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Mechanism of Action
US Drug Names
Initially, 0.75 to 9 mg/day PO, given in 2 to 4 divided doses. Adjust according to patient response. NOTE: Parenteral therapy may be needed in acute insufficiency. Hydrocortisone and cortisone are preferred for these conditions; dexamethasone has no mineralocorticoid properties. Dosages required may be variable.
0.15 to 0.375 mg/m2/day PO once daily has been recommended for patients with congenital adrenal hyperplasia.  Although most experts recommend hydrocortisone as first-line treatment of adrenal insufficiency in pediatric patients whose linear growth is incomplete due to a lower incidence of growth suppression, other authors have stated that dexamethasone may be used safely with close monitoring and individualization of dose based on growth, bone age, and hormone levels. Liquid formulations of dexamethasone are recommended for more precise titration of doses.  0.02 to 0.3 mg/kg/day or 0.6 to 9 mg/m2/day PO given in 3 to 4 divided doses is the FDA-approved general dosage range. Parenteral therapy may be needed in acute insufficiency.
Initially, 0.5 to 9 mg/day IV or IM, divided every 6 to 12 hours. Adjust according to patient response. NOTE: Hydrocortisone and cortisone are preferred for these conditions; dexamethasone has no mineralocorticoid properties. Dosages required may be variable.
0.02 to 0.3 mg/kg/day or 0.6 to 9 mg/m2/day IV or IM given in 3 to 4 divided doses is the FDA-approved general dosage range.  Adjust according to patient response.
0.5 mg/kg/dose IV (Maximum: 10 mg/dose IV) every 6 hours for 6 doses with the first dose given 6 to 12 hours prior to extubation has been studied with mixed results.  One prospective, randomized study (n = 153) found no significant difference in the risk of postextubation stridor, the average number of racemic epinephrine treatments, or the number of patients requiring reintubation in patients receiving dexamethasone compared to those receiving placebo. Another prospective, randomized study (n = 66) found that dexamethasone-treated patients had a significantly lower rate of postextubation stridor at 10 minutes, 6 hours, and 12 hours but not 24 hours and fewer patients requiring epinephrine or reintubation compared to placebo-treated patients. A systematic review of clinical trials of dexamethasone for the prevention of postextubation stridor concluded that therapy may be beneficial in high-risk patients, such as those with underlying airway anomalies or multiple airway manipulations.
Various regimens have been used. 0.25 mg/kg/dose IV every 8 hours for 3 doses with the first dose given approximately 4 hours prior to scheduled extubation was studied in a prospective, randomized trial in 50 premature neonates (mean gestational age, 27.7 to 28.7 weeks) who were at high risk for airway edema. The rate of postextubation stridor and reintubation was significantly lower in the dexamethasone group compared to the placebo group. A systematic review of clinical trials of dexamethasone for the prevention of extubation failure recommends therapy be reserved for use in high risk neonates, such as those with repeated or prolonged intubations, due to a lack of benefit in low risk neonates and the risk of adverse effects. Use preservative-free products for administration to neonates when possible.
10 mg IV or IM as a single dose, followed by 4 mg IV or IM every 6 hours, until symptoms subside, then reduce dosage. A response should be seen within 12 to 24 hours, and a gradual dose reduction begun after 2 to 4 days, reducing over another 5 to 7 days. Replace with oral dosage as soon as possible. For palliative maintenance therapy when oral therapy is not feasible, 2 mg IM or IV can be given 2 to 3 times per day, if needed. Use is not a substitute for neurosurgical evaluation and definitive management such as neurosurgery, etc.
For cerebral edema, 1 to 3 mg PO three times daily, can follow parenteral therapy; then, taper off over a period of 5 to 7 days. For palliative management of recurrent or inoperable brain tumors, maintenance with 2 mg PO given 2 or 3 times daily may be effective.
A bolus of 8 to 10 mg dexamethasone (or equivalent) PO or IV, followed by 16 mg/day PO (usually in twice-daily to four-times-daily doses for tolerance) is a typical dose; doses are adjusted to patient condition and are either maintained or tapered over a few weeks dependent on radiation therapy cycles and/or anticipated surgery. A broad dosage range of 16 to 100 mg/day has been used depending on the presence of paraparesis, etc. Higher quality data are needed to establish the benefits vs. risks and optimal dose and duration of therapy. Experts generally agree that patients who have neurologic deficits should receive dexamethasone; many patients with MSCC require corticosteroids to help preserve neurologic function, such as ambulation. 
0.15 mg/kg/dose IV every 6 hours for 2 to 4 days; the first dose should be given 10 to 20 minutes before or concomitantly with the first dose of antimicrobial agent. The Infectious Diseases Society of America (IDSA) recommends dexamethasone for the treatment of proven or suspected pneumococcal meningitis due to S. pneumoniae. The IDSA suggests dexamethasone in these patients may reduce neuronal injury mediated by proinflammatory cytokine expression. Adjunctive dexamethasone should not be administered to patients who have already received antimicrobial therapy as this is unlikely to improve patient outcome. The IDSA does not routinely recommend dexamethasone as adjunctive therapy for meningitis caused by any other bacterial pathogens. For the treatment of tuberculous (TB) meningitis, use doses for adjunctive treatment of TB.
0.15 mg/kg/dose IV every 6 hours for 2 to 4 days is recommended by the Infectious Diseases Society of America (IDSA) for the treatment of meningitis due to H. influenzae type B; administer the first dose 10 to 20 minutes before or concomitantly with the first dose of antimicrobial agent. The IDSA suggests dexamethasone in these patients may reduce hearing impairment and neuronal injury mediated by proinflammatory cytokine expression. Do not administer adjunctive dexamethasone to patients who have already received antimicrobial therapy as this is unlikely to improve patient outcome. The IDSA and the American Academy of Pediatrics (AAP) do not recommend routine dexamethasone as adjunctive therapy for meningitis caused by bacterial pathogens other than H. influenzae type B in pediatric patients. The use of dexamethasone in pneumococcal meningitis (S. pneumoniae) is controversial and may be considered in patients older than 6 weeks of age after weighing the possible benefits and risks.
The Infectious Diseases Society of America (IDSA) does not recommend adjunctive steroid therapy for neonates with bacterial meningitis due to insufficient data.
0.15 mg/kg/dose PO every 6 hours for 2 to 4 days; the first dose should be given 10 to 20 minutes before or concomitantly with the first dose of antimicrobial agent. The Infectious Diseases Society of America (IDSA) recommends dexamethasone for the treatment of proven or suspected pneumococcal meningitis due to S. pneumoniae. The IDSA suggests dexamethasone in these patients may reduce neuronal injury mediated by proinflammatory cytokine expression. Adjunctive dexamethasone should not be administered to patients who have already received antimicrobial therapy as this is unlikely to improve patient outcome. The IDSA does not routinely recommend dexamethasone as adjunctive therapy for meningitis caused by any other bacterial pathogens. For the treatment of tuberculous (TB) meningitis, use doses for adjunctive treatment of TB.
0.15 mg/kg/dose PO every 6 hours for 2 to 4 days is recommended by the Infectious Diseases Society of America (IDSA) for the treatment of meningitis due to H. influenzae type B; administer the first dose 10 to 20 minutes before or concomitantly with the first dose of antimicrobial agent. The IDSA suggests dexamethasone in these patients may reduce hearing impairment and neuronal injury mediated by proinflammatory cytokine expression. Do not administer adjunctive dexamethasone to patients who have already received antimicrobial therapy as this is unlikely to improve patient outcome. The IDSA and the American Academy of Pediatrics (AAP) do not recommend routine dexamethasone as adjunctive therapy for meningitis caused by bacterial pathogens other than H. influenzae type B in pediatric patients. The use of dexamethasone in pneumococcal meningitis (S. pneumoniae) is controversial and may be considered in patients older than 6 weeks of age after weighing the possible benefits and risks.
Initially, 0.5 to 9 mg/day IV or IM, in divided doses. Adjust according to patient response. Renal transplant guidelines recommend corticosteroids for the initial treatment of acute rejection. 
0.06 to 0.3 mg/kg/day or 1.2 to 10 mg/m2/day IM or IV in divided doses every 6 to 12 hours. Renal transplant guidelines recommend corticosteroids for the initial treatment of acute rejection. 
Instill 3 or 4 drops (ophthalmic solution) into the aural canal 2 to 3 times per day. When a favorable response is obtained, reduce dosage gradually and eventually discontinue. If preferred, the aural canal may be packed with a gauze wick saturated with solution. Keep the wick moist with solution and remove from the ear after 12 to 24 hours. May repeat as needed at the discretion of the prescriber. There is no specific otic solution preparation; use ophthalmic solution. Used for steroid responsive inflammatory conditions of the external auditory meatus, such as allergic otitis externa, selected purulent and nonpurulent infective otitis externa when the hazard of steroid use is accepted to decrease edema and inflammation.
