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Medication Safety Issues
Sound-alike/look-alike issues:
Dexamethasone may be confused with desoximetasone, dextroamphetamine
Decadron® may be confused with Percodan®
Maxidex® may be confused with Maxzide®
Pronunciation
(deks a METH a sone)
U.S. Brand Names
Index Terms
Generic Available
Yes: Excludes ophthalmic suspension
Canadian Brand Names
Pharmacologic Category
Pharmacologic Category Synonyms
Use: Labeled Indications
Systemic: Primarily as an anti-inflammatory or immunosuppressant agent in the treatment of a variety of diseases including those of allergic, dermatologic, endocrine, hematologic, inflammatory, neoplastic, nervous system, renal, respiratory, rheumatic, and autoimmune origin; may be used in management of cerebral edema, septic shock, chronic swelling, as a diagnostic agent, diagnosis of Cushing's syndrome, antiemetic
Ophthalmic: Treatment of palpebral and bulbar conjunctivitis; corneal injury from chemical, radiation, thermal burns, or foreign body penetration
Otic: Treatment of inflammation of external auditory meatus; treatment of edema associated with infective otitis externa
Use: Dental
Treatment of a variety of oral diseases of allergic, inflammatory or autoimmune origin
Use: Unlabeled/Investigational
Dexamethasone suppression test: General indicator consistent with depression and/or suicide
Pregnancy Risk Factor
C
Pregnancy Considerations
Adverse events have been observed with corticosteroids in animal reproduction studies. Dexamethasone crosses the placenta; and is partially metabolized to an inactive metabolite by placental enzymes. Due to its positive effect on stimulating fetal lung maturation, the injection is often used in patients with premature labor (24-34 weeks gestation). Some studies have shown an association between first trimester systemic corticosteroid use and oral clefts; adverse events in the fetus/neonate have been noted in case reports following large doses of systemic corticosteroids during pregnancy. Women exposed to dexamethasone during pregnancy for the treatment of an autoimmune disease may contact the OTIS Autoimmune Diseases Study at 877-311-8972.
Lactation
Excretion in breast milk unknown/use caution
Breast-Feeding Considerations
Corticosteroids are excreted in human milk; information specific to dexamethasone has not been located.
Contraindications
Hypersensitivity to dexamethasone or any component of the formulation; systemic fungal infections, cerebral malaria; ophthalmic use in viral (active ocular herpes simplex), fungal, or tuberculosis diseases of the eye
Warnings/Precautions
Concerns related to adverse effects:
• Adrenal suppression: May cause hypercorticism or suppression of hypothalamic-pituitary-adrenal (HPA) axis, particularly in younger children or in patients receiving high doses for prolonged periods. HPA axis suppression may lead to adrenal crisis. Withdrawal and discontinuation of a corticosteroid should be done slowly and carefully. Particular care is required when patients are transferred from systemic corticosteroids to inhaled products due to possible adrenal insufficiency or withdrawal from steroids, including an increase in allergic symptoms. Patients receiving >20 mg per day of prednisone (or equivalent) may be most susceptible. Fatalities have occurred due to adrenal insufficiency in asthmatic patients during and after transfer from systemic corticosteroids to aerosol steroids; aerosol steroids do not provide the systemic steroid needed to treat patients having trauma, surgery, or infections.
• Immunosuppression: Prolonged use of corticosteroids may also increase the incidence of secondary infection, mask acute infection (including fungal infections), prolong or exacerbate viral infections, or limit response to vaccines. Exposure to chickenpox should be avoided; corticosteroids should not be used to treat ocular herpes simplex. Corticosteroids should not be used for cerebral malaria or viral hepatitis. Close observation is required in patients with latent tuberculosis and/or TB reactivity; restrict use in active TB (only in conjunction with antituberculosis treatment).
• Kaposi's sarcoma: Prolonged treatment with corticosteroids has been associated with the development of Kaposi's sarcoma (case reports); if noted, discontinuation of therapy should be considered.
• Myopathy: Acute myopathy has been reported with high dose corticosteroids, usually in patients with neuromuscular transmission disorders; may involve ocular and/or respiratory muscles; monitor creatine kinase; recovery may be delayed.
• Psychiatric disturbances: Corticosteroid use may cause psychiatric disturbances, including depression, euphoria, insomnia, mood swings, and personality changes. Pre-existing psychiatric conditions may be exacerbated by corticosteroid use.
Disease-related concerns:
• Adrenal insufficiency: Dexamethasone does not provide adequate mineralocorticoid activity in adrenal insufficiency (may be employed as a single dose while cortisol assays are performed). The lowest possible dose should be used during treatment; discontinuation and/or dose reductions should be gradual.
• Cardiovascular disease: Use with caution in patients with HF; long-term use has been associated with fluid retention and hypertension.
• Diabetes: Use with caution in patients with diabetes mellitus; may alter glucose production/regulation leading to hyperglycemia.
• Gastrointestinal disease: Use with caution in patients with GI diseases (diverticulitis, peptic ulcer, ulcerative colitis) due to perforation risk.
• Hepatic impairment: Use with caution in patients with hepatic impairment, including cirrhosis; long-term use has been associated with fluid retention.
