alendronate, risedronate), and a weight-bearing exercise program that maintains muscle mass are suitable first-line therapies aimed at reducing the risk of adverse bone effects.

Calcitonin may be considered as second-line therapy for patients who refuse or do not tolerate bisphosphonate therapy or in whom the drugs are contraindicated.

Fluid and Electrolyte Disturbances

Sodium retention with resultant edema, potassium loss, and elevation of BP may occur but is less common with betamethasone than with average or large doses of cortisone or hydrocortisone. Risk is increased with high-dose synthetic glucocorticoids for prolonged periods. Edema and CHF (in susceptible patients) may occur.

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

Increased calcium excretion and possible hypocalcemia.

Ocular Effects

Prolonged use may result in posterior subcapsular and nuclear cataracts (particularly in children), exophthalmos, and/or increased intraocular pressure (IOP) which may result in glaucoma or may occasionally damage the optic nerve.

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

Use cautiously in patients with active ocular herpes simplex infections since corneal perforation may develop.

Transient blindness, amblyopia, acute retinal necrosis syndrome, intraocular hemorrhage, and cortical blindness have occurred following epidural glucocorticoid injection.

Endocrine and Metabolic Effects

Administration over a prolonged period may produce various endocrine disorders including hypercorticism (cushingoid state) and amenorrhea or other menstrual difficulties.

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

May decrease glucose tolerance, produce hyperglycemia, and aggravate or precipitate diabetes mellitus, especially in patients predisposed to diabetes mellitus. If glucocorticoid therapy is required in patients with diabetes mellitus, changes in insulin or oral antidiabetic agent dosage or diet may be necessary.

Administer by epidural injection with caution in patients with diabetes mellitus.

Exaggerated response to the glucocorticoids in hypothyroidism.

Cardiovascular Effects

Use with extreme caution in recent MI since an association between use of glucocorticoids and left ventricular free-wall rupture has been suggested.

Administer by epidural injection with caution in patients with CHF.

Use with caution in patients with hypertension.

Sensitivity Reactions

Anaphylactic or anaphylactoid reactions with or without circulatory collapse, cardiac arrest, or bronchospasm. Take appropriate precautionary measures prior to administration, especially in patients with a history of allergy to any drug.

Benzalkonium Chloride Sensitivity

Injectable suspension contains benzalkonium chloride that has been associated with neurotoxic effects in animals or humans when used epidurally or intrathecally.

General Precautions


Prior to initiation of long-term glucocorticoid therapy, perform baseline ECGs, BPs, chest and spinal radiographs, glucose tolerance tests, and evaluations of HPA-axis function in all patients.

Perform upper GI radiographs in patients predisposed to GI disorders, including those with known or suspected peptic ulcer disease.

During long-term therapy, perform periodic height, weight, chest and spinal radiographs, hematopoietic, electrolyte, glucose tolerance, and ocular and BP evaluations.

GU Effects

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

GI Effects

Corticosteroids should be used with caution in patients with diverticulitis, nonspecific ulcerative colitis (if there is a probability of impending perforation, abscess, or other pyogenic infection), or those with recent intestinal anastomoses.

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

Use of Fixed Combination

When used in fixed combination with other agents, consider the cautions, precautions, and contraindications associated with the concomitant agents.

Specific Populations


Category C.

Observe neonates born from mothers receiving prolonged therapy for signs of hypoadrenalism.

Fluoroscopy (recommended for ensuring proper needle placement for epidural injections) is contraindicated in pregnant women.


Distributed into milk and could suppress growth, interfere with endogenous glucocorticoid production, or cause other adverse effects in nursing infants.

Pediatric Use

With long-term use, may delay growth and maturation in children and adolescents. Monitor carefully the growth and development of pediatric patients receiving prolonged corticosteroid therapy. Titrate dosage to the lowest effective level. Alternate-day therapy with short-acting glucocorticoids (e.g., prednisone, prednisolone, methylprednisolone) may minimize growth suppression and should be instituted if growth suppression occurs.

Glucocorticoid-induced osteoporosis and associated fractures are common in children and adolescents receiving long-term systemic therapy. In addition, may prevent achievement of peak bone mass during adolescence by inhibiting bone formation. Methods for monitoring bone mineralization (e.g., dual-energy x-ray absorptiometry [DXA]) in children and adolescents are similar to those in adults.

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

Geriatric Use

With prolonged therapy, muscle wasting, muscle pain or weakness, delayed wound healing, and atrophy of the protein matrix of the bone resulting in osteoporosis, vertebral compression fractures, aseptic necrosis of femoral or humeral heads, or pathologic fractures of long bones may occur. May be especially serious in geriatric or debilitated patients.

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

Hepatic Impairment

Glucocorticoids should be used with caution in patients with cirrhosis because such patients often show exaggerated response to the drugs.

Renal Impairment

Use with caution.

Common Adverse Effects

Intra-articular and soft-tissue injection: Soft-tissue atrophy, hypopigmentation or hyperpigmentation, facial erythema, thin, fragile skin.

Interactions for Betamethasone (Systemic)

Inhibits and is metabolized by CYP3A4.

