Brand name: Kenalog
Drug class: Adrenals

Medically reviewed by Drugs.com on Nov 10, 2024. Written by ASHP.

Introduction

Synthetic glucocorticoid; virtually no mineralocorticoid activity.^c

Uses for Triamcinolone Acetonide

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.^b

Usually inadequate alone for adrenocortical insufficiency because essentially devoid of mineralocorticoid activity.^{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.^b

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

Adrenogenital Syndrome

Lifelong glucocorticoid treatment of congenital adrenogenital syndrome.^b

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, is continued for long-term therapy after early childhood.^b

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

Hypercalcemia

Treatment of hypercalcemia associated with malignancy.^b

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

Treatment of hypercalcemia associated with sarcoidosis^{† [off-label]}.^{b m}

Treatment of hypercalcemia associated with vitamin D intoxication^{† [off-label]}.^b

Not effective for hypercalcemia caused by hyperparathyroidism^{† [off-label]}.^b

Thyroiditis

Treatment of granulomatous (subacute, nonsuppurative) thyroiditis.^{107 b} Anti-inflammatory actions relieve fever, acute thyroid pain, and swelling.^b

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

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

Rheumatic Disorders and Collagen Diseases

Short-term adjunctive treatment of acute episodes or exacerbations of rheumatic disorders (e.g., rheumatoid arthritis, juvenile rheumatoid arthritis, psoriatic arthritis, acute gouty arthritis, synovitis of osteoarthritis, epicondylitis, acute nonspecific tenosynovitis, ankylosing spondylitis, acute and subacute bursitis, Reiter syndrome^{† [off-label]m} , rheumatic fever^{† [off-label]} [especially with carditis]^m ) and collagen diseases (e.g., acute rheumatic carditis, systemic lupus erythematosus, polyarteritis nodosa^†m , vasculitis^†m ) refractory to more conservative measures.^{106 107 b c}

Relieves inflammation and suppresses symptoms but not disease progression.^b

Rarely indicated as maintenance therapy.^b

Local injection (intra-articular or soft-tissue administration) can provide 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.^{106 107 b}

Primary treatment to control symptoms and prevent severe, often life-threatening complications in patients with polyarteritis nodosa^†, relapsing polychondritis^†, polymyalgia rheumatica^†, 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

Dermatologic Diseases

Treatment of pemphigus and pemphigoid^†m , bullous dermatitis herpetiformis, severe erythema multiforme (Stevens-Johnson syndrome), exfoliative dermatitis, uncontrollable eczema^†m , cutaneous sarcoidosis^†m , mycosis fungoides, lichen planus, severe psoriasis, and severe seborrheic dermatitis.^{106 107 b}

For control of severe or incapacitating allergic conditions (e.g., contact dermatitis, atopic dermatitis) intractable to adequate trials of conventional treatment.¹⁰⁷

Chronic skin disorders seldom an indication for systemic glucocorticoids.^b

Intralesional or sublesional injections occasionally indicated for localized chronic skin disorders including keloids, psoriatic plaques, alopecia areata, discoid lupus erythematosus, necrobiosis lipoidica diabeticorum, granuloma annulare, or lichen simplex chronicus (neurodermatitis)¹⁰⁶ unresponsive to topical therapy.^{106 b}

Rarely indicated systemically for alopecia (areata, totalis, or universalis).^b 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 serum sickness, drug hypersensitivity reactions, and severe seasonal or perennial rhinitis.^{107 b}

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, sympathetic ophthalmia).^{107 b}

Sarcoidosis

Management of symptomatic sarcoidosis.^{107 b}

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

Tuberculosis

Treatment of fulminating or disseminated pulmonary tuberculosis when used concurrently with appropriate antituberculous therapy.^{107 b}

Hematologic Disorders

Management of acquired (autoimmune) hemolytic anemia, idiopathic thrombocytopenic purpura (ITP), secondary thrombocytopenia, erythroblastopenia, or congenital (erythroid) hypoplastic anemia.¹⁰⁷

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

Glucocorticoids may not affect or prevent renal complications in Henoch-Schoenlein purpura.^b

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

GI Diseases

Short-term palliative therapy for acute exacerbations and systemic complications of ulcerative colitis, regional enteritis, and Crohn's disease^†.^{107 m b}

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) 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

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).¹⁰⁷

Treatment of breast cancer^†m ; glucocorticoids alone not as effective as other agents (e.g., cytotoxic agents, hormones, antiestrogens) and should be reserved for unresponsive disease.^b

