Medication Guide App

Hydrocortisone Acetate

Pronunciation

Class: Adrenals
Note: This monograph also contains information on Hydrocortisone, Hydrocortisone Sodium Phosphate, Hydrocortisone Sodium Succinate
ATC Class: H02AB09
VA Class: HS051
CAS Number: 50-23-7
Brands: A-hydroCort, Cortef, Hydrocortone, Solu-Cortef

Warning(s)

Special Alerts:

[Posted 03/31/2014] ISSUE: FDA is warning that injection of corticosteroids into the epidural space of the spine may result in rare but serious adverse events, including loss of vision, stroke, paralysis, and death. The injections are given to treat neck and back pain, and radiating pain in the arms and legs. The effectiveness and safety of epidural administration of corticosteroids have not been established, and FDA has not approved corticosteroids for this use.

FDA is requiring the addition of a Warning to the drug labels of injectable corticosteroids to describe these risks.

BACKGROUND: To raise awareness of the risks of epidural corticosteroid injections in the medical community, FDA’s Safe Use Initiative convened a panel of experts, including pain management experts to help define the techniques for such injections which would reduce preventable harm. The expert panel’s recommendations will be released when they are finalized. FDA will convene an Advisory Committee meeting of external experts in late 2014 to discuss the benefits and risks of epidural corticosteroid injections and to determine if further FDA actions are needed.

RECOMMENDATION: Patients should discuss the benefits and risks of epidural corticosteroid injections with their health care professionals, along with the benefits and risks associated with other possible treatments. See the Drug Safety Communication for a Data Summary and additional information for both patients and healthcare professionals.

Healthcare professionals and patients are encouraged to report adverse events or side effects related to the use of these products to the FDA's MedWatch Safety Information and Adverse Event Reporting Program.

For more information visit the FDA website at: and .

Introduction

Glucocorticoid secreted by the adrenal cortex; also exhibits mineralocorticoid activity.a

Uses for Hydrocortisone Acetate

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.a b

When used for anti-inflammatory and immunosuppressant properties, synthetic glucocorticoids that have minimal mineralocorticoid activity are preferred.b

Adrenocortical Insufficiency

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

Hydrocortisone or cortisone (in conjunction with liberal salt intake) is usually the corticosteroid of choice for replacement therapy in patients with adrenocortical insufficiency, because these drugs have both glucocorticoid and mineralocorticoid properties.a b Concomitant administration of a more potent mineralocorticoid (fludrocortisone) may be required in some patients.b

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

In shock, IV therapy in conjunction with other therapy for shock is essential; hydrocortisone is preferred.b

Adrenogenital Syndrome

Lifelong glucocorticoid treatment of congenital adrenogenital syndrome.a c d f

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

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

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

Hypercalcemia

Treatment of hypercalcemia associated with malignancy.a b c d e f

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

Treatment of hypercalcemia associated with sarcoidosis.b

Treatment of hypercalcemia associated with vitamin D intoxication.b

Not effective for hypercalcemia caused by hyperparathyroidism.b

Thyroiditis

Treatment of granulomatous (subacute, nonsuppurative) thyroiditis.a c d e f

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

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

Usually reserved for palliative therapy in severly ill patients unresponsive to salicylates and thyroid homones.b

Rheumatic Disorders and Collagen Diseases

Short-term palliative treatment of acute episodes or exacerbations and systemic complications of rheumatic disorders (e.g., rheumatoid arthritis, juvenile arthritis, psoriatic arthritis, acute gouty arthritis, posttraumatic osteoarthritis, synovitis of osteoarthritis, epicondylitis, acute nonspecific tenosynovitis, ankylosing spondylitis, Reiter syndrome, rheumatic fever [especially with carditis]) and collagen diseases (e.g., acute rheumatic carditis, systemic lupus erythematosus, dematomyositis [polymyositis], polyareteristis nodosa, vasculitis) refractory to more conservative measures.a c d f

Relieves inflammation and suppresses symptoms but not disease progression.b

Rarely indicated as maintenance therapy.b

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.a b c d f

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

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

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

Controls acute manifestations of rheumatic carditis more rapidly than salicylates and may be life-saving; cannot prevent valvular damage and no better than salicylates for long-term treatment.b

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

Primary treatment to control symptoms and prevent severe, often life-threatening complications of dermatomyositis and polymyositis, polyarteritis nodosa, relapsing polychondritis, polymyalgia rheumatica and giant-cell (temporal) arteritis, 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

Slideshow: Can Prescription Drugs Lead to Weight Gain?

