HYDROCORTISONE
  • HYDROCORTISONE

  • (Generic for CORTEF)
  • QTY 28 • 2.5 % • Cream (g) • Near 77381

HYDROCORTISONE (hye droe KOR ti sone) is a corticosteroid. It is used on the skin to reduce swelling, redness, itching, and allergic reactions.

HYDROCORTISONE Pediatric Monographs
  • General Administration Information
    For storage information, see the specific product information within the How Supplied section.

    Route-Specific Administration

    Oral Administration
    -Administer with meals to minimize indigestion or GI irritation. If given once daily, administer in the morning to coincide with the body's normal cortisol secretion.
    Oral Solid Formulations
    -Tablets may be crushed and mixed with a small amount of liquid just prior to administration for patient's unable to swallow tablets. Crushed tablets are recommended over oral suspension in patients with congenital adrenal hyperplasia due to results of a study showing hydrocortisone cypionate suspension (Cortef) was not bioequivalent to the tablets.

    Oral Liquid Formulations
    Oral Suspension
    -Shake well before administering. Measure dosage with calibrated measuring device.

    Extemporaneous Compounding-Oral
    Extemporaneous 2.5 mg/mL Hydrocortisone Oral Suspension Preparation
    -Dissolve 0.02 g of methyl hydroxybenzoate, 0.08 g of propyl hydroxybenzoate, 0.6 g of citric acid monohydrate, and 10 mL of syrup BP in hot water to make the vehicle.
    -Triturate the cooled vehicle with 1 g of sodium carboxymethylcellulose and allow the solution to stand overnight.
    -Weigh out 250 mg of hydrocortisone powder or grind twelve and one-half (12.5) 20 mg hydrocortisone tablets into a fine powder in a glass mortar.
    -Combine the ground tablets or the 250 mg of hydrocortisone powder with 0.5 mL of polysorbate 80 and triturate.
    -Add the vehicle to the hydrocortisone powder mixture and transfer to amber plastic bottles.
    -Add enough water to bring the total volume to 100 mL.
    -Storage: The resulting suspension is chemically stable at 5 and 25 degrees Celsius for 90 days; however, a 30-day expiration is suggested due to the lack of antimicrobial preservative.



    Injectable Administration
    -Visually inspect parenteral products for particulate matter and discoloration prior to administration whenever solution and container permit.
    -Some injectable formulations contain benzyl alcohol; avoid the use of these formulations in premature neonates, and use with caution in neonates.
    -Reconstitute hydrocortisone sodium phosphate or hydrocortisone sodium succinate with the diluent provided by the manufacturer (Act-O-Vial) or with 2 mL bacteriostatic water or saline for injection (100 mg plain vial).
    -Storage: Store reconstituted solution at room temperature (68 to 77 degrees F [20 to 25 degrees C]). Discard unused solution after 3 days.
    -Only hydrocortisone sodium phosphate or hydrocortisone sodium succinate may be administered intravenously. NEVER administer hydrocortisone acetate suspension intravenously.
    Intravenous Administration
    IV Push
    -Use only hydrocortisone sodium phosphate or hydrocortisone sodium succinate.
    -Inject each 100 mg of the reconstituted solution over at least 30 seconds. For doses of 500 mg or greater, administer over at least 10 minutes.

    Intermittent IV Infusion
    -Add the desired dose of the reconstituted injection to 50 to 1,000 mL of 5% Dextrose Injection, 0.9% Sodium Chloride Injection, or 5% Dextrose and 0.9% Sodium Chloride Injection.
    -Diluted solutions are stable for at least 4 hours.

    Intramuscular Administration
    -Use only hydrocortisone, hydrocortisone sodium phosphate, or hydrocortisone sodium succinate.
    -Inject deeply into a large muscle mass (e.g., anterolateral thigh). Rotate sites of injection.
    -Do NOT administer hydrocortisone IM into the deltoid muscle as subcutaneous atrophy occurs with high frequency after such use.
    -In general, IM administration of drugs in very low birth weight premature neonates is not practical due to small muscle mass, and absorption is unreliable due to hemodynamic instability that is relatively common in this population.



    Topical Administration
    Cream/Ointment/Lotion Formulations
    -Cream, lotion, or ointment: Apply sparingly as a thin film and rub gently into the cleansed affected area. Occlusive dressings may be necessary for severe conditions. However, occlusive dressings should be used very cautiously, if at all, in young pediatric patients due to increased systemic absorption.

    Other Topical Formulations
    -Solution or gel: Apply sparingly in a thin film and rub gently into the cleansed affected area. Occlusive dressings may be necessary for severe conditions. However, occlusive dressings should be used very cautiously, if at all, in young pediatric patients due to increased systemic absorption.
    -Aerosol: Shake the container gently once or twice each time before using. Spray each 4 square inch area for about 1 to 2 seconds from a distance of about 15 cm.



    Rectal Administration
    -Suppository: Instruct patient or caregiver about the proper use of suppository. Unwrap the suppository prior to insertion. Moisten the suppository with water prior to insertion. If suppository is too soft because of storage in a warm place, chill in the refrigerator for 30 minutes or run cold water over it before removing the wrapper.

    Prolonged systemic administration of physiologic replacement dosages of corticosteroid therapy usually does not cause adverse effects. The severity of the adverse effects associated with prolonged administration of pharmacological dosages of corticosteroids increases with duration and frequency of therapy. Short-term administration of large doses typically does not cause adverse effects, but long-term administration can lead to adrenocortical atrophy and generalized protein depletion.

    Pharmacologic doses of systemic corticosteroids administered for prolonged periods can result in physiological dependence due to hypothalamic-pituitary-adrenal (HPA) suppression. Pediatric patients may absorb proportionally larger amounts of topical corticosteroids compared to adults due to a larger skin surface to body mass ratio and, therefore, may be at increased risk of systemic adverse reactions, especially if applied to a large surface area and/or if occlusive dressings are used. HPA axis suppression and increased intracranial pressure have been reported in pediatric patients receiving topical corticosteroids. Increased intracranial pressure with papilledema (i.e., pseudotumor cerebri) has also been reported with withdrawal of glucocorticoid therapy. Exogenously administered corticosteroids exert a negative feedback effect on the pituitary, inhibiting the secretion of adrenocorticotropin (ACTH). This results in a decrease in ACTH-mediated synthesis of endogenous corticosteroids and androgens by the adrenal cortex. The severity of secondary adrenocortical insufficiency varies among individuals and is dependent on the dose, frequency, time of administration, and duration of therapy. Systemic administration of drug on alternate days may help to alleviate this adverse effect. Patients with HPA axis suppression will require increased doses of corticosteroid therapy during periods of physiologic stress. Acute adrenal insufficiency and even death can occur with abrupt discontinuation of therapy. Gradual discontinuation of prolonged oral corticosteroid therapy is recommended, since HPA suppression can last for up to 12 months following cessation of therapy. Patients may continue to need supplemental corticosteroid treatment during periods of physiologic stress or infectious conditions, even after the drug has been discontinued. A withdrawal syndrome unrelated to adrenocortical insufficiency can occur following sudden discontinuance of corticosteroid therapy. This syndrome includes symptoms such as fever, arthralgia, myalgia, and malaise. These effects are believed to be due to the sudden change in corticosteroid concentration rather than to low corticosteroid levels.

    Prolonged corticosteroid therapy can result in manifestations of Cushing's syndrome. Cushing's syndrome is characterized by truncal obesity, moon face, acne vulgaris, abdominal striae, increased blood pressure, decreased ability to tolerate carbohydrates, protein catabolism, psychiatric disturbances, skeletal changes, menstrual irregularity including amenorrhea or dysmenorrhea, and hirsutism.

    Corticosteroids, such as hydrocortisone, are responsible for protein metabolism, and prolonged therapy can result in various musculoskeletal manifestations, including: myopathy (myalgia, muscle wasting, muscle weakness), bone matrix atrophy (osteopenia, osteoporosis), bone fractures such as vertebral compression fractures or fractures of long bones, and avascular necrosis of femoral or humoral heads. Because of retardation of bone growth, pediatric patients receiving prolonged corticosteroid therapy may have growth inhibition. In a population based study, the risk of fractures was increased in children and adolescents (age 4-17 years) receiving > 4 courses of oral corticosteroids or doses >= 30 mg/day of prednisone. Because bone development is critical in pediatric patients, monitoring is warranted in patients receiving high-doses or chronic corticosteroid treatment. Glucocorticoids interact with calcium metabolism at many sites, including decreasing the synthesis by osteoblasts of the principle proteins of bone matrix, malabsorption of calcium in both the nephron and the gut, and reduction of sex hormone concentrations. Although all of these actions probably contribute to glucocorticoid-induced osteoporosis, the actions on osteoblasts are the most important. Glucocorticoids do not modify vitamin D metabolism. Intra-articular injections of corticosteroids can cause Charcot-like arthropathy and postinjection flare. Atrophy at the site of injection has been reported following administration of soluble glucocorticoids. Tendon rupture has also been reported.