Low Back Pain

Systemic corticosteroids have been used symptomatic relief of low back pain^†, however current evidence suggests that corticosteroids do not seem to be effective for improving radicular or nonradicular low back pain.^{574 b}

Organ Transplants

In massive dosage, used concomitantly with other immunosuppressive drugs to prevent rejection of transplanted organs^†.^{b m}

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

Nephrotic Syndrome and Lupus Nephritis

Treatment of idiopathic nephrotic syndrome without uremia.¹⁰⁷

Can induce diuresis and remission of proteinuria in nephrotic syndrome¹⁰⁷ secondary to primary renal disease, especially when there is minimal renal histologic change.^b

Treatment of lupus nephritis.¹⁰⁷

Carpal Tunnel Syndrome

Local injection of glucocorticoids 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^†.⁵⁷³

Triamcinolone Acetonide Dosage and Administration

General

• Dosage depends on the condition being treated and patient response.^c

• Individualize dosage carefully according to the diagnosis, severity, prognosis and probable duration of the disease, and patient response and tolerance.^{106 107 b}

• Long-term therapy should not be initiated without due consideration of its risks.^b If necessary, administer in the smallest dosage possible.^b Continual monitoring is recommended for signs that indicate dosage adjustment is necessary (e.g., remission or exacerbations of the disease and stress [surgery, infection, trauma]).^b

Alternate-Day Therapy

• Alternate-day therapy in which a single dose is administered every other morning is the dosage regimen of choice for long-term oral glucocorticoid treatment of most conditions.^b This regimen provides relief of symptoms while minimizing adrenal suppression, protein catabolism, and other adverse effects.^b

• Some conditions (e.g., rheumatoid arthritis, ulcerative colitis) require daily glucocorticoid therapy because symptoms of the underlying disease cannot be controlled by alternate-day therapy.^b

Discontinuance of Therapy

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

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

• Very gradually withdraw systemic glucocorticoids until recovery of HPA-axis function occurs following long-term therapy with pharmacologic dosages.^b

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

• In one suggested regimen, decrease by 2–4 mg every 3–7 days until the physiologic dose (4 mg) is reached.^b

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

• When a physiologic dosage has been reached, single 20-mg oral morning doses of hydrocortisone can be substituted for whatever glucocorticoid the patient has been receiving.^b After 2–4 weeks, may decrease hydrocortisone dosage by 2.5 mg every week until a single morning dosage of 10 mg daily is reached.^b

• For certain acute allergic conditions (e.g., contact dermatitis such as poison ivy) or acute exacerbations of chronic allergic conditions, glucocorticoids may be administered short term (e.g., for 6 days).^b Administer an initially high dose on the first day of therapy, and then withdraw therapy by tapering the dose over several days.^b

Administration

Administer by IM injection.^{107 c} Not for IV injection.^{106 107}

Administer for local effect by intra-articular, intrabursal, intrasynovial, intralesional (intradermal), sublesional, or soft-tissue injection.^{106 107}

Kenalog-10 indicated for intra-articular or intralesional use only; not for IV, IM, intraocular, epidural or intrathecal use.¹⁰⁶

Kenalog-40 and Kenalog-80 indicated for IM or intra-articular use only; not for IV, intradermal, intraocular, epidural, or intrathecal use.¹⁰⁷

Generally reserve IM therapy for patients who are not able to take oral therapy.^{107 c}

IM Administration

Triamcinolone Acetonide

Administer 40-mg/mL and 80-mg/mL sterile suspension by deep IM injection into gluteal muscle.¹⁰⁷ The 10-mg/mL sterile suspension is not suitable for IM administration.¹⁰⁶

Shake vial before use to insure uniform suspension.¹⁰⁷ For adults, a minimum needle length of 1.5 inches recommended; a longer needle may be required in obese patients.¹⁰⁷ Use alternate sites for subsequent injections.¹⁰⁷

Because it is slowly absorbed, IM administration is not indicated when an immediate effect or short duration is required.^c

Do not administer IM for conditions prone to bleeding (e.g., ITP).¹⁰⁷

Intra-articular, Intrabursal, Intrasynovial, Intralesional, or Soft-tissue Administration

For treatment of joints, consult standard textbooks for administration techniques.^{106 107}

Triamcinolone Acetonide

Administer by intra-articular, intrabursal, intrasynovial, soft-tissue, intralesional, or sublesional injection.^{106 107 c}