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

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

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

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.a c d f

Usually reserved for acute exacerbations unresponsive to conservative therapy.b

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

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

Chronic skin disorders seldom an indication for systemic glucocorticoids.b

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

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

Rarely indicated for alopecia (areata, totalis, or universalis); 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 anaphylactic and anaphylactoid reactions, angioedema, acute noninfectious laryngeal edema, serum sickness, allergic symptoms of trichinosis, urticarial transfusion reactions, drug hypersensitivity reactions, and severe seasonal or perennial rhinitis.a b c d f

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 patients with 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).a c d

Acute optic neuritis optimally treated with intial high-dose IV therapy followed by chronic oral therapy.b Can slow progression to clinically definite multiple sclerosis.b

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

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

Asthma

Adjunctively for moderate to severe exacerbations of asthma and for maintenance in persistent asthma.b j

Systemically (oral or IV) for treatment of moderate to severe acute exacerbations of asthma (oral prednisone usually preferred); speeds resolution of airflow obstruction and reduces rate of relapse.j

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

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

In hospital management of an acute asthma exacerbation, may give 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.b

For severe persistent asthma once intial control is achieved, high dosages of inhaled corticosteroids are preferable to oral glucocorticoids 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 asthmab (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).b

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.b

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

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.

Sarcoidosis

Management of symptomatic sarcoidosis.a b c d f

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

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.a

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.b

Lipid Pneumonitis

Promotes the breakdown or dissolution of pulmonary lesions and eliminates sputum lipids in lipid pneumonitis.b

Pneumocystis jiroveci Pneumonia

Systemic adjunctive glucocorticoids decrease the likelihood of deterioration of oxygenation, respiratory failure, and/or death in moderate to severe Pneumocystis jiroveci (Pneumocystis carinii) pneumonia in acquired immunodeficiency syndrome (AIDS).

Prevents early deterioration in oxygenation associated with antipneumocystis therapy; initiate adjunctive glucocorticoid therapy as early as possible in moderate to severe pneumocystis pneumonia.

Not known whether patients with mild pneumocystis pneumonia (arterial oxygen pressure >70 mm Hg or arterial-alveolar gradient <35 mm Hg on room air) will have clinically important benefit with adjunctive glucocorticoid therapy.

Other glucocorticoids (e.g., oral prednisone, parenteral methylprednisolone) generally are preferred.

Loeffler’s Syndrome

Symptomatic relief of acute manifestations of symptomatic Loeffler’s syndrome not manageable by other means.a b c d e f

Berylliosis

Symptomatic relief of acute manifestations of berylliosis.a b c d e f

Aspiration Pneumonitis

Symptomatic relief of acute manifestations of aspiration pneumonitis.a b c d e f

Anthrax

Adjunct to anti-infective therapy in the treatment of anthrax in an attempt to ameliorate toxin-mediated effects associated with Bacillus anthracis infections.

For cutaneous anthrax if there are signs of systemic involvement or extensive edema involving the neck and thoracic region, anthrax meningitis, and inhalational anthrax that occurs as the result of exposure to anthrax spores in the context of biologic warfare or bioterrorism if extensive edema, respiratory compromise, or meningitis is present.

Antenatal Use in Preterm Labor

Short-course IM betamethasone or dexamethasone are preferred in selected women with preterm labor to hasten fetal maturation (e.g., lungs, cerebral blood vessels), including women with preterm premature rupture of membranes, preeclampsia, or third-trimester hemorrhage. Insufficient experience to evaluate efficacy of hydrocortisone.

Postnatal Use for Bronchopulmonary Dysplasia

Has been used for prevention or treatment of bronchopulmonary dysplasia in very low-birth-weight infants (i.e., <1.5 kg) who require mechanical ventilation. However, the AAP states that routine use of systemic glucocorticoids in such patients is not recommended.

May provide short-term pulmonary benefits but does not reduce mortality and is associated with an increased risk of serious adverse effects (e.g., hyperglycemia, hypertension, GI bleeding or intestinal perforation, hypertrophic obstructive cardiomyopathy, poor weight gain, poor growth of head circumference) and long-term sequelae (e.g., neurodevelopmental delay, cerebral palsy, impaired cognitive function, and stunted growth at or before school age).

Hematologic Disorders

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

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

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

May not affect or prevent renal complications in Henoch-Schoenlein purpura.b

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

Shock

Although IV glucocorticoids may be life-saving in shock secondary to adrenocortical insufficiency (see Adrenocortical Insufficiency under Uses), the value of the drugs in the treatment of shock resulting from other causes is controversial.b

Management of shock should be based on specific treatment of the primary cause and secondary abnormalities, and glucocorticoids, if used, should be regarded only as adjunctive supportive treatment.

Value in adjunctive treatment of septic shock is particularly controversial. Conflicting evidence regarding effects of high-dose regimens on morbidity and mortality in septic shock.

Pericarditis

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

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

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

Consider possibility that cardiac rupture may account for recurrent pain since use of glucocorticoids may be a risk factor in its development.

Glucocorticoids may cause thinning of developing scar and myocardial rupture.

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 celiac disease.a b c d f

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, celiac disease) 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

Crohn’s Disease

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

Some experts state that conventional glucocorticoids should not be used for the management of mildly to moderately active disease, because of the high incidence of adverse effects and their use should be reserved for patients with moderately to severely active disease.

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

Glucocorticoids should not be used for maintenance therapy of Crohn’s disease, because they usually do not prevent relapses and the drugs may produce severe adverse reactions with long-term administration.

Glucocorticoids have been used in the management of moderately to severely active Crohn’s disease and in mild esophageal or gastroduodenal Crohn’s disease in pediatric patients.