American Society of Clinical Oncology (ASCO) guideline-based dosage regimens are stratified according to patient risk. HIGHLY EMETOGENIC CHEMOTHERAPY: 12 mg PO or IV prior to chemotherapy, then 8 mg PO or IV on days 2 to 3 or days 2 to 4. If an NK1 receptor antagonist is not included in the anti-emetic regimen, increase to dexamethasone 20 mg PO or IV prior to chemotherapy, then 16 mg PO or IV on days 2 to 3 or days 2 to 4. MODERATELY EMETOGENIC CHEMOTHERAPY: 8 mg PO or IV prior to chemotherapy, then 8 mg PO or IV on days 2 and 3. LOW EMOTOGENIC RISK CHEMOTHERAPY: 8 mg PO or IV as a single dose prior to chemotherapy. (NOTE: Other regimens have been used historically during chemotherapy - e.g., 10 to 20 mg IV before administration of chemotherapy, with additional, lower doses given for 24 to 72 hours, as needed).
10 to 14 mg/m2/dose IV is usually used prior to chemotherapy. A 5-HT3 antagonist is usually given along with dexamethasone for highly-emetogenic chemotherapy. An example regimen: dexamethasone 10 mg/m2/dose IV once daily, along with ondansetron. Some patients receive repeat dexamethasone every 12 hours, either IV or PO, but optimal regimens for repeat dosing are not established. For chemotherapy that is less emetogenic, doses as low as 6 mg/m2/dose PO have been given. The optimal dose of steroids for chemotherapy-induced nausea/vomiting (CINV) in children is not determined, and there are safety considerations. 
Initially, 0.75 to 9 mg/day PO, given in 2 to 4 divided doses. Adjust according to patient response.
0.02 to 0.3 mg/kg/day or 0.6 to 9 mg/m2/day PO given in 3 to 4 divided doses is the FDA-approved general dosage range. Adjust according to patient response.
Initially, 0.5 to 9 mg/day IV or IM, in 2 to 4 divided doses. Adjust maintenance dosage according to patient response.
Dosage ranges from 2 to 4 mg for large joints and 0.8 to 1 mg for small joints. Injection into intervertebral joints should not be attempted at any time and hip joint injection cannot be recommended as an office procedure. Intrasynovial should be employed only when affected areas are limited to 1 or 2 sites. May repeat from once every 3 to 5 days to once every 2 to 3 weeks.
The 4 mg/mL injection strength may be used for intralesional and soft tissue administration. Doses range from 0.2 mg to 4 mg injected as a single dose at the appropriate site. For soft tissue and bursal injections a dose of 2 to 4 mg is recommended. Ganglia require a dose of 1 to 2 mg. A dose of 0.4 to 1 mg is used for injection into tendon sheaths. Usually employed when condition to be treated is limited to 1 or 2 sites. Dosage dependent upon degree of inflammation, size, disease state, and location of affected area. Repeat doses may be given from once every 3 to 5 days to once every 2 to 3 weeks.
Initially, 0.75 to 9 mg/day PO, given in 2 to 4 divided doses. For many conditions, the dosing of corticosteroids is highly variable. Adjust according to patient response. In an open study of 10 patients with ITP, pulse dosing produced a sustained improvement in platelet count with a total daily dose of 40 mg/day PO for 4 consecutive days out of each 28 day cycle for 6 consecutive cycles.
Initially, 0.5 to 9 mg/day IV or IM, given in 2 to 4 divided doses. For many conditions, the dosing of corticosteroids is highly variable. Adjust according to patient response.
Initially, 0.75 to 9 mg/day PO, given in 2 to 4 divided doses. Dosage of corticosteroids can be highly variable, depending on patient condition. Adjust according to patient response.
0.02 to 0.3 mg/kg/day or 0.6 to 9 mg/m2/day PO given in 3 to 4 divided doses is the FDA-approved general dosage range. Adjust according to patient response. Administer dexamethasone IV or IM initially for the treatment of severe respiratory conditions or those compromising the airway.
Initially, 0.5 to 9 mg/day IV or IM, in 2 to 4 divided doses. Dosage of corticosteroids can be highly variable, depending on patient condition. Adjust according to patient response.
0.02 to 0.3 mg/kg/day or 0.6 to 9 mg/m2/day IV or IM given in 3 to 4 divided doses is the FDA-approved general dosage range.  Adjust according to patient response. Administer dexamethasone IV or IM initially for the treatment of severe respiratory conditions or those compromising the airway.
Initially, 0.5 to 9 mg/day IV or IM, in 2 to 4 divided doses. Adjust according to patient response.
0.06 to 0.3 mg/kg/day or 1.2 to 10 mg/m2/day IV or IM, in divided doses every 6 to 12 hours.
0.6 mg/kg/dose PO, IV, or IM (Max: 8 to 20 mg/dose depending on study) as a single dose is the most commonly used regimen; however, lower doses of 0.15 mg/kg/dose PO, IV, or IM (Max: 3 mg/dose) have been shown to have similar efficacy.    
Initially, 0.75 to 9 mg/day PO, given in 2 to 4 divided doses. Adjust according to patient response. Use of dexamethasone for longer than 2 days may increase the potential for metabolic side effects. Use parenteral dexamethasone dosage for severe respiratory conditions or those compromising the airway. Although prednisone, prednisolone, or methylprednisolone are the systemic corticosteroids of choice for the management of moderate to severe asthma exacerbations, other corticosteroids such as dexamethasone, given in equipotent daily doses are likely to be as effective.
0.6 mg/kg/dose PO as a single dose or once daily for 2 days. Max: 16 mg/dose.     Administer dexamethasone IV or IM initially for the treatment of severe respiratory conditions or those compromising the airway. Single or 2-day regimens of dexamethasone have shown similar efficacy, less vomiting, and improved compliance when compared to a 5-day course of oral prednisone or prednisolone.    Use of dexamethasone for longer than 2 days may increase the potential for metabolic side effects. Although prednisone, prednisolone, or methylprednisolone are the systemic corticosteroids of choice for the management of moderate to severe asthma exacerbations, other corticosteroids such as dexamethasone, given in equipotent daily doses are likely to be as effective. Of note, 0.02 to 0.3 mg/kg/day or 0.6 to 9 mg/m2/day PO given in 3 to 4 divided doses is the FDA-approved initial dosage range for dexamethasone; however, this is significantly lower than the range used in clinical practice.
Initially, 0.5 to 9 mg/day IV or IM, in 2 to 4 divided doses. Adjust according to patient response. Use of dexamethasone for longer than 2 days may increase the potential for metabolic side effects. Although prednisone, prednisolone, or methylprednisolone are the systemic corticosteroids of choice for the management of moderate to severe asthma exacerbations, other corticosteroids such as dexamethasone, given in equipotent daily doses are likely to be as effective.
0.6 mg/kg/dose IV or IM as a single dose or once daily for 2 days. Max: 16 mg/dose.   Single-dose regimens ranging from 0.3 to 1.7 mg/kg/dose have been reported. Max: 36 mg/dose. In a study of young children with moderate exacerbations, a single day regimen of parenteral dexamethasone resulted in similar efficacy as a 5-day course of oral prednisolone. Use of dexamethasone for longer than 2 days may increase the potential for metabolic side effects. Although prednisone, prednisolone, or methylprednisolone are the systemic corticosteroids of choice for the management of moderate to severe asthma exacerbations, other corticosteroids such as dexamethasone, given in equipotent daily doses are likely to be as effective. Of note, 0.5 to 9 mg per day IV or IM is the FDA-approved initial dosage range depending on the condition being treated; however, higher doses are sometimes used in clinical practice. 
6 mg IM every 12 hours for 4 doses in all pregnant women between 24 and 34 weeks gestation who are at risk for preterm delivery within 7 days. A single course of corticosteroids may also be considered starting at 23 weeks gestation for pregnant women who are at risk of preterm delivery within 7 days, regardless of membrane status. If labor is impending and further doses are unlikely, the first dose of dexamethasone should still be given because treatment with corticosteroids for less than 24 hours is still associated with a significant reduction in neonatal morbidity/mortality. However, no additional benefit has been demonstrated for courses of antenatal steroids with shorter dosage intervals than those recommended, often referred to as accelerated dosing, even when delivery is imminent. A repeat or rescue course of corticosteroids may be considered in women who are less than 34 weeks gestation, who are at risk of preterm delivery within the next 7 days, and whose prior course of antenatal corticosteroids was administered more than 14 days previously. Rescue course corticosteroids could be provided as early as 7 days from the prior dose if indicated by the clinical situation. Dexamethasone is comparable to betamethasone in preventing adverse outcomes and reducing neonatal intensive care unit (NICU) stays.