    Spontaneous intestinal perforation (GI perforation) has occurred in premature neonates receiving hydrocortisone for the prevention of chronic lung disease. Enrollment in 2 prospective, placebo-controlled trials (n = 51-360) was stopped early due to a significantly higher incidence of intestinal perforation in premature neonates receiving hydrocortisone (9-16%) compared to patients receiving placebo (0-2%); the majority of patients with intestinal perforation also received indomethacin or ibuprofen. Adverse gastrointestinal (GI) effects associated with systemic corticosteroid administration include abdominal distension, hepatomegaly, appetite stimulation with weight gain, pancreatitis, esophageal ulceration, and nausea. Peptic ulcers with possible subsequent GI bleeding and GI perforation have been reported. Elevated hepatic enzymes, usually reversible upon discontinuation of therapy, have also occurred with systemic corticosteroids. Bladder and bowel dysfunction have been reported after intrathecal administration. Although it was once believed that corticosteroids contributed to the development of peptic ulcer disease, in a published review of 93 studies of corticosteroid use, the incidence of peptic ulcer disease was not found to be higher in steroid recipients compared to control groups.

    Topical preparations of hydrocortisone may be associated with local adverse effects and skin irritation including acneiform rash, allergic contact dermatitis, erythema, folliculitis, hypertrichosis, miliaria, perioral dermatitis, pruritus, skin atrophy, skin hypopigmentation, telangiectasia, and xerosis. Various adverse dermatologic effects reported during systemic corticosteroid therapy include acne, alopecia, xerosis, erythema, skin hypopigmentation, skin hyperpigmentation, rash (unspecified), skin atrophy, suppression of reactions to skin tests, diaphoresis, facial erythema, petechiae, ecchymosis, and easy bruising. Hypersensitivity reactions may manifest as allergic dermatitis, urticaria, angioedema, and/or anaphylactoid reactions. Parenteral corticosteroid therapy has also produced scarring and other types of injection site reaction (e.g., induration, delayed pain or soreness, subcutaneous and cutaneous atrophy, and sterile abscesses). Avoid injection of hydrocortisone into the deltoid muscle due to high incidence of subcutaneous atrophy. Paresthesias (burning or tingling) in the perineal area may occur following IV injection of corticosteroids.

    In general, excessive use of systemic or topical corticosteroids can lead to impaired wound healing. Do not apply hydrocortisone directly on or near healing wounds. Use of topical corticosteroids in patients with markedly impaired circulation may lead to skin ulcer development.

    Corticosteroid therapy (systemic or topical) can mask the symptoms of infection and may result in secondary systemic or localized infections. Avoid systemic use of corticosteroids, such as hydrocortisone, in patients with an active infection unless adequately controlled by anti-infective agents. Leukocytosis is a common physiologic effect of systemic corticosteroid therapy and may need to be differentiated from the leukocytosis that occurs with inflammatory or infectious processes. Immunosuppression is most likely to occur in patients receiving high-dose systemic corticosteroid therapy for any period of time, particularly in conjunction with corticosteroid-sparing drugs (e.g., troleandomycin) and/or concomitant immunosuppressant agents; however, patients receiving moderate dosages of systemic corticosteroids for short periods or low dosages for prolonged periods also may be at risk. Corticosteroids can reactivate tuberculosis and should not be used in patients with a history of active tuberculosis except when chemoprophylaxis is instituted concomitantly. Patients receiving immunosuppressive doses of corticosteroids should be advised to avoid exposure to measles or varicella (chickenpox) and, if exposed to these diseases, to seek medical advice immediately. Additionally, health care providers should monitor steroid recipients for signs of an opportunistic fungal infection as cases of candidiasis have been reported with the use of corticosteroids. The development of Kaposi's sarcoma has been associated with prolonged administration of corticosteroids.

    Systemic administration of corticosteroids, such as hydrocortisone, can result in edema, fluid retention, sodium retention, electrolyte disturbances (hypokalemia, hypokalemic metabolic alkalosis, hypernatremia, hypocalcemia), and hypertension. Congestive heart failure can occur in susceptible patients. In a review of 93 studies of corticosteroid use, hypertension was found to develop 4 times as often in steroid recipients compared to control groups. Other cardiovascular adverse reactions reported with systemic corticosteroids include bradycardia, cardiac arrest, cardiac arrhythmias, cardiac enlargement, circulatory collapse, hypertrophic cardiomyopathy (premature neonates), myocardial rupture after recent myocardial infarction, pulmonary edema, syncope, sinus tachycardia, thromboembolism, phlebitis, and vasculitis.

    Ocular effects, such as exophthalmos, posterior subcapsular cataracts, retinopathy, central serous chorioretinopathy (CSCR), or ocular hypertension, can result from prolonged use of corticosteroids and could result in glaucoma, or ocular nerve damage including optic neuritis. Secondary bacterial, fungal, and viral infections of the eye can be exacerbated by corticosteroid therapy. Monitor intraocular pressure in patients receiving corticosteroid therapy for more than 6 weeks. Case reports describe visual impairment in patients using topical corticosteroids for eczema of the face. The visual impairment was secondary to the onset of ocular hypertension. Such adverse effects, if they occur, could lead to blindness. Cataracts have also been reported, usually with large doses or therapy duration greater than 6 months. The mechanism of corticosteroid-induced cataract formation is uncertain but may involve disruption of sodium-potassium pumps in the lens epithelium leading to accumulation of water in lens fibers and agglutination of lens proteins.

    Prolonged corticosteroid therapy can result in glycosuria, hyperglycemia, and aggravation of diabetes mellitus in susceptible patients. Insulin or oral hypoglycemic dosages may require adjustment. In a review of 93 studies of corticosteroid use, the development of diabetes mellitus was determined to occur 4 times more frequently in steroid recipients compared to control groups.

    Adverse neurologic effects have been reported during prolonged corticosteroid therapy, such as hydrocortisone, including headache, insomnia, vertigo, restlessness, ischemic peripheral neuropathy, neuritis, seizures, and EEG changes. Arachnoiditis, meningitis, paresis, paraplegia, and sensory disturbances have been reported after intrathecal administration. Mental status changes including depression, anxiety, euphoria, personality changes, mood swings, and psychosis also have been reported. Emotional lability and psychotic problems can be exacerbated by corticosteroid therapy.

    Tolerance (tachyphylaxis) may occur with the prolonged use of topical corticosteroids. Tolerance is usually described as a decreased acute vasoconstrictive response to the agent after a period of days to weeks. This may explain the dramatic responses noted initially by patients early in topical corticosteroid treatment and an apparent diminished response with time. Tolerance is reversible and may be attenuated by interrupted or cyclic schedules of application (e.g., hydrocortisone is given for 2-3 weeks, followed by a 1-week intermission). It is unclear if tolerance or tachyphylaxis actually occurs or is due to patient adherence to topical corticosteroid regimen.

    Systemic corticosteroid therapy, such as hydrocortisone, can mask the symptoms of infection. Although the FDA-approved product labeling states that systemic hydrocortisone is contraindicated in patients with systemic fungal infections , most clinicians believe that systemic corticosteroids can be administered to these patients as long as appropriate therapy is administered simultaneously. Avoid use of systemic hydrocortisone in patients with a fungal infection or bacterial infection that is not adequately controlled with anti-infective agents. Activation of latent disease or exacerbation of intercurrent infection due to pathogens such as Amoeba, Candida, Cryptococcus, Mycobacterium, Nocardia, Pneumocystis, or Toxoplasma can occur in patients receiving systemic corticosteroids. Rule out infection with latent or active amebiasis before initiating corticosteroid therapy in patients who have spent time in the tropics or who have unexplained diarrhea. Use corticosteroids with caution in patients with known or suspected Strongyloides (threadworm) infestation as the immunosuppressive effects may lead to disseminated infection, severe enterocolitis, and sepsis. Avoid use of systemic corticosteroids in patients with cerebral malaria. Reserve systemic corticosteroid therapy in active tuberculosis for patients with fulminating or disseminated disease and only in conjunction with appropriate antituberculosis therapy. Reactivation of tuberculosis may occur in patients with latent tuberculosis or tuberculin reactivity; close observation for disease reactivation is needed if corticosteroids are indicated in such patients. Further, chemoprophylaxis is advised if prolonged corticosteroid therapy is needed. Advise patients receiving immunosuppressive doses of systemic corticosteroids to avoid exposure to viral infections (i.e., measles or varicella) because these diseases may be more serious or even fatal in immunosuppressed patients. Instruct patients to get immediate medical advice if exposure occurs. If exposed to chicken pox, prophylaxis with varicella zoster immune globulin may be indicated. Pediatric patients dependent on systemic corticosteroids should undergo anti-varicella-zoster virus antibody testing. If exposed to measles, prophylaxis with pooled intramuscular immunoglobulin may be indicated. Use corticosteroids with caution in patients with ocular herpes infection due to the risk of corneal perforation; avoid the use of corticosteroids in active ocular herpes infection. Initiate or continue therapy with topical corticosteroids to areas of infection, including tuberculosis of the skin, dermatologic fungal infection, and cutaneous or systemic viral infection (e.g., herpes infection, measles, varicella), only if the appropriate anti-infective treatment is instituted. If the infection does not respond to the antimicrobial therapy, discontinue the concurrent use of the topical corticosteroid until the infection is controlled.