• Myasthenia gravis: Use with caution in patients with myasthenia gravis; exacerbation of symptoms has occurred especially during initial treatment with corticosteroids.
• Myocardial infarction (MI): Use with caution following acute MI; corticosteroids have been associated with myocardial rupture.
• Ocular disease: Use with caution in patients with cataracts and/or glaucoma; increased intraocular pressure, open-angle glaucoma, and cataracts have occurred with prolonged use. Consider routine eye exams in chronic users.
• Osteoporosis: Use with caution in patients with osteoporosis; high doses and/or long-term use of corticosteroids have been associated with increased bone loss and osteoporotic fractures.
• Renal impairment: Use with caution in patients with renal impairment; fluid retention may occur.
• Seizure disorders: Use with caution in patients with a history of seizure disorder; seizures have been reported with adrenal crisis.
• Thyroid disease: Changes in thyroid status may necessitate dosage adjustments; metabolic clearance of corticosteroids increases in hyperthyroid patients and decreases in hypothyroid ones.
Special populations:
• Elderly: Because of the risk of adverse effects, systemic corticosteroids should be used cautiously in the elderly in the smallest possible effective dose for the shortest duration.
• Pediatrics: May affect growth velocity; growth should be routinely monitored in pediatric patients.
Other warnings/precautions:
• Discontinuation of therapy: Withdraw therapy with gradual tapering of dose.
Adverse Reactions
Frequency not defined.
Cardiovascular: Arrhythmia, bradycardia, cardiac arrest, cardiomyopathy, CHF, circulatory collapse, edema, hypertension, myocardial rupture (post-MI), syncope, thromboembolism, vasculitis
Central nervous system: Depression, emotional instability, euphoria, headache, intracranial pressure increased, insomnia, malaise, mood swings, neuritis, personality changes, pseudotumor cerebri (usually following discontinuation), psychic disorders, seizure, vertigo
Dermatologic: Acne, allergic dermatitis, alopecia, angioedema, bruising, dry skin, erythema, fragile skin, hirsutism, hyper-/hypopigmentation, hypertrichosis, perianal pruritus (following I.V. injection), petechiae, rash, skin atrophy, skin test reaction impaired, striae, urticaria, wound healing impaired
Endocrine & metabolic: Adrenal suppression, carbohydrate tolerance decreased, Cushing's syndrome, diabetes mellitus, glucose intolerance decreased, growth suppression (children), hyperglycemia, hypokalemic alkalosis, menstrual irregularities, negative nitrogen balance, pituitary-adrenal axis suppression, protein catabolism, sodium retention
Gastrointestinal: Abdominal distention, appetite increased, gastrointestinal hemorrhage, gastrointestinal perforation, nausea, pancreatitis, peptic ulcer, ulcerative esophagitis, weight gain
Genitourinary: Altered (increased or decreased) spermatogenesis
Hepatic: Hepatomegaly, transaminases increased
Local: Postinjection flare (intra-articular use), thrombophlebitis
Neuromuscular & skeletal: Arthropathy, aseptic necrosis (femoral and humoral heads), fractures, muscle mass loss, myopathy (particularly in conjunction with neuromuscular disease or neuromuscular-blocking agents), neuropathy, osteoporosis, parasthesia, tendon rupture, vertebral compression fractures, weakness
Ocular: Cataracts, exophthalmos, glaucoma, intraocular pressure increased
Renal: Glucosuria
Respiratory: Pulmonary edema
Miscellaneous: Abnormal fat deposition, anaphylactoid reaction, anaphylaxis, avascular necrosis, diaphoresis, hiccups, hypersensitivity, impaired wound healing, infections, Kaposi's sarcoma, moon face, secondary malignancy
Metabolism/Transport Effects
Substrate of CYP3A4 (major); Induces CYP2A6 (weak), 2B6 (weak), 2C8 (weak), 2C9 (weak), 3A4 (strong)
Drug Interactions
Acetylcholinesterase Inhibitors: Corticosteroids (Systemic) may enhance the adverse/toxic effect of Acetylcholinesterase Inhibitors. Increased muscular weakness may occur. Risk C: Monitor therapy
Aminoglutethimide: May increase the metabolism of Corticosteroids (Systemic). Risk C: Monitor therapy
Amphotericin B: Corticosteroids (Systemic) may enhance the hypokalemic effect of Amphotericin B. Risk C: Monitor therapy
Antacids: May decrease the bioavailability of Corticosteroids (Oral). Risk D: Consider therapy modification
Antidiabetic Agents: Corticosteroids (Systemic) may diminish the hypoglycemic effect of Antidiabetic Agents. In some instances, corticosteroid-mediated HPA axis suppression has led to episodes of acute adrenal crisis, which may manifest as enhanced hypoglycemia, particularly in the setting of insulin or other antidiabetic agent use. Risk C: Monitor therapy
