Triamcinolone Acetonide and CNS depression

• Generic Name: triamcinolone
• Dosage Forms: n.a.
• Other Brand Names: Aristocort, Azmacort, Kenalog-40, Zilretta

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.

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.

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.

Treatment of hypercalcemia associated with malignancy.

Usually ameliorates hypercalcemia associated with bone involvement in multiple myeloma.

Treatment of hypercalcemia associated with sarcoidosis.

Treatment of hypercalcemia associated with vitamin D intoxication.

Not effective for hypercalcemia caused by hyperparathyroidism.

Treatment of granulomatous (subacute, nonsuppurative) thyroiditis. Anti-inflammatory 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).

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 , rheumatic fever [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.

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.

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.

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.

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.

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.

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.

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.

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

Symptomatic relief of acute manifestations of berylliosis.

Symptomatic relief of acute manifestations of aspiration pneumonitis.

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.

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.)

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.

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.

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.

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.

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

In massive dosage, used concomitantly with other immunosuppressive drugs to prevent rejection of transplanted organs.

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

Treatment of trichinosis with neurologic or myocardial involvement.

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.

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.