Triamcinolone (Systemic) Monograph for Professionals - Drugs.com

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# Triamcinolone (Systemic)

Brand names: Aristocort, Aristospan, Azmacort, Kenalog
Drug class: Adrenals
VA class: RE101
CAS number: 124-94-7

Medically reviewed by Drugs.com on Dec 27, 2022. Written by ASHP.

## Introduction

Synthetic glucocorticoid; virtually no mineralocorticoid activity.

## Uses for Triamcinolone (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 essentially devoid of 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 triamcinolone is used, must also administer a mineralocorticoid (fludrocortisone), particularly in infants.

### Adrenogenital Syndrome

Lifelong glucocorticoid treatment of congenital adrenogenital syndrome.

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. A glucocorticoid, usually alone, is continued 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 because of tendency toward overdosage and growth retardation.

### Hypercalcemia

Treatment of hypercalcemia associated with malignancy.

Usually ameliorates hypercalcemia associated with bone involvement in multiple myeloma.

Treatment of hypercalcemia associated with sarcoidosis† [off-label].

Treatment of hypercalcemia associated with vitamin D intoxication† [off-label].

Not effective for hypercalcemia caused by hyperparathyroidism† [off-label].

### Thyroiditis

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

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

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

### 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 rheumatoid arthritis, psoriatic arthritis, acute gouty arthritis, posttraumatic osteoarthritis, synovitis of osteoarthritis, epicondylitis, acute nonspecific tenosynovitis, ankylosing spondylitis, acute and subacute bursitis, Reiter syndrome† [off-label] , rheumatic fever† [off-label] [especially with carditis] ) and collagen diseases (e.g., acute rheumatic carditis, systemic lupus erythematosus, polyarteritis nodosa† , vasculitis† ) refractory to more conservative measures.

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. However, glucocorticoid withdrawal is extremely difficult in these patients; 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 is 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 polyarteritis nodosa†, relapsing polychondritis†, polymyalgia rheumatica†, 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.

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, uncontrollable eczema† , cutaneous sarcoidosis† , mycosis fungoides, lichen planus, severe psoriasis, and severe seborrheic dermatitis.

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

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 including keloids, psoriatic plaques, alopecia areata, discoid lupus erythematosus, necrobiosis lipoidica diabeticorum, granuloma annulare, or lichen simplex chronicus (neurodermatitis) unresponsive to topical therapy.

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 serum sickness, 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 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).

Acute optic neuritis optimally treated with initial high-dose IV therapy (e.g., methylprednisolone) followed by chronic oral therapy. Can slow progression to clinically definite multiple sclerosis.

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

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

### Asthma

Used by oral inhalation for the long-term prevention of bronchospasm in patients with asthma.

Used orally for severe bronchial asthma intractable to conventional treatment.

Used orally for treatment of moderate to severe acute exacerbations of asthma (oral prednisone usually preferred). Speeds resolution of airflow obstruction and reduces rate of relapse.

Because onset of effects is delayed, do not use alone for emergency treatment.

Early systemic glucocorticoid therapy particularly important for asthma exacerbations in infants and children.

In hospital management of an acute asthma exacerbation, systemic adjunctive glucocorticoids if response to oral inhalation therapy is not immediate, if oral corticosteroids were used as self-medication prior to hospitalization, or if the episode is severe.

For severe persistent asthma once initial control is achieved, high dosages of inhaled corticosteroids are preferable to oral corticosteroids for maintenance because inhaled corticosteroids have fewer systemic effects.

Maintenance therapy with low doses of an orally inhaled corticosteroid is preferred treatment for adults and children with mild persistent asthma (i.e., patients with daytime symptoms of asthma more than twice weekly but less than once daily, and nocturnal symptoms of asthma more than twice per month).

A long-acting β2-agonist (e.g., formoterol, salmeterol) added to low- to medium-dose inhaled corticosteroids is the preferred therapy in patients with moderate persistent asthma (i.e., patients with daily asthmatic symptoms); alternatively, may increase (e.g., double) maintenance dosage of inhaled corticosteroid within medium-dosage range in such patients.

Orally as an adjunct to other therapy to speed resolution of all but the mildest exacerbations of asthma when response to a short-acting inhaled β2-agonist is not prompt or sustained after 1 hour or in those who have a history of severe exacerbations.