Antifungal Agents (Azole Derivatives, Systemic): May decrease the metabolism of Corticosteroids (Systemic). Risk C: Monitor therapy
Aprepitant: May increase the serum concentration of Corticosteroids (Systemic). Risk D: Consider therapy modification
Barbiturates: May increase the metabolism of Corticosteroids (Systemic). Risk C: Monitor therapy
Bile Acid Sequestrants: May decrease the absorption of Corticosteroids (Oral). Risk C: Monitor therapy
Calcitriol: Corticosteroids (Systemic) may diminish the therapeutic effect of Calcitriol. Risk C: Monitor therapy
Calcium Channel Blockers (Nondihydropyridine): May decrease the metabolism of Corticosteroids (Systemic). Risk C: Monitor therapy
Caspofungin: Inducers of Drug Clearance may decrease the serum concentration of Caspofungin. Management: Consider using an increased caspofungin dose of 70mg daily in adults (or 70mg/m2, up to a maximum of 70mg, daily in pediatric patients) when coadministered with known inducers of drug clearance. Risk D: Consider therapy modification
Corticorelin: Corticosteroids may diminish the therapeutic effect of Corticorelin. Specifically, the plasma ACTH response to corticorelin may be blunted by recent or current corticosteroid therapy. Risk C: Monitor therapy
CycloSPORINE: Corticosteroids (Systemic) may increase the serum concentration of CycloSPORINE. CycloSPORINE may increase the serum concentration of Corticosteroids (Systemic). Risk C: Monitor therapy
CYP3A4 Inducers (Strong): May increase the metabolism of CYP3A4 Substrates. Risk C: Monitor therapy
CYP3A4 Inhibitors (Moderate): May decrease the metabolism of CYP3A4 Substrates. Risk C: Monitor therapy
CYP3A4 Inhibitors (Strong): May decrease the metabolism of CYP3A4 Substrates. Risk D: Consider therapy modification
CYP3A4 Substrates: CYP3A4 Inducers (Strong) may increase the metabolism of CYP3A4 Substrates. Risk C: Monitor therapy
Dabigatran Etexilate: P-Glycoprotein Inducers may decrease the serum concentration of Dabigatran Etexilate. Risk C: Monitor therapy
Echinacea: May diminish the therapeutic effect of Immunosuppressants. Risk D: Consider therapy modification
Estrogen Derivatives: May increase the serum concentration of Corticosteroids (Systemic). Risk C: Monitor therapy
Fluconazole: May decrease the metabolism of Corticosteroids (Systemic). Risk C: Monitor therapy
Fosaprepitant: May increase the serum concentration of Corticosteroids (Systemic). The active metabolite aprepitant is likely responsible for this effect. Risk D: Consider therapy modification
Herbs (CYP3A4 Inducers): May increase the metabolism of CYP3A4 Substrates. Risk C: Monitor therapy
Isoniazid: Corticosteroids (Systemic) may decrease the serum concentration of Isoniazid. Risk C: Monitor therapy
Lenalidomide: Dexamethasone may enhance the thrombogenic effect of Lenalidomide. Risk D: Consider therapy modification
Loop Diuretics: Corticosteroids (Systemic) may enhance the hypokalemic effect of Loop Diuretics. Risk C: Monitor therapy
Macrolide Antibiotics: May decrease the metabolism of Corticosteroids (Systemic). Exceptions: Azithromycin; Dirithromycin [Off Market]; Spiramycin. Risk D: Consider therapy modification
Maraviroc: CYP3A4 Inducers may decrease the serum concentration of Maraviroc. Risk D: Consider therapy modification
Natalizumab: Immunosuppressants may enhance the adverse/toxic effect of Natalizumab. Specifically, the risk of concurrent infection may be increased. Risk X: Avoid combination
Neuromuscular-Blocking Agents (Nondepolarizing): May enhance the adverse/toxic effect of Corticosteroids (Systemic). Increased muscle weakness, possibly progressing to polyneuropathies and myopathies, may occur. Risk D: Consider therapy modification
Nilotinib: CYP3A4 Inducers (Strong) may decrease the serum concentration of Nilotinib. Risk X: Avoid combination
Nisoldipine: CYP3A4 Inducers (Strong) may decrease the serum concentration of Nisoldipine. Risk X: Avoid combination
NSAID (COX-2 Inhibitor): Corticosteroids (Systemic) may enhance the adverse/toxic effect of NSAID (COX-2 Inhibitor). Risk C: Monitor therapy
NSAID (Nonselective): Corticosteroids (Systemic) may enhance the adverse/toxic effect of NSAID (Nonselective). Risk C: Monitor therapy
P-Glycoprotein Inducers: May decrease the serum concentration of P-Glycoprotein Substrates. P-glycoprotein inducers may also further limit the distribution of p-glycoprotein substrates to specific cells/tissues/organs where p-glycoprotein is present in large amounts (e.g., brain, T-lymphocytes, testes, etc.). Risk C: Monitor therapy
P-Glycoprotein Inhibitors: May increase the serum concentration of P-Glycoprotein Substrates. P-glycoprotein inhibitors may also enhance the distribution of p-glycoprotein substrates to specific cells/tissues/organs where p-glycoprotein is present in large amounts (e.g., brain, T-lymphocytes, testes, etc.). Risk C: Monitor therapy