    Systemic corticosteroids, such as hydrocortisone, can aggravate Cushing's syndrome; avoid use in patients with Cushing's syndrome. Prolonged administration of pharmacological doses of systemic corticosteroids or topical preparations (resulting in systemic absorption) may result in hypothalamic-pituitary-adrenal (HPA) suppression and/or manifestations of Cushing's syndrome in some patients.Adrenal suppression and increased intracranial pressure have been reported with the use and/or withdrawal of systemic and topical corticosteroids in pediatric patients. Acute adrenal insufficiency and even death may occur following abrupt discontinuation of prolonged systemic therapy. In addition, a withdrawal syndrome unrelated to adrenocortical insufficiency may occur following sudden discontinuation of corticosteroid therapy. These effects are thought to be due to the sudden change in glucocorticoid concentration rather than to low corticosteroid levels. Withdraw prolonged systemic corticosteroid therapy (> 2 weeks) gradually. HPA axis suppression can last for up to 12 months following cessation of systemic therapy. Recovery of HPA axis function is generally prompt and complete upon discontinuation of the topical corticosteroid. HPA axis-suppressed patients may need supplemental corticosteroid treatment during periods of physiologic stress, such as surgery, acute blood loss, or infection, even after the corticosteroid has been discontinued. Encourage patients currently receiving chronic corticosteroid therapy or who have had corticosteroids discontinued within the last 12 months to carry identification advising the need for administration of hydrocortisone in situations of increased stress. Conditions that increase systemic absorption of topical corticosteroids include use over large surface areas, prolonged use, use in areas where the epidermal barrier is disrupted (i.e., skin abrasion), and the use of an occlusive dressing. Pediatric patients may absorb proportionally larger amounts of topical corticosteroids compared to adults due to a larger skin surface to body mass ratio and, therefore, may be at increased risk of systemic adverse reactions. Evaluate patients receiving large doses of hydrocortisone applied to a large surface area periodically for evidence of HPA axis suppression and/or manifestations of Cushing's syndrome. If these effects are noted, attempt withdrawal of the drug, a reduction in the frequency of application, or substitution of a less potent corticosteroid.

    Patients receiving high-dose systemic corticosteroid therapy, such as hydrocortisone, for any period of time are at risk to develop immunosuppression; patients receiving moderate doses of systemic corticosteroids for short periods or low doses for prolonged periods may also be at risk. When given in combination with other immunosuppressive agents, there is a risk of over-immunosuppression.

    Do not use topical corticosteroids to treat acne vulgaris, acne rosacea, or perioral dermatitis as they may exacerbate these conditions. Topical corticosteroids may delay the healing of non-infected wounds, such as venous stasis ulcers. Use topical hydrocortisone preparations with caution in patients with markedly impaired circulation or peripheral vascular disease; skin ulceration has been reported in these patients following topical corticosteroid use.

    Corticosteroid therapy, such as hydrocortisone, has been associated with left ventricular free-wall rupture in patients with recent myocardial infarction; use cautiously in these patients.

    Systemic corticosteroids, such as hydrocortisone, can cause edema and weight gain. Use with caution in patients with congestive heart failure, hypertension, or renal disease as this can cause an exacerbation of their condition.

    Chronic corticosteroid therapy, such as hydrocortisone, in pediatric patients may cause growth inhibition due to hypothalamic-pituitary-adrenal axis suppression and inhibition of bone growth. Because bone development is critical in pediatric patients, monitoring is warranted in patients receiving high-dose or chronic corticosteroid treatment. Prolonged systemic corticosteroid therapy can lead to osteoporosis, vertebral compression fractures, aseptic necrosis of femoral and humoral heads, and pathologic fractures of long bones secondary to decreased bone formation, increased bone resorption, and protein catabolism. A high-protein diet may alleviate or prevent the adverse effects associated with protein catabolism.

    Systemic corticosteroids, such as hydrocortisone, may decrease glucose tolerance, produce hyperglycemia, and aggravate or precipitate diabetes mellitus. This may especially occur in patients predisposed to diabetes mellitus. When corticosteroid therapy is necessary in patients with diabetes mellitus, changes in insulin, oral antidiabetic agent dosage, and/or diet may be required. Use topical corticosteroids with caution in patients with diabetes mellitus. Exacerbation of diabetes may occur with systemic absorption of the topical corticosteroid. Use of topical corticosteroids may further delay healing of skin ulcers in diabetic patients.

    Oral corticosteroids, such as hydrocortisone, can cause gastrointestinal (GI) irritation. Use systemic corticosteroids with caution in patients with active or latent peptic ulcer disease, GI disease, diverticulitis, nonspecific ulcerative colitis, or intestinal anastomosis (because of the possibility of perforation). While used for the short-term treatment of acute exacerbations of chronic inflammatory bowel disease such as ulcerative colitis and Crohn's disease, avoid use of corticosteroids in patients where there is a possibility of impending GI perforation, abscess, or pyogenic infection. Some patients may require long-term corticosteroid therapy to suppress disease activity, but generally this practice is not recommended.

    Use systemic corticosteroids, such as hydrocortisone, with extreme caution in patients with psychosis, emotional instability, and seizure disorder because the drugs can exacerbate these conditions. Do not use high doses of systemic corticosteroids for the treatment of traumatic brain injury. An increase in early mortality (at 2 weeks) and late mortality (at 6 months) was noted in patients with head trauma who were determined not to have other clear indications for corticosteroid treatment; in the trial, patients received methylprednisolone hemisuccinate.

    Use systemic corticosteroids, such as hydrocortisone, with caution in patients with myasthenia gravis who are being treated with anticholinesterase agents. A generalized acute myopathy has been reported with the use of high-dose corticosteroids in patients with disorders of neuromuscular transmission, such as myasthenia gravis. Ocular and respiratory muscles may be involved and may result in quadriparesis; elevations in creatine kinase may also occur. Recovery from the myopathy after discontinuation of corticosteroids may take weeks to years.

    Systemic corticosteroids rarely may increase blood coagulability, causing intravascular thrombosis, thrombophlebitis, and thromboembolism. Therefore, use systemic corticosteroids, such as hydrocortisone, with caution in patients with preexisting coagulopathy (e.g., hemophilia) or thromboembolic disease. Hydrocortisone use via IM administration for immune thrombocytopenia/idiopathic thrombocytopenic purpura (ITP) is contraindicated.

    Administration of live or live, attenuated vaccines is contraindicated in patients receiving immunosuppressive doses of systemic corticosteroids, such as hydrocortisone. Killed or inactivated vaccines may be administered to patients receiving immunosuppressive doses of corticosteroids; however, the response to vaccination may be diminished. The immunosuppressive effects of steroid treatment differ, but many clinicians consider a dose equivalent to either 2 mg/kg/day or 20 mg/day of prednisone as sufficiently immunosuppressive to raise concern about the safety of immunization with live-virus vaccines. Corticosteroid therapy usually does not contraindicate vaccination with live-virus vaccines when such therapy is of short-term (< 2 weeks); low to moderate dose; long-term alternate day treatment with short-acting preparations; maintenance physiologic doses (replacement therapy); or administration topically (skin or eye), by aerosol, or by intra-articular, bursal or tendon injection. When cancer chemotherapy or immunosuppressive therapy is being considered (e.g., for patients with Hodgkin's disease or organ transplantation), vaccination should precede the initiation of chemotherapy or immunotherapy by >= 2 weeks. Consider patients vaccinated while on immunosuppressive therapy or in the 2 weeks prior to starting therapy unimmunized and revaccinate at least 3 months after discontinuation of therapy. In patients who have received high-dose, systemic corticosteroids for >= 2 weeks, it is recommended to wait at least 3 months after discontinuation of therapy before administering a live-virus vaccine.

    Some commercially available formulations of hydrocortisone injection may contain sulfites. Sulfites may cause allergic reactions in some people. Use these formulations with caution in patients with known sulfite hypersensitivity. Patients with asthma are more likely to experience this sensitivity reaction than non-asthmatic patients.