Numerous dosing schedules have been studied. The Dexamethasone: A Randomized Trial (DART) study (n = 70, median gestational age 25 weeks) used the following tapering dose schedule over 10 days: 0.075 mg/kg/dose IV twice daily for 3 days, 0.05 mg/kg/dose IV twice daily for 3 days, 0.025 mg/kg/dose IV twice daily for 2 days, and 0.01 mg/kg/dose IV twice daily for 2 days. This dosing regimen facilitated extubation by day 10 but did not significantly improve mortality or oxygen dependence at 36 weeks; follow-up at 2 years of age did not indicate any significant adverse neurodevelopmental outcomes in patients treated with dexamethasone.  Use is somewhat controversial, and most experts suggest using low doses and careful patient selection. The American Academy of Pediatrics (AAP) recommends against the use of high-dose dexamethasone (greater than 0.5 mg/kg/day) due to the risk of short- and long-term adverse effects, including neurodevelopmental effects. Late corticosteroid therapy (initiated after 7 days of age) may be preferred over early therapy (initiated at less than 7 days of age). Late therapy may reduce neonatal mortality without significantly increasing potential adverse long-term neurodevelopmental outcomes. 
Initially, 0.75 to 9 mg/day PO, given in 2 to 4 divided doses. For many conditions, the dosing of corticosteroids is highly variable. Adjust to patient response.
Initially, 0.75 to 9 mg/day PO, given in 2 to 4 divided doses. Adjust according to patient response until urine is protein-free, then slowly taper as indicated. Some patients may require long-term dosing.
Initially, 0.75 to 9 mg/day PO, given in 2 to 4 divided doses. Dosing can be quite variable, depending on the patient's condition. Adjust according to patient response.
Dosages vary depending upon the chemotherapy protocol. Common doses include 1.5 to 6 mg/m2/day PO for 8 to 21 days or 8 mg PO every 8 hours for 10 days.
6 to 10 mg/m2/day PO for 14 days as part of induction, consolidation, or intensification combination regimens.
0.02 to 0.3 mg/kg/day or 0.6 to 9 mg/m2/day PO given in 3 to 4 divided doses is the FDA-approved general dosage range ; however, doses may vary according to the specific protocol used.
Initially, 0.5 to 9 mg IV or IM daily; dose is dependent on the disease being treated and should be individualized based on patient response. Maintenance therapy may be given; use the lowest dose that produces an adequate response. Taper dexamethasone gradually in patients receiving parenteral therapy for more than a few days; do not abruptly stop treatment.
0.02 to 0.3 mg/kg/day or 0.6 to 9 mg/m2/day IV or IM given in 3 to 4 divided doses is the FDA-approved general dosage range  ; however, doses may vary according to the specific protocol used.
NOTE: Dexamethasone has been designated an orphan drug by the FDA for the treatment of multiple myeloma.
30 mg/day PO for 7 days, followed by doses of 4 to 12 mg PO every other day for 1 month have been shown to be effective. Controlled clinical trials have shown corticosteroids to be effective in speeding the resolution of acute exacerbations, they do not show that they affect the ultimate outcome or natural history of the disease.
Initially, 0.75 to 9 mg/day PO, given in 2 to 4 divided doses. 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. 
0.02 to 0.3 mg/kg/day or 0.6 to 9 mg/m2/day PO given in 3 to 4 divided doses 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. 
Initially, 0.5 to 9 mg/day IV or IM, in 2 to 4 divided doses. 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. 
0.02 to 0.3 mg/kg/day or 0.6 to 9 mg/m2/day IV or IM given in 3 to 4 divided doses 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. 
Instill 1 or 2 drops of 0.1% ophthalmic solution in the affected eye(s) every hour during the day and every 2 hours at night; reduce application to every 4 hours (while awake) once a favorable response occurs. Later, further reduction in dosage to 1 drop 3 or 4 times daily may suffice to control symptoms. The duration of treatment will vary with the type of lesion and may extend from a few days to several weeks, according to therapeutic response. Relapses, more common in chronic active lesions than in self-limited conditions, usually respond to treatment.
Instill 1 or 2 drops of 0.1% ophthalmic suspension in the affected eye(s). In severe disease, drops may be used hourly, being tapered to discontinuation as the inflammation subsides. In mild disease, drops may be used up to 4 to 6 times daily.
Initially, 0.75 to 9 mg/day PO, given in 2 to 4 divided doses. Adjust according to patient response.
Initially, 0.5 to 9 mg/day IV or IM, in 2 to 4 divided doses. Adjust according to patient response. 
Inject the implant (containing 0.7 mg dexamethasone in a solid polymer delivery system) intravitreally. Monitor the patient for elevated intraocular pressure and endophthalmitis. According to the American Diabetes Association (ADA), intravitreous steroid injections are considered second-line alternative treatment options for central-involved diabetic macular edema (CIDME). These drugs are rarely used as first-line treatment options, because when compared against intravitreal injections of anti-vascular endothelial growth factor (anti-VEGF) agents, steroid therapies are associated with inferior visual acuity outcomes and increased rate of cataracts and glaucoma.
Inject the implant (containing 0.7 mg dexamethasone in a solid polymer delivery system) intravitreally. Monitor the patient for elevated intraocular pressure and endophthalmitis.
4 mg PO, IV, or IM every 6 hours for the treatment of acute altitude sickness without high altitude cerebral edema (HACE) or 8 mg PO, IV, or IM once followed by 4 mg PO, IV, or IM every 6 hours for the treatment of HACE is recommended by clinical practice guidelines.  Descent is the preferred initial treatment. When descent is not possible or effective, symptomatic treatment (e.g., analgesics and antiemetics), oxygen, and other treatments, including dexamethasone, should be considered. Dexamethasone is more reliably effective than acetazolamide for acute altitude sickness of any degree, especially moderate to severe illness. Consideration can be given to adding acetazolamide for persons with HACE. Continue treatment until symptoms resolve. Of note, dexamethasone does not facilitate acclimatization.
0.15 mg/kg/dose PO, IV, or IM every 6 hours (Max: 4 mg/dose).  Descent is the preferred initial treatment, particularly for younger children and infants. When descent is not effective or not possible, dexamethasone is the preferred pharmacologic therapy, especially for moderate to severe disease. Symptomatic treatment (e.g., analgesics and antiemetics), oxygen, and other treatments, including acetazolamide, should also be considered. Dexamethasone does not facilitate acclimatization; advise patients to delay further ascent until they are asymptomatic off medication. If the drug is discontinued at altitude before acclimatization, rebound can occur. 
2 mg PO every 6 hours or 4 mg PO every 12 hours is recommended by clinical practice guidelines.  4 mg PO every 6 hours may be considered for very high risk situations necessitating immediate physical performance after being airlifted to high altitudes (e.g., military or search and rescue operations). Prophylactic medications should be considered in addition to slow ascent for moderate- to high-risk situations, and acetazolamide is preferred. Dexamethasone may be used in individuals with a history of intolerance or allergy to acetazolamide, or in emergency circumstances that require very rapid ascent, dexamethasone may be considered for concomitant use with acetazolamide. Start prophylaxis with dexamethasone the day of the ascent and continue prophylaxis for 2 to 3 days after reaching the target altitude or until descent is initiated. Duration of use should not exceed 10 days to prevent glucocorticoid toxicity or adrenal suppression.
0.5 mg PO once daily at bedtime, administered on cycle days 3 to 12, days 5 to 9, or starting on day 5 and continuing through conception, in combination with clomiphene (doses ranging from 50 to 200 mg/day) has been studied.   Alternatively, dexamethasone 2 mg PO once daily on cycle days 5 to 14 in combination with clomiphene 200 mg/day or dexamethasone 1 mg PO twice daily on cycle days 3 to 12 in combination with clomiphene 100 mg/day PO has also been studied; HCG was administered to augment ovulation.  Optimal timing and dose of dexamethasone is not clear and has varied from study to study. Combination therapy has been shown to increase ovulation rates (range, 75% to 100%) and pregnancy rates (range, 38% to 74%) in women with both normal and elevated DHEA-S concentrations and in those women with or without polycystic ovary syndrome (PCOS). A Cochrane's review indicates that dexamethasone-clomiphene combination is one of the few adjunctive therapies for infertility that has been shown to improve pregnancy rates (fixed OR 11.3, 95% CI 5.3 to 24; NNT 2.7, 95% CI 2.1 to 3.6) ; the 2 studies in this review used differing doses of 0.5 mg PO at bedtime on days 5 to 9 or 2 mg PO/day on days 5 to 14.  Several theories on the mechanism of dexamethasone in infertility exist. One theory is that dexamethasone enhances folliculogenesis by suppressing adrenal androgen hypersecretion, which should augment the actions of clomiphene. Dexamethasone may increase FSH concentrations thereby facilitating folliculogenesis. Finally, dexamethasone may decrease the elevated LH concentrations in patients with PCOS.
