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Indications/Uses
Corticosteroid.
Use in certain endocrine and non-endocrine disorders responsive to corticosteroid therapy.
Systemic administration: Dexamethasone sodium phosphate Injection is recommended for systemic administration by intravenous or intramuscular injection when oral therapy is not feasible or desirable in the following conditions.
Endocrine disorders: Primary or secondary adrenocortical insufficiency: (hydrocortisone or cortisone is the first choice, but synthetic analogues may be used with mineralocorticoids where applicable and, in infancy, mineralocorticoid supplementation is particularly important.)
Non-endocrine disorders: Dexamethasone sodium phosphate may be used in the treatment of non-endocrine corticosteroid responsive conditions including: Allergy and anaphylaxis: Angioneurotic edema and anaphylaxis.
Gastro-intestinal: Crohn's disease and ulcerative colitis.
Infection (with appropriate chemotherapy): Miliary tuberculosis and endotoxic shock.
Neurological disorders: Raised intracranial pressure secondary to cerebral tumors and infantile spasms.
Respiratory: Bronchial asthma and aspiration pneumonitis.
Skin disorders: Toxic epidermal necrolysis.
Shock: Adjunctive treatment where high pharmacological doses are needed. Treatment is an adjunct to, and not a substitute for specific supportive measures the patient may require. Dexamethasone has been shown to be beneficial when used in the early treatment of shock, but it may not influence overall survival.
Local administration: Dexamethasone sodium phosphate Injection is suitable for intra-articular or soft-tissue injection as adjunctive therapy for short-term administration in: Soft-tissue disorders such as carpal tunnel syndrome and tenosynovitis.
Intra-articular disorders such as rheumatoid arthritis and osteoarthritis with an inflammatory component. Dexamethasone sodium phosphate injection may be injected intralesionally in selected skin disorders such as cystic acne vulgaris, localized lichen simplex, and keloids.
Use in certain endocrine and non-endocrine disorders responsive to corticosteroid therapy.
Systemic administration: Dexamethasone sodium phosphate Injection is recommended for systemic administration by intravenous or intramuscular injection when oral therapy is not feasible or desirable in the following conditions.
Endocrine disorders: Primary or secondary adrenocortical insufficiency: (hydrocortisone or cortisone is the first choice, but synthetic analogues may be used with mineralocorticoids where applicable and, in infancy, mineralocorticoid supplementation is particularly important.)
Non-endocrine disorders: Dexamethasone sodium phosphate may be used in the treatment of non-endocrine corticosteroid responsive conditions including: Allergy and anaphylaxis: Angioneurotic edema and anaphylaxis.
Gastro-intestinal: Crohn's disease and ulcerative colitis.
Infection (with appropriate chemotherapy): Miliary tuberculosis and endotoxic shock.
Neurological disorders: Raised intracranial pressure secondary to cerebral tumors and infantile spasms.
Respiratory: Bronchial asthma and aspiration pneumonitis.
Skin disorders: Toxic epidermal necrolysis.
Shock: Adjunctive treatment where high pharmacological doses are needed. Treatment is an adjunct to, and not a substitute for specific supportive measures the patient may require. Dexamethasone has been shown to be beneficial when used in the early treatment of shock, but it may not influence overall survival.
Local administration: Dexamethasone sodium phosphate Injection is suitable for intra-articular or soft-tissue injection as adjunctive therapy for short-term administration in: Soft-tissue disorders such as carpal tunnel syndrome and tenosynovitis.
Intra-articular disorders such as rheumatoid arthritis and osteoarthritis with an inflammatory component. Dexamethasone sodium phosphate injection may be injected intralesionally in selected skin disorders such as cystic acne vulgaris, localized lichen simplex, and keloids.
Dosage/Direction for Use
Dexamethasone sodium phosphate can be given without mixing and dilution, but if preferred, can be added without loss of potency to sodium chloride injection or dextrose injection and given by intravenous drip. The infusion mixture must be used within 24 hours, and the usual aseptic techniques for injections should be observed.