    Several commercial formulations of hydrocortisone injection are contraindicated in premature neonates because these products contain benzyl alcohol. Use these formulations of hydrocortisone with caution in neonates. Administration of benzyl alcohol to neonates can result in 'gasping syndrome,' which is a potentially fatal condition characterized by metabolic acidosis and CNS, respiratory, circulatory, and renal dysfunction; it is also characterized by high concentrations of benzyl alcohol and its metabolites in the blood and urine. While the minimum amount of benzyl alcohol at which toxicity may occur is not known, 'gasping syndrome' has been associated with benzyl alcohol dosages >99 mg/kg/day in neonates and low-birth-weight neonates. Additional symptoms may include gradual neurological deterioration, seizures, intracranial hemorrhage, hematologic abnormalities, skin breakdown, hepatic failure, renal failure, hypotension, bradycardia, and cardiovascular collapse. Rare cases of death, primarily in premature neonates, have been reported. Further, an increased incidence of kernicterus, especially in small, premature neonates has been reported. Practitioners administering this and other medications containing benzyl alcohol should consider the combined daily metabolic load of benzyl alcohol from all sources. Premature neonates, neonates with a low birth weight, and patients who receive a high dose may be more likely to develop toxicity.

    Hydrocortisone is contraindicated in patients with hypersensitivity to the drug or any of its components. True corticosteroid hypersensitivity reactions are rare. While a hypersensitivity reaction could be to a specific salt of the corticosteroid (i.e., hydrocortisone sodium succinate), administer any form of hydrocortisone with extreme caution in patients who have demonstrated a prior hypersensitivity reaction to hydrocortisone. It is possible, though also rare, that such patients will display cross-hypersensitivity to other corticosteroids; there have been reports that a cross-sensitivity between hydrocortisone and methylprednisolone may exist. It is advisable that patients who have a hypersensitivity reaction to any corticosteroid undergo skin testing, which, although not a conclusive predictor, may help to determine if hypersensitivity to another corticosteroid exists. Carefully monitor such patients during and after the administration of any corticosteroid.

    Use corticosteroids with caution in patients with glaucoma or any other visual disturbance. Corticosteroids are well known to cause cataracts and can exacerbate glaucoma during long-term administration. Assess patients receiving chronic corticosteroid therapy periodically for cataract formation. There is also an increase in the propensity for secondary fungal, viral, or bacterial ocular infection. Avoid ophthalmic administration of topical hydrocortisone preparations. Visual impairment, ocular hypertension, and worsened cataracts have been reported with ocular exposure to other high potency topical corticosteroids. Preexisting glaucoma may be aggravated if hydrocortisone is applied in the periorbital area.

    Injection of hydrocortisone may result in dermal and/or subdermal changes forming depressions in the skin at the injection site. In order to minimize the incidence of subdermal and dermal atrophy, care must be exercised not to exceed recommended doses in injections. Injection into the deltoid muscle should be avoided because of a high incidence of subcutaneous atrophy. Use topical corticosteroids, such as hydrocortisone, for brief periods, or under close medical supervision in patients with evidence of pre-existing skin atrophy. Prolonged use of a topical corticosteroid, and the application of the steroid to thin areas of skin appear to increase the risk for atrophy. Use of lower potency topical corticosteroids may be necessary in some patients.

    In utero exposure to hydrocortisone can lead to hypoadrenalism in neonates. Monitor neonates born to mothers who have taken substantial doses of corticosteroids during pregnancy for signs of hypoadrenalism.

    Epidural administration of corticosteroids such as hydrocortisone should be used with great caution. Rare, but serious adverse events, including cortical blindness, stroke, spinal cord infarction, paralysis, seizures, nerve injury, brain edema, and death have been reported after epidural administration of corticosteroid injections. These events have been reported with and without the use of fluoroscopy. Many cases were temporally associated with epidural corticosteroid administration, with events occurring within minutes to 48 hours after administration. Some cases of neurologic events were confirmed using magnetic resonance imaging (MRI) or computed tomography (CT) scan. Many patients did not recover from the reported adverse effects. Discuss the benefits and risks of epidural corticosteroid injections with patients. If the decision is made to proceed with epidural administration, counsel patients to seek medical attention immediately if they experience symptoms such as vision changes, tingling in arms or legs, any symptoms of stroke, or seizures. In addition, intrathecal administration of hydrocortisone sodium succinate injection is contraindicated. Severe medical events, including arachnoiditis, meningitis, paraparesis, paraplegia, and sensory disturbances, have been reported after intrathecal administration.

    Use hydrocortisone with caution in patients with hypothyroidism or hyperthyroidism. The metabolic clearance of corticosteroids is decreased in patients with hypothyroidism and increased in patients with hyperthyroidism. Doses of hydrocortisone may need to be adjusted in patients with changes in thyroid status.

    The metabolic clearance of corticosteroids, such as hydrocortisone, is decreased in patients with hepatic disease, such as cirrhosis. Use with caution in patients with hepatic disease.

    Use hydrocortisone with caution in patients with diagnosed or suspected pheochromocytoma. Pheochromocytoma crisis, which can be fatal, has been reported after administration of systemic corticosteroids. Consider the risk of pheochromocytoma crisis prior to administering corticosteroids in any patients with suspected pheochromocytoma.

    Description: Hydrocortisone is a steroid hormone secreted by the adrenal cortex. Commercially, it is available as the unchanged hormone and as various salts. Hydrocortisone is the preferred glucocorticoid for replacement therapy in pediatric patients with acute and chronic adrenal insufficiency due to its mineralocorticoid activity. In pediatric patients with chronic adrenal insufficiency, hydrocortisone is preferred over more potent corticosteroids, such as dexamethasone, due to a lower risk of adverse reactions, especially growth suppression. Some patients with adrenal insufficiency may require concomitant administration of a more potent mineralocorticoid, such as fludrocortisone. Systemic hydrocortisone is also used off-label in pediatric patients for refractory hypotension due to shock, prevention of chronic lung disease (neonates), and refractory hypoglycemia (neonates). Pediatric guidelines state hydrocortisone may or may not be used for fluid- and vasopressor-refractory septic shock. Low potency topical corticosteroids, such as hydrocortisone base and acetate formulations, are the safest for chronic use and may be used on the face or intertriginous areas, with occlusion, and in infants and young children. Systemic corticosteroids may be added to other long-term maintenance medications in the management of uncontrolled severe persistent asthma. Once stabilization of asthma is achieved, regular attempts should be made to reduce or eliminate the use of systemic corticosteroids due to the adverse reactions associated with chronic administration. Short courses of treatment may be used in the management of asthma exacerbations. Systemic formulations of hydrocortisone are FDA-approved in pediatric patients (age not specified); other formulations are approved for use in patients of varying ages depending on the specific product.

    General dosing information for systemic therapy:
    -Dosage requirements are variable. Individualize dosage based on the condition being treated and the response of the patient.
    -Closer monitoring may be required in pediatric patients receiving hydrocortisone suspension. Crushed tablets are recommended over oral suspension in pediatric patients with CAH due to results of a study showing hydrocortisone cypionate suspension (Cortef) was not bioequivalent to the tablets.
    -Gradual withdrawal of hydrocortisone after high-dose or prolonged therapy is recommended due to the possibility of hypothalamic-pituitary-adrenal (HPA) axis suppression. The following recommendations for withdrawal of corticosteroids based on the duration of therapy have been made: less than 2 weeks - may abruptly discontinue; 2 to 4 weeks - taper dose over 1 to 2 weeks; more than 4 weeks - taper slowly over 1 to 2 months to physiologic dose (approximately 10 mg/m2/day of hydrocortisone) and discontinue after assessment of adrenal function has demonstrated recovery.