2 to 4 mg IV once for established post-operative nausea/vomiting (PONV), per treatment guidelines; readministration of longer-acting drugs, such as dexamethasone, is not recommended. If PONV prophylaxis was either inadequate or not initially given, dexamethasone is an appropriate rescue treatment option if not initially used for PONV prophylaxis. Of note, the 5-HT3 antagonists are the only class of drugs that have been adequately studied for the treatment of established PONV.
4 to 5 mg IV at anesthesia induction is recommended by treatment guidelines for patients at an increased risk for post-operative nausea and vomiting (PONV); administration at induction rather than at the end of surgery is preferred. Some studies suggest that 8 mg IV is associated with a dose-dependent increase in quality of recovery, including reduced fatigue, postoperative pain, and need for opioid analgesia; however, further confirmation is necessary before larger doses are universally recommend. Safety data regarding the perioperative use of dexamethasone point to a possible increased risk of wound infection and/or increased blood glucose in some patients. A single dexamethasone dose (4 to 8 mg IV) is, however, considered safe for PONV prophylaxis. For patients with labile glucose control, dexamethasone use is relatively contraindicated.
0.15 to 1 mg/kg/dose IV (Max: 8 to 25 mg/dose IV) given as a single intraoperative dose reduces the incidence of postoperative nausea/vomiting in the first 24 hours, improves postoperative pain control, and decreases the time to resumption of soft/solid diet without adverse effects and is recommended in patients undergoing tonsillectomy.  A lower dose of 0.015 mg/kg/dose (Max: 5 mg/dose) in combination with ondansetron 0.1 mg/kg/dose (Max: 4 mg) is recommended first-line for postoperative vomiting prophylaxis in children by the Society for Ambulatory Anesthesiology.
Due to the lack of consistent efficacy data and the high risk of adverse effects, the American Academy of Pediatrics does not recommend systemic corticosteroids for the management of bronchiolitis in any setting. However, other authors state corticosteroids may be beneficial in severely ill or mechanically ventilated patients. One randomized trial of 800 infants seen in the emergency department used 1 mg/kg PO once (Max: 10 mg/dose) followed by 0.6 mg/kg/dose PO once daily (Max: 10 mg/dose) for 5 days. Dexamethasone in combination with nebulized epinephrine was effective in reducing hospital admissions by day 7 of illness compared to treatment with dexamethasone alone, epinephrine alone, or placebo. In a study of 200 infants (median age 3.5 months) with an asthma risk, as determined by eczema or a family history of asthma in a first-degree relative, dexamethasone 1 mg/kg (single dose) PO then 0.6 mg/kg/dose PO once daily for 4 more days was administered with salbutamol. In infants receiving dexamethasone with salbutamol, the time to readiness for discharge was 18.6 hours vs. 27.1 hours in patients not receiving dexamethasone (p = 0.015). In contrast, 1 mg/kg/dose PO (Max: 12 mg/dose) given as a single dose did not reduce hospitalization rates, Respiratory Assessment Change Scores (RACS), length of hospitalization for those patients who required admission, or subsequent hospitalizations within 7 days compared to placebo in another large, randomized trial (n = 600).
Due to the lack of consistent efficacy data and the high risk of adverse effects, the American Academy of Pediatrics does not recommend systemic corticosteroids for the management of bronchiolitis in any setting. However, other authors state corticosteroids may be beneficial in severely ill or mechanically ventilated patients. 0.15 mg/kg/dose IV every 6 hours for 48 hours with the first dose administered within 24 hours of mechanical ventilation was used in patients with respiratory syncytial virus. In a post hoc analysis of patients with bronchiolitis (n = 39), the mean duration of mechanical ventilation and of supplemental oxygen were significantly shorter in patients receiving dexamethasone compared to those receiving placebo (4.9 and 7.7 days vs. 9.2 and 11.3 days, respectively); no differences were seen in the length of intensive care unit or hospital stay.
Systemic dosage may need adjustment depending on the degree of hepatic insufficiency, but quantitative recommendations are not available.
Specific guidelines for dosage adjustments in renal impairment are not available; it appears that no dosage adjustments are needed.
Dexamethasone and its derivatives, dexamethasone sodium phosphate and dexamethasone acetate, are synthetic glucocorticoids used as anti-inflammatory or immunosuppressive agents. Dexamethasone is available as oral, parenteral, as well as topical ophthalmic and intraocular dosage forms. Dexamethasone is used for many conditions in adult and pediatric patients, including cerebral edema, prevention of transplant rejection, and many allergic, dermatologic, ophthalmic, and systemic inflammatory conditions. Systemic dexamethasone is usually selected for the management of cerebral edema because of its superior ability to penetrate the CNS. Dexamethasone is also commonly used in antiemetic regimens for chemotherapy patients and is included in the American Society of Clinical Oncology (ASCO) guideline-based dosage regimens. In general, prednisone is more commonly prescribed as an oral corticosteroid when systemic treatment is needed for most conditions. Dexamethasone has little to no mineralocorticoid activity and is therefore not used by itself in the management of adrenal insufficiency. 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 side effects associated with chronic administration. Short courses of treatment may be used in the management of asthma exacerbations.
Updates for coronavirus disease 2019 (COVID-19):
The National Institutes of Health (NIH) COVID-19 treatment guidelines have released recommendations for the use of corticosteroids that are based on disease severity.
The World Health Organization strongly recommends the use of systemic corticosteroids, including dexamethasone, in patients with severe or critical COVID-19; but suggests against use in patients with non-severe COVID-19.
These recommendations are based on preliminary results from the Randomized Evaluation of COVID-19 Therapy (RECOVERY) trial. The RECOVERY trial is a multicenter, open-label study that found dexamethasone reduced deaths in patients with severe respiratory complications to COVID-19. When compared to patients receiving usual care alone (n = 4,321), treatment with dexamethasone (n = 2,104) reduced deaths in ventilated patients (29.3% vs. 41.4%; RR 0.64; 95% CI, 0.51 to 0.81) and in other patients receiving oxygen only (23.3% vs. 26.2%; RR 0.82; 95% CI, 0.72 to 0.94). No benefit was observed in patients not requiring respiratory support (17.8% vs. 14%; RR 1.19; 95% CI, 0.91 to 1.55). Overall, significantly fewer dexamethasone patients than usual care patients died within 28 days (22.9% vs. 25.7%; RR 0.83; 95% CI, 0.75 to 0.93; p less than 0.001). Another randomized, open-label, multicenter study compared the efficacy of dexamethasone plus standard care (n = 151) against standard care alone (n = 148) in adults on mechanical ventilation for COVID-19 induced acute respiratory distress syndrome (ARDS). The study's primary outcome of ventilator-free days during the first 28 days was significantly higher in the dexamethasone group (6.6 days vs. 4 days; difference, 2.26; 95% CI, 0.2 to 4.38; p = 0.4). Additionally, a secondary outcome of the mean Sequential Organ Failure Assessment (SOFA) score at day 7 was significantly lower in the dexamethasone group (6.1 vs. 7.5; difference, -1.16; 95% CI, -1.94 to -0.38; p = 0.004). There was no difference in the other secondary outcomes of 28-day all-cause mortality, clinical status at day 15, ICU-free days during the first 28 days, and mechanical ventilation duration at day 28.
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Dexamethasone Intensol (Oral Solution Concentrate)
Direct IV injection:
Intermittent or continuous IV infusion:
Intra-articular, Soft tissue, or Intralesional injection
Ophthalmic solution or suspension:
Dexycu Intraocular Suspension
Preparation of intraocular suspension:
Dextenza Ophthalmic Insert
Otic Administration of Ophthalmic Solution:
Intravitreal Implant Administration
Pharmacologic doses of systemic corticosteroids (e.g. dexamethasone) administered for prolonged periods can result in physiological dependence due to hypothalamic-pituitary-adrenal (HPA) suppression. 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 the drug on alternate days may help to alleviate this adverse effect. Patients with HPA 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. Discontinuation of prolonged oral corticosteroid therapy should be gradual 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 appetite loss, malaise, lethargy, nauseousness, head pain/ache, joint pain, muscle pain, fever, exfoliative dermatitis, loss of weight, and hypotension. These effects are believed to be due to the sudden change in corticosteroid concentration rather than to low corticosteroid levels. Increased intracranial pressure with papilledema (i.e., pseudotumor cerebri) has also been reported with glucocorticoids usually after treatment withdrawal.  