Shake vial before use to insure uniform suspension.^{106 107}

For intralesional (or sublesional) injection, use the 10-mg/mL sterile suspension;¹⁰⁶ the 40 mg/mL and 80 mg/mL sterile suspension is not intended for intralesional (intradermal) use.¹⁰⁷

Use a tuberculin syringe to facilitate intralesional or sublesional dosage measurement.^c May inject multiple sites if they are ≥1 cm apart.^c

For intra-articular, intrabursal, intrasynovial, or soft-tissue injection, may use either the 10, 40, or 80-mg/mL sterile suspension.^{106 107} A local anesthetic (e.g., procaine hydrochloride) may be infiltrated into soft tissue surrounding the joint and/or injected into the joint before administration of triamcinolone acetonide.^{107 c}

Dosage

Available as triamcinolone acetonide; dosage expressed in terms of the salt.^{106 107}

After a satisfactory response is obtained, decrease dosage in small decrements to the lowest level that maintains an adequate clinical response, and discontinue the drug as soon as possible.^{b c}

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

High dosages may be required for acute situations of certain rheumatic disorders and collagen diseases; after a response has been obtained, drug often must be continued for long periods at low dosage.^b

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

Pediatric Patients

Base pediatric dosage on severity of the disease and patient response rather than on strict adherence to dosage indicated by age, body weight, or body surface area.^c

Usual Dosage

IM

In pediatric patients, the initial dose of triamcinolone may vary depending on the specific condition being treated.¹⁰⁷ The range of initial doses is 0.11 mg/kg daily to 1.6 mg/kg daily in 3 or 4 divided doses (3.2 mg/m² bsa/day to 48 mg/m² bsa/day).¹⁰⁷

Adults

Usual Dosage

IM

Triamcinolone acetonide: Usually, 60 mg initially (using the 40-mg/mL or 80-mg/mL sterile suspension).^{107 c} May administer additional doses of 20–100 mg when signs and symptoms recur.^c Manufacturer states dosage is usually adjusted within the range of 40–80 mg depending on patient response.¹⁰⁷ Some clinicians recommend administration at 6-week intervals, if possible, to minimize HPA suppression.^c Some patients may be well controlled with doses ≤20 mg.¹⁰⁷

Intra-articular, Intrabursal, Intrasynovial, or Soft-tissue Injection

Dosage varies depending on location, size, and degree of inflammation.^{106 107 b}

Triamcinolone acetonide: Initially, 5–15 mg for large joints; 2.5–5 mg for small joints.^{106 107 c} Symptom relief generally occurs with dosages ≤40 mg for large joints and ≤10 mg for small joints.^{106 107} For soft-tissue injection in treatment of tendon sheath inflammation, 2.5–10 mg.^c Repeat when signs and symptoms recur.^{106 107 b}

Intra-articular or Soft-tissue Injection

Dosage varies depending on location, size, and degree of inflammation.^c

Intralesional or Sublesional Injection

Dosage varies depending on location, size, and degree of inflammation.^{106 107}

May inject intralesionally into multiple sites if ≥1 cm apart, but do not exceed total dosage of 30 mg at any one time.^c

Cautions for Triamcinolone Acetonide

Contraindications

• Known hypersensitivity to triamcinolone or any ingredient in the formulation.¹⁰⁶

• Concurrent administration of live virus vaccines in patients receiving immunosuppressive dosages of corticosteroids. ¹⁰⁶

• IM administration for idiopathic thrombocytopenic purpura.¹⁰⁶

Warnings/Precautions

Warnings

Nervous System Effects

Serious neurologic events, some resulting in death, have been reported with epidural injection of corticosteroids.^{106 107} May precipitate mental disturbances ranging from euphoria, insomnia, mood swings, depression and anxiety, and personality changes to frank psychoses.^{106 107} Use may aggravate emotional instability or psychotic tendencies.^{106 107}

Use with caution in patients with seizure disorders and patients with myasthenia gravis receiving anticholinesterase therapy.^{107 b}

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.^{1000 1001 1002 1003}

FDA states efficacy and safety of epidural glucocorticoid administration not established; not FDA-labeled for this use.^{1000 1001}

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).^b

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

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

Withdraw triamcinolone very gradually following long-term therapy with pharmacologic dosages.^b

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

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

If the disease flares up during withdrawal, dosage may need to be increased and followed by a more gradual withdrawal.^b

Immunosuppression

Increased susceptibility to infections secondary to glucocorticoid-induced immunosuppression. Certain infections (e.g., varicella [chickenpox], measles) can have a more serious or even fatal outcome in such patients.^{106 107}

Administration of live virus vaccines, including smallpox, is contraindicated in patients receiving immunosuppressive dosages of glucocorticoids.^{106 107}

Increased Susceptibility to Infection

Corticosteroids 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; reactivation of latent infections may occur.