All dosage recommendations are given in units of Dexamethasone phosphate.
Intravenous and intramuscular injection: General considerations: Dosage must be individualized on the basis of the disease and the response of the patient. In order to minimize side effects, the lowest possible dosage adequate to control the disease process should be used (see Side Effects).
Usually the parenteral dosage ranges are one-third to one-half the oral dose, given every 12 hours.
The usual initial dosage is 0.5-20 mg (0.125-5 mL) a day. In situations of less severity, lower doses will generally suffice. However, in certain overwhelming, acute, life-threatening situations, administration of dosages exceeding the usual dosages may be justified. In these circumstances, the slower rate of absorption by intramuscular administration should be recognized.
The initial dosage must be maintained or adjusted until a satisfactory response is noted. Both the dose in the evening, which is useful in alleviating morning stiffness, and the divided dosage regimen are associated with greater suppression of the hypothalamo-pituitary-adrenal axis. After a favorable response is noted, the proper maintenance dosage should be determined by decreasing the initial dosage by small amounts at appropriate intervals to the lowest dosage which will maintain an adequate clinical response. Chronic dosage should preferably not exceed 500 micrograms dexamethasone daily.
Close monitoring of drug is needed.
If Dexamethasone sodium phosphate injection is to be stopped after it has been given for more than a few days, it should be withdrawn gradually rather than stopped abruptly.
Whenever possible, the intravenous route should be used for the initial dose and for as many subsequent doses are given while the patient is in shock (because of the irregular rate of absorption of any medicament administered by any other route in such patients).
When the blood pressure responds, use the intramuscular route until oral therapy can be substituted. For the comfort of the patient, not more than 2 mL should be injected intramuscularly at any one site.
In emergencies, the usual dose of Dexamethasone sodium phosphate injection by intravenous or intramuscular injection is 4-20 mg (1-5 mL), depending on the severity of the condition (see also Shock as follows).
This dose may be repeated until adequate response is noted.
After initial improvement, single doses of 2-4 mg (0.5-1 mL) repeated as necessary, should be sufficient. The total daily dosage usually need not exceed 80 mg (20 mL), even in severe conditions. When constant maximal effects is desired, dosage must be repeated at three-hour or four-hour intervals, or maintained by slow intravenous drip. Intravenous and intramuscular injections are advised in acute illness. When the acute stage has passed, oral steroid therapy should be substituted as soon as feasible.
Shock (of hemorrhagic, traumatic or surgical): Usually 2 to 6 mg/kg body weight as a single intravenous injection. This may be repeated in two to six hours if shock persists.
Alternatively, this may be followed immediately by the same dose in an intravenous infusion. Therapy with Dexamethasone sodium phosphate injection is an adjunct to, and not a replacement for conventional therapy.
Administration of these high doses should be continued only until the patient's condition has stabilized and usually no longer than 48-72 hours.
Cerebral edema: Associated with primary or metastatic brain tumor, pre-operative preparation of patients with increased intracranial pressure secondary to brain tumor: initially 10 mg (2.5 mL) intravenously, followed by 4 mg (1 mL) intramuscularly every six hours until symptoms of cerebral edema subside. Response is usually noted within 12-24 hours; dosage may be reduced after two to four days and gradually discontinued over five to seven days.
High doses of Dexamethasone sodium phosphate Injection are recommended for initiating short-term intensive therapy for acute life-threatening cerebral edema. Following the high loading dose schedule of the first day of therapy, the dose is scaled down over the seven-to-ten day period of intensive therapy and subsequently reduced to zero over the next seven to ten days. When maintenance therapy is required, substitute oral Dexamethasone as soon as possible (see Table 1 as follows).
Palliative management of recurrent or inoperable brain tumors: Maintenance therapy should be determined for each patient; 2 mg (0.5 mL) two to three times a day may be effective.
The smallest dosage necessary to control cerebral edema should be used.