Drugs Affecting Hepatic Microsomal Enzymes

Inhibitors of CYP3A4: Potential pharmacokinetic interaction (decreased betamethasone clearance).

Inducers of CYP3A4: Potential pharmacokinetic interaction (increased betamethasone clearance).

Specific Drugs




Analgesics, opiate

Epidural injection: Potential for serious injuries (e.g., brain damage, death) when glucocorticoids are combined with opiate analgesics

Improve patient safety by excluding typical epidural doses (volumes in excess of intrathecal test doses) of opiate analgesics from epidural glucocorticoid injections

Anesthetics, local

Epidural injection: Potential for serious injuries (e.g., brain damage, death) when glucocorticoids are combined with local anesthetics

Improve patient safety by excluding typical epidural doses (volumes in excess of intrathecal test doses) of local anesthetics from epidural glucocorticoid injections

Antidiabetic therapy

Increased blood glucose concentrations in diabetes mellitus

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


Increased clearance of betamethasone

Increase dosage of betamethasone

Diuretics, potassium-depleting

Enhances the potassium-wasting effects of glucocorticoids

Monitor for development of hypokalemia


Decreased clearance of betamethasone

Reduce dosage of betamethasone to avoid potential adverse effects


Increases the risk of GI ulceration

Decreased serum salicylate concentrations; when corticosteroids are discontinued, serum salicylate concentration may increase possibly resulting in salicylate intoxication

Use concurrently with caution

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

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

Use concurrently with aspirin with caution in hypoprothrombinemia


Increased clearance of betamethasone

Increase dosage of betamethasone


Increased clearance of betamethasone

Increase dosage of betamethasone


Decreased clearance of betamethasone

Reduce dosage of betamethasone to avoid potential adverse effects

Vaccines and toxoids

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

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

Can aggravate neurologic reactions to some vaccines (supraphysiologic dosages)

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

Betamethasone (Systemic) Pharmacokinetics



Following intra-articular administration, systemic absorption of the soluble portion (betamethasone sodium phosphate) of the injectable suspension is rapid.

Following IM administration, peak plasma concentrations occurred at 1 hour.


IM administration: Anti-inflammatory effects may appear within 1–3 hours.


IM administration: Anti-inflammatory effects or HPA suppression may persist for 7 days.



Most glucocorticoids are removed rapidly from the blood and distributed to muscles, liver, skin, intestines, and kidneys.

Distributes into breast milk and crosses the placenta.

Plasma Protein Binding

Low affinity for transcortin binding protein.



Metabolized in most tissues, but mainly in the liver, to inactive compounds.

Elimination Route

Cleared mainly by the liver, with a small amount excreted by the kidney.


In pregnant women, 7–9 hours.





25°C (may be exposed to 15–30°C). Protect from light.


Suspension for Injection

20–25°C (may be exposed to 15–30°C). Protect from light.


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


Do not mix with diluents or local anesthetics containing preservatives (e.g., parabens, phenol) because flocculation of suspension may result.


  • Principally an anti-inflammatory agent.

  • Exhibits potent anti-inflammatory activity and minimal mineralocorticoid properties.

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

  • Inhibits macrophage accumulation in inflamed areas.

  • Reduces capillary wall permeability and edema formation.

  • Antagonizes histamine activity and release of kinin from substrates.

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

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

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

  • Reduces intestinal absorption and increases renal excretion of calcium.

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

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

  • Depresses reactivity of tissue to antigen-antibody interactions.

Advice to Patients

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

  • Importance of notifying a clinician of any infections, signs of infections (e.g., fever, sore throat, pain during urination, muscle aches), or injuries that develop during therapy or within 12 months after therapy is discontinued.

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

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

  • In immunosuppressed patients, importance of avoiding exposure to certain infections (e.g., chickenpox, measles) and of obtaining medical advice if such exposure occurs.

  • When considering epidural glucocorticoid injections for pain relief, importance of understanding potential benefits and risks of epidural injections and alternative treatments. Importance of immediately seeking emergency medical attention if unusual symptoms (e.g., loss of or changes in vision, tingling in extremities, sudden weakness or numbness affecting face or occurring unilaterally or bilaterally in arms or legs, dizziness, severe headache, seizures) occur after epidural injection.

  • Importance of informing clinicians of existing or contemplated concomitant therapy, including prescription and OTC drugs.

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

  • Importance of informing patients of other important precautionary information. (See Cautions.)


Excipients in commercially available drug preparations may have clinically important effects in some individuals; consult specific product labeling for details.

Please refer to the ASHP Drug Shortages Resource Center for information on shortages of one or more of these preparations.



Dosage Forms


Brand Names




0.6 mg/5mL

Celestone Syrup


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

Betamethasone Sodium Phosphate and Betamethasone Acetate


Dosage Forms


Brand Names



Injectable suspension

Betamethasone Sodium Phosphate 3 mg (of betamethasone) per mL with Betamethasone Acetate 3 mg/mL*

Celestone Soluspan


AHFS DI Essentials™. © Copyright 2022, Selected Revisions January 5, 2015. American Society of Health-System Pharmacists, Inc., 4500 East-West Highway, Suite 900, Bethesda, Maryland 20814.

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

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