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

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

Some infections (e.g., varicella [chickenpox], measles) can have a more serious or even fatal outcome, particularly in children.¹⁰⁶

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.¹⁰⁶

If exposure to varicella or measles occurs in susceptible patients, treat appropriately (e.g., VZIG, IG, acyclovir).¹⁰⁶

Use with great care in patients with known or suspected Strongyloides (threadworm) infection.¹⁰⁶ Immunosuppression may lead to Strongyloides hyperinfection and dissemination with widespread larval migration, often accompanied by severe enterocolitis and potentially fatal gram-negative septicemia.¹⁰⁶

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

Can reactivate tuberculosis.¹⁰⁶ Include chemoprophylaxis in patients with a history of active tuberculosis undergoing prolonged glucocorticoid therapy.^{106 b} Observe closely for evidence of reactivation.¹⁰⁶

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.^{107 b} These adverse effects may be especially serious in geriatric or debilitated patients.^b A high-protein diet may help to prevent adverse effects associated with protein catabolism.^b

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).¹⁰⁶

Osteoporosis and related fractures are one of the most serious adverse effects of long-term glucocorticoid therapy.⁵⁷² The American College of Rheumatology (ACR) has published guidelines on prevention and treatment of glucocorticoid-induced osteoporosis.⁵⁷² Recommendations are made according to a patient's risk of fracture.⁵⁷²

Ocular Effects

Prolonged use may result in posterior subcapsular and nuclear cataracts (particularly in children), exophthalmos, and/or increased IOP which may result in glaucoma or may occasionally damage the optic nerve.^{553 b}

Do not use in patients with active ocular herpes simplex infections for fear of corneal perforation.^b

Transient blindness, amblyopia, acute retinal necrosis syndrome, intraocular hemorrhage, and cortical blindness have occurred following epidural glucocorticoid injection.^{1001 1002 1003}

Endocrine and Metabolic Effects

Administration over a prolonged period may produce various endocrine disorders including hypercorticism (cushingoid state) and amenorrhea or other menstrual difficulties.^{106 b}

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

Exaggerated glucocorticoid response in patients with hypothyroidism.^{106 b}

Cardiovascular Effects

Possible association between use of glucocorticoids and left ventricular free-wall rupture; use with extreme caution in patients with recent MI.^b

Use with caution in patients with CHF or hypertension.¹⁰⁶

Sensitivity Reactions

Some commercially available injections of triamcinolone contain benzyl alcohol as a preservative and are not for use in neonates.^{106 107} Administration of injections preserved with benzyl alcohol has been associated with toxicity in neonates (gasping syndrome).¹⁰⁷

Anaphylaxis reported rarely in patients receiving corticosteroid therapy. Cases of serious anaphylaxis, including death, reported in individuals receiving triamcinolone acetonide injection, regardless of route of administration.¹⁰⁶ Take appropriate precautionary measures prior to administration, especially in patients with a history of allergy to any drug.¹⁰⁶

General Precautions

Monitoring

Prior to initiation of long-term glucocorticoid therapy, perform baseline ECGs, BP, chest and spinal radiographs, glucose tolerance tests, and evaluations of HPA-axis function in all patients.^{107 b}

Perform upper GI radiographs in patients predisposed to GI disorders, including those with known or suspected peptic ulcer disease or appreciable dyspepsia.^{107 b}

GU Effects

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

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.¹⁰⁷

Use with caution in patients with active or latent peptic ulcer.¹⁰⁷ Manifestations of peritoneal irritation following GI perforation may be minimal or absent in patients receiving corticosteroids.^b Suggest concurrent administration of antacids between meals to prevent peptic ulcer formation in patients receiving high dosages of corticosteroids.^b

Hematologic Effects

Cortisone reported rarely to increase blood coagulability and to precipitate intravascular thrombosis, thromboembolism, and thrombophlebitis; use corticosteroids with caution in patients with thromboembolic disorders.^{106 107 b}

Specific Populations

Pregnancy

Corticosteroids have been shown to be teratogenic in many species when administered in clinical doses.¹⁰⁶ No adequate and well-controlled studies in pregnant women.¹⁰⁶ Use during pregnancy only potential benefit justifies potential risk to fetus.¹⁰⁶