Prolonged dexamethasone therapy can adversely affect the endocrine system, resulting in hypercorticism (Cushing's syndrome including fat abnormalities such as buffalo hump and moon face), hypertrichosis or hirsutism, menstrual irregularity including amenorrhea, postmenopausal bleeding, or dysmenorrhea, a decrease or increase in motility and number of spermatozoa, hyperthyroidism, hypothyroidism, glycosuria, hyperglycemia, and aggravation of diabetes mellitus in susceptible patients. 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.   
Because of retardation of bone growth, children receiving prolonged systemic corticosteroid therapy, like dexamethasone, may have growth inhibition. Growth inhibition has been observed in the absence of laboratory evidence of hypothalamic-pituitary-adrenal (HPA) suppression, suggesting that growth velocity is a more sensitive indicator of systemic corticosteroid exposure in pediatric patients.  
Endogenous glucocorticoids are responsible for protein metabolism; prolonged therapy with pharmaceutical glucocorticoids like dexamethasone can result in various musculoskeletal and joint manifestations, including myopathy (myalgia, muscle wasting, muscle weakness or myasthenia, and quadriplegia), arthralgia, tendon rupture, bone matrix atrophy (osteoporosis and osteopenia), bone fractures such as vertebral compression fractures or fractures of long bones, and avascular necrosis of femoral or humeral heads. These effects are more likely to occur in older or debilitated patients. Of note, abrupt cessation of corticosteroids can cause arthralgia and myalgia. Glucocorticoids interact with calcium metabolism at many sites, including: decreasing the synthesis by osteoblasts of the principal 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 most important. Glucocorticoids do not modify vitamin D metabolism. Intra-articular injections of corticosteroids can cause Charcot-like arthropathy and post-injection flare. Atrophy at the site of injection has been reported following administration of soluble glucocorticoids.   
Adverse gastrointestinal (GI) effects associated with systemic corticosteroid (e.g., dexamethasone) administration include nausea and vomiting. Abdominal pain or distention, appetite stimulation, weight gain, pancreatitis, gastritis, hiccups, peptic ulcer with possible GI perforation and GI bleeding, perforation of the small and large bowel (particularly in patients with inflammatory bowel disease), and esophageal ulceration (ulcerative esophagitis) have also been reported.   Although it was once believed that corticosteroids contributed to the development of peptic ulcer disease, in a 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. While most of these studies did not utilize endoscopy, it is unlikely that corticosteroids contribute to the development of peptic ulcer disease.
Corticosteroid therapy including dexamethasone can mask the symptoms of infection and should generally be avoided during an acute viral, fungal, or bacterial infection. 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 from corticosteroids is most likely to occur in patients receiving high-dose (e.g., equivalent to 1 mg/kg or more of prednisone daily), 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 may also be at risk. Corticosteroid-induced immunosuppression may result in the activation of latent viral (e.g., herpes) or bacterial (e.g., tuberculosis) infections and should not be used in patients with an active infection except when appropriate anti-infective therapy 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. Monitoring systemic corticosteroid recipients for signs of opportunistic fungal infection is recommended, as cases of oropharyngeal candidiasis have been reported. Development of Kaposi's sarcoma has also been associated with prolonged administration of corticosteroids; discontinuation of the corticosteroid may result in clinical improvement.   Bronchitis was noted in 5% of dexamethasone ophthalmic implant recipients during clinical trials and at an incidence higher than with placebo; secondary ophthalmic infection or exacerbation of infection has also been reported with other ophthalmic and intraocular dosage forms.  
Various adverse dermatologic effects reported during systemic corticosteroid therapy include skin atrophy (thin fragile skin), increased sweating (hyperhidrosis), acne vulgaris, striae, acneiform rash, alopecia, xerosis, perineal pain and irritation, purpura, rash (unspecified), telangiectasia, facial erythema, petechiae, ecchymosis or easy bruising, and suppression of reactions to skin tests. An increased susceptibility to skin ulcer may occur in patients with impaired circulation. Hypersensitivity reactions may manifest as allergic dermatitis, urticaria, anaphylactoid reactions, and/or angioedema. Burning or tingling in the perineal area may occur following IV injection of corticosteroids. Parenteral corticosteroid therapy has also produced skin hypopigmentation, skin hyperpigmentation, scarring, and other types of injection site reaction (e.g., induration, delayed pain or soreness, subcutaneous and cutaneous atrophy, and sterile abscesses).  
In general, systemic corticosteroids like dexamethasone can lead to impaired wound healing.  
Prolonged administration of systemic dexamethasone can result in edema and fluid retention due to sodium retention; electrolyte disturbances (hypokalemia, hypokalemic metabolic alkalosis, hypernatremia, hypocalcemia); and hypertension.   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. In another study, an increased risk of heart failure was observed for medium-dose glucocorticoid use as compared with nonuse. At the beginning of the study, patients were at least 40 years of age and had not been hospitalized for cardiovascular disease. Medium exposure was defined as less than 7.5 mg daily of prednisolone or the equivalent given orally, rectally, or parenterally. Increased blood pressure was noted in 13% of dexamethasone ophthalmic insert recipients for one of the products during clinical trials.
Adverse neurologic effects have been reported during prolonged systemic dexamethasone administration and include insomnia, vertigo or dizziness, restlessness, amnesia and memory impairment, increased motor activity, impaired cognition, paresthesias, ischemic peripheral neuropathy, seizures, neuritis, and EEG changes. Mental disturbances, including depression, anxiety, euphoria, personality changes, emotional lability, delirium, dementia, hallucinations, irritability, mania, mood swings, schizophrenic reactions, withdrawn behavior, and psychosis have also been reported; emotional lability and psychotic problems can be exacerbated by corticosteroid therapy. Headache may be a sign of elevated intracranial pressure.   Arachnoiditis, meningitis, paresis, paraplegia, and sensory disturbances have occurred after intrathecal administration. Serious neurologic events, some resulting in death, have been reported with epidural injection of corticosteroids. Specific events reported include, but are not limited to, spinal cord infarction, paraplegia, quadriplegia, cortical blindness, and stroke. Headache was noted in 1% to 4% of dexamethasone ophthalmic insert/implant recipients during clinical trials, at incidences higher than with placebo. 