Suggested high dose schedule in cerebral edema: See Table 1.
All dosage recommendations are given in units of Dexamethasone phosphate.
Intravenous and intramuscular injection: General considerations: Dosage must be individualized on the basis of the disease and the response of the patient. In order to minimize side effects, the lowest possible dosage adequate to control the disease process should be used (see Side Effects).
Usually the parenteral dosage ranges are one-third to one-half the oral dose, given every 12 hours.
The usual initial dosage is 0.5-20 mg (0.125-5 mL) a day. In situations of less severity, lower doses will generally suffice. However, in certain overwhelming, acute, life-threatening situations, administration of dosages exceeding the usual dosages may be justified. In these circumstances, the slower rate of absorption by intramuscular administration should be recognized.
The initial dosage must be maintained or adjusted until a satisfactory response is noted. Both the dose in the evening, which is useful in alleviating morning stiffness, and the divided dosage regimen are associated with greater suppression of the hypothalamo-pituitary-adrenal axis. After a favorable response is noted, the proper maintenance dosage should be determined by decreasing the initial dosage by small amounts at appropriate intervals to the lowest dosage which will maintain an adequate clinical response. Chronic dosage should preferably not exceed 500 micrograms dexamethasone daily.
Close monitoring of drug is needed.
If Dexamethasone sodium phosphate injection is to be stopped after it has been given for more than a few days, it should be withdrawn gradually rather than stopped abruptly.
Whenever possible, the intravenous route should be used for the initial dose and for as many subsequent doses are given while the patient is in shock (because of the irregular rate of absorption of any medicament administered by any other route in such patients).
When the blood pressure responds, use the intramuscular route until oral therapy can be substituted. For the comfort of the patient, not more than 2 mL should be injected intramuscularly at any one site.
In emergencies, the usual dose of Dexamethasone sodium phosphate injection by intravenous or intramuscular injection is 4-20 mg (1-5 mL), depending on the severity of the condition (see also Shock as follows).
This dose may be repeated until adequate response is noted.
After initial improvement, single doses of 2-4 mg (0.5-1 mL) repeated as necessary, should be sufficient. The total daily dosage usually need not exceed 80 mg (20 mL), even in severe conditions. When constant maximal effects is desired, dosage must be repeated at three-hour or four-hour intervals, or maintained by slow intravenous drip. Intravenous and intramuscular injections are advised in acute illness. When the acute stage has passed, oral steroid therapy should be substituted as soon as feasible.
Shock (of hemorrhagic, traumatic or surgical): Usually 2 to 6 mg/kg body weight as a single intravenous injection. This may be repeated in two to six hours if shock persists.
Alternatively, this may be followed immediately by the same dose in an intravenous infusion. Therapy with Dexamethasone sodium phosphate injection is an adjunct to, and not a replacement for conventional therapy.
Administration of these high doses should be continued only until the patient's condition has stabilized and usually no longer than 48-72 hours.
Cerebral edema: Associated with primary or metastatic brain tumor, pre-operative preparation of patients with increased intracranial pressure secondary to brain tumor: initially 10 mg (2.5 mL) intravenously, followed by 4 mg (1 mL) intramuscularly every six hours until symptoms of cerebral edema subside. Response is usually noted within 12-24 hours; dosage may be reduced after two to four days and gradually discontinued over five to seven days.
High doses of Dexamethasone sodium phosphate Injection are recommended for initiating short-term intensive therapy for acute life-threatening cerebral edema. Following the high loading dose schedule of the first day of therapy, the dose is scaled down over the seven-to-ten day period of intensive therapy and subsequently reduced to zero over the next seven to ten days. When maintenance therapy is required, substitute oral Dexamethasone as soon as possible (see Table 1 as follows).
Palliative management of recurrent or inoperable brain tumors: Maintenance therapy should be determined for each patient; 2 mg (0.5 mL) two to three times a day may be effective.
The smallest dosage necessary to control cerebral edema should be used.