Lactation

Distributed into milk.¹⁰⁶ Caution if used in nursing women.¹⁰⁶

Pediatric Use

Efficacy and safety of corticosteroids in pediatric patients are based on the well-established course of effect of corticosteroids.¹⁰⁷ Adverse effects of corticosteroids in pediatric patients are similar to those in adults.¹⁰⁷

Published studies provide evidence of efficacy and safety in pediatric patients for treatment of nephrotic syndrome (>2 years of age), and aggressive lymphomas and leukemias (>1 month of age).¹⁰⁷ Other indications for pediatric use of corticosteroids (e.g., severe asthma) are based on adequate and well-controlled trials conducted in adults.¹⁰⁷

Carefully observe pediatric patients with frequent measurements of BP, weight, height, intraocular pressure, and clinical evaluation for infection, psychosocial disturbances, thromboembolism, peptic ulcers, cataracts, and osteoporosis.¹⁰⁷ Pediatric patients who are treated with corticosteroids by any route, including systemically administered corticosteroids, may experience a decrease in growth velocity.¹⁰⁷

Geriatric Use

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

Hepatic Impairment

Exaggerated glucocorticoid response in patients with cirrhosis.^b

Renal Impairment

Use with caution in patients with renal insufficiency.¹⁰⁷

Common Adverse Effects

Associated with long-term therapy: bone loss, cataracts, indigestion, muscle weakness, back pain, bruising, oral candidiasis.^{k l}

Drug Interactions

Metabolized by CYP3A4.^{b f}

Drugs Affecting Hepatic Microsomal Enzymes

Inhibitors of CYP3A4: potential pharmacokinetic interaction (increased plasma triamcinolone concentrations).^b

Inducers of CYP3A4: potential pharmacokinetic interaction (decreased plasma triamcinolone concentrations).^b

Specific Drugs and Laboratory Tests

Triamcinolone Acetonide Pharmacokinetics

Absorption

Duration

Following IM administration of a single dose of 40–80 mg of triamcinolone acetonide, the duration of HPA suppression is 2–4 weeks.^b

Following oral administration of a single dose (40 mg) of triamcinolone, the duration of HPA-axis suppression is 2.25 days.^b

Following intra-articular administration, anti-inflammatory effects may be maintained for several weeks.^c

Distribution

Extent

Most glucocorticoids are removed rapidly from the blood and distributed to muscles, liver, skin, intestines, and kidneys.^b Glucocorticoids cross the placenta and may be distributed into milk.^b

Plasma Protein Binding

Lower affinity for transcortin than prednisolone.^b

Stability

Storage

Parenteral

Injectable Suspension

Triamcinolone acetonide: 20–25°C; avoid freezing.^{106 107} Protect from light.^{106 107}

Actions

• Principally an anti-inflammatory or immunosuppressant agent.¹⁰⁶

• Exhibits potent anti-inflammatory activity and virtually no mineralocorticoid properties.^b

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

• Inhibits macrophage accumulation in inflamed areas.^b

• Reduces capillary wall permeability and edema formation.^b

• Antagonizes histamine activity and release of kinin from substrates.^b

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

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

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

• Reduces intestinal absorption and increases renal excretion of calcium.^b

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

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

• Depresses reactivity of tissue to antigen-antibody interactions.^b

Advice to Patients

• Importance of providing the patient a copy of the manufacturer's patient information.^b

• Importance of avoiding exposure to chickenpox or measles and, if exposed, of immediately consulting clinician.¹⁰⁶

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

• 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 long-term therapy is discontinued.^b

• When considering epidural glucocorticoid injections for pain relief, importance of understanding potential benefits and risks of epidural injections and alternative treatments.^{1000 1001} 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.¹⁰⁰¹

• Importance of informing clinicians of existing or contemplated concomitant therapy, including prescription and OTC drugs.¹⁰⁶

• Importance of women informing clinicians if they are or plan to become pregnant or plan to breast-feed.¹⁰⁶

• Importance of informing patients of other important precautionary information.¹⁰⁶

Additional Information

The American Society of Health-System Pharmacists, Inc. represents that the information provided in the accompanying monograph was formulated with a reasonable standard of care, and in conformity with professional standards in the field. Readers are advised that decisions regarding use of drugs are complex medical decisions requiring the independent, informed decision of an appropriate health care professional, and that the information contained in the monograph is provided for informational purposes only. The manufacturer’s labeling should be consulted for more detailed information. The American Society of Health-System Pharmacists, Inc. does not endorse or recommend the use of any drug. The information contained in the monograph is not a substitute for medical care.

Preparations

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.

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