Neoplastic Diseases

Alone or as a component of various chemotherapeutic regimens in the palliative treatment of neoplastic diseases of the lymphatic system (e.g., leukemias and lymphomas in adults and acute leukemias in children).a b c d e f

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.b

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

Head Injury

Efficacy of glucocorticoid therapy is not established in patients with head injury; such therapy can be detrimental and is associated with a substantial increase in risk of death. Use to improve outcome or reduce intracranial pressure not recommended in patients with head injury.

Cerebral Malaria

Glucocorticoids are not effective and can have detrimental effects in the management of cerebral malaria caused by Plasmodium falciparum; no longer recommended for this condition.b

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.

Parenterally for the treatment of myasthenic crisis.

Organ Transplants

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

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

Trichinosis

Treatment of trichinosis with neurologic or myocardial involvement.a c d f

Nephrotic Syndrome and Lupus Nephritis

Treatment of idiopathic nephrotic syndrome without uremia.a c d f f

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

Treatment of lupus nephritis.a b c d

Hydrocortisone Acetate Dosage and Administration

General

  • Route of administration and dosage depend on the condition being treated and the patient response.a 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, and myalgia can develop following abrupt discontinuance.b d Symptoms often occur without evidence of adrenal insufficiency (while plasma glucocorticoid concentrations were still high but were falling rapidly).b d

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

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

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

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

  • In one suggested regimen, decrease by 10–20 mg every 3–7 days until the physiologic dose (20 mg) is reached.b

  • Other recommendations state that decrements usually should not exceed 10 mg every 1–2 weeks.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).a b Administer an initially high dose on the first day of therapy, and then withdraw therapy by tapering the dose over several days.a b

Administration

Administer orally, by IV injection or infusion, or IM or sub-Q injection.a

Administer for local effect by intra-articular, intralesional, or soft-tissue injection.g

Generally reserve IM or IV therapy for patients who are not able to take the drug orally or for use in an emergency situation.b d After the initial emergency period, consider a longer-acting injectable corticosteroid preparation or oral administration of a corticosteroid.d

Oral Administration

Hydrocortisone

Administer orally as tablets.a

IV Administration

Hydrocortisone Sodium Phosphate

Administer by IV injection or by IV infusion.a Usually given parenterally at 12-hour intervals.

Dilution of Hydrocortisone Sodium Phosphate

When administered by IV infusion, the drug can be added to dextrose or sodium chloride injections.a

Hydrocortisone Sodium Succinate

Administer by IV injection or by IV infusion.a

Reconstitution of Hydrocortisone Sodium Succinate

Reconstitute for IV injection with bacteriostatic water for injection or bacteriostatic 0.9% sodium chloride injection according to the manufacturer’s instructions.a

Dilution of Hydrocortisone Sodium Succinate

For IV infusion, further dilute the reconstituted hydrocortisone sodium succinate solutions with 5% dextrose, 0.9% sodium chloride, or 5% dextrose in 0.9% sodium chloride injection to a concentration of 0.1–1 mg/mL.a

Rate of Administration of Hydrocortisone Sodium Succinate

When the drug is administered by direct IV injection, administer over a period of at least 30 seconds.a

IM Injection

Hydrocortisone Sodium Phosphate

Administer by IM injection.a Usually the drug is given parenterally at 12-hour intervals.a

Hydrocortisone Sodium Succinate

Administer by IM injection.a

Reconstitution of Hydrocortisone Sodium Succinate

Reconstitute for IM injection with bacteriostatic water for injection or bacteriostatic 0.9% sodium chloride injection according to the manufacturer’s instructions.a

Sub-Q Administration

Hydrocortisone Sodium Phosphate

Administer by sub-Q injection.a Usually the drug is given parenterally at 12-hour intervals.a

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

Hydrocortisone Acetate

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

Systemic absorption of hydrocortisone acetate from intra-articular injection sites is usually complete within 24–48 hours.a

A local anesthetic, such as procaine hydrochloride, may be infiltrated into the soft tissue surrounding the joint and/or injected into the joint before the administration of hydrocortisone acetate.a Alternatively, the local anesthetic may be mixed in the syringe with hydrocortisone acetate suspension immediately prior to administration.a

Dosage

Available as hydrocortisone, hydrocortisone acetate, hydrocortisone sodium phosphate, and hydrocortisone sodium succinate; dosage of hydrocortisone sodium phosphate and sodium succinate is expressed in terms of hydrocortisone and dosage of hydrocortisone acetate is expressed in terms of hydrocortisone acetate.c d e f g m

After a satisfactory response is obtained, dosage should be decreased in small decrements to the lowest level that maintains an adequate clinical response, and discontinue the drug as soon as possible.a b

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.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

Massive dosages may be required for the treatment of shock.b

If used orally for prolonged anti-inflammatory therapy, consider an alternate-day dosage regimen.a Following long-term therapy, withdraw gradually.a

Pediatric Patients

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

Usual Dosage
Oral

Hydrocortisone: 0.56–8 mg/kg daily or 16–240 mg/m2 daily, administered in 3 or 4 divided doses.a

IV

Hydrocortisone sodium succinate: 0.16–1 mg/kg or 6–30 mg/m2 IV 1 or 2 times daily.a