Suggested high dose schedule in cerebral edema: See Table 1.
Intrasynovial, intralesional, and soft-tissue injection: In general, these injections are employed when only one or two joints or areas are affected.
Some of the usual single doses are: See Table 2.
Some of the usual single doses are: See Table 2.
Frequency of injection: once every three to five days to once every two to three weeks, depending on response.
Use in children: Dosage should be limited to a single dose on alternate days to minimize suppression of the hypothalamo-pituitary-adrenal axis.
Use in the elderly: Treatment of elderly patients, particularly if long term, should be planned bearing in mind the more serious consequences of the common side effects of corticosteroids in old age, especially osteoporosis, diabetes, hypertension, susceptibility to infection and thinning of the skin.
Close clinical supervision is required to avoid life-threatening reactions (see Side Effects).
Use in children: Dosage should be limited to a single dose on alternate days to minimize suppression of the hypothalamo-pituitary-adrenal axis.
Use in the elderly: Treatment of elderly patients, particularly if long term, should be planned bearing in mind the more serious consequences of the common side effects of corticosteroids in old age, especially osteoporosis, diabetes, hypertension, susceptibility to infection and thinning of the skin.
Close clinical supervision is required to avoid life-threatening reactions (see Side Effects).
Overdosage
Reports of acute toxicity and/or death following overdosage with glucocorticoids are rare. No antidote is available. Treatment is probably not indicated for reactions due to chronic poisoning unless the patient has a condition that would render a patient unusually susceptible to ill effects from corticosteroids. In this case symptomatic treatment should be instituted as necessary. Anaphylactic and hypersensitivity reactions may be treated with adrenaline, positive-pressure artificial respiration and aminophylline. The patient should be kept warm and quiet.
The biological half-life of Dexamethasone in plasma is about 190 minutes.
The biological half-life of Dexamethasone in plasma is about 190 minutes.
Contraindications
Systemic fungal infection; systemic infection unless specific anti-infective therapy is employed; hypersensitivity to any component of this medication.
Administration of live virus vaccines (see Precautions).
Administration of live virus vaccines (see Precautions).
Warnings
Frequent intra-articular injections over a prolonged period may lead to joint destruction with bone necrosis. Intra-articular injection of corticosteroid may produce systemic adverse reactions including adrenal suppression.
Dexamethasone sodium phosphate injection contains sodium metabisulfite, a sulfite that may cause allergic-type reactions, including anaphylactic symptoms and life-threatening or less severe asthmatic episodes in certain susceptible people. The overall prevalence of sulfite sensitivity in the general population is unknown and probably low. Sulfite sensitivity is seen more frequently in asthmatic than in non-asthmatic people.
Dexamethasone sodium phosphate injection contains sodium metabisulfite, a sulfite that may cause allergic-type reactions, including anaphylactic symptoms and life-threatening or less severe asthmatic episodes in certain susceptible people. The overall prevalence of sulfite sensitivity in the general population is unknown and probably low. Sulfite sensitivity is seen more frequently in asthmatic than in non-asthmatic people.
Special Precautions
Undesirable effects may be minimized by using lowest effective dose for the minimum period. Frequent patient review is required to appropriately titrate the dose against disease activity. Where reduction in dosage is possible, the reduction should be gradual. (see Dosage & Administration)
Corticosteroids may exacerbate systemic fungal infections and therefore, should not be used in the presence of such infections unless they are needed to control drug reactions due to amphotericin.
Moreover, there have been cases reported in which concomitant use of amphotericin and hydrocortisone was followed by cardiac enlargement and congestive failure.
Average and large doses of hydrocortisone or cortisone can cause elevation of blood pressure, retention of salt and water, and increased excretion of potassium, but these effects are less likely to occur with synthetic derivatives, except when in large dose. Dietary salt restriction and potassium supplementation may be necessary. All corticosteroids increase calcium excretion.