P-Glycoprotein Substrates: P-Glycoprotein Inducers may decrease the serum concentration of P-Glycoprotein Substrates. P-glycoprotein inducers may also further limit the distribution of p-glycoprotein substrates to specific cells/tissues/organs where p-glycoprotein is present in large amounts (e.g., brain, T-lymphocytes, testes, etc.). Risk C: Monitor therapy
Primidone: May increase the metabolism of Corticosteroids (Systemic). Risk C: Monitor therapy
Quinolone Antibiotics: May enhance the adverse/toxic effect of Corticosteroids (Systemic). Risk of tendon-related side effects, including tendonitis and rupture, may be enhanced. Risk C: Monitor therapy
Ranolazine: CYP3A4 Inducers (Strong) may decrease the serum concentration of Ranolazine. Risk X: Avoid combination
Rifamycin Derivatives: May increase the metabolism of Corticosteroids (Systemic). Risk C: Monitor therapy
Salicylates: May enhance the adverse/toxic effect of Corticosteroids (Systemic). These specifically include gastrointestinal ulceration and bleeding. Corticosteroids (Systemic) may decrease the serum concentration of Salicylates. Withdrawal of corticosteroids may result in salicylate toxicity. Risk C: Monitor therapy
Sorafenib: CYP3A4 Inducers (Strong) may decrease the serum concentration of Sorafenib. Risk D: Consider therapy modification
Thalidomide: Dexamethasone may enhance the dermatologic adverse effect of Thalidomide. Dexamethasone may enhance the thrombogenic effect of Thalidomide. Risk D: Consider therapy modification
Thiazide Diuretics: Corticosteroids (Systemic) may enhance the hypokalemic effect of Thiazide Diuretics. Risk C: Monitor therapy
Trastuzumab: May enhance the neutropenic effect of Immunosuppressants. Risk C: Monitor therapy
Vaccines (Inactivated): Immunosuppressants may diminish the therapeutic effect of Vaccines (Inactivated). Risk C: Monitor therapy
Vaccines (Live): Immunosuppressants may enhance the adverse/toxic effect of Vaccines (Live). Vaccinal infections may develop. Immunosuppressants may also decrease therapeutic response to vaccines. Risk X: Avoid combination
Warfarin: Corticosteroids (Systemic) may enhance the anticoagulant effect of Warfarin. Risk C: Monitor therapy
Ethanol/Nutrition/Herb Interactions
Ethanol: Avoid ethanol (may enhance gastric mucosal irritation).
Food: Dexamethasone interferes with calcium absorption. Limit caffeine.
Herb/Nutraceutical: Avoid cat's claw, echinacea (have immunostimulant properties).
Storage
Injection solution: Store at room temperature; protect from light and freezing.
Stability of injection of parenteral admixture at room temperature (25°C): 24 hours.
Stability of injection of parenteral admixture at refrigeration temperature (4°C): 2 days; protect from light and freezing.
Reconstitution
Injection should be diluted in 50-100 mL NS or D5W.
Compatibility
Stable in D5W, NS.
Y-site administration: Compatible: Acyclovir, allopurinol, amifostine, amikacin, amphotericin B cholesteryl sulfate complex, amsacrine, aztreonam, cefepime, cefpirome, cisatracurium, cisplatin, cladribine, cyclophosphamide, cytarabine, docetaxel, doxorubicin, doxorubicin liposome, etoposide phosphate, famotidine, filgrastim, fluconazole, fludarabine, foscarnet, gatifloxacin, gemcitabine, granisetron, heparin, heparin with hydrocortisone sodium succinate, levofloxacin, linezolid, lorazepam, melphalan, meperidine, meropenem, morphine, ondansetron, paclitaxel, piperacillin/tazobactam, potassium chloride, propofol, remifentanil, sargramostim, sodium bicarbonate, sufentanil, tacrolimus, teniposide, theophylline, thiotepa, vinorelbine, vitamin B complex with C, zidovudine. Incompatible: Ciprofloxacin, idarubicin, midazolam, topotecan. Variable (consult detailed reference): Methotrexate.
Compatibility in syringe: Compatible: Granisetron, metoclopramide, palonosetron, ranitidine, sufentanil. Incompatible: Doxapram, glycopyrrolate. Variable (consult detailed reference): Diphenhydramine, hydromorphone, ondansetron.
Compatibility when admixed: Compatible: Aminophylline, bleomycin, cimetidine, floxacillin, furosemide, granisetron, lidocaine, meropenem, mitomycin, nafcillin, netilmicin, ondansetron, palonosetron, prochlorperazine edisylate, ranitidine, verapamil. Incompatible: Daunorubicin, diphenhydramine with lorazepam and metoclopramide, metaraminol, vancomycin. Variable (consult detailed reference): Amikacin.
Mechanism of Action
Decreases inflammation by suppression of neutrophil migration, decreased production of inflammatory mediators, and reversal of increased capillary permeability; suppresses normal immune response. Dexamethasone's mechanism of antiemetic activity is unknown.