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

Do not use oral inhalation for the treatment of nonasthmatic bronchitis or for relief of acute bronchospasm.

### COPD

For severe exacerbations of COPD†, a short (e.g., 1–2 weeks) course of oral glucocorticoids can be added to existing therapy.

Effects in stable COPD are much less dramatic than in asthma, and role of glucocorticoids in the management of stable COPD is limited to very specific indications.

Inhaled corticosteroids are not appropriate in the treatment of acute exacerbations of COPD.

### Sarcoidosis

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.

Systemic adjunctive glucocorticoid therapy rapidly reduces the size of pericardial effusions and the need for drainage procedures and decreases mortality (probably through control of hemodynamically threatening effusion) in acute tuberculous pericarditis.

Hastens the resolution of pain, dyspnea, and fever associated with tuberculous pleurisy.

### Loeffler’s Syndrome

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

### Berylliosis

Symptomatic relief of acute manifestations of berylliosis.

### Aspiration Pneumonitis

Symptomatic relief of acute manifestations of aspiration pneumonitis.

### Hematologic Disorders

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

High or even massive glucocorticoid 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.

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

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

### Pericarditis

To reduce the pain, fever, and inflammation of pericarditis†, including that associated with MI.

Glucocorticoids can provide effective symptomatic relief, but aspirin considered the treatment of choice for post-MI pericarditis because of greater evidence establishing benefit.

Important to distinguish between pain caused by pericarditis and that caused by ischemia since management will differ.

Glucocorticoids may cause thinning of developing scar and myocardial rupture. Consider possibility that cardiac rupture may account for recurrent pain since use of glucocorticoids may be a risk factor in its development. (See Cardiovascular Effects under Cautions.)

Management of tuberculous pericarditis. (See Advanced Pulmonary and Extrapulmonary Tuberculosis under Uses.)

### GI Diseases

Short-term palliative therapy for acute exacerbations and systemic complications of ulcerative colitis, regional enteritis, and Crohn's disease† .

Do not use if a probability of impending perforation, abscess, or other pyogenic infection.

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.

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

### 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.

Glucocorticoids 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 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.

### Multiple Sclerosis

Glucocorticoids are drugs of choice for the management of acute relapses of multiple sclerosis.

Anti-inflammatory and immunomodulating effects accelerate neurologic recovery by restoring the blood-brain barrier, reducing edema, and possibly improving axonal conduction.

Shortens the duration of relapse and accelerates recovery; remains to be established whether the overall degree of recovery improves or the long-term course is altered.

### Myasthenia Gravis

Management of myasthenia gravis†, usually when there is an inadequate response to anticholinesterase therapy.

### 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.

### Trichinosis

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 secondary to primary renal disease, especially when there is minimal renal histologic change.

Treatment of lupus nephritis.

### 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†.

## Related/similar drugs

Taltz, amlodipine, aspirin, prednisone, lisinopril, metoprolol, furosemide

## Triamcinolone (Systemic) Dosage and Administration

### General

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

- Individualize dosage carefully according to the diagnosis, severity, prognosis and probable duration of the disease, and patient response and tolerance.

- Long-term therapy should not be initiated without due consideration of its risks. If necessary, administer in the smallest dosage possible. 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]).

#### 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. This regimen provides relief of symptoms while minimizing adrenal suppression, protein catabolism, and other adverse effects.

- Although triamcinolone's HPA-axis suppression persists for 2.25 days, the manufacturer recommends that an alternate-day dosage regimen may be considered for some patients receiving long-term oral therapy. However, most authorities consider only a “short-acting” glucocorticoid that suppresses the HPA axis <1.5 days after a single oral dose (e.g., prednisone, prednisolone, methylprednisolone) to be suitable.

- 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, myalgia can develop following abrupt discontinuance. Symptoms often occur without evidence of adrenal insufficiency (while plasma glucocorticoid concentrations were still high but were 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 Warnings.)

- Exercise caution when transferring from systemic glucocorticoid to oral or nasal inhalation corticosteroid therapy. (See Conversion to Orally Inhaled Therapy in Patients Receiving Systemic Corticosteroids under Dosage and Administration.)

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

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

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

- 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. 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.

- 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). Administer an initially high dose on the first day of therapy, and then withdraw therapy by tapering the dose over several days.