IM

Hydrocortisone sodium phosphate: 0.16–1 mg/kg or 6–30 mg/m2 IM 1 or 2 times daily.a

Hydrocortisone sodium succinate: 0.16–1 mg/kg or 6–30 mg/m2 IM 1 or 2 times daily.a

Adults

Usual Dosage
Oral

Hydrocortisone: Initially, 10–320 mg daily (usually administered in 3 or 4 divided doses), depending on the disease being treated.a

IV

Hydrocortisone sodium phosphate: Initially, 15–240 mg IV daily depending on the disease being treated.a In life-threatening situations, extremely high parenteral dosage may be justified and may be a multiple of the usual oral dosage.a

Hydrocortisone sodium succinate: 100 mg to 8 g daily.a 100–500 mg IV initially, and every 2–10 hours as needed.a

IM

Hydrocortisone sodium phosphate: 15–240 mg IM daily, depending on the disease being treated.a In life-threatening situations, extremely high parenteral dosage may be justified and may be a multiple of the usual oral dosage.a

Hydrocortisone sodium succinate: 100 mg to 8 g daily.a 100–500 mg IM initially and every 2–10 hours as needed.a

Sub-Q

Hydrocortisone sodium phosphate: 15–240 mg daily depending on the disease being treated.a In life-threatening situations, extremely high parenteral dosage may be justified and may be a multiple of the usual oral dosage.a

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

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

Large joints (e.g., knee): 25–50 mg of hydrocortisone acetate; may repeat once every 1–4 weeks.a

Smaller joints: 10–25 mg of hydrocortisone acetate; may repeat once every 1–4 weeks.a

Bursae: 25–50 mg of hydrocortisone acetate; may repeat once every 3–5 days.a

Ganglia: 10–25 mg;a repeat as needed.

Soft-tissues: 5–12.5 mg for tendon sheath inflammation and 25–75 mg for soft tissue infiltration;a repeat as needed.

Shock
IV

Life-threatening shock: Massive doses of hydrocortisone sodium succinate such as 50 mg/kg by direct IV injection (over a period of one to several minutes) initially and repeated in 4 hours and/or every 24 hours if needed.a

Alternatively, 0.5–2 g by direct IV injection (over a period of one to several minutes) initially and repeated at 2- to 6-hour intervals as required.a

In such cases, administer by direct IV injection over a period of one to several minutes.a

Continue high-dose therapy only until the patient’s condition has stabilized and usually not beyond 48–72 hours.a

If massive corticosteroid therapy is needed beyond 72 hours, use a corticosteroid which causes less sodium retention (e.g., methylprednisolone sodium succinate or dexamethasone sodium phosphate) to minimize the risk of hypernatremia.a

Cautions for Hydrocortisone Acetate

Contraindications

  • Known hypersensitivity to hydrocortisone, any ingredient in the respective formulation, or any other corticosteroid.b

  • Systemic fungal infectionsb unless needed to control drug reactions due to amphotericin B.d

  • Concurrent administration of live virus vaccines in patients receiving immunosuppressive doses of corticosteroids.g

  • IM administration for conditions prone to bleeding (e.g., idiopathic thrombocytopenic purpura [ITP]).

  • Hydrocortisone sodium succinate injection preparations containing benzyl alcohol in premature infants.c (See Pediatric Use under Cautions.)

Warnings/Precautions

Warnings

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 d

Withdraw hydrocortisone very gradually following long-term therapy with pharmacologic dosages.b c (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.b c

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

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 immunosupression.c f Certain infections (e.g., varicella [chickenpox], measles) can have a more serious or even fatal outcome in such patients.c f (See Increased Susceptibility to Infection under Warnings.)

Administration of live virus vaccines, including smallpox, is contraindicated in patients receiving immunosuppressive dosages of glucocorticoids.c f If inactivated viral or bacterial vaccines are administered to such patients, the expected serum antibody response may not be obtained.c f May undertake immunization procedures in patients receiving glucocorticoids as replacement therapy (e.g., Addison’s disease).c f

Increased Susceptibility to Infection

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

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.c f

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

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.c f

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.c f

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

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 infection unless needed to control drug reactions to amphotericin B; however, cases of cardiac enlargement and CHF have been reported with concomitant use of hydrocortisone and amphotericin B.d

Not effective and can have detrimental effects (prolongation of coma, higher incidence of pneumonia and GI bleeding) in the management of cerebral malaria.b d f

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

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

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.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).c

Tendon rupture, particularly of the Achilles tendon.c

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.b

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

Glucocorticoid-induced bone loss can be both prevented and treated. Baseline measurement of bone mass density (BMD) at the lumbar spine and/or hip should be obtained when initiating long-term (e.g., exceeding 6 months) glucocorticoid therapy and appropriate preventive therapy should be initiated. Longitudinal measurements may be repeated as often as every 6 months to detect possible bone loss. Less frequent (e.g., 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, and trabecular bone is affected to a greater degree than is cortical bone.