Pharmacodynamics/Kinetics
Onset of action: Acetate: Prompt
Duration of metabolic effect: 72 hours; acetate is a long-acting repository preparation
Metabolism: Hepatic
Half-life elimination: Normal renal function: 1.8-3.5 hours; Biological half-life: 36-54 hours
Time to peak, serum: Oral: 1-2 hours; I.M.: ?8 hours
Excretion: Urine and feces
Dosage
Refer to individual protocols.
Children:
Antiemetic (prior to chemotherapy): I.V.: 10 mg/m2 (initial dose) followed by 5 mg/m2 every 6 hours as needed or 5-20 mg given 15-30 minutes before treatment
Anti-inflammatory immunosuppressant: Oral, I.M., I.V.: 0.08-0.3 mg/kg/day or 2.5-10 mg/m2/day in divided doses every 6-12 hours
Extubation or airway edema: Oral, I.M., I.V.: 0.5-2 mg/kg/day in divided doses every 6 hours beginning 24 hours prior to extubation and continuing for 4-6 doses afterwards
Cerebral edema: I.V.: Loading dose: 1-2 mg/kg/dose as a single dose; maintenance: 1-1.5 mg/kg/day (maximum: 16 mg/day) in divided doses every 4-6 hours, taper off over 1-6 weeks
Bacterial meningitis in infants and children >2 months: I.V.: 0.6 mg/kg/day in 4 divided doses every 6 hours for the first 4 days of antibiotic treatment; start dexamethasone at the time of the first dose of antibiotic
Physiologic replacement: Oral, I.M., I.V.: 0.03-0.15 mg/kg/day or 0.6-0.75 mg/m2/day in divided doses every 6-12 hours
Adults:
Antiemetic:
Prophylaxis: Oral, I.V.: 10-20 mg 15-30 minutes before treatment on each treatment day
Continuous infusion regimen: Oral or I.V.: 10 mg every 12 hours on each treatment day
Mildly emetogenic therapy: Oral, I.M., I.V.: 4 mg every 4-6 hours
Delayed nausea/vomiting: Oral: 4-10 mg 1-2 times/day for 2-4 days or
8 mg every 12 hours for 2 days; then
4 mg every 12 hours for 2 days or
20 mg 1 hour before chemotherapy; then
10 mg 12 hours after chemotherapy; then
8 mg every 12 hours for 4 doses; then
4 mg every 12 hours for 4 doses
Anti-inflammatory:
Oral, I.M., I.V. (injections should be given as sodium phosphate): 0.75-9 mg/day in divided doses every 6-12 hours
Intra-articular, intralesional, or soft tissue (as sodium phosphate): 0.4-6 mg/day
Ophthalmic:
Solution: Instill 1-2 drops into conjunctival sac every hour during the day and every other hour during the night; gradually reduce dose to every 3-4 hours, then to 3-4 times/day
Suspension: Instill 1-2 drops into conjunctival sac up to 4-6 times per day; may use hourly in severe disease; taper prior to discontinuation
Otic: Instill 3-4 drops 2-3 times a day; reduce dose gradually prior to discontinuation
Multiple myeloma: Oral, I.V.: 40 mg/day, days 1 to 4, 9 to 12, and 17 to 20, repeated every 4 weeks (alone or as part of a regimen)
Cerebral edema: I.V. 10 mg stat, 4 mg I.M./I.V. every 6 hours until response is maximized, then switch to oral regimen, then taper off if appropriate; dosage may be reduced after 24 days and gradually discontinued over 5-7 days
Extubation or airway edema: Oral, I.M., I.V. (injections should be given as sodium phosphate): 0.5-2 mg/kg/day in divided doses every 6 hours beginning 24 hours prior to extubation and continuing for 4-6 doses afterwards
Dexamethasone suppression test (depression/suicide indicator) (unlabeled use): Oral: 1 mg at 11 PM, draw blood at 8 AM the following day for plasma cortisol determination
Cushing's syndrome, diagnostic: Oral: 1 mg at 11 PM, draw blood at 8 AM; greater accuracy for Cushing's syndrome may be achieved by the following:
Dexamethasone 0.5 mg by mouth every 6 hours for 48 hours (with 24-hour urine collection for 17-hydroxycorticosteroid excretion)
Differentiation of Cushing's syndrome due to ACTH excess from Cushing's due to other causes: Oral: Dexamethasone 2 mg every 6 hours for 48 hours (with 24-hour urine collection for 17-hydroxycorticosteroid excretion)
Multiple sclerosis (acute exacerbation): 30 mg/day for 1 week, followed by 4-12 mg/day for 1 month
Physiological replacement: Oral, I.M., I.V. (should be given as sodium phosphate): 0.03-0.15 mg/kg/day or 0.6-0.75 mg/m2/day in divided doses every 6-12 hours
Treatment of shock:
Addisonian crisis/shock (ie, adrenal insufficiency/responsive to steroid therapy): I.V. (given as sodium phosphate): 4-10 mg as a single dose, which may be repeated if necessary
Unresponsive shock (ie, unresponsive to steroid therapy): I.V. (given as sodium phosphate): 1-6 mg/kg as a single I.V. dose or up to 40 mg initially followed by repeat doses every 2-6 hours while shock persists
Hemodialysis: Supplemental dose is not necessary
Peritoneal dialysis: Supplemental dose is not necessary
Dosage: Combination Regimens
Leukemia, acute lymphocytic:
Hyper-CVAD + Imatinib
Hyper-CVAD (Leukemia, Acute Lymphocytic)
TVTG
VAD/CVAD
Leukemia, acute myeloid: TVTG
Lymphoma, non-Hodgkin's:
DHAP
Hyper - CVAD (Lymphoma, non-Hodgkin's)
m-BACOD
Lymphoma, non-Hodgkin's (Mantle cell): Hyper-CVAD + Rituximab
Multiple myeloma:
Bortezomib-Dexamethasone
Bortezomib-Doxorubicin-Dexamethasone
Bortezomib-Doxorubicin (Liposomal)-Dexamethasone
DTPACE
Doxorubicin (Liposomal) - Vincristine - Dexamethasone
Hyper - CVAD (Multiple Myeloma)
Lenalidomide-Dexamethasone
Lenalidomide-Dexamethasone (Low Dose)
Thalidomide-Dexamethasone
VAD
Prostate cancer: Cyclophosphamide + Vincristine + Dexamethasone
Administration: Oral
Administer oral formulation with meals to decrease GI upset.