#### Conversion to Orally Inhaled Therapy in Patients Receiving Systemic Corticosteroids

- When switching from systemic corticosteroids to orally inhaled triamcinolone acetonide in patients with asthma, asthma should be reasonably stable before initiating treatment with the oral inhalation.

- Initially, administer the aerosol concurrently with the maintenance dosage of the systemic corticosteroid. After about 1 week, gradually withdraw systemic corticosteroid by reducing the daily or alternate daily dosage. Generally, decrease dosage in decrements of ≤2 mg of triamcinolone acetonide after intervals of 1–2 weeks, depending on patient response.

- Death has occurred in some individuals in whom systemic corticosteroids were withdrawn too rapidly. (See Adrenocortical Insufficiency under Warnings.)

- During withdrawal of oral therapy, symptoms of systemic corticosteroid withdrawal may occur, despite maintenance or even improvement in pulmonary function; continue oral inhalation therapy but monitor for objective signs of adrenal insufficiency. If evidence of adrenal insufficiency occurs, increase systemic corticosteroid dosage temporarily and then continue withdrawal more slowly.

- If exacerbations of asthma occur during oral inhalation therapy after systemic corticosteroids have been withdrawn, administer short courses of systemic corticosteroids, then taper dosage as symptoms subside. Supplemental systemic corticosteroid therapy may also be required during periods of stress.

### Administration

Administer orally, by oral inhalation, or by IM injection. Not for IV injection.

Administer for local effect by intra-articular, intrabursal, intrasynovial, intralesional (intradermal), sublesional, soft-tissue, or epidural† injection.

Generally reserve IM therapy for patients who are not able to take the drug orally.

#### Oral Administration

##### Triamcinolone

Administer orally as tablets.

#### Oral Inhalation

##### Triamcinolone Acetonide

Prime inhaler prior to first use and after a period of nonuse >3 days by shaking upright inhaler gently and then pressing the canister firmly (away from eyes) and quickly to release spray; repeat procedure so a total of 2 sprays are released.

Shake well immediately before each use and invert inhaler prior to actuation. Exhale as completely as possible and place the mouthpiece of the inhaler well into the mouth with lips closed firmly around it. Inhale slowly and deeply through the mouth while pressing the metal canister down with the forefinger. After holding the breath for as long as possible (about 10 seconds), remove the mouthpiece and exhale very slowly. If additional inhalations are required, wait ≥1 minute between inhalations, shake the inhaler again, and repeat the procedure.

Following each treatment, rinse mouth thoroughly with water or mouthwash to remove drug deposited in the oropharyngeal area.

Clean inhaler once daily by removing canister from the inhaler, pulling apart the 2 plastic parts of inhaler, removing mouthpiece cap, and gently washing in lukewarm water; dry thoroughly.

#### IM Administration

##### Triamcinolone Acetonide

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

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

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

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

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

For treatment of joints, consult standard textbooks for administration techniques.

##### Triamcinolone Acetonide

Administer by intra-articular, intrabursal, intrasynovial, soft-tissue, intralesional, or sublesional injection.

Shake vial before use to insure uniform suspension.

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

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

For intra-articular, intrabursal, intrasynovial, or soft-tissue injection, may use either the 10- or 40-mg/mL sterile suspension. 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.

##### Triamcinolone Hexacetonide

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

For intralesional (or sublesional) injection, use the 5-mg/mL sterile suspension. For intra-articular or soft-tissue injection, use the 20-mg/mL sterile suspension.

##### Dilution of Triamcinolone Hexacetonide

May dilute with a local anesthetic (e.g., 1% or 2% lidocaine hydrochloride) prior to intra-articular or intralesional injection. May dilute with sterile water for injection, 0.9% sodium chloride injection, or 5 or 10% dextrose in 0.9% sodium chloride injection prior to intralesional injection.

Determine optimum dilution by nature and location of lesion, lesion size, depth of injection, and necessary volume; generally, perform more superficial injections with greater dilution.

Avoid diluents containing preservatives (e.g., parabens, phenols).

#### 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.

### Dosage

Available as triamcinolone, triamcinolone acetonide, and triamcinolone hexacetonide. Dosage of triamcinolone acetonide or hexacetonide is expressed in terms of the respective salt.

Triamcinolone acetonide oral aerosol inhaler delivers about 100 mcg of drug per metered spray. Commercially available aerosol delivers at least 240 metered sprays; do not use after 240 actuations.