Dexamethasone can cause increased intraocular pressure or ocular hypertension, the magnitude of which depends on the formulation used, indication for use, and the frequency and duration of dosing. Ocular hypertension can occur after 1 to 6 weeks of topical ophthalmic therapy, and it is usually reversible upon discontinuance of the drug. Use of the intravitreal implant has resulted in ocular hypertension (glaucoma) in 5% of patients in clinical trials and increased ocular pressure (IOP) occurred in 25% to 35% of patients receiving the intravitreal implant. In retinal vein occlusion (RVO) and uveitis trials, IOP peaked at 60 days, returning to baseline by day 180. During the initial treatment period with the intravitreal implant for RVO and uveitis, 1% of patients required laser or surgical procedures to manage elevated IOP. In a 2-year observational study with the intravitreal implant, among patients who received more than 2 injections, increased IOP was reported in 24% (n = 68) patients. Frequently check IOP during receipt of ophthalmic preparations of dexamethasone. In diseases that cause thinning of the cornea or sclera, topical ocular steroids have been known to cause perforation. Intravitreal injections have also been associated with endophthalmitis, ocular inflammation, and retinal detachment. In clinical trials, the use of the intravitreal implant has resulted in ocular hemorrhage (conjunctival hemorrhage) (22% to 23%), ocular pain (8%), conjunctival hyperemia (7%), conjunctivitis (6%), vitreous floaters (5%), conjunctival edema (5%), xerophthalmia (5%), vitreous opacities (3%), retinal aneurysm (3%), foreign body sensation (2%), corneal erosion (2%), keratitis (2%), anterior chamber inflammation (2%), retinal tear (2%), eyelid ptosis (2%), vitreous hemorrhage (ocular hemorrhage, 6%), and vitreous detachment (2% to 4%). Postmarketing, complication of device insertion resulting in ocular tissue injury including sclera, subconjunctiva, lens and retina (implant misplacement), device dislocation with or without corneal edema, and ocular hypotonia (associated with vitreous leakage due to injection) were noted. Patients with an absent or torn posterior capsule of the lens are at increased risk of migration of the intravitreal implant into the anterior chamber. The most common ocular adverse reactions that occurred in patients treated with dexamethasone ophthalmic insert were: anterior chamber inflammation including iritis and iridocyclitis (10%), increased intraocular pressure (6%), reduced visual acuity (2%), ocular pain (1%), cystoid macular edema (1%), corneal edema (1%), and conjunctival hyperemia (1%). Ocular irritation including transient stinging, burning, or tearing and keratoconjunctivitis may occur during use of ophthalmic dexamethasone. Allergic reactions have also been reported; ocular pruritus can occur. Ocular discomfort (10%) and eye irritation (1%) were the most frequently reported adverse reactions in clinical studies with dexamethasone ophthalmic suspension. All other adverse reactions from these studies occurred with a frequency less than 1% including keratitis, conjunctivitis, dry eye (xerophthalmia), photophobia, blurred vision, ocular pruritus, foreign body sensation, increased lacrimation, abnormal ocular sensation, eyelid margin crusting, and ocular hyperemia. Postmarketing adverse reactions with dexamethasone topical ophthalmic suspension use include corneal erosion, dizziness, ocular pain, eyelid ptosis, headache, hypersensitivity reactions, and mydriasis. In patients receiving dexamethasone intraocular suspension for injection, the most common adverse reactions occurring in 5% to 15% of patients included intraocular pressure or ocular hypertension, corneal edema and iritis. Other ocular adverse reactions occurring in 1% to 5% of patients included corneal endothelial cell loss, blepharitis, ocular pain, cystoid macular edema, xerophthalmia, ocular inflammation, posterior capsule opacification, blurred vision, reduced visual acuity, vitreous floaters, foreign body sensation, photophobia, and vitreous detachment. Prolonged use of dexamethasone therapy by any route can result in ocular nerve damage including optic neuritis and visual defects. Temporary or permanent visual impairment, including blurred vision and blindness, has been reported with glucocorticoid administration by several routes of administration including intranasal and ophthalmic administration. Other ocular adverse reactions resulting from systemic corticosteroid therapy can include corneal perforation, exophthalmos, slowing of corneal wound healing, increased intraocular pressure, glaucoma with possible damage to the optic nerves, blurred vision, or retinopathy.   Consider referring patients who develop ocular symptoms or use systemic corticosteroid-containing products for more than 6 weeks to an ophthalmologist for evaluation.      Dexamethasone (by any route) can reduce host resistance to infection. Secondary fungal and viral infections of the eye (ocular infection) can be masked or exacerbated by corticosteroid therapy. Investigate the possibility of fungal infection if patients have persistent corneal ulceration. Prolonged use of dexamethasone therapy by any route has resulted in posterior subcapsular cataracts.    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. The incidence of cataracts with initial use of the intravitreal implant in clinical trials of patients with RVO or uveitis was 5% within the first 6 months; however, the overall incidence after a second intravitreal implant injection was higher after 1 year. In diabetic macular edema (DME) trials, the incidence of cataract development in patients who had a phakic study eye was higher in the dexamethasone group (68%) compared with sham (21%). Among these patients, 61% of dexamethasone subjects vs. 8% of sham-controlled subjects underwent cataract surgery. In a 2 year observational study, among patients who received more than 2 injections, the most frequent adverse reaction was cataract 54% (n = 96 out of 178 phakic eyes at baseline).
Hypercholesterolemia, atherosclerosis, fat embolism, palpitations, sinus tachycardia, bradycardia, syncope, vasculitis, necrotizing angiitis, thrombosis, thromboembolism, and phlebitis, specifically, thrombophlebitis, have been associated with systemic corticosteroid therapy such as dexamethasone. Systemic glucocorticoid use appears to increase the risk of cardiovascular events such as myocardial infarction, left ventricular rupture (in persons who recently experienced a myocardial infarction), angina, angioplasty, coronary revascularization, stroke, transient ischemic attack, cardiomegaly, arrhythmia exacerbation and ECG changes, hypertrophic cardiomyopathy (in premature infants), congestive heart failure and pulmonary edema, cardiac arrest or cardiovascular death.   As determined from observational data, the rate of cardiovascular events was 17 per 1,000 person-years among 82,202 non-users of glucocorticoids. In contrast, the rate was 23.9 per 1,000 person-years among 68,781 glucocorticoid users. Furthermore, the rate of cardiovascular events was 76.5 per 1,000 person-years for high exposure patients. After adjustment for known covariates by multivariate analysis, high-dose glucocorticoid use was associated with a 2.56-fold increased risk of cardiovascular events as compared with nonuse. At the beginning of the study, patients were at least 40 years of age and had not been hospitalized for cardiovascular disease. High glucocorticoid exposure was defined as at least 7.5 mg daily of prednisolone (or equivalent) given orally, rectally, or parenterally whereas medium exposure was defined as less than the above dosage by any of the 3 routes. Low-dose exposure was defined as inhaled, topical, or nasal usage only.
Cases of elevated hepatic enzymes (usually reversible upon discontinuation) and hepatomegaly have been associated with corticosteroid receipt such as dexamethasone.  
Epidural administration of corticosteroids should be used with great caution. Rare, but serious adverse reactions, including cortical blindness, stroke, spinal cord infarction, paralysis, seizures, nerve injury, brain edema, and death have been associated with epidural administration of injectable corticosteroids. These events have been reported with and without the use of fluoroscopy. Many cases were temporally associated with the corticosteroid injection; reactions occurred within minutes to 48 hours after injection. Some cases of neurologic events were confirmed through 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 the patient before treatment. If a decision is made to proceed with corticosteroid epidural administration, counsel patients to seek emergency medical attention if they experience symptoms after injection such as vision changes, tingling in the arms or legs, dizziness, severe headache, seizures, or sudden weakness or numbness of face, arm, or leg. 
Dexamethasone is contraindicated in patients with a hypersensitivity to the drug or any of its components. Although true corticosteroid hypersensitivity is rare, it is possible, though also rare, that such patients will display cross-hypersensitivity to other corticosteroids. 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. Such patients should be carefully monitored during and following the administration of any corticosteroid.         
Prolonged administration of pharmacological doses of systemic, nasal, inhaled or topical corticosteroids (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 various corticosteroid formulations in pediatric patients.  Acute adrenal insufficiency and even death may occur following abrupt discontinuation of 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 concentrations. Withdraw prolonged systemic corticosteroid therapy (duration of treatment of more than 2 weeks) gradually. HPA 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-suppressed patients may need supplemental corticosteroid treatment during periods of physiologic stress, such as post-surgical stress, acute blood loss, or infectious conditions, 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 corticosteroids in situations of increased stress.    
Potential adverse effects of chronic corticosteroid therapy should be weighed against the clinical benefits obtained and the availability of other treatment alternatives. Prolonged systemic corticosteroid therapy can lead to osteopenia, osteoporosis, vertebral compression fractures, aseptic necrosis of femoral and humeral heads, and pathologic fractures of long bones secondary to decreased bone formation, increased bone resorption, and protein catabolism in any patient.   A high-protein diet may alleviate or prevent the adverse effects associated with protein catabolism. The elderly, post-menopausal, and pediatric patients may be more susceptible to the effects on bone. Chronic systemic dexamethasone therapy may cause growth inhibition in pediatric patients due to hypothalamic-pituitary-adrenal axis suppression and inhibition of bone growth. Corticosteroids should be titrated to the lowest effective dose. Because bone development is critical in pediatric patients, monitoring is warranted in patients receiving high-dose or chronic corticosteroid treatment. Use of the lowest effective dose is recommended to minimize the occurrence of systemic adverse effects. Monitor growth routinely.   
Patients receiving high-dose (e.g., equivalent to 1 mg/kg or more of prednisone daily) or systemic corticosteroid therapy, such as dexamethasone, for any period of time, particularly in conjunction with corticosteroid-sparing drugs (e.g., troleandomycin) are at risk to develop immunosuppression; however, patients receiving moderate dosages of systemic corticosteroids for short periods or low dosages for prolonged periods also may be at risk. Treatment with topical or inhaled corticosteroids lessens the risk of immunosuppression; although localized effects may be seen in some patients. When given in combination with other immunosuppressive agents, there is a risk of over-immunosuppression.   Intra-articularly injected corticosteroids are systemically absorbed and may cause immunosuppression. Advise patients to contact their health care provider if they develop fever or other signs or symptoms of an infectious process. Local injection of a corticosteroid into a previously infected joint is not usually recommended. Examine any joint fluid to exclude a septic process. Injection into unstable joints is generally not recommended.
If surgery is required, patients should advise their physician that they received prolonged systemic corticosteroid therapy, such as dexamethasone, within the last 12 months and state the disease for which they were being treated. For systemic therapy, identification cards that include disease state, type and dose of corticosteroid, and physician should always be carried with the patient. Long-acting dexamethasone injection preparations, which are no longer marketed in the U.S., are not suitable for use in acute stress situations. To avoid drug-induced adrenal insufficiency, a supportive corticosteroid dosage may be required in times of stress (such as trauma, surgery, or severe illness) both during treatment with these injections and for a year afterward.  