Administration: I.V.
Administer as a 5-10 minute bolus; rapid injection is associated with a high incidence of perineal discomfort.
Administration: Topical
Topical formulation is for external use. Do not use on open wounds.
Administration: Other
Ophthalmic: Remove soft contact lenses prior to using solutions containing benzalkonium chloride. Do not touch tip of container to eye.
Otic: Use ophthalmic solution for otic administration. Instill directly into aural canal or may pack canal with gauze saturated with solution. Keep wick moist and remove after 12-24 hours.
Administration: I.V. Detail
pH: 7.0-8.5
Monitoring Parameters
Hemoglobin, occult blood loss, serum potassium, and glucose; intraocular pressure (with use >6 weeks)
Reference Range
Dexamethasone suppression test, overnight: 8 AM cortisol <6 mcg/100 mL (dexamethasone 1 mg); plasma cortisol determination should be made on the day after giving dose
Dietary Considerations
May be taken with meals to decrease GI upset. May need diet with increased potassium, pyridoxine, vitamin C, vitamin D, folate, calcium, and phosphorus.
Patient Education
Do not take any new medication during therapy unless approved by prescriber. Take exactly as directed, do not increase dose or discontinue abruptly without consulting prescriber.
Oral: Take with or after meals. Avoid alcohol and limit intake of caffeine or stimulants. Prescriber may recommend increased dietary vitamins, minerals, or iron. If you have diabetes, monitor glucose levels closely (antidiabetic medication may need to be adjusted). Inform prescriber if you are experiencing greater-than-normal levels of stress (medication may need adjustment). You may be more susceptible to infection (avoid crowds and persons with contagious or infective conditions and do not have any vaccinations unless approved by prescriber). Some forms of this medication may cause GI upset (small frequent meals and frequent mouth care may help). Report promptly excessive nervousness or sleep disturbances; signs of infection (eg, sore throat, unhealed injuries); excessive growth of body hair or loss of skin color; vision changes; excessive or sudden weight gain (>3 lb/week); swelling of face or extremities; respiratory difficulty; muscle weakness; tarry stool, persistent abdominal pain; worsening of condition or failure to improve. Pregnancy/breast-feeding precautions: Inform prescriber if you are or intend to become pregnant. Consult prescriber if breast-feeding.
Ophthalmic: For use in eyes only. Wash hands before using. Lie down or tilt your head back and look upward. Put drops of suspension or solution inside lower eyelid. Close eye and roll eyeball in all directions. Do not blink for 1/2 minute. Apply gentle pressure to inner corner of eye for 30 seconds. Do not use any other eye preparation for at least 10 minutes. Do not let tip of applicator touch eye; do not contaminate tip of applicator (may cause eye infection, eye damage, or vision loss). Do not share medication with anyone else. Wear sunglasses when in sunlight; you may be more sensitive to bright light. Inform prescriber if condition worsens, fails to improve, or if you experience eye pain, disturbances of vision, or other adverse eye response.
Geriatric Considerations
Because of the risk of adverse effects, systemic corticosteroids should be used cautiously in the elderly in the smallest possible dose, and for the shortest possible time.
Additional Information
Effects of inhaled/intranasal steroids on growth have been observed in the absence of laboratory evidence of HPA axis suppression, suggesting that growth velocity is a more sensitive indicator of systemic corticosteroid exposure in pediatric patients than some commonly used tests of HPA axis function. The long-term effects of this reduction in growth velocity associated with orally-inhaled and intranasal corticosteroids, including the impact on final adult height, are unknown. The potential for “catch up” growth following discontinuation of treatment with inhaled corticosteroids has not been adequately studied.
Withdrawal/tapering of therapy: Corticosteroid tapering following short-term use is limited primarily by the need to control the underlying disease state; tapering may be accomplished over a period of days. Following longer-term use, tapering over weeks to months may be necessary to avoid signs and symptoms of adrenal insufficiency and to allow recovery of the HPA axis. Testing of HPA axis responsiveness may be of value in selected patients. Subtle deficits in HPA response may persist for months after discontinuation of therapy, and may require supplemental dosing during periods of acute illness or surgical stress.