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.

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.

#### 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.

##### Usual Dosage

###### Oral

Some clinicians recommend 0.117–1.66 mg/kg daily or 3.3–50 mg/m2 daily, administered in 4 divided doses.

###### IM

Triamcinolone acetonide in children <6 years of age: Dosage not established; insufficient clinical experience to recommend use in this age group.

Triamcinolone acetonide in children 6–12 years of age: Initially, 40 mg depending on the severity of the condition. Some clinicians recommend 0.03–0.2 mg/kg or 1–6.25 mg/m2 at 1- to 7-day intervals.

Triamcinolone acetonide in children >12 years of age: Initially, 60 mg (using the 40-mg/mL sterile suspension). May administer additional doses of 20–100 mg (usually 40–80 mg) when signs and symptoms recur; some clinicians recommend administration at 6-week intervals, if possible, to minimize HPA suppression. Some patients may be well controlled on doses ≤20 mg.

###### Intra-articular or Soft-tissue Injection

Triamcinolone hexacetonide: Initially, 0.11–1.6 mg/kg daily or 3.2–48 mg/m2 daily, administered in 3–4 divided doses; dosage may vary depending on disease being treated.

##### Asthma

###### Oral Inhalation

Triamcinolone acetonide in children <6 years of age: manufacturer does not recommended use in this age group.

Triamcinolone acetonide in children 6–12 years of age: Initially, 100 or 200 mcg (1 or 2 sprays) 3 or 4 times daily (300–800 mcg total) or 200–400 mcg (2–4 sprays) twice daily (400–800 mcg total); adjust dosage according to patient response. Maximum dosage recommended by manufacturer is 1200 mcg (12 sprays) daily; some experts state that higher dosages may be used in children with severe persistent asthma.

Continually monitor patients for signs that indicate dosage adjustment is necessary (e.g., remissions or exacerbations of disease and stress [surgery, infection, trauma]). (See Conversion to Orally Inhaled Therapy in Patients Receiving Systemic Corticosteroids under Dosage and Administration.)

##### Neoplastic Diseases

###### Oral

In children with acute leukemia, usually 1 mg/kg daily, but up to 2 mg/kg may be necessary. Initial response usually observed within 6–21 days and therapy continued for 4–6 weeks.

#### Adults

##### Usual Dosage

###### Oral

Initially, 4–48 mg daily, usually administered in 1–4 doses, depending on disease being treated.

###### IM

Triamcinolone acetonide: Usually, 60 mg (using the 40-mg/mL sterile suspension). May administer additional doses of 20–100 mg (usually 40–80 mg) when signs and symptoms recur. Some clinicians recommend administration at 6-week intervals, if possible, to minimize HPA suppression. Some patients may be well controlled with doses ≤20 mg.

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

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

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

###### Intra-articular or Soft-tissue Injection

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

Triamcinolone hexacetonide: 10–20 mg for large joints; 2–6 mg for small joints. Determine subsequent dosage and frequency based on patient response. Repeat every 3–4 weeks as necessary; more frequent administration is not recommended.

###### Intralesional or Sublesional Injection

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

Triamcinolone acetonide: ≤1 mg per injection site; may repeat at intervals of ≥1 week, depending on patient response. May inject intralesionally into multiple sites if ≥1 cm apart, but do not exceed total dosage of 30 mg at any one time.

Triamcinolone hexacetonide: average dose ≤0.5 mg per square inch of affected skin. Administer additional injections according to patient response.

##### Asthma

###### Oral Inhalation

Triamcinolone acetonide: Initially, 200 mcg (2 sprays) 3 or 4 times daily (600 or 800 mcg total) or 400 mcg (4 sprays) twice daily. In adults with severe asthma, it may be advisable to start with 12–16 sprays daily (1200–1600 mcg total), and then reduce dosage to the lowest effective level. Maximum 1600 mcg (16 sprays) daily recommended by manufacturer, but some experts state that higher dosages may be used.

###### Oral

For severe or incapacitating asthma, 8–16 mg daily.

##### Adrenocortical Insufficiency

###### Oral

Usually, 4–12 mg daily in addition to mineralocorticoid therapy.