    For the treatment of primary adrenocortical insufficiency (e.g., Addison's Disease, congenital adrenal hyperplasia) or secondary adrenocortical insufficiency:
    Oral dosage:
    Neonates: 8 to 20 mg/m2/day PO given in 3 divided doses initially; individualize dosage to minimize symptoms of adrenal insufficiency while avoiding growth retardation and Cushingoid symptoms that occur with overdosage. A usual dose of 2.5 to 5 mg/day PO 3 times daily has been recommended by the American Academy of Pediatrics (AAP). Doses more than 20 mg/m2/day PO have been associated with loss of height and shorter adult height. Patients with primary adrenal insufficiency may require higher initial doses than those with secondary adrenal insufficiency. Hydrocortisone cypionate suspension (Cortef) and hydrocortisone tablets are not bioequivalent; therefore, the suspension is not recommended for the treatment of patients with congenital adrenal hyperplasia (CAH). Neonates and infants with classic CAH also require treatment with fludrocortisone (0.05 to 0.3 mg/day PO given in 1 to 2 divided doses) and sodium chloride supplementation (1 to 2 g/day or 17 to 34 mEq/day PO divided and given with several feedings).
    Infants: 8 to 20 mg/m2/day PO given in 3 divided doses initially; individualize dosage to minimize symptoms of adrenal insufficiency while avoiding growth retardation and Cushingoid symptoms that occur with overdosage. A usual dose of 2.5 to 5 mg/day PO 3 times daily has been recommended by the American Academy of Pediatrics (AAP). Doses more than 20 mg/m2/day PO have been associated with loss of height and shorter adult height. Patients with primary adrenal insufficiency may require higher initial doses than those with secondary adrenal insufficiency. Hydrocortisone cypionate suspension (Cortef) and hydrocortisone tablets are not bioequivalent; therefore, the suspension is not recommended for the treatment of patients with congenital adrenal hyperplasia (CAH). Neonates and infants with classic CAH also require treatment with fludrocortisone (0.05 to 0.3 mg/day PO given in 1 to 2 divided doses) and sodium chloride supplementation (1 to 2 g/day or 17 to 34 mEq/day PO divided and given with several feedings).
    Children and Adolescents: 8 to 20 mg/m2/day PO given in 3 divided doses initially; individualize dosage to minimize symptoms of adrenal insufficiency while avoiding growth retardation and Cushingoid symptoms that occur with overdosage. A usual dose of 5 to 10 mg/day PO 3 times daily has been recommended by the American Academy of Pediatrics. Doses more than 17 mg/m2/day in adolescents have been associated with loss of height and shorter adult height. Patients with primary adrenal insufficiency may require higher initial doses than those with secondary adrenal insufficiency. Hydrocortisone cypionate suspension (Cortef) and hydrocortisone tablets are not bioequivalent; therefore, the suspension is not recommended for the treatment of patients with congenital adrenal hyperplasia (CAH). Patients with classic CAH also require treatment with fludrocortisone (0.05 to 0.3 mg/day PO given in 1 to 2 divided doses).
    -for adrenal crisis prophylaxis in patients with known or suspected adrenal insufficiency with other acute stressors (e.g., febrile illness more than 38.5 degrees Celsius, gastroenteritis with dehydration, major trauma):
    Intramuscular or Intravenous Dosage:
    Neonates: 50 mg/m2 IM will provide 6 to 8 hours of coverage. If the patient's condition does not improve or worsens during this time, initiate IV stress dosing (3 to 4 times the daily maintenance dose divided every 6 hours). Alternatively, an initial dose of 25 mg IM has been recommended for patients with congenital adrenal hyperplasia.
    Infants: 50 mg/m2 IM will provide 6 to 8 hours of coverage. If the patient's condition does not improve or worsens during this time, initiate IV stress dosing (3 to 4 times the daily maintenance dose divided every 6 hours). Alternatively, an initial dose of 25 mg IM has been recommended for patients with congenital adrenal hyperplasia.
    Children 1 to 5 years: 50 mg/m2 IM will provide 6 to 8 hours of coverage. If the patient's condition does not improve or worsens during this time, initiate IV stress dosing (3 to 4 times the daily maintenance dose divided every 6 hours). Alternatively, an initial dose of 50 mg IM has been recommended for patients with congenital adrenal hyperplasia.
    Children and Adolescents 6 to 17 years: 50 mg/m2 IM will provide 6 to 8 hours of coverage. If the patient's condition does not improve or worsens during this time, initiate IV stress dosing (3 to 4 times the daily maintenance dose divided every 6 hours). Alternatively, an initial dose of 100 mg IM has been recommended for patients with congenital adrenal hyperplasia.
    Oral dosage:
    Neonates: 30 to 50 mg/m2/day PO given in 3 to 4 divided doses (approximately triple the daily maintenance dose) is commonly recommended. Varying recommendations of increases in the daily maintenance dose anywhere from 2 to 10 times have been made depending on the level of stress and the patient's individual needs. Hydrocortisone cypionate suspension (Cortef) and hydrocortisone tablets are not bioequivalent; therefore, the suspension is not recommended for the treatment of patients with congenital adrenal hyperplasia (CAH).
    Infants, Children, and Adolescents: 30 to 50 mg/m2/day PO given in 3 to 4 divided doses (approximately triple the daily maintenance dose) is commonly recommended. Varying recommendations of increases in the daily maintenance dose anywhere from 2 to 10 times have been made depending on the level of stress and the patient's individual needs. Hydrocortisone cypionate suspension (Cortef) and hydrocortisone tablets are not bioequivalent; therefore, the suspension is not recommended for the treatment of patients with congenital adrenal hyperplasia (CAH).
    Rectal dosage*:
    Infants, Children, and Adolescents: 100 mg/m2/dose PR every 8 hours has been recommended as an alternative to parenteral administration in patients who cannot tolerate oral administration due to illness. Due to large interindividual differences in bioavailability, higher doses (150 to 200 mg/m2/dose PR) may be required in patients who do not show an adequate response (serum cortisol concentration more than 1,000 nmol/L 3 hours after administration). It is recommended that the patient's response to rectal hydrocortisone be tested prior to use during illness. In a study of patients with adrenal insufficiency (n = 57, age 1 month to 17 years), 43 patients responded adequately to a dose of 100 mg/m2 rectally. Risk factors for failed response included younger age and obesity. Suppositories used in this study were compounded in a Witepsol W45 base.
    -for adrenal crisis prophylaxis in patients with known or suspected adrenal insufficiency undergoing surgery accompanied by general anesthesia:
    Intravenous or Intramuscular dosage:
    Neonates: 50 mg/m2 IV 30 to 60 minutes prior to induction of anesthesia with repeat doses of 50 mg/m2/dose IV every 6 hours or as a continuous infusion until the patient has recovered. For patients with congenital adrenal hyperplasia (CAH), 2 mg/kg/dose IV at induction of anesthesia with repeat doses every 4 hours or as a continuous IV infusion for prolonged procedures or recovery times has also been recommended. Alternatively, an initial stress dose of 25 mg IM followed by IV doses equivalent to 3 to 4 times the daily maintenance dose divided every 6 hours has been recommended.
    Infants: 50 mg/m2 IV 30 to 60 minutes prior to induction of anesthesia with repeat doses of 50 mg/m2/dose IV every 6 hours or as a continuous infusion until the patient has recovered. For patients with congenital adrenal hyperplasia (CAH), 2 mg/kg/dose IV at induction of anesthesia with repeat doses every 4 hours or as a continuous IV infusion for prolonged procedures or recovery times has also been recommended. Alternatively, an initial stress dose of 25 mg IM followed by IV doses equivalent to 3 to 4 times the daily maintenance dose divided every 6 hours has been recommended.
    Children 1 to 5 years: 50 mg/m2 IV 30 to 60 minutes prior to induction of anesthesia with repeat doses of 50 mg/m2/dose IV every 6 hours or as a continuous infusion until the patient has recovered. For patients with congenital adrenal hyperplasia (CAH), 2 mg/kg/dose IV at induction of anesthesia with repeat doses every 4 hours or as a continuous IV infusion for prolonged procedures or recovery times has also been recommended. Alternatively, an initial stress dose of 50 mg IM followed by IV doses equivalent to 3 to 4 times the daily maintenance dose divided every 6 hours has been recommended.
    Children and Adolescents 6 to 17 years: 50 mg/m2 IV 30 to 60 minutes prior to induction of anesthesia with repeat doses of 50 mg/m2/dose IV every 6 hours or as a continuous infusion until the patient has recovered. For patients with congenital adrenal hyperplasia (CAH), 2 mg/kg/dose IV at induction of anesthesia with repeat doses every 4 hours or as a continuous IV infusion for prolonged procedures or recovery times has also been recommended. Alternatively, an initial stress dose of 100 mg IM followed by IV doses equivalent to 3 to 4 times the daily maintenance dose divided every 6 hours has been recommended.
    -for the treatment of acute adrenocortical insufficiency:
    Intravenous or Intramuscular dosage:
    Neonates: 2 mg/kg/dose [weight-based], 10 to 25 mg/dose [flat dose], or 50 to 100 mg/m2/dose [BSA-based] IV or IM load, followed by 10 to 25 mg/day [flat dose] or 50 to 100 mg/m2/day [BSA-based] IV or IM in divided doses at 6-hour intervals for 24 hours.
    Infants: 2 mg/kg/dose [weight-based], 10 to 25 mg/dose [flat dose], or 50 to 100 mg/m2/dose [BSA-based] IV or IM load, followed by 10 to 25 mg/day [flat dose] or 50 to 100 mg/m2/day [BSA-based] IV or IM in divided doses at 6-hour intervals for 24 hours.
    Children 1 to 5 years: 2 mg/kg/dose (Max: 100 mg) [weight-based], 25 to 50 mg/dose [flat dose], or 50 to 100 mg/m2/dose [BSA-based] IV or IM load, followed by 25 to 50 mg/day [flat dose] or 50 to 100 mg/m2/day [BSA-based] IV or IM in divided doses at 6-hour intervals for 24 hours.
    Children and Adolescents 6 to 17 years: 2 mg/kg/dose (Max: 100 mg) [weight-based], 50 to 100 mg/dose [flat dose], or 50 to 100 mg/m2/dose [BSA-based] IV or IM load, followed by 50 to 100 mg/day [flat dose] or 50 to 100 mg/m2/day [BSA-based] IV or IM in divided doses at 6-hour intervals for 24 hours.