Administration of live virus vaccines is contraindicated in individuals receiving immunosuppressive doses of corticosteroids. If inactivated viral or bacterial vaccines are administered to individuals receiving immunosuppressive doses of corticosteroids, the expected serum antibody response may not be obtained, however, immunization procedures may be undertaken in patients who are receiving corticosteroids as replacement therapy, e.g. for Addison's disease.
Literature reports suggest an apparent association between use of corticosteroids and left ventricular free wall rupture after a recent myocardial infarction, therefore, therapy with corticosteroids should be used with great caution in these patients. The use of Dexamethasone sodium phosphate injection in active tuberculosis should be restricted to those cases of fulminating or disseminated tuberculosis in which the corticosteroid is used for the management of the disease in conjunction with an appropriate antituberculosis regimen. If the corticosteroids are indicated in patients with latent tuberculosis or tuberculin reactivity, close observation is necessary as reactivation may occur. During prolonged corticosteroid therapy, these patients should receive prophylactic chemotherapy. Corticosteroids may mask some signs of infection and new infections may appear during their use.
Suppression of the inflammatory response and immune function increases the susceptibility to infections and their severity. The clinical presentation may often be atypical, and serious infections such as septicemia and tuberculosis may be masked and reach an advanced stage before being recognized. There may be decreased resistance, and inability to localize infection.
A report shows that the use of corticosteroids in cerebral malaria is associated with a prolonged coma and an increased incidence of pneumonia and gastro-intestinal bleeding. Chickenpox is of particular concern, since this normally minor illness may be fatal in immune suppressed patients. Patients (or parents of children) without a definite history of chickenpox should be advised to avoid close personal contact with chickenpox or herpes zoster, and if exposed they should seek urgent medical attention. Passive immunization with varicella/zoster immunoglobulin (VZIG) is needed by exposed non-immune patients who are receiving systemic corticosteroids or who have used them within the previous 3 months, this should be given within 10 days of exposure to chickenpox. If a diagnosis of chickenpox is confirmed, the illness warrants specialist care and urgent treatment. Corticosteroids should not be stopped and the dose may need to be increased.
Measles can have a more serious or even fatal course in immune suppressed patients. In such children or adults particular care should be taken to avoid exposure to measles. If exposed, prophylaxis with intramuscular pooled immunoglobulin (IG) may be indicated. Exposed patients should be advised to seek medical advice without delay. Corticosteroids may activate latent amoebiasis or strongyloidiasis or exacerbate active disease. Therefore, it is recommended that latent or active amoebiasis and strongyloidiasis be ruled out before initiating corticosteroids therapy in any patient at risk or with symptoms of either condition. Prolonged use of corticosteroids may produce posterior subcapsular cataracts, glaucoma with possible damage to the optic nerves, and may enhance the establishment of secondary ocular infections due to fungi or viruses. Corticosteroids may increase or decrease motility and number of spermatozoa.
Special precautions: Particular care is required when considering use of systemic corticosteroids in patients with the following conditions, and frequent patient monitoring is necessary; renal insufficiency; hypertension, diabetes or in those with a family history of diabetes, congestive heart failure, osteoporosis, previous steroid myopathy, glaucoma (or family history of glaucoma), myasthenia gravis, non-specific ulcerative colitis, diverticulitis, fresh intestinal anastomoses, active or latent peptic ulcer existing or previous history of severe affective disorder (especially previous steroid psychosis), liver failure, and epilepsy. Signs of peritoneal irritation following gastro-intestinal perforation in patients receiving large doses of corticosteroids may be minimal or absent.
Fat embolism has been reported as a possible complication of hypercortisonism.
There is an enhanced effect or corticosteroids in patients with hypothyroidism and in those with cirrhosis.
Corticosteroids should be used cautiously in patients with ocular herpes simplex because of possible corneal perforation.
Local steroid injection should be undertaken in an aseptic environment to reduce the particular risk of bacterial infection. Injection of a steroid into an infected site should be avoided.
Appropriate examination of joint fluid is necessary to exclude a septic process.