Corticosteroids may increase the risks related to infections with any pathogen, including viral, bacterial, fungal, protozoan, or helminth infection. The degree to which the dose, route, and duration of corticosteroid administration correlate with the specific risks of infection is not well characterized, however, with increasing doses of corticosteroids, the rate of occurrence of infectious complications increases. Corticosteroids may also mask some signs of current infection. Although the FDA-approved product labeling states that corticosteroids are 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 the use of dexamethasone 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. Cases of severe and disseminated strongyloidiasis have been reported following use of corticosteroids in combination with tocilizumab to treat patients with coronavirus disease 2019 (COVID-19). Before giving these drugs together to patients from strongyloidiasis endemic areas, consider administering ivermectin as prophylactic treatment. 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. Furthermore, chemoprophylaxis is advised if prolonged corticosteroid therapy is needed. Advise patients receiving immunosuppressive doses of systemic corticosteroids to avoid exposure to persons with a viral infection (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 chickenpox, prophylaxis with varicella-zoster immune globulin may be indicated. If exposed to measles, prophylaxis with pooled intramuscular immunoglobulin may be indicated. Avoid the use of corticosteroids in active ocular herpes infection due to the risk of corneal perforation. Corticosteroids should not be used in cerebral malaria.    The use of ophthalmic dexamethasone formulations is contraindicated in most forms of cornea and conjunctiva viral infection including epithelial herpes simplex keratitis (dendritic keratitis), vaccinia, and varicella, and also in mycobacterial infection of the eye and fungal diseases of ocular structures.    
Do not use high doses of systemic corticosteroids such as dexamethasone 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.
Corticosteroid therapy, including systemic dexamethasone therapy, has been associated with left ventricular free-wall rupture in patients with recent myocardial infarction, and should therefore be used cautiously in these patients. As sodium retention with resultant edema and potassium loss may occur in patients receiving systemic corticosteroids, these agents should be used with caution in patients with congestive heart failure, hypertension, or renal disease or insufficiency.  
Systemic corticosteroids, such as dexamethasone, 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 for patients with diabetes mellitus, changes in insulin, oral antidiabetic agent dosage, and/or diet may be required.  
An acute myopathy has been observed with the use of high doses of systemic corticosteroids, most often occurring in patients with neuromuscular disease disorders (e.g., myasthenia gravis), or in patients receiving concomitant therapy with neuromuscular blocking drugs. This acute myopathy is generalized, may involve ocular and respiratory muscles, and may result in quadriparesis. Elevation of creatinine kinase may occur. Clinical improvement or recovery after stopping corticosteroids may require weeks to years.  
Existing emotional instability or psychosis may be aggravated by corticosteroids. Psychiatric derangements may appear when corticosteroids are used, ranging from euphoria, insomnia, mood swings, personality changes, and severe depression, to frank psychosis. Use dexamethasone with caution in patients with a seizure disorder; systemic steroids can lower the seizure threshold.  
Metabolic clearance of corticosteroids is decreased in hypothyroidism and increased in hyperthyroidism. Changes in thyroid disease status of a patient may necessitate an adjustment in systemic dexamethasone dosage.  
Systemic corticosteroids should be used with caution in patients with active or latent peptic ulcer disease, diverticulitis, fresh intestinal anastomoses, and nonspecific ulcerative colitis, since steroids may increase the risk of a gastrointestinal (GI) perforation. Signs of peritoneal irritation following GI perforation in patients receiving corticosteroids may be minimal or absent. Corticosteroids should not be used in patients where there is a possibility of impending GI perforation, abscess, or pyogenic infection. There is an enhanced effect due to decreased metabolism of systemic corticosteroids in patients with severe hepatic disease with cirrhosis.  
Systemic corticosteroids, like dexamethasone, may cause impaired wound healing. Ophthalmic and ocular dosage forms may cause impairment of wound healing within or near the site of application.       
Prolonged use of corticosteroids including dexamethasone may result in glaucoma with damage to the optic nerve, defects in visual acuity and fields of vision. Corticosteroids can cause cataracts and exacerbate pre-existing glaucoma. Periodically assess patients receiving corticosteroids chronically for cataract formation, visual disturbance, or increased intraocular pressure. Consider referring patients who develop ocular symptoms or use systemic corticosteroid-containing products for more than 6 weeks to an ophthalmologist for evaluation.   Ophthalmic dexamethasone is more likely than other ophthalmic agents to increase intraocular pressure, so intraocular pressure should be measured every 2 to 4 weeks for the first 2 months of therapy, and every 1 to 2 months thereafter. Ophthalmic dexamethasone therapy should be undertaken with caution in patients with a history of open-angle glaucoma, myopia, Krukenberg's spindle, or diabetes because these patients have an increased risk of developing ocular hypertension during therapy. There is also an increase in the propensity for secondary ocular infection caused by fungal or viral infections. Ophthalmic dexamethasone should be used with caution in patients with corneal abrasion.     The dexamethasone intravitreal implant is contraindicated in patients with glaucoma who have cup to disc ratio more than 0.8. Dexamethasone intravitreal implant is also contraindicated in patients who have a tear or a rupture of posterior ocular lens capsule; these patients with an absent or torn posterior capsule of the lens are at increased risk of migration of the intravitreal implant into the anterior chamber. Laser posterior capsulotomy in pseudophakic patients is not a contraindication for the dexamethasone intravitreal implant. The safety and efficacy of dexamethasone intravitreal implant. ophthalmic injection suspension, and ophthalmic insert have not been established in pediatric patients.  
Corticosteroid therapy usually does not contraindicate vaccination with live-virus vaccines when such therapy is of short-term (less than 2 weeks); low to moderate dose; long-term alternate-day treatment with short-acting preparations; maintenance physiologic doses (replacement therapy); ophthalmic administration, or by intra-articular, bursal or tendon injection. 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 a concern about the safety of immunization with live-virus vaccines. In general, patients with severe immunosuppression due to large doses of corticosteroids should not receive vaccination with live-virus vaccines. 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 or more weeks. Patients vaccinated while on immunosuppressive therapy or in the 2 weeks prior to starting therapy should be considered unimmunized and should be revaccinated at least 3 months after discontinuation of therapy. In patients who have received high-dose, systemic corticosteroids for 2 or more weeks, it is recommended to wait at least 3 months after discontinuation of therapy before administering a live-virus vaccine. 
There are no adequate, well-controlled studies for the use of dexamethasone in pregnant women; therefore, the manufacturers recommend that the drug be used during pregnancy only if the potential benefit to the mother outweighs the potential risk to the fetus. Corticosteroids have been shown to be teratogenic in many species when given in systemic doses equivalent to the human dose. Animal studies in which corticosteroids have been given to pregnant mice, rats, and rabbits have yielded an increased incidence of cleft palate in the offspring.   In addition, dexamethasone has been shown to be teratogenic in mice and rabbits following topical ophthalmic application in multiples of the therapeutic dose. Topical ocular administration of dexamethasone to pregnant mice and rabbits during organogenesis produced embryofetal lethality, cleft palate and multiple visceral malformations.  Topical and otic corticosteroids should not be used in large amounts, on large areas, or for prolonged periods of time in pregnant women. Dexamethasone injections have been used medically later in pregnancy to induce fetal lung maturation in patients at risk for pre-term delivery; use is for select circumstances and for a limited duration of time.   An infant who is born to a woman receiving large doses of systemic corticosteroids during pregnancy should be monitored for signs of adrenal insufficiency, and appropriate therapy should be initiated, if necessary.
Systemic use of dexamethasone has not been studied during breast-feeding; corticosteroids appear in human milk and could suppress growth, interfere with endogenous corticosteroid production, or cause other untoward effects. Caution is warranted, and some manufacturers recommend to discontinue breast-feeding if systemic dexamethasone treatment is needed.   However, experts generally consider inhaled corticosteroids and oral corticosteroids (e.g., prednisone and prednisolone), acceptable to use during breast-feeding.   There is no information regarding dexamethasone effects on breastfed infants or milk production or its presence in human milk following placement of the intravitreal implant or intracanalicular insert to inform risk to an infant during lactation.  However, the systemic concentration of dexamethasone following administration of the intracanalicular insert is low. It is not known whether topical ophthalmic administration of dexamethasone could result in sufficient systemic absorption to produce detectable quantities in breast milk.  Consider the benefits of breast-feeding, the risk of potential infant drug exposure, and the risk of an untreated or inadequately treated condition.