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

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

Fluid and Electrolyte Disturbances

Sodium retention with resultant edema, potassium loss, and elevation of blood pressure may occur with average or large doses of hydrocortisone.b c Edema and CHF (in susceptible patients) may occur.b c

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

Increased calcium excretion and posible hypocalcemia.b c

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.b

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

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

Endocrine and Metabolic Effects

Administration over a prolonged period may produce various endocrine disorders including hypercorticism (cushingoid state) and amenorrhea or other menstrual difficulties.b Corticosteroids have also been reported to increase or decrease motility and number of sperm in some men.c

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 response to the glucocorticoids in hypothyroidism.b c

Cardiovascular Effects

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

Sensitivity Reactions

Anaphylactic and hypersensitivity reactions.b d

Tartrazine Sensitivity

Certain tablet formulations contain the dye tartrazine (FD&C yellow No. 5), which may cause allergic reactions including bronchial asthma in susceptible individuals. Although the incidence of tartrazine sensitivity is low, it frequently occurs in patients who are sensitive to aspirin.

Sulfite Sensitivity

Some commercially available formulations contain sulfites that may cause allergic-type reactions, including anaphylaxis and life-threatening or less severe asthmatic episodes, in certain susceptible individuals.b Overall prevalence of sulfite sensitivity in the general population is unknown but probably low; appears to occur more frequently in asthmatic than in nonasthmatic individuals.b

General Precautions

Monitoring

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

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

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

GU Effects

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

Nervous System Effects

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

Use with caution in patients with myasthenia gravisc receiving anticholinesterase therapy.

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.c

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.b

Dermatologic Effects

Various dermatologic effects (i.e., impaired wound healing, skin atrophy and thinning, acne, increased sweating, hirsutism, facial erythema, striae, petechiae, ecchymoses, easy bruising) are associated with systemic glucocorticoids.b

Kaposi’s sarcoma reported in patients receiving glucocorticoids; discontinuance may result in clinical remission.c d

Specific Populations

Pregnancy

Category C.d

Lactation

Glucocorticoids are distributed into milk and could suppress growth, interfere with endogenous glucocorticoid production, or cause other adverse effects in nursing infants.d Discontinue nursing (in mothers taking pharmacologic doses) because of potential risk to nursing infants.c d

Pediatric Use

With long-term use, may delay growth and maturation in children and adolescents.b c Monitor carefully the growth and development of pediatric patients receiving prolonged corticosteroid therapy.a c d Titrate dosage to the lowest effective level.b Alternate-day therapy may minimize growth suppression and should be instituted if growth suppression occurs.b

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 adequate calcium and vitamin D either through diet or supplementation.

Some commercially available injections contain benzyl alcohol as a preservative.b Administration of injections preserved with benzyl alcohol has been associated with toxicity in neonates (when large amounts administered [100–400 mg/kg daily]), although causal relationship not established.b

Some manufacturers state that benzyl alcohol-containing injectable preparations are contraindicated in premature infants and use should be avoided whenever possible; AAP states that presence of small amounts in a commercially available injection should not proscribe its use when the medication is indicated in neonates and comparable benzyl alcohol-free preparations are not available.b

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

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

Use with caution in patients with osteoporosis.d

Hepatic Impairment

Patients with cirrhosis show an exaggerated response to glucocorticoids.b c

Renal Impairment

Use with caution.c

Common Adverse Effects

Associated with long-term therapy: bone loss, cataracts, indigestion, muscle weakness, back pain, bruising, oral candidiasis.h i (See Warnings/Precautions under Cautions.)

Interactions for Hydrocortisone Acetate

Drugs Affecting Hepatic Microsomal Enzymes

Inhibitors of CYP3A4: potential pharmacokinetic interaction (decreased hydrocortisone clearance).c e

Inducers of CYP3A4: potential pharmacokinetic interaction (increased hydrocortisone clearance).a c

Specific Drugs

Drug

Interaction

Comments

Amphotericin B

Cases of cardiac enlargement and CHF reported with use of hydrocortisone to control adverse reactions to amphotericin Bd

Anticoagulants, oral

Conflicting reports of alterations in the anticoagulant responsec

Monitor prothrombin time frequentlyc

Antidiabetic therapy

Increased blood glucose concentrations in diabetes mellitus

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

Barbiturates

Possible increase in metabolic clearance of hydrocortisoned

Increased hydrocortisone dosage may be necessaryd

Diuretics, potassium-depleting

Enhance the potassium-wasting effects of glucocorticoidsb

Monitor for development of hypokalemiac

Ephedrine

Possible increase in metabolic clearance of hydrocortisoned

Increased hydrocortisone dosage may be necessaryd

Estrogens

Estrogens may potentiate effects of hydrocortisoneb

Dosage adjustment of hydrocortisone may be required if estrogens are added to or withdrawn from a stable dosage regimenb

Ketoconazole

Possible decrease in metabolic clearance of hydrocortisonef

Inhibits adrenal corticosteroid synthesis, causing adrenal insufficiency during corticosteroid withdrawalf

May need a reduction in dosage of hydrocortisone to avoid potential adverse effectsf

Macrolide antibiotics

Possible decrease in metabolic clearance of hydrocortisonef

May need a reduction in dosage of hydrocortisone to avoid potential adverse effectsf