A marked increase in pain accompanied by local swelling, further restriction of joint motion, fever and malaise are suggestive of septic arthritis. If this complication occurs and the diagnosis of sepsis is confirmed, appropriate antimicrobial therapy should be instituted. Patients should understand the great importance of not overusing joints that are still diseased despite symptomatic improvement. Corticosteroids should not be injected into unstable joints.
Frequent intra-articular injections have been reported to cause development of Charcot-like arthropathies.
Use in pregnancy and lactation: There is inadequate evidence of safety in human pregnancy and there may be a very small risk of cleft palate and intra-uterine growth retardation in the fetus; there is evidence of harmful effect on pregnancy in animals. Infants born of mothers who have received substantial doses of corticosteroids during pregnancy should be carefully observed for signs of hypoadrenalism. When corticosteroids are essential however, patients with normal pregnancies may be treated as though they were in the non-gravid state. Patients with pre-eclampsia or fluid retention require close monitoring. Corticosteroids appear in breast milk and could suppress growth, interfere with endogenous corticosteroid production, or cause other unwanted effects. Mothers taking pharmacological doses of corticosteroids should be advised not to breast-feed.
Children: Corticosteroids cause growth retardation in infancy, childhood and adolescence, which may be irreversible. Treatment should be limited to the minimum dosage for the shortest possible time, in order to minimize suppression of the hypothalamic-pituitary adrenal axis and growth retardation, treatment should be limited, where possible, to a single dose on alternate days.
Growth and development of infants and children or prolonged corticosteroid therapy should be carefully monitored.
Corticosteroids may exacerbate systemic fungal infections and therefore, should not be used in the presence of such infections unless they are needed to control drug reactions due to amphotericin.
Moreover, there have been cases reported in which concomitant use of amphotericin and hydrocortisone was followed by cardiac enlargement and congestive failure.
Average and large doses of hydrocortisone or cortisone can cause elevation of blood pressure, retention of salt and water, and increased excretion of potassium, but these effects are less likely to occur with synthetic derivatives, except when in large dose. Dietary salt restriction and potassium supplementation may be necessary. All corticosteroids increase calcium excretion.
Administration of live virus vaccines is contraindicated in individuals receiving immunosuppressive doses of corticosteroids. If inactivated viral or bacterial vaccines are administered to individuals receiving immunosuppressive doses of corticosteroids, the expected serum antibody response may not be obtained, however, immunization procedures may be undertaken in patients who are receiving corticosteroids as replacement therapy, e.g. for Addison's disease.
Literature reports suggest an apparent association between use of corticosteroids and left ventricular free wall rupture after a recent myocardial infarction, therefore, therapy with corticosteroids should be used with great caution in these patients. The use of Dexamethasone sodium phosphate injection in active tuberculosis should be restricted to those cases of fulminating or disseminated tuberculosis in which the corticosteroid is used for the management of the disease in conjunction with an appropriate antituberculosis regimen. If the corticosteroids are indicated in patients with latent tuberculosis or tuberculin reactivity, close observation is necessary as reactivation may occur. During prolonged corticosteroid therapy, these patients should receive prophylactic chemotherapy. Corticosteroids may mask some signs of infection and new infections may appear during their use.
Suppression of the inflammatory response and immune function increases the susceptibility to infections and their severity. The clinical presentation may often be atypical, and serious infections such as septicemia and tuberculosis may be masked and reach an advanced stage before being recognized. There may be decreased resistance, and inability to localize infection.
A report shows that the use of corticosteroids in cerebral malaria is associated with a prolonged coma and an increased incidence of pneumonia and gastro-intestinal bleeding. Chickenpox is of particular concern, since this normally minor illness may be fatal in immune suppressed patients. Patients (or parents of children) without a definite history of chickenpox should be advised to avoid close personal contact with chickenpox or herpes zoster, and if exposed they should seek urgent medical attention. Passive immunization with varicella/zoster immunoglobulin (VZIG) is needed by exposed non-immune patients who are receiving systemic corticosteroids or who have used them within the previous 3 months, this should be given within 10 days of exposure to chickenpox. If a diagnosis of chickenpox is confirmed, the illness warrants specialist care and urgent treatment. Corticosteroids should not be stopped and the dose may need to be increased.