The routine use of high-dose (greater than 0.5 mg/kg/day) dexamethasone for either the prevention or treatment of chronic lung disease in premature neonates is not recommended by the American Academy of Pediatrics (AAP) due to a lack of survival benefit and concern about long-term adverse outcomes, particularly increased rates of cerebral palsy. Studies utilizing lower doses of dexamethasone (less than 0.2 mg/kg/day) have not reported increased rates of adverse neurodevelopmental effects; however, due to the small number of patients included in these studies, the AAP states that there is insufficient evidence to recommend the use of low-dose dexamethasone and further study is warranted. In a geographical cohort study of 148 extremely premature pediatric patients (born less than 28 weeks gestation), 55 (27%) received postnatal dexamethasone (mean cumulative dose 7.7 mg/kg) during the neonatal period. Patients receiving dexamethasone had smaller total brain tissue volume (mean difference -3.6%, p value = 0.04) and smaller white matter, thalami, and basal ganglia volumes (p is less than 0.05 for all) when compared with participants who did not receive postnatal dexamethasone. There was also a trend of smaller total brain and white matter volumes with an increased dose of postnatal dexamethasone. Avoid the use of dexamethasone injectable formulations containing benzyl alcohol in premature neonates and 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 daily benzyl alcohol exposure above 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 low birth weight, and patients who receive a high dose may be more likely to develop toxicity.
Use systemic corticosteroids with caution in the geriatric patient; the risks and benefits of therapy should be considered for any individual patient. Geriatric and debilitated patients are especially susceptible to corticosteroid-induced decreases in bone mineral density and resultant fractures. Detrimental effects on bone metabolism, such as osteoporosis, are a risk with chronic, systemically-administered corticosteroids.   According to the Beers Criteria, systemic corticosteroids are considered potentially inappropriate medications (PIMs) for use in geriatric patients with delirium or at high risk for delirium and should be avoided in these patient populations due to the possibility of new-onset delirium or exacerbation of the current condition. The Beers expert panel notes that oral and parenteral corticosteroids may be required for conditions such as exacerbation of chronic obstructive pulmonary disease (COPD) but should be prescribed in the lowest effective dose and for the shortest possible duration. The federal Omnibus Budget Reconciliation Act (OBRA) regulates medication use in residents of long-term care facilities (LTCFs); the need for continued use of a systemic glucocorticoid should be documented, along with monitoring for adverse consequences with intermediate or longer-term use.
Some commercially available formulations of dexamethasone injection or ophthalmic solution may contain sulfites; some parenteral products also contain benzyl alcohol. Sulfites and benzyl alcohol may cause allergic reactions in some people. They should be used with caution in patients with known sulfite hypersensitivity or benzyl alcohol hypersensitivity. Patients who have asthma are more likely to experience a sulfite sensitivity reaction than non-asthmatic patients. 
Dexamethasone ophthalmic solutions are sometimes used off-label in the ear for otic conditions. Otic dexamethasone use is contraindicated for use in patients with tympanic membrane perforation.
Glucocorticoids are naturally occurring hormones that 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 the 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 an immune response. The degree of clinical effect is normally related to the dose administered. 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. Likewise, the numerous adverse effects related to corticosteroid use usually depend on the dose administered and the duration of therapy.
Dexamethasone is administered via oral, intravenous, intramuscular, intraarticular, intravitreal, ophthalmic, and otic routes. Certain dosage forms, like inhalational products, have been removed from marketing. Circulating drug binds weakly to plasma proteins, with only the unbound portion of a dose being active. Systemic dexamethasone is quickly distributed into the kidneys, intestines, skin, liver, and muscle. Corticosteroids distribute into breast milk and cross the placenta. Systemic dexamethasone 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 plasma elimination half-life of dexamethasone is approximately 1.8 to 3.5 hours whereas the biological half-life is 36 to 54 hours.
Affected cytochrome P450 (CYP450) isoenzymes and drug transporters: CYP3A4, P-glycoprotein (P-gp)
Dexamethasone is an inducer of CYP3A4 and is a substrate for both P-glycoprotein (P-gp) and CYP3A4.
Dexamethasone is rapidly and well absorbed after oral administration. In adults, bioavailability has been reported to be in the range of approximately 60% to 100%, with no significant differences between the elixir and tablet formulations. Peak concentrations occur 1 to 2 hours after oral administration. However, 1 study of 13 patients (aged 14 to 28 years) with congenital adrenal hyperplasia reported a mean time to peak concentrations for oral dexamethasone of 45 minutes (range 30 to 120 minutes).
Peak concentrations were reached approximately 60 minutes after single-dose administration of IV dexamethasone in neonates.
The onset and duration of action of dexamethasone injection ranges from 2 days to 3 weeks and is dependent on whether the drug is administered by intra-articular or IM injection and by the extent of the local blood supply.
Following ophthalmic administration, dexamethasone is absorbed through the aqueous humor and distribute into the local tissues, with only minimal systemic absorption occurring. Ophthalmic doses are metabolized locally.
Intravitreal Implant Route
After the insertion of the dexamethasone intravitreal implant (0.35 mg or 0.7 mg) in 21 patients, plasma concentrations were obtained on days 1, 7, 30, 60, and 90. Overall, the majority of dexamethasone plasma concentration measurements were below the lower limit of quantitation (LLOQ = 50 pg/mL). Ten of the 73 samples in the patients receiving the 0.7 mg dose and 2 of the 42 samples in the patients receiving the 0.35 mg dose were above the LLOQ (range, 52 to 94 pg/mL). The highest plasma concentration (94 pg/mL) was observed in one patient who had received the 0.7 mg dose. Age, body weight, and gender did not affect the plasma dexamethasone concentrations. In vitro metabolism studies of the intravitreal implant showed no metabolites.
Systemic exposure to dexamethasone was evaluated in a subgroup of patients enrolled in 2 studies (n = 25 for the first study and n = 13 for the second study). The patients received a single intraocular injection of dexamethasone containing 342 mcg or 517 mcg of dexamethasone at the end of cataract surgery and blood samples were collected prior to surgery and at the several time points post-surgery between Day 1 and up to Day 30. In the first study, the dexamethasone plasma concentrations on post-surgery Day 1 ranged from 0.09 to 0.86 ng/mL and from 0.07 to 1.16 ng/mL following administration of dexamethasone 342 mcg and 517 mcg, respectively. In the second study, dexamethasone plasma concentrations on post-surgery Day 1 ranged from 0.349 to 2.79 ng/mL following administration of dexamethasone 517 mcg. In both the studies, dexamethasone plasma concentrations declined over time and very few patients had quantifiable dexamethasone plasma concentrations at the final time point of sampling (Day 15 or Day 30).
Systemic exposure to dexamthasone was evaluated in 16 healthy volunteers. Plasma samples were obtained prior to and at several time points on Days 1 to 29. Dexamethasone plasma concentrations were detectable (above 50 pg/mL, the lower limit of quantification of the assay) in 11% of samples (21 of 189), and ranged from 0.05 ng/mL to 0.81 ng/mL.
In adult patients with chronic liver disease, dexamethasone clearance is reduced and the elimination half-life is prolonged. Pharmacokinetic data are unavailable in pediatric patients with hepatic impairment.
In adult patients with renal impairment, dexamethasone clearance is increased and the elimination half-life is shorter. This is due to decreased protein binding of dexamethasone to albumin in uremic patients. Pharmacokinetic data are unavailable in pediatric patients with renal impairment.
Infants, Children, and Adolescents
Pharmacokinetics of dexamethasone in pediatric patients are similar to adults. In a pharmacokinetic study in 12 pediatric patients (4 months to 16 years) who received IV dexamethasone (0.1 to 0.3 mg/kg/dose), the mean elimination half-life of dexamethasone was 4.34 hours (range 2.33 to 9.54 hours), which is similar to that reported in adults. The mean volume of distribution (Vd) was 2.07 L/kg (range 0.48 to 8.99 L/kg). Another study that included adolescents and adults (14 to 28 years) reported a mean elimination half-life of 3.53 hours (range 2.18 to 4.5 hours) after dexamethasone administration.
Clearance of dexamethasone in neonates is a function of gestational age (GA) with premature neonates having a slower clearance. In a pharmacokinetic study in 9 neonates (mean GA 27.3 weeks [range 25 to 30 weeks]; mean postnatal age 21.8 days), mean clearance was 1.69 mL/kg/minute in neonates with a GA less than 27 weeks compared with 7.57 mL/kg/minute in neonates with a GA more than 27 weeks. Corresponding elimination half-life values were 10.2 and 4.9 hours, respectively. The mean Vd was 1.78 L/kg, which was also correlated with GA (1.26 vs 2.19 L/kg for neonates with GA less than 27 weeks and more than 27 weeks, respectively). The mean Vd was higher than what has been reported in adults (0.77 L/kg). Another study in 7 extremely low birth weight neonates (mean GA 25.6 weeks; mean birthweight 735 g) found similar results after administration of single-dose IV dexamethasone. In this study, mean values for clearance, Vd, and elimination half-life were 2.4 mL/kg/minute, 1.9 L/kg, and 9.26 hours, respectively.
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