NSAIAs

Increases the risk of GI ulcerationb

Decreased serum salicylate concentrations.b When corticosteroids are discontinued, serum salicylate concentration may increase possibly resulting in salicylate intoxicationb

Use concurrently with cautionb

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

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

Use aspirin and corticosteroids with caution in hypoprothrombinemiad

Phenytoin

Possible increase in metabolic clearance of hydrocortisoned

Increased dosage of hydrocortisone may be necessaryd

Rifampin

Possible increase in metabolic clearance of hydrocortisoned

Increased dosage of hydrocortisone may be necessaryd

Vaccines and toxoids

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

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

Can aggravate neurologic reactions to some vaccines (supraphysiologic dosages) b

Live virus vaccines contraindicated in individuals receiving immunosuppressive hydrocortisone dosesc

Defer routine administration of vaccines or toxoids until corticosteroid therapy is discontinuedb

May need serologic testing to ensure adequate antibody response for immunization;b additional doses of the vaccine or toxoid may be necessaryb

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

Hydrocortisone Acetate Pharmacokinetics

Absorption

Bioavailability

Readily absorbed after oral administration.b Following IM administration, absorption of the water-soluble sodium phosphate and sodium succinate salts is rapid; the rate of absorption of the lipid-soluble acetate is much slower.b

Duration

The duration of anti-inflammatory activity of hydrocortisone approximately equals the duration of HPA-axis suppression, about 1.25–1.5 days for a single 250-mg oral dose.b

Distribution

Extent

Most glucocorticoids are removed rapidly from the blood and distributed to muscle, liver, skin, intestines, and kidneys.b Glucocorticoids appear in breast milk and cross the placenta.b

Plasma Protein Binding

Extensively bound to corticosteroid-binding globulin (transcortin) and albumin.b

Special Populations

Patients with low serum albumin concentrations may be more susceptible to effects of glucocorticoids than those with normal serum albumin concentrations.b

Elimination

Metabolism

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

Elimination Route

Inactive metabolites are excreted by the kidneys, primarily as glucuronides and sulfates, but also as unconjugated products.b Small amounts of unmetabolized drugs are also excreted in urine.b

Half-life

Following oral or IV administration of hydrocortisone, 1.5–3.5 hours.pkin1 pkin2

Special Populations

Metabolic clearance may be decreased in patients with hypothyroidism and increased in those with hyperthyroidism.b

Stability

Storage

Oral

Tablets

Well-closed containers at 20–25°C.a f

Parenteral

Injectable Suspension

Hydrocortisone acetate: <40°C, preferably between 15–30°C.b Avoid freezing.m Sensitive to heat; do not autoclave.m

Injection

Hydrocortisone sodium phosphate: <40°C, preferably between 15–30°C.b Sensitive to heat; do not autoclave.d

Powder for Injection

Hydrocortisone sodium succinate: Store unreconstituted at 20–25°C.c

Store reconstituted solution at 20–25°C; protect from light.c Discard unused solutions after 3 days.c

Compatibility

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

Parenteral

Injections of hydrocortisone and its esters have been reported to be incompatible with various drugs, but the compatibility depends on several factors (e.g., concentration of the drugs, resulting pH, temperatures).a Specialized references should be consulted for more specific compatibility information.a

Hydrocortisone Sodium Phosphate

Solution CompatibilityHID

Compatible

Fat emulsion 10%, IV

Drug Compatibility
Admixture CompatibilityHID

Compatible

Amikacin sulfate

Amphotericin B

Amphotericin B with heparin sodium

Bleomycin sulfate

Metaraminol bitartrate

Verapamil HCl

Variable

Mitoxantrone HCl

Y-Site CompatibilityHID

Compatible

Allopurinol sodium

Amifostine

Aztreonam

Cefepime HCl

Cladribine

Clarithromycin

Docetaxel

Etoposide phosphate

Famotidine

Filgrastim

Fluconazole

Fludarabine phosphate

Gemcitabine HCl

Granisetron HCl

Melphalan HCl

Ondansetron HCl

Paclitaxel

Piperacillin sodium–tazobactam sodium

Teniposide

Thiotepa

Vinorelbine tartrate

Incompatible

Sargramostim

Hydrocortisone Sodium Succinate

Solution CompatibilityHID

Compatible

Alcohol 5%, dextrose 5%

Dextran 40,000

Dextran 6% in dextrose 5%

Dextran 6% in sodium chloride 0.9%

Dextrose–Ringer’s injection combinations

Dextrose–Ringer’s injection, lactated, combinations

Dextrose 5% in Ringer’s injection, lactated

Dextrose–saline combinations

Dextrose 5% in sodium chloride 0.9%

Dextrose 2½, 5, 10, or 20% in water

Fat emulsion 10%, IV

Fructose 10% in sodium chloride 0.9%

Fructose 10% in water

Invert sugar 10% in Electrolyte #1 or #2

Invert sugar 5 and 10% in sodium chloride 0.9%

Invert sugar 5 and 10% in water

Ionosol products (except as noted below)