Anesthesia and Critical Care Concerns/Other Considerations
Dexamethasone is a long-acting corticosteroid with minimal sodium-retaining potential. Corticosteroids and muscle relaxants appear to trigger some types of ICU myopathy; avoid or administer at the lowest dose possible.
Patients will often have steroid-induced adverse effects on glucose tolerance and lipid profiles. In discontinuing steroid therapy in patients on long-term steroid supplementation, it is important that the steroid therapy be discontinued gradually. Abrupt withdrawal may result in adrenal insufficiency with hypotension and hyperkalemia. Patients on long-term steroid supplementation will require higher corticosteroid doses when subject to stress (ie, trauma, surgery, severe infection).
Oral and intravenous steroid therapy in patients with heart failure should be administered cautiously with special attention given to signs and symptoms of fluid retention.
The 2008 Surviving Sepsis Campaign guidelines recommend doses of corticosteroids comparable to >300 mg hydrocortisone daily not be used in severe sepsis or septic shock for the purpose of treating septic shock (Grade 1A). They also recommend corticosteroids not be administered for the treatment of sepsis in the absence of shock. There is, however, no contraindication to continuing maintenance steroid therapy or to using stress dose steroids if the patient's endocrine or corticosteroid administration history warrants (Grade 1D).
Cardiovascular Considerations
Oral and intravenous steroid therapy in patients with heart failure should be administered cautiously with special attention given to signs and symptoms of fluid retention. Avoid use in acute myocardial infarction; may cause wall rupture.
Although glucocorticoids can provide relief from pericarditis postmyocardial infarctions, these drugs may cause thinning of the developing scar and myocardial rupture.
Dental Health: Effects on Dental Treatment
No significant effects or complications reported
Dental Health: Vasoconstrictor/Local Anesthetic Precautions
No information available to require special precautions
Mental Health: Effects on Mental Status
Insomnia and nervousness are common; may cause euphoria, confusion, or hallucinations
Mental Health: Effects on Psychiatric Treatment
Barbiturates and carbamazepine may decrease dexamethasone effects
Nursing: Physical Assessment/Monitoring
Assess potential for interactions with other prescriptions, OTC medications, or herbal products patient may be taking. Assess results of laboratory tests, therapeutic response, and adverse effects, according to indications for therapy, dose, route, and duration of therapy. When used for long-term therapy (>10-14 days), do not discontinue abruptly; decrease dosage incrementally. With systemic administration, caution patients with diabetes to monitor glucose levels closely (corticosteroids may alter glucose levels). Teach patient proper use (according to formulation), side effects/appropriate interventions, and symptoms to report.
Oncology: Emetic Potential
Very low (<10%); may cause nausea/indigestion if taken orally on an empty stomach
Oncology: Vesicant
No
Dosage Forms
Excipient information presented when available (limited, particularly for generics); consult specific product labeling.
Elixir, as base: 0.5 mg/5 mL (240 mL)
Injection, solution, as sodium phosphate: 4 mg/mL (1 mL, 5 mL, 30 mL); 10 mg/mL (10 mL)
Injection, solution, as sodium phosphate [preservative free]: 10 mg/mL (1 mL)
Solution, ophthalmic, as sodium phosphate [drops]: 0.1% (5 mL)
Solution, oral: 0.5 mg/5 mL (500 mL)
Solution, oral [concentrate]:
Dexamethasone Intensol™: 1 mg/mL (30 mL) [dye free, sugar free; contains alcohol 30% and propylene glycol]
Suspension, ophthalmic [drops]:
Maxidex®: 0.1% (5 mL) [contains benzalkonium chloride]
Tablet [scored]: 0.5 mg, 0.75 mg, 1 mg, 1.5 mg, 2 mg, 4 mg, 6 mg
DexPak® 10 Day TaperPak®: 1.5 mg [35 tablets on taper dose card]
DexPak® TaperPak®: 1.5 mg [51 tablets on taper dose card]
Pricing: U.S. (www.drugstore.com)
Elixir (Dexamethasone)
0.5 mg/5 mL (120): $47.70
Solution (Dexamethasone Sodium Phosphate)
0.1% (5): $19.99
4 mg/mL (25): $41.99
Suspension (Maxidex)
0.1% (5): $45.08
0.1% (15): $86.99
Tablets (Dexamethasone)
1 mg (30): $19.99
2 mg (30): $21.99
6 mg (30): $22.99
References
American Academy of Pediatrics Committee on Infectious Diseases, “Dexamethasone Therapy for Bacterial Meningitis in Infants and Children,” Pediatrics, 1990, 86(1):130-3.
Bahal N and Nahata MC, “The Role of Corticosteroids in Infants and Children With Bacterial Meningitis,” DICP, 1991, 25(5):542-5.
Brophy TR, McCafferty J, Tyrer JH, et al, “Bioavailability of Oral Dexamethasone During High Dose Steroid Therapy in Neurological Patients,” Eur J Clin Pharmacol, 1983, 24(1):103-8.