Measles can have a more serious or even fatal course in immune suppressed patients. In such children or adults particular care should be taken to avoid exposure to measles. If exposed, prophylaxis with intramuscular pooled immunoglobulin (IG) may be indicated. Exposed patients should be advised to seek medical advice without delay. Corticosteroids may activate latent amoebiasis or strongyloidiasis or exacerbate active disease. Therefore, it is recommended that latent or active amoebiasis and strongyloidiasis be ruled out before initiating corticosteroids therapy in any patient at risk or with symptoms of either condition. Prolonged use of corticosteroids may produce posterior subcapsular cataracts, glaucoma with possible damage to the optic nerves, and may enhance the establishment of secondary ocular infections due to fungi or viruses. Corticosteroids may increase or decrease motility and number of spermatozoa.
Special precautions: Particular care is required when considering use of systemic corticosteroids in patients with the following conditions, and frequent patient monitoring is necessary; renal insufficiency; hypertension, diabetes or in those with a family history of diabetes, congestive heart failure, osteoporosis, previous steroid myopathy, glaucoma (or family history of glaucoma), myasthenia gravis, non-specific ulcerative colitis, diverticulitis, fresh intestinal anastomoses, active or latent peptic ulcer existing or previous history of severe affective disorder (especially previous steroid psychosis), liver failure, and epilepsy. Signs of peritoneal irritation following gastro-intestinal perforation in patients receiving large doses of corticosteroids may be minimal or absent.
Fat embolism has been reported as a possible complication of hypercortisonism.
There is an enhanced effect or corticosteroids in patients with hypothyroidism and in those with cirrhosis.
Corticosteroids should be used cautiously in patients with ocular herpes simplex because of possible corneal perforation.
Local steroid injection should be undertaken in an aseptic environment to reduce the particular risk of bacterial infection. Injection of a steroid into an infected site should be avoided.
Appropriate examination of joint fluid is necessary to exclude a septic process.
A marked increase in pain accompanied by local swelling, further restriction of joint motion, fever and malaise are suggestive of septic arthritis. If this complication occurs and the diagnosis of sepsis is confirmed, appropriate antimicrobial therapy should be instituted. Patients should understand the great importance of not overusing joints that are still diseased despite symptomatic improvement. Corticosteroids should not be injected into unstable joints.
Frequent intra-articular injections have been reported to cause development of Charcot-like arthropathies.
Use in pregnancy and lactation: There is inadequate evidence of safety in human pregnancy and there may be a very small risk of cleft palate and intra-uterine growth retardation in the fetus; there is evidence of harmful effect on pregnancy in animals. Infants born of mothers who have received substantial doses of corticosteroids during pregnancy should be carefully observed for signs of hypoadrenalism. When corticosteroids are essential however, patients with normal pregnancies may be treated as though they were in the non-gravid state. Patients with pre-eclampsia or fluid retention require close monitoring. Corticosteroids appear in breast milk and could suppress growth, interfere with endogenous corticosteroid production, or cause other unwanted effects. Mothers taking pharmacological doses of corticosteroids should be advised not to breast-feed.
Children: Corticosteroids cause growth retardation in infancy, childhood and adolescence, which may be irreversible. Treatment should be limited to the minimum dosage for the shortest possible time, in order to minimize suppression of the hypothalamic-pituitary adrenal axis and growth retardation, treatment should be limited, where possible, to a single dose on alternate days.
Growth and development of infants and children or prolonged corticosteroid therapy should be carefully monitored.