Polysal M with dextrose 5%

Ringer’s injection

Ringer’s injection, lactated

Sodium chloride 0.45 or 0.9%

Sodium lactate (1/6) M

Incompatible

Ionosol B with invert sugar 10%

Drug Compatibility
Admixture CompatibilityHID

Compatible

Amikacin sulfate

Aminophylline

Amphotericin B

Calcium chloride

Calcium gluconate

Chloramphenicol sodium succinate

Clindamycin phosphate

Corticotropin

Daunorubicin HCl

Diphenhydramine HCl

Dopamine HCl

Erythromycin lactobionate

Lidocaine HCl

Magnesium sulfate

Metronidazole HCl with sodium bicarbonate

Mitomycin

Mitoxantrone HCl

Norepinephrine bitartrate

Penicillin G potassium

Penicillin G sodium

Polymyxin B sulfate

Potassium chloride

Procaine HCl

Theophylline

Thiopental sodium

Vancomycin HCl

Verapamil HCl

Vitamin B complex with C

Incompatible

Bleomycin sulfate

Colistimethate sodium

Ephedrine sulfate

Hydralazine HCl

Nafcillin sodium

Pentobarbital sodium

Phenobarbital sodium

Prochlorperazine edisylate

Promethazine HCl

Variable

Amobarbital sodium

Ampicillin sodium

Antithymocyte globulin (rabbit) with heparin sodium

Cytarabine

Dimenhydrinate

Furosemide

Heparin sodium

Kanamycin sulfate

Metaraminol bitartrate

Metronidazole

Y-Site CompatibilityHID

Compatible

Acyclovir sodium

Allopurinol sodium

Amifostine

Aminophylline

Amphotericin B cholesteryl sulfate complex

Ampicillin sodium

Amsacrine

Antihymocyte globulin (rabbit)

Argatroban

Atracurium besylate

Atropine sulfate

Aztreonam

Betamethasone sodium phosphate

Bivalirudin

Calcium gluconate

Cefepime HCl

Chlordiazepoxide HCl

Chlorpromazine HCl

Cladribine

Cyanocobalamin

Cytarabine

Dexamethasone sodium phosphate

Digoxin

Diphenhydramine HCl

Docetaxel

Dopamine HCl

Doxorubicin HCl liposome injection

Droperidol

Edrophonium chloride

Enalaprilat

Epinephrine HCl

Esmolol HCl

Estrogens, conjugated

Ethacrynate sodium

Etoposide phosphate

Famotidine

Fenoldopam mesylate

Fentanyl citrate

Filgrastim

Fludarabine phosphate

Fluorouracil

Foscarnet sodium

Furosemide

Gallium nitrate

Gemcitabine HCl

Granisetron HCl

Heparin sodium

Hetastarch in lactated electrolyte injection (Hextend)

Hydralazine HCl

Inamrinone lactate

Isoproterenol HCl

Kanamycin sulfate

Lidocaine HCl

Linezolid

Lorazepam

Magnesium sulfate

Melphalan HCl

Meperidine HCl

Methoxamine HCl

Methylergonovine maleate

Morphine sulfate

Neostigmine methylsulfate

Nicardipine HCl

Norepinephrine bitartrate

Ondansetron HCl

Oxacillin sodium

Oxaliplatin

Oxytocin

Paclitaxel

Pancuronium bromide

Penicillin G potassium

Pentazocine lactate

Phytonadione

Piperacillin sodium–tazobactam sodium

Procainamide HCl

Prochlorperazine edisylate

Propofol

Propranolol HCl

Pyridostigmine bromide

Remifentanil HCl

Scopolamine HBr

Sodium bicarbonate

Succinylcholine chloride

Tacrolimus

Teniposide

Theophylline

Thiotepa

Trimethobenzamide HCl

Vecuronium bromide

Vinorelbine tartrate

Incompatible

Ciprofloxacin

Diazepam

Idarubicin HCl

Lansoprazole

Midazolam HCl

Phenytoin sodium

Sargramostim

Variable

Diltiazem HCl

Methylprednisolone sodium succinate

Promethazine HCl

Actions

  • Principally an anti-inflammatory or immunosuppressant agent.b

  • Exhibits potent anti-inflammatory activity and some mineralocorticoid properties.a b c f

  • 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.

  • 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

  • In pharmacologic doses, suppresses release of corticotropin (ACTH) from the pituitary, thus, the adrenal cortex ceases secretion of endogenous corticosteroids (secondary adrenalcortical insufficiency); degree and duration of HPA axis suppression depends on dose, frequency, and time of administration, and duration of therapy.b

Advice to Patients

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

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

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

  • 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).b

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

  • 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 clinician. 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.