    For the treatment of septic shock* and/or hypotension* in patients whose blood pressure is poorly responsive to adequate fluid resuscitation and vasopressor therapy:
    Intravenous dosage (hydrocortisone sodium succinate):
    Neonates: 1 mg/kg/dose IV every 8 to 12 hours for 1 to 5 days has been studied (combined n from 3 studies = 89, gestational age 23 to 40 weeks). An initial loading dose of 2 mg/kg IV was used in 1 retrospective study and another prospective, observational study used a higher maintenance dose of 3 to 6 mg/kg/day IV divided 2 to 4 times daily in a small number of patients (n = 5) with severe capillary leak syndrome and/or previous steroid treatment. Guidelines state hydrocortisone may or may not be used for fluid- and vasopressor-refractory septic shock.
    Infants and Children 1 month to 2 years: 2 mg/kg [weight-based], 25 mg [flat-dose], or 100 mg/m2 [BSA-based] IV bolus, followed by 1 to 2 mg/kg/day [weight-based] or 50 to 100 mg/m2/day [BSA-based] IV in divided doses at 6-hour intervals or as a continuous IV infusion. Infusions up to 50 mg/kg/day may be required to reverse shock short-term; however, this recommendation is based on very limited data that did not demonstrate improvement in mortality. Guidelines state hydrocortisone may or may not be used for fluid- and vasopressor-refractory septic shock.
    Children 3 to 12 years: 2 mg/kg (Max: 100 mg) [weight-based], 50 mg [flat-dose], or 100 mg/m2 [BSA-based] IV bolus, followed by 1 to 2 mg/kg/day [weight-based] or 50 to 100 mg/m2/day [BSA-based] IV in divided doses at 6-hour intervals or as a continuous IV infusion. Infusions up to 50 mg/kg/day may be required to reverse shock short-term; however, this recommendation is based on very limited data that did not demonstrate improvement in mortality. Guidelines state hydrocortisone may or may not be used for fluid- and vasopressor-refractory septic shock.
    Adolescents: 2 mg/kg (Max: 100 mg) [weight-based], 100 mg [flat-dose], or 100 mg/m2 [BSA-based] IV bolus, followed by 1 to 2 mg/kg/day [weight-based] or 50 to 100 mg/m2/day [BSA-based] IV in divided doses at 6-hour intervals or as a continuous IV infusion. Infusions up to 50 mg/kg/day may be required to reverse shock short-term; however, this recommendation is based on very limited data that did not demonstrate improvement in mortality. Guidelines state hydrocortisone may or may not be used for fluid- and vasopressor-refractory septic shock.

    For the treatment of acute episodes or exacerbation of inflammatory bowel disease (Crohn's disease or ulcerative colitis):
    Intramuscular or Intravenous dosage:
    Children and Adolescents: 0.56 to 8 mg/kg/day or 20 to 240 mg/m2/day IM or IV given in 3 to 4 divided dose is the FDA-approved general dosage range. Adjust according to patient response. Because of the potential complications of steroid use, steroids should be used selectively and in the lowest dose possible for the shortest duration as possible.
    Oral dosage:
    Children and Adolescents: A general dose range of 0.56 to 8 mg/kg/day or 16 to 240 mg/m2/day PO given in 3 to 4 divided doses has been recommended. Adjust according to patient response. Because of the potential complications of steroid use, steroids should be used selectively and in the lowest dose possible for the shortest duration as possible.

    For the treatment of rheumatic and related disorders such as acute rheumatic carditis, systemic dermatomyositis (polymyositis), systemic lupus erythematosus (SLE), temporal arteritis, and symptomatic sarcoidosis or for adjunctive therapy in the treatment of acute gouty arthritis, ankylosing spondylitis, rheumatoid arthritis, juvenile rheumatoid arthritis (JRA)/juvenile idiopathic arthritis (JIA), post-traumatic osteoarthritis, or psoriatic arthritis:
    Oral dosage:
    Infants, Children, and Adolescents: A general dose range of 0.56-8 mg/kg/day or 16-240 mg/m2/day PO given in 3-4 divided doses has been recommended. Adjust according to patient response.
    Intramuscular or Intravenous dosage:
    Infants, Children, and Adolescents: 0.56-8 mg/kg/day or 20-240 mg/m2/day IM or IV given in 3-4 divided dose is the FDA-approved general dosage range. Adjust according to patient response.

    For the treatment of acute episodes or exacerbation of non-rheumatic inflammation including acute and subacute bursitis, epicondylitis, and acute non-specific tenosynovitis:
    Oral dosage:
    Infants, Children, and Adolescents: A general dose range of 0.56-8 mg/kg/day or 16-240 mg/m2/day PO given in 3-4 divided doses has been recommended. Adjust according to patient response.

    For the management of nephrotic syndrome to induce diuresis or decrease proteinuria:
    Oral dosage:
    Infants, Children, and Adolescents: A general dose range of 0.56-8 mg/kg/day or 16-240 mg/m2/day PO given in 3-4 divided doses has been recommended. Adjust according to patient response.
    Intramuscular or Intravenous dosage:
    Infants, Children, and Adolescents: 0.56-8 mg/kg/day or 20-240 mg/m2/day IM or IV given in 3-4 divided dose is the FDA-approved general dosage range. Adjust according to patient response.

    For the treatment of allergic disorders including anaphylaxis, anaphylactic shock, or anaphylactoid reactions, angioedema, acute noninfectious laryngeal edema, hypersensitivity reactions (drug or food allergy), transfusion-related reactions, urticaria, serum sickness, and severe perennial allergies or seasonal allergies, including allergic rhinitis:
    -for the urgent treatment of severe conditions such as anaphylaxis, angioedema, acute noninfectious laryngeal edema, or transfusion-related reactions:
    Intravenous dosage (hydrocortisone sodium succinate injection):
    Infants, Children, and Adolescents: The FDA-approved general dosage range is 0.56 to 8 mg/kg/day or 20 to 240 mg/m2/day IV given in 3 to 4 divided doses. However, in certain acute, life-threatening situations, higher doses may be justified. Adjust according to patient response. Corticosteroids are not indicated as initial treatment for anaphylaxis, but can be given as adjunctive therapy after the administration of epinephrine.
    -for the non-emergent treatment of hypersensitivity or allergic conditions:
    Oral dosage:
    Infants, Children, and Adolescents: A general dose range of 0.56 to 8 mg/kg/day or 16 to 240 mg/m2/day PO given in 3 to 4 divided doses has been recommended. Adjust according to patient response.

    For the treatment of corticosteroid-responsive dermatologic disorders (e.g., alopecia areata, atopic dermatitis, bullous dermatitis herpetiformis, contact dermatitis including Rhus dermatitis due to poison ivy, poison oak, poison sumac, discoid lupus erythematosus, eczema, exfoliative dermatitis, insect bites or stings, granuloma annulare, keloids, lichen striatus, lichen planus, lichen simplex, necrobiosis lipoidica diabeticorum, pemphigus, pityriasis rosea, polymorphous light eruption, pompholyx (dyshidrosis), pruritus, psoriasis, sarcoidosis, seborrheic dermatitis, or xerosis):
    -for mild-to-moderate corticosteroid responsive dermatoses:
    Topical dosage (hydrocortisone or hydrocortisone acetate):
    Infants and Children less than 2 years: Only for use with a prescriber's prescription. Apply sparingly to affected areas 2 to 4 times per day. Follow the directions on the specific product labeling. Occlusive dressings may be used for the management of psoriasis or refractory conditions; however, occlusive dressings can increase absorption as much as 10 to 100 times which may increase the risk of systemic adverse reactions. Avoid the use of tight-fitting diapers or plastic pants in patients being treated in the diaper area as these may act as an occlusive dressing.
    Children and Adolescents 2 to 17 years: Apply sparingly to affected areas 2 to 4 times per day. Follow the directions on the specific product labeling. Occlusive dressings may be used for the management of psoriasis or refractory conditions; however, occlusive dressings can increase absorption as much as 10 to 100 times which may increase the risk of systemic adverse reactions. Advise caregivers to avoid the use of tight-fitting diapers or plastic pants in patients being treated in the diaper area as these may act as an occlusive dressing. For self-medication, apply a 0.5% or 1% non-prescription product to affected areas not more than 3 to 4 times per day. If condition worsens, or if symptoms persist for more than 7 days or clear up and occur again within a few days, discontinue therapy.
    Topical dosage (hydrocortisone butyrate):
    Infants, Children, and Adolescents: Apply sparingly to affected areas 2 to 3 times per day. According to the product labeling, occlusive dressings may be used for the management of psoriasis or refractory conditions; however, occlusive dressings can increase absorption as much as 10 to 100 times which may increase the risk of systemic adverse reactions. Advise caregivers to avoid the use of tight-fitting diapers or plastic pants in patients being treated in the diaper area as these may act as an occlusive dressing.
    -for mild to moderate atopic dermatitis:
    Topical dosage (hydrocortisone butyrate lotion or Lipocream):
    Infants 3 months and older, Children, and Adolescents: Apply sparingly to affected areas twice daily; if no improvement after 2 weeks, reassess diagnosis. Safety and efficacy have not been established beyond 4 weeks of therapy.