##### Rheumatic Disorders and Collagen Diseases

###### Oral

In patients with rheumatoid arthritis, acute gouty arthritis, ankylosing spondylitis, select cases of psoriatic arthritis, acute and subacute bursitis, or acute nonspecific tenosynovitis, initially, 8–16 mg once daily (morning) or on alternate days. Occasionally, more effective relief achieved with administration 2–4 times daily.

In patients with systemic lupus erythematosus, initially, 20–32 mg daily until desired response is achieved, then reduce to maintenance dosage. In patients with more severe symptoms, ≥48 mg daily initially and higher maintenance dosages may be required.

In patients with acute rheumatic carditis, initially, 20–60 mg daily until desired clinical response achieved. Reduce dosage and continue maintenance therapy for ≥6–8 weeks (seldom required for >3 months).

##### Dermatologic Diseases

###### Oral

In patients with pemphigus, bullous dermatitis herpetiformis, severe erythema multiforme, exfoliative dermatitis, or mycosis fungoides, initially, 8–16 mg daily. Alternatively, alternative-day therapy is well tolerated and may be associated with fewer adverse effects.

In patients with severe psoriasis, 8–16 mg daily. Maintenance period depends on clinical response.

##### Allergic Conditions

###### Oral

In patients with acute seasonal or perennial allergic rhinitis, 8–12 mg daily to alleviate acute distress; intractable cases may require high initial and maintenance dosages.

In patients with contact dermatitis or atopic dermatitis, short-courses of 8–16 mg daily to supplement topical therapy.

##### Ocular Disorders

###### Oral

In patients with allergic conjunctivitis, keratitis, iridocyclitis, chorioretinitis, anterior segment inflammation, diffuse posterior uveitis and choroiditis, optic neuritis, or sympathetic ophthalmia, initially, 12–40 mg daily for short duration, depending on severity of condition.

##### Hematologic Disorders

###### Oral

16–60 mg daily, with dosage reduction after adequate clinical response.

##### Neoplastic Diseases

###### Oral

In patients with acute leukemia and lymphoma, usually, 16–40 mg daily; dosages as high as 100 mg daily may be necessary for treatment of leukemia.

##### Nephrotic Syndrome and Lupus Nephritis

###### Oral

Average 16–20 mg (up to 48 mg) daily, until diuresis occurs. After diuresis begins, continue treatment until maximal or complete remission occurs, then reduce dosage gradually and discontinue. In less severe disease, maintenance dosage as low as 4 mg may be adequate.

##### Tuberculous Meningitis

###### Oral

Average 32–48 mg daily in single or divided doses.

### Prescribing Limits

#### Pediatric Patients

##### Asthma

###### Oral Inhalation

Triamcinolone acetonide in children 6–12 years of age: Manufacturer recommends that dosage not exceed 1200 mcg (12 sprays) daily.

#### Adults

##### Usual Dosage

###### Intra-articular or Soft-tissue Injection

Triamcinolone hexacetonide: Administer no more frequently than every 3–4 weeks.

###### Intralesional or Sublesional Injection

Triamcinolone acetonide: Maximum 1 mg per injection site; may repeat at intervals of ≥1 week, depending on patient response. May inject intralesionally into multiple sites if ≥1 cm apart, but do not exceed total dosage of 30 mg at any one time.

##### Asthma

###### Oral Inhalation

Triamcinolone acetonide: Manufacturer recommends that dosage not exceed 1600 mcg (16 sprays) daily.

### Special Populations

#### Geriatric Patients

Generally, initiate oral inhalation therapy at low end of dosage range, reflecting greater frequency of decreased hepatic, renal, or cardiac function, and of concomitant disease or other drug therapy.

Detailed Triamcinolone dosage information

## Cautions for Triamcinolone (Systemic)

### Contraindications

- Known hypersensitivity to triamcinolone or any ingredient in the formulation.

- Oral or parenteral administration in presence of systemic fungal infections. (See Increased Susceptibility to Infection under Cautions.)

- Concurrent administration of live virus vaccines in patients receiving immunosuppressive dosages of glucocorticoids (oral or parenteral formulations). (See Immunosuppression under Cautions.)

- IM administration for conditions prone to bleeding (e.g., ITP).

- Oral inhalation for primary treatment of severe acute asthmatic attacks or status asthmaticus when intensive measures are required.

- 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.