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

Hydrocortisone

Routes

Dosage Forms

Strengths

Brand Names

Manufacturer

Bulk

Powder

Oral

Tablets

5 mg

Cortef (scored)

Pfizer

10 mg

Cortef (scored)

Pfizer

Hydrocortone (scored)

Merck

20 mg*

Cortef (scored)

Pfizer

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

Hydrocortisone Acetate

Routes

Dosage Forms

Strengths

Brand Names

Manufacturer

Bulk

Powder

Parenteral

Injectable suspension

25 mg/mL*

50 mg/mL*

Hydrocortone Acetate (with benzyl alcohol)

Merck

Hydrocortisone Sodium Phosphate

Routes

Dosage Forms

Strengths

Brand Names

Manufacturer

Parenteral

Injection

50 mg (of hydrocortisone) per mL

Hydrocortone Phosphate (with parabens and sodium bisulfite)

Merck

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

Hydrocortisone Sodium Succinate

Routes

Dosage Forms

Strengths

Brand Names

Manufacturer

Parenteral

For injection

100 mg (of hydrocortisone)*

A-hydroCort (with benzyl alcohol 18 mg in Univial)

Hospira

Solu-Cortef (preservative-free in vials or with benzyl alcohol 18 mg in Act-O-Vial)

Pfizer

250 mg (of hydrocortisone)*

A-hydroCort (with benzyl alcohol 18 mg in Univial)

Hospira

Solu-Cortef (with benzyl alcohol 16.4 mg in Act-O-Vial)

Pfizer

500 mg (of hydrocortisone)*

A-hydroCort (with benzyl alcohol 36 mg in Univial)

Hospira

Solu-Cortef (with benzyl alcohol 33.4 mg in Act-O-Vial)

Pfizer

1 g (of hydrocortisone)*

A-hydroCort (with benzyl alcohol 72 mg in Univial)

Hospira

Solu-Cortef (with benzyl alcohol 66.9 mg in Act-O-Vial)

Pfizer

Comparative Pricing

This pricing information is subject to change at the sole discretion of DS Pharmacy. This pricing information was updated 05/2014. Actual costs to patients will vary depending on the use of specific retail or mail-order locations and health insurance copays.

Cortef 10MG Tablets (PFIZER U.S.): 30/$29.99 or 90/$66.97

Cortef 20MG Tablets (PFIZER U.S.): 30/$48.37 or 90/$145.10

Cortef 5MG Tablets (PFIZER U.S.): 50/$29.99 or 100/$48.97

Hydrocortisone 10MG Tablets (QUALITEST): 100/$59.99 or 200/$109.98

Hydrocortisone 20MG Tablets (QUALITEST): 30/$39.99 or 90/$95.97

Hydrocortisone 5MG Tablets (GLADES PHARMACEUTICALS): 50/$23.99 or 100/$36.98

AHFS DI Essentials. © Copyright, 2004-2014, Selected Revisions August 1, 2007. American Society of Health-System Pharmacists, Inc., 7272 Wisconsin Avenue, Bethesda, Maryland 20814.

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

References

HID. Trissel LA. Handbook on injectable drugs. 14th ed. Bethesda, MD: American Society of Health-System Pharmacists; 2007:882-900.

a. AHFS drug information 2004. McEvoy GK, ed. Hydrocortisone. Bethesda, MD: American Society of Health-System Pharmacists; 2003:2912-3.

b. AHFS drug information 2004. McEvoy GK, ed. Corticosteroids general statement. Bethesda, MD: American Society of Health-System Pharmacists; 2004:2886-98.

c. Pharmacia & Upjohn. Solu-Cortef(hydrocortisone sodium succinate) for injection prescribing information. Kalamazoo, MI; 2003 Apr.

d. Merck & Co, Inc. Hydrocortone phosphate (hydrocortisone sodium phosphate) injection prescribing information. Whitehouse Station, NJ; 2001 Nov.

e. Abbott Laboratories. A-Hydrocort (hydrocortisone sodium succinate) for injection prescribing information. Chicago, IL; 1996 Apr.

f. Pharmacia & Upjohn. Cortef (hydrocortisone) tablets prescribing information. Kalamazoo, MI; 2002 Dec.

g. Merck & Co, Inc. Hydrocortone (hydrocortisone) tablets prescribing information. Whitehouse Station, NJ; 2001 Nov.

h. Walsh LJ, Wong CA, Oborne J et al. Adverse effects of oral corticosteroids in relation to dose in patients with lung disease. Thorax. 2001; 56:279-84. [PubMed 11254818]

i. Bello CE, Garrett SD. Therapeutic issues in oral glucocorticoid use. Lippincotts Prim Care Pract. 1999; 3:333-41. [PubMed 10711134]

j. In: Behrman RE, Kliegman RM, Jenson HB, eds. Nelson textbook of pediatrics. 17th ed. Philadelphia: Saunders; 2004:1407-8.

k. National Asthma Education and Prevention Program. Expert panel report II: guidelines for the diagnosis and management of asthma. Bethesda, MD: National Institutes of Health National Heart Lung, and Blood Institute. (NIH publication No. 97-4051) 1997 Jul.

l. Health and Public Policy Committee American College of Physicians. The dexamethasone suppression test for the detection, diagnosis, and managemnt of depression. Ann Intern Med. 1984; 100:307-8. [IDIS 181319] [PubMed 6691676]

m. Hydrocortone Acetate

pkin1. Hellman L, Bradlow HL, Frazell EL et al. Tracer studies of the absorption and fate of steroid hormones in man. J Clin Invest. 35; 1033-44, 1956.

pkin2. Peterson RE, Wyngaarden JB, Guerra SL et al. The physiological disposition and metabolic fate of hydrocortisone in man. J Clin Invest. 34; 1779-94, 1955.

Hide
(web1)