Committee on Obstetric Practice, “ACOG Committee Opinion: Antenatal Corticosteroid Therapy for Fetal Maturation,” Obstet Gynecol, 2002, 99(5 Pt 1):871-3.
Coryell WH, “Clinical Assessment of Suicide Risk in Depressive Disorder,” CNS Spectr, 2006, 11(6):455-61.
Couser RJ, Ferrara TB, Falde B, et al, “Effectiveness of Dexamethasone in Preventing Extubation Failure in Preterm Infants at Increased Risk for Airway Edema,” J Pediatr, 1992, 121(4):591-6.
Dellinger RP, Levy MM, Carlet JM, et al, “Surviving Sepsis Campaign: International Guidelines for Management of Severe Sepsis and Septic Shock: 2008,” Intensive Care Med, 2008, 34(1): 17-60. Available at http://www.survivingsepsis.org/system/files/images/2008_20International_20SSC_20Guidelines_1_.pdf
de los Reyes RA, Ausman JI, and Diaz FG, “Agents for Cerebral Edema,” Clin Neurosurg, 1981, 28:98-107.
“Dexamethasone, Granisetron, or Both for the Prevention of Nausea and Vomiting During Chemotherapy for Cancer. The Italian Group for Antiemetic Research,” N Engl J Med, 1995, 332(1):1-5.
Duggan DE, Matalia N, Ditzler, CA, et al, “Bioavailability of Oral Dexamethasone,” Clin Pharmacol Ther, 1975, 18(2):205-9.
Durand M, Sardesai S, and McEvoy C, “Effects of Early Dexamethasone Therapy on Pulmonary Mechanics and Chronic Lung Disease in Very Low Birth Weight Infants: A Randomized, Controlled Trial,” Pediatrics, 1995, 95(4):584-90.
Goedert JJ, Vitale F, Lauria C, et al, “Risk Factors for Classical Kaposi's Sarcoma,” J Natl Cancer Inst, 2002, 94(22):1712-8.
Kyle RA and Rajkumar SV, “Multiple Myeloma,” N Engl J Med, 2004, 351(18): 1860-73.
Kris MG, Baltzer L, Pisters KM, et al, “Enhancing the Effectiveness of the Specific Serotonin Antagonists. Combination Antiemetic Therapy With Dexamethasone,” Cancer, 1993, 72(11 Suppl):3436-42.
Latreille J, Stewart D, Laberge F, et al, “Dexamethasone Improves the Efficacy of Granisetron in the First 24 h Following High-Dose Cisplatin Chemotherapy,” Support Care Cancer, 1995, 3(5):307-12.
Mann JJ, Currier D, Stanley B, et al, “Can Biological Tests Assist Prediction of Suicide in Mood Disorders?” Int J Neuropsychopharmacol, 2006, 9(4):465-74.
McDonnell M and Evans N, “Upper and Lower Gastrointestinal Complications With Dexamethasone Despite H2 Antagonists,” J Paediatr Child Health, 1995, 31(2):152-4.
McGee S and Hirschmann J, “Use of Corticosteroids in Treating Infectious Diseases,” Arch Intern Med, 2008, 168(10):1034-46.
Ng PC, “The Effectiveness and Side Effects of Dexamethasone in Preterm Infants With Bronchopulmonary Dysplasia,” Arch Dis Child, 1993, 68(3 Spec No):330-6.
Ostensen M, “Optimisation of Antirheumatic Drug Treatment in Pregnancy,” Clin Pharmacokinet, 1994, 27(6):486-503.
Peterson C, Hursti TJ, Borjeson S, et al, “Single High-Dose Dexamethasone Improves the Effect of Ondansetron on Acute Chemotherapy-Induced Nausea and Vomiting But Impairs the Control of Delayed Symptoms,” Support Care Cancer, 1996, 4(6):440-6.
Pradat P, Robert-Gnansia E, Di Tanna GL, et al, “First Trimester Exposure to Corticosteroids and Oral Clefts,” Birth Defects Res A Clin Mol Teratol, 2003, 67(12):968-70.
Randin D, Vollenweider P, Tappy L, et al, “Suppression of Alcohol-Induced Hypertension by Dexamethasone,” N Engl J Med, 1995, 332(26):1733-7.
Ruvinsky ED, Douvas SG, Roberts WE, et al, “Maternal Administration of Dexamethasone in Severe Pregnancy-Induced Hypertension,” Am J Obstet Gynecol, 1984, 149(7):722-6.
Trissel LA and Zhang Y, “Compatibility and Stability of Aloxi (Palonosetron Hydrochloride) Admixed With Dexamethasone Sodium Phosphate,” Intl J Pharm Compounding, 2004, 8(5):398-403.
Wald ER, Kaplan SL, and Mason, EO Jr, “Dexamethasone Therapy for Children With Bacterial Meningitis,” Pediatrics, 1995, 95(1):21-8.
Yerevanian BI, Feusner JD, Koek RJ, et al, “The Dexamethasone Suppression Test as a Predictor of Suicidal Behavior in Unipolar Depression,” J Affect Disord, 2004, 83(2-3):103-8.
International Brand Names
Lexi-Comp.com
Last full review/revision September 2008
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