    For the treatment of corticosteroid-responsive hematologic disorders, like acquired (autoimmune) hemolytic anemia, erythroblastopenia, and congenital hypoplastic anemia; OR for the palliative treatment of acute leukemias of childhood including acute lymphocytic leukemia (ALL), chronic lymphocytic leukemia (CLL), Hodgkin's disease, non-Hodgkin's lymphoma (NHL), or cutaneous T-cell lymphoma (CTCL) (aka mycosis fungoides):
    Oral dosage:
    Infants, Children, and Adolescents: A general dose range of 0.56-8 mg/kg/day or 16-240 mg/m2/day PO given in 3-4 divided doses has been recommended. Adjust according to patient response.
    Intramuscular or Intravenous dosage:
    Infants, Children, and Adolescents: 0.56-8 mg/kg/day or 20-240 mg/m2/day IM or IV given in 3-4 divided dose is the FDA-approved general dosage range. Adjust according to patient response.

    For the treatment of respiratory inflammatory conditions including aspiration pneumonitis, berylliosis, or Loeffler's syndrome:
    Oral dosage:
    Infants, Children, and Adolescents: A general dose range of 0.56 to 8 mg/kg/day or 16 to 240 mg/m2/day PO given in 3 to 4 divided doses has been recommended. Administer hydrocortisone IV or IM initially for the treatment of severe respiratory conditions or those compromising the airway.
    Intramuscular or Intravenous dosage (hydrocortisone sodium succinate injection):
    Infants, Children, and Adolescents: 0.56 to 8 mg/kg/day or 20 to 240 mg/m2/day IM or IV given in 3 to 4 divided dose is the FDA-approved general dosage range. Adjust according to patient response.

    For the prevention of chronic lung disease (CLD)* in mechanically ventilated patients:
    Intravenous dosage:
    Premature neonates: 0.5 mg/kg/dose IV every 12 hours for 9-12 days followed by 0.25 mg/kg/day IV every 12 hours for 3 days started within the first 48 hours of life has been studied (combined n from 3 studies = 450, birth weight 500-1249 g). The rate of survival without chronic lung disease (CLD) was significantly increased in 2 studies in patients receiving hydrocortisone compared to those receiving placebo. Although the largest study (n = 360) did not find a significantly increased rate of survival without CLD in the overall study group, the rate of survival without CLD was significantly improved in a subset of patients receiving hydrocortisone who were exposed to chorioamnionitis. This study was terminated early due to a higher incidence of intestinal perforation in patients receiving hydrocortisone and indomethacin (vs. indomethacin plus placebo). The American Academy of Pediatrics states that hydrocortisone at a dose of 1 mg/kg/day IV given for the first 2 weeks of life may increase the rate of survival without CLD, especially in neonates delivered in a setting of prenatal inflammation, without adverse effects on neurodevelopment.

    For the treatment of corticosteroid-responsive ophthalmic disorders, including allergic conjunctivitis (not controlled topically), allergic marginal corneal ulcer, anterior segment inflammation, chorioretinitis, herpes zoster ocular infection (herpes zoster ophthalmicus), iritis, keratitis, optic neuritis, diffuse posterior uveitis and choroiditis, or sympathetic ophthalmia:
    Oral dosage:
    Infants, Children, and Adolescents: A general dose range of 0.56-8 mg/kg/day or 16-240 mg/m2/day PO given in 3-4 divided doses has been recommended. Adjust according to patient response.
    Intramuscular or Intravenous dosage:
    Infants, Children, and Adolescents: 0.56-8 mg/kg/day or 20-240 mg/m2/day IM or IV given in 3-4 divided dose is the FDA-approved general dosage range. Adjust according to patient response.

    For the treatment of hypercalcemia associated with cancer:
    Intramuscular or Intravenous dosage (hydrocortisone sodium succinate injection):
    Infants, Children, and Adolescents: 0.56 to 8 mg/kg/day or 20 to 240 mg/m2/day IM or IV given in 3 to 4 divided dose is the FDA-approved general dosage range. Adjust according to patient response.

    For the treatment of refractory neonatal hypoglycemia*:
    Intravenous or Oral dosage:
    Neonates: 5 mg/kg/day IV or PO given in 2 divided doses has been recommended in patients not responding to glucose infusions of 12 to 15 mg/kg/minute.

    For the treatment of fulminating or disseminated pulmonary tuberculosis infection or tuberculosis meningitis with subarachnoid block or impending block in conjunction with appropriate antituberculosis therapy:
    Oral dosage:
    Infants, Children, and Adolescents: A general dose range of 0.56-8 mg/kg/day or 16-240 mg/m2/day PO given in 3-4 divided doses has been recommended. Adjust according to patient response.
    Intramuscular or Intravenous dosage:
    Infants, Children, and Adolescents: 0.56-8 mg/kg/day or 20-240 mg/m2/day IM or IV given in 3-4 divided dose is the FDA-approved general dosage range. Adjust according to patient response.

    For the treatment of neurologic or myocardial involvement associated with trichinosis:
    Oral dosage:
    Infants, Children, and Adolescents: A general dose range of 0.56-8 mg/kg/day or 16-240 mg/m2/day PO given in 3-4 divided doses has been recommended. Adjust according to patient response.
    Intramuscular or Intravenous dosage:
    Infants, Children, and Adolescents: 0.56-8 mg/kg/day or 20-240 mg/m2/day IM or IV given in 3-4 divided dose is the FDA-approved general dosage range. Adjust according to patient response.

    For the treatment of nonsuppurative thyroiditis:
    Oral dosage:
    Infants, Children, and Adolescents: A general dose range of 0.56 to 8 mg/kg/day or 16 to 240 mg/m2/day PO given in 3 to 4 divided doses has been recommended. Adjust according to patient response.
    Intramuscular or Intravenous dosage (hydrocortisone sodium succinate injection):
    Infants, Children, and Adolescents: 0.56 to 8 mg/kg/day or 20 to 240 mg/m2/day IM or IV given in 3 to 4 divided dose is the FDA-approved general dosage range. Adjust according to patient response.

    For the systemic treatment of severe inflammatory dermatoses, like severe exfoliative dermatitis, erythema multiforme, Stevens-Johnson syndrome, or psoriasis unresponsive to topical treatment:
    Intramuscular or Intravenous dosage (hydrocortisone sodium succinate):
    Infants, Children, and Adolescents: 0.56 to 8 mg/kg/day or 20 to 240 mg/m2/day IM or IV given in 3 to 4 divided dose is the FDA-approved general dosage range. Adjust according to patient response.
    Oral dosage:
    Infants, Children, and Adolescents: A general dose range of 0.56 to 8 mg/kg/day or 16 to 240 mg/m2/day PO given in 3 to 4 divided doses has been recommended. Adjust according to patient response.

    For asthma exacerbation:
    Oral dosage:
    Children 6 to 11 years: Usual dose is 1 to 2 mg/kg/day PO (Max: 40 mg/day), given in divided doses. A 3 to 5-day course is usually sufficient for most pediatric patients. Titrate to patient response up to 8 mg/kg/day, given in divided doses. Administer hydrocortisone IV or IM initially for the treatment of severe respiratory conditions or those compromising the airway. Although prednisone, prednisolone, or methylprednisolone are the systemic corticosteroids of choice, other corticosteroids such as hydrocortisone, given in equipotent daily doses are likely to be as effective.
    Children and Adolescents 12 years and older: Usual pediatric dose is 1 to 2 mg/kg/day PO (Adult Usual: 200 mg/day), given in divided doses. A 3 to 5-day course is usually sufficient. FDA-approved Dose Range: 20 to 240 mg/day PO, given in 2 to 4 divided doses. Titrate to patient response. Administer hydrocortisone IV or IM initially for the treatment of severe respiratory conditions or those compromising the airway. Although prednisone, prednisolone, or methylprednisolone are the systemic corticosteroids of choice, other corticosteroids such as hydrocortisone, given in equipotent daily doses are likely to be as effective.
    Intravenous or Intramuscular dosage (hydrocortisone sodium succinate injection):
    Infants and Children: 0.56 to 8 mg/kg/day or 20 to 240 mg/m2/day IM or IV given in 3 to 4 divided dose is the FDA-approved general dosage range. Adjust according to patient response. A 3 to 5-day course of corticosteroids is usually sufficient for most pediatric patients. An initial dose of 6 mg/kg IV followed by 8 to 10 mg/kg/day IV given in 4 divided doses for 1 to 2 days was used in 2 studies (age 2 months to 11 years) of pediatric patients with acute asthma. Although prednisone, prednisolone, or methylprednisolone are the systemic corticosteroids of choice for the management of moderate to severe asthma exacerbations, other corticosteroids such as hydrocortisone, given in equipotent daily doses are likely to be as effective.
    Adolescents: 0.56 to 8 mg/kg/day or 20 to 240 mg/m2/day IM or IV given in 3 to 4 divided dose is the FDA-approved general dosage range. Adjust according to patient response. A 3 to 5-day course of corticosteroids is usually sufficient for most pediatric patients. Although prednisone, prednisolone, or methylprednisolone are the systemic corticosteroids of choice for the management of moderate to severe asthma exacerbations, other corticosteroids such as hydrocortisone, given in equipotent daily doses are likely to be as effective.