Use In Pregnancy & Lactation
Since adequate human reproduction studies have not been done with corticosteroids, use of these drugs in pregnancy or in women of childbearing potential requires that the anticipated benefits be weighed against the possible hazards to the mother and embryo or fetus. Infants born of mothers who have received substantial doses of corticosteroids during pregnancy should be carefully observed for signs of hypoadrenalism.
Corticosteroids appear in breast milk and could suppress growth, interfere with endogenous corticosteroid production, or cause other unwanted effects. Mothers taking pharmacologic doses of corticosteroids should be advised not to nurse.
Corticosteroids appear in breast milk and could suppress growth, interfere with endogenous corticosteroid production, or cause other unwanted effects. Mothers taking pharmacologic doses of corticosteroids should be advised not to nurse.
Adverse Reactions
Na & fluid retention, CHF, K loss, hypokalemic alkalosis, HTN, increased Ca excretion; muscle weakness, steroid myopathy, loss of muscles mass, osteoporosis, vertebral compression fractures, aseptic necrosis of femoral & humeral heads, pathological fracture of long bones, tendon rupture & post inj flare (intra-articular); peptic ulcer w/ possible perforation & hemorrhage, small & large bowel perforation, pancreatitis, abdominal distension, ulcerative esophagitis, dyspepsia, esophageal candidiasis; impaired wound healing, thin fragile skin, petechiae & ecchymoses, erythema, striae, telangiectasia, acne, increased sweating, possible suppression of skin tests, burning or tingling in the perineal area (IV), allergic dermatitis, urticaria, angioneurotic edema & hypo- or hyper-pigmentation; convulsions, increased intracranial pressure w/ papilloedema, vertigo, headache, psychic disturbances (eg, euphoria, psychological dependence, depression, insomnia); menstrual irregularities, amenorrhea, development of Cushingoid state, suppression of growth in childn & adolescents, secondary adrenocortical & pituitary unresponsiveness (in times of stress), decreased carbohydrate tolerance, latent DM, increased insulin requirement or oral hypoglycemic agents in diabetes, hirsutism; opportunistic infections, recurrence of dormant TB; posterior subcapsular cataracts, IOP, papilloedema, corneal or scleral thinning, exacerbation of ophth viral disease, glaucoma, exophthalmos. -ve nitrogen balance due to protein catabolism, -ve Ca balance; hypertrophic cardiomyopathy in low birth-wt infants; hypersensitivity (anaphylaxis), leucocytosis, thromboembolism, wt gain, increased appetite, nausea, malaise, hiccups & sterile abscess; acute adrenal insufficiency, hypotension & death.
Drug Interactions
Aspirin should be used in conjunction with corticosteroids in hypoprothrombinemia.
The renal clearance of salicylates is increased by corticosteroids and therefore salicylate dosage should be reduced along with steroids withdrawal. As phenytoin, barbiturates, ephedrine, rifabutin, carbamazepine, rifampicin, and aminogluthetimide may enhance the metabolic clearance of corticosteroid, resulting in decreased blood levels and reduced physiological activity the dosage may have to be adjusted. These interactions may interfere with dexamethasone suppression tests which should be interpreted with caution during administration of these drugs.
False negative results in patients being treated with indomethacin have been reported.
The efficacy of coumarin anticoagulants may be changed by concurrent corticosteroid treatment. The prothrombin time should be checked frequently in patients who are receiving corticosteroids and coumarin anticoagulants at the same time in order to avoid spontaneous bleeding. The desired effects of hypoglycemic agents (including insulin), are antagonized by corticosteroids.
When corticosteroids are administered concomitantly with potassium-depleting diuretics, patients should be observed closely for development of hypokalemia.
Corticosteroids may affect the nitrobluetetrazolium test for bacterial infection and produce false-negative results.
The renal clearance of salicylates is increased by corticosteroids and therefore salicylate dosage should be reduced along with steroids withdrawal. As phenytoin, barbiturates, ephedrine, rifabutin, carbamazepine, rifampicin, and aminogluthetimide may enhance the metabolic clearance of corticosteroid, resulting in decreased blood levels