Dexamethasone Sodium Phosphate Injection USP
Dexamethasone is a synthetic adrenocortical steroid. Dexamethasone possesses the actions and effects of other glucocorticoids and is among the most active member of its class. Adrenocorticosteroids act on the HPA at specific receptors on the plasma membrane. On other tissues the adrenocorticoids diffuse across cell membranes and complex with specific cytoplasmic receptors which enter the cell nucleus and stimulate protein synthesis. Adrenocorticoids have anti-allergic, antitoxic, antishock, antipyretic and immunosuppressive properties. Dexamethasone has only minor mineralocorticoid activities and does therefore, not induce water and sodium retention. Dexamethasone decrease inflammation by suppression of neutrophil migration. It decreases the production of inflammatory mediators and reversal of increased capillary permeability. It also suppresses normal immune response.
Dexamethasone Sodium Phosphate is 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, and renal, respiratory, rheumatic and autoimmune origin. It may be used in management of cerebral edema, chronic swelling, as a diagnostic agent, diagnosis of Cushing’s syndrome, antiemetic.
- Hypersensitivity to Dexamethasone or any component of the formulation
- Systemic fungal infections
- Cerebral malaria.
- Local injection of a glucocorticoid is contraindicated in bactraemia and systemic fungal infections, unstable joints, infection at the injection site e.g. septic arthritis resulting from gonorrhea or tuberculosis.
Special warnings and precautions
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. 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 increasing in allergic symptoms.
Immunosuppression: prolonged use of corticosteroids may also increase the incidence of secondary infection, mask acute infection (including fungal infections), prolonged or exacerbate viral infections, or limit response to vaccines.
Adrenal insufficiency: dexamethasone does not provide adequate mineralocorticoid activity in adrenal insufficiency. 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 heart failure; long-term use has been associated with fluid retention and hypertension.
Diabetes: use with caution in patients with diabetes mellitus; may alter glucose production or regulation leading to hyperglycemia.
Gastrointestinal disease: use with caution in patients with Gastrointestinal disease (peptic ulcer, ulcerative colitis) due to perforation risk.
Head injury: high-dose corticosteroids should not be used for the management of head injury
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: 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 has 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 thyroid ones.
Discontinuation of therapy: withdrawal therapy with gradual tapering of dose
Pregnancy: dexamethasone crosses the placenta; and is partially metabolized to inactive metabolites by placenta enzyme.
Lactation: corticosteroids may pass into breast milk, although no data are available for Dexamethasone. Infants of mothers taking high doses of systemic corticosteroids for prolonged periods may have a degree of adrenal suppression.
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.
Dosage and directions for use
Dosage must be individualized on the basis of the disease and the response of the patient.
Adults: usual adult initial dosage is 0.5mg-20mg a day
In emergencies, the usual dose of Dexamethasone Sodium Phosphate 4mg/ml solution for injection by intravenous or intramuscular injection is 4mg-20mg (in shock use only the I.V route). This dose may be repeated until adequate response is noted.
After initial improvement, single doses of 2mg-4mg. repeated as necessary, should be suffiecient. The total daily dosage usually need not exceed 80mg, even in severe conditions.
Cerebral oedema associated with malignancy: I.V 10mg initially, then 4mg by intramuscular injection every 6 hours as required for 2-4 days then gradually reduced and stopped over 5-7 days.
Mildly emetogenic therapy: I.M., I.V. 4mg every 4-6 hours
Treatment of shock: Addisonian crisis/shock (e.g. adrenal insufficiency/responsive to steroid therapy): I.V 4-10mg as a single dose, which may be repeated if necessary.
Pediatric: 200-400 micrograms/kg daily.
Rifampicin, rifabutin, ephedrine, carbamazepine, phenylbutazone, Phenobarbital, phenytoin, primidone and aminoglutethimide enhance the mechanism of corticosteroids and its therapeutic effects may be reduced.
The effects of anticholinesterases are antagonized by corticosteroids in myasthenia gravis.
The desired effects of hypogylcaemic agents (including insulin), anti hypertensives, cardiac glycosides and diuretics are antagonized by corticosteroids and the hypokalaemic effects of acetazolamide, loop diuretics, thiazide diuretics and carbenoxolone are enhanced.
The effect of coumarin anticoagulants may be enhanced by concurrent corticosteroid therap.
The renal clearance of salicylates is increased by corticosteroids and steroid withdrawal may result in salicylate intoxication. There may be interaction with salicylates in patients with hypoprothrombinaemia.
Reports of acute toxicity and/or death following overdosage of glucocorticoids are rare. In the event of overdosage, no specific antidote is available; treatment is supportive and symptomatic.