    Maximum Dosage Limits:
    Corticosteroid dosage must be individualized and is highly variable depending on the nature and severity of the disease, route of administration, and patient response.

    Patients with Hepatic Impairment Dosing
    Systemic dosage may need adjustment depending on the degree of hepatic insufficiency, but quantitative recommendations are not available.

    Patients with Renal Impairment Dosing
    Specific guidelines for dosage adjustments in renal impairment are not available; it appears that no dosage adjustments are needed.

    *non-FDA-approved indication

    Monograph content under development

    Mechanism of Action: Endogenous corticosteroids are secreted by the adrenal cortex, and their effects are believed to be due to enzyme modification rather than to a direct hormone-induced action. Corticosteroids are loosely classified into two categories, mineralocorticoids and glucocorticoids, depending on their primary pharmacological activity. Mineralocorticoids alter electrolyte and fluid balance by facilitating sodium resorption and hydrogen and potassium excretion at the level of the distal renal tubule, resulting in edema and hypertension. Glucocorticoids exert some mineralocorticoid effects but are also involved in a number of other metabolic pathways including regulation of protein, carbohydrate, lipid, and nucleic acid metabolism; maintenance of cardiac and vascular response to vasoconstrictors; regulation of extracellular water and promotion of free water excretion; suppression of the inflammatory response; lowering of capillary permeability; and modulation of central nervous system processing and behavior. Hydrocortisone possesses both mineralocorticoid actions and glucocorticoid actions.

    Glucocorticoids prevent or suppress inflammation and immune responses when administered at pharmacological doses. At the molecular level, unbound glucocorticoids readily cross cell membranes and bind with high affinity to specific cytoplasmic receptors. This binding induces a response by modifying transcription and, ultimately, protein synthesis to achieve the steroid's intended action. Such actions can include: inhibition of leukocyte infiltration at the site of inflammation, interference in the function of mediators of inflammatory response, and suppression of humoral immune responses. Some of the net effects include reduction in edema or scar tissue and a general suppression in immune response. The anti-inflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, collectively called lipocortins. Lipocortins, in turn, control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes by inhibiting the release of the precursor molecule arachidonic acid. The degree of clinical effect and the numerous adverse effects related to corticosteroid use usually depend on the dose administered and the duration of therapy.

    Early anti-inflammatory effects of topical corticosteroids include the inhibition of macrophage and leukocyte movement and activity in the inflamed area by reversing vascular dilation and permeability. Later inflammatory processes such as capillary production, collagen deposition, and keloid (scar) formation also are inhibited by corticosteroids. Clinically, these actions correspond to decreased edema, erythema, pruritus, plaque formation and scaling of the affected skin.

    In the treatment of asthma, corticosteroids block the late phase allergic response to allergens. Mediators involved in the pathogenesis of asthma include histamine, leukotrienes (slow releasing substance of anaphylaxis, SRS-A), eosinophil chemotactic factor of anaphylaxis (ECF-A), neutrophil chemotactic factor (NCF), cytokines, hydroxyeicosatetraenoic acids, prostaglandin-generating factor of anaphylaxis (PGF-A), prostaglandins, major basic protein, bradykinin, adenosine, peroxides, and superoxide anions. Different cell types are responsible for release of these mediators including airway epithelium, eosinophils, basophils, lung parenchyma, lymphocytes, macrophages, mast cells, neutrophils, and platelets. Corticosteroids inhibit the release of these mediators as well as inhibit IgE synthesis, attenuate mucous secretion and eicosanoid generation, up-regulate beta-receptors, promote vasoconstriction, and suppress inflammatory cell influx and inflammatory processes. Clinical effects in asthma include a reduction in bronchial hyperresponsiveness to allergens, a decreased number of asthma exacerbations, and an improvement in FEV1, peak-flow rate, and respiratory symptoms. Since corticosteroid effects take several hours to days to become clinically noticeable, they are ineffective for primary treatment of severe acute bronchospastic attacks or for status asthmaticus.

    Pharmacokinetics: Hydrocortisone is administered via oral, parenteral, topical, and rectal routes. Circulating drug binds extensively to plasma proteins (92% to 93%), and only the unbound portion of a dose is active. Systemic hydrocortisone is quickly distributed into the kidneys, intestines, skin, liver, and muscle. Systemic hydrocortisone is metabolized by the liver to inactive metabolites. These inactive metabolites, as well as a small portion of unchanged drug, are excreted in the urine. The biological half-life of hydrocortisone is 8 to 12 hours.

    Affected cytochrome P450 isoenzymes: none


    -Route-Specific Pharmacokinetics
    Oral Route
    Hydrocortisone is rapidly absorbed after an oral dose with an absolute bioavailability of 96% in adult subjects. Peak effects occur within 1 to 2 hours.

    Intravenous Route
    Peak effects of hydrocortisone after IV administration occur within 1 hour. Excretion of the dose is nearly complete within 12 hours.

    Intramuscular Route
    After intramuscular administration of hydrocortisone, the onset and duration of action depend on the type of injection and the extent of the local blood supply.

    Topical Route
    Systemic absorption after topical application of hydrocortisone is dependant on the vehicle, the state of the skin at the application site, the use of occlusive dressings, and the age of the patient. Absorption is increased in areas that have skin damage, inflammation, or where the stratum corneum is thin such as the eyelids, genitalia, and face. Factors that can increase systemic absorption of topical hydrocortisone include occlusive dressings, large surface area, frequent application, longer duration of treatment, increased humidity or temperature, and younger age. In a study of pediatric patients (n = 38, age 1 month to 14.4 years) with mild, moderate, or severe atopic or seborrheic dermatitis percutaneous absorption of hydrocortisone cream, assessed by the maximum post-application serum cortisol, was significantly higher in patients younger than 18 months of age and in patients with severe disease.

    Other Route(s)
    Rectal Route
    When a suppository containing hydrocortisone acetate is administered rectally, about 26% of a dose is absorbed in normal subjects; absorption may vary across abraded or inflamed surfaces. Hydrocortisone rectal suspension is partially absorbed after rectal administration. In patients with ulcerative colitis, up to 50% of hydrocortisone was absorbed when administered as the rectal suspension.

    Intra-articular Route
    The onset and duration of action depend on type of hydrocortisone injection and the extent of the local blood supply.


    -Special Populations
    Pediatrics
    Neonates
    The half-life of hydrocortisone is prolonged in premature (8 to 12 hours) and term (4 hours) neonates compared to adults (1.7 to 2.1 hours).

    Children and Adolescents
    Cortisol clearance was significantly increased in pubertal patients (n = 20, age 10.6 to 16.8 years) compared to prepubertal (n = 14, age 6.1 to 11 years) and postpubertal patients (n = 6, age 17.2 to 20.3 years) with congenital adrenal hyperplasia. Volume of distribution was higher in pubertal patients compared to prepubertal and postpubertal patients; however, only the difference between pubertal and prepubertal patients reached statistical significance. The mean clearance and volume distribution of free cortisol after a single dose of hydrocortisone 15 mg/m2 IV were 4,787.7 mL/minute and 540.7 L, respectively, in the pubertal group. Mean clearance in the prepubertal and postpubertal groups was 2,477.4 mL/minute and 3,001.8 mL/minute, respectively; mean volume of distribution in these 2 groups was 237 L and 276.6 L, respectively. There were no significant differences in half-life between the 3 groups (mean half-life 67.2 minutes, 77.1 minutes, and 62.5 minutes in the prepubertal, pubertal, and postpubertal groups, respectively).

    Hepatic Impairment
    The metabolic clearance of corticosteroids, such as hydrocortisone, is decreased in patients with hepatic disease, such as cirrhosis.

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