### Warnings/Precautions

#### Warnings

##### Nervous System Effects

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

Use with caution in patients with seizure disorders and patients with myasthenia gravis receiving anticholinesterase therapy.

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 triamcinolone 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. With recommended dosages administered by oral inhalation, suppression of the HPA axis has occurred within 6–12 weeks in some patients.

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. Since mineralocorticoid secretion may be impaired, sodium chloride and/or a mineralocorticoid should also be administered.

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

##### 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. (See Increased Susceptibility to Infection under Warnings.)

Administration of live virus vaccines, including smallpox, is contraindicated in patients receiving immunosuppressive dosages of glucocorticoids. If inactivated or killed vaccines are administered to such patients, the expected antibody response may not be obtained. May undertake immunization procedures in patients receiving glucocorticoids as replacement therapy (e.g., Addison’s disease). (See Specific Drugs and Laboratory Tests under Interactions.)

##### 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, acyclovir).

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.

May exacerbate fungal infections and should not be used in the presence of such infections unless needed to control drug reactions.

Some clinicians recommend avoidance of glucocorticoid inhalation therapy when risk of activating bronchopulmonary mycoses appears high, as in patients with bronchiectasis or inadequate immunologic responses.

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).

Possible 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. Topical and inhaled preparations should be used whenever possible.

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. Obtain baseline measurement of bone mass density (BMD) at the lumbar spine and/or hip when initiating long-term (e.g., >6 months) glucocorticoid therapy and initiate appropriate preventive therapy. Longitudinal measurements may be repeated as often as every 6 months to detect possible bone loss. Less frequent (e.g., annually) 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; 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 triamcinolone 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 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 IOP which may result in glaucoma or may occasionally damage the optic nerve.

Increased risk of ocular hypertension or open-angle glaucoma observed in patients receiving the maximum dosage of oral inhalation for 3 or more months.

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

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

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.

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 glucocorticoid response in patients with hypothyroidism.

##### Cardiovascular Effects

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

Use with caution in patients with CHF or hypertension.

Administer by epidural injection with caution in patients with CHF.

##### Respiratory Effects

Bronchospasm, and/or wheezing may occur with oral inhalation therapy.

If bronchospasm occurs, treat immediately with a short-acting bronchodilator, and discontinue treatment with triamcinolone acetonide and institute alternative therapy.

Unknown long-term, systemic, and local effects of the drug in humans, particularly developmental or immunologic processes in the mouth, pharynx, trachea, and lung.

#### Sensitivity Reactions

Some commercially available injections of triamcinolone contain benzyl alcohol as a preservative. Administration of injections preserved with benzyl alcohol has been associated with toxicity in neonates (gasping syndrome).

Anaphylactic or anaphylactoid reactions have occurred with parenteral corticosteroids. Take appropriate precautionary measures prior to administration, especially in patients with a history of allergy to any drug.

#### 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.

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

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

Because systemic absorption possible with orally inhaled corticosteroids, carefully observe patients for systemic effects.

##### 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 of corticosteroids.

##### 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.

#### Specific Populations

##### Pregnancy

Category C.

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

##### Lactation

Distributed into milk. Caution if used in nursing women.

##### Pediatric Use

Insufficient experience with triamcinolone acetonide IM injection or inhalation aerosol in children <6 years of age; use not recommended.

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. Weigh potential growth effects of prolonged therapy against the clinical benefits and availability of treatment alternatives.

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.

Do not use preparations containing benzyl alcohol in newborn infants.

##### Geriatric Use

Triamcinolone acetonide: Insufficient experience with oral inhalation in patients ≥65 years of age to determine whether geriatric patients respond differently than younger adults. (See Special Populations under Dosage and Administration.)

Triamcinolone hexacetonide: No substantial differences in safety and efficacy relative to younger adults, but increased sensitivity cannot be ruled out.

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. (See Musculoskeletal Effects under Cautions.)

Before initiating glucocorticoid therapy in postmenopausal women, consider that such women are especially prone to osteoporosis. Use with caution in patients with osteoporosis. (See Musculoskeletal Effects under Cautions.)

##### Hepatic Impairment

Exaggerated glucocorticoid response in patients with cirrhosis.

##### Renal Impairment

Use with caution in patients with renal insufficiency, acute glomerulonephritis, or chronic nephritis.

### Common Adverse Effects

With oral inhalation, sinusitis, pharyngitis, headache, flu syndrome, back pain.

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

## Interactions for Triamcinolone (Systemic)

Metabolized by CYP3A4.

### Drugs Affecting Hepatic Microsomal Enzymes

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

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

### Specific Drugs and Laboratory Tests

Drug or Test | Interaction | Comments
--- | --- | ---
Aminoglutethimide | Possible loss of corticosteroid-induced adrenal suppression |
Amphotericin B | Enhanced potassium-wasting effects of glucocorticoids | Monitor for development of hypokalemia
Analgesics, opiate | Epidural injection: Potential for serious injuries (e.g., brain damage, death) when glucocorticoids are combined with local anesthetics and/or opiate analgesics for epidural injection | Improve patient safety by excluding typical epidural doses (volumes in excess of intrathecal test doses) of local anesthetics and/or 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 and/or opiate analgesics for epidural injection | Improve patient safety by excluding typical epidural doses (volumes in excess of intrathecal test doses) of local anesthetics and/or opiate analgesics from epidural glucocorticoid injections
Antibiotics, macrolide | Increased plasma concentrations of triamcinolone | May require a decrease in dosage of triamcinolone
Anticholinesterase agents | Possible severe weakness in patients with myasthenia gravis receiving concomitant anticholinesterase and corticosteroid therapy | If possible, withdraw anticholinesterase agents ≥24 hours before initiating corticosteroid therapy
Anticoagulants, oral | Potential altered anticoagulant effects | Monitor coagulation indices
Antidiabetic agents | Glucocorticoids may increase blood glucose concentrations in patients with diabetes mellitus | Adjust insulin and/or antidiabetic dosages as needed
Barbiturates | Possible increased triamcinolone metabolism | Increased triamcinolone dosage may be necessary
Carbamazepine | Possible increased triamcinolone metabolism | Increased triamcinolone dosage may be necessary
Cardiac glycosides | Possible increased risk of cardiac arrhythmias due to hypokalemia |
Cholestyramine | Possible increased clearance of triamcinolone |
Cyclosporine | Possible increased activity of cyclosporine and corticosteroids Convulsions reported with concomitant use |
Diuretics, potassium-depleting | Possible enhanced potassium-wasting effects of glucocorticoids | Monitor for development of hypokalemia
Estrogens (i.e., oral contraceptives) | Possible decreased metabolism and enhanced effects of triamcinolone |
Isoniazid | Possible decreased serum isoniazid concentrations |
Ketoconazole | Potential decreased clearance and increased risk of adverse effects of triamcinolone | Decreased triamcinolone dosage may be necessary

NSAIAs

Possible increased risk of GI ulceration

Possible 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 aspirin and corticosteroids with caution in patients with hypoprothrombinemia

Phenytoin | Possible increased triamcinolone metabolism | Increased triamcinolone dosage may be necessary
Rifampin | Possible increased triamcinolone metabolism | Increased triamcinolone dosage may be necessary
Skin Tests | Possible suppression of reactions to skin tests |

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)

Generally, defer routine administration of vaccines or toxoids until corticosteroid therapy is discontinued

May need serologic testing to ensure adequate antibody response for immunization. Additional doses of the vaccine or toxoid may be necessary

May undertake immunization procedures in patients receiving nonimmunosuppressive doses of glucocorticoids or in patients receiving glucocorticoids as replacement therapy (e.g., Addison’s disease)

Triamcinolone drug interactions (more detail)

## Triamcinolone (Systemic) Pharmacokinetics

### Absorption

#### Bioavailability

Triamcinolone acetonide: Absorbed relatively rapidly after oral administration.

Triamcinolone hexacetonide: Absorbed slowly from injection site after intra-articular, intralesional, or sublesional injection.

#### Onset

Following oral administration in children with acute leukemia, response usually seen within 16–21 days.

Following oral administration in patients with nephrotic syndrome and lupus nephritis, diuresis usually occurs by day 14.

Following oral inhalation, appreciable improvement may occur by 1 week, but maximum benefit may not be achieved for ≥2 weeks.

#### Duration

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

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

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

### Distribution

#### Extent

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

#### Plasma Protein Binding

Lower affinity for transcortin than prednisolone.

Triamcinolone acetonide: Approximately 68%.

### Elimination

#### Metabolism

Triamcinolone acetonide: Metabolized rapidly to 3 less active metabolites.

#### Elimination Route

After oral administration, approximately 40 and 60% of triamcinolone acetonide dose recovered in urine and feces, respectively.

#### Half-life

Triamcinolone acetonide: Approximately 88 minutes after IV administration of triamcinolone acetonide phosphate.

#### Special Populations

In patients with hypothyroidism or hyperthyroidism, metabolic clearance of corticosteroids may decrease or increase, respectively.

## Stability

### Storage

#### Oral

##### Tablets

15–30°C.

#### Oral Inhalation

##### Aerosol

20–25°C. Contents of oral inhaler are under pressure; do not puncture, use or store aerosol container near heat or an open flame, expose to temperatures >49°C, or place into a fire or incinerator for disposal.

#### Parenteral

##### Injectable Suspension

Triamcinolone acetonide: 20–25°C; avoid freezing. Protect triamcinolone acetonide injectable suspension (Kenalog-10) from light.

Triamcinolone hexacetonide: room temperature; do not freeze. Following dilution, discard after 7 days.

### Compatibility

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

#### Parenteral

##### Triamcinolone Hexacetonide

May dilute with a local anesthetic (e.g., 1 or 2% lidocaine hydrochloride) prior to intra-articular or intralesional injection. May dilute with sterile water for injection, 0.9% sodium chloride injection, or 5 or 10% dextrose in 0.9% sodium chloride injection prior to intralesional injection.

## Actions

- Principally an anti-inflammatory or immunosuppressant agent.

- Exhibits potent anti-inflammatory activity and virtually no 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

- Importance of providing the patient a copy of the manufacturer's patient information.

- Carefully instruct patients in the use of the oral inhaler. Advise that oral inhalation must be used at regular intervals to be therapeutically effective and that although improvement may occur within the first week, at least 2 weeks of continuous therapy may be required for optimal effectiveness.

- Importance of not exceeding the recommended dosage of oral inhalation. Importance of discarding the aerosol inhaler after 240 actuations.

- Advise that orally inhaled drug should not be used as a bronchodilator and is not indicated for emergency use (e.g., relief of acute bronchospasm).

- Importance of contacting a clinician immediately when asthmatic attacks that are not controlled by bronchodilator therapy occur.

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

- 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 long-term therapy is discontinued.

- Advise patients receiving orally inhaled glucocorticoid therapy who are currently being withdrawn or who have been withdrawn from systemic therapy to immediately resume full therapeutic dosages of systemic glucocorticoids and to contact their clinician for further instructions during stressful periods (e.g., severe infection, severe asthmatic attack).

- 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.

- Patients should carry identification cards listing the diseases for which they are being treated, the glucocorticoid they are receiving and its dosage, and the name and telephone number of their physician. Patients being transferred from systemic corticosteroid to oral inhalation therapy should carry special identification (e.g., card, bracelet) indicating the need for supplementary systemic corticosteroids during periods of stress.

- 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.)

## 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.

Triamcinolone
Routes | Dosage Forms | Strengths | Brand Names | Manufacturer
--- | --- | --- | --- | ---
Oral | Tablets | 4 mg | Aristocort (scored) | Astellas

Triamcinolone Acetonide
Routes | Dosage Forms | Strengths | Brand Names | Manufacturer
--- | --- | --- | --- | ---
Parenteral | Injectable suspension | 10 mg/mL | Kenalog | Bristol-Myers Squibb
|  | 40 mg/mL | Kenalog | Bristol-Myers Squibb

Triamcinolone Acetonide (Microcrystalline)
Routes | Dosage Forms | Strengths | Brand Names | Manufacturer
--- | --- | --- | --- | ---
Oral Inhalation | Aerosol | 100 mcg/metered spray | Azmacort Oral Inhaler | Kos

Triamcinolone Hexacetonide (Microcrystalline)
Routes | Dosage Forms | Strengths | Brand Names | Manufacturer
--- | --- | --- | --- | ---
Parenteral | Injectable suspension | 5 mg/mL | Aristospan Intralesional | Sandoz
|  | 20 mg/mL | Aristospan Intra-articular | Sandoz

AHFS DI Essentials™. © Copyright 2023, Selected Revisions January 6, 2015. American Society of Health-System Pharmacists, Inc., 4500 East-West Highway, Suite 900, Bethesda, Maryland 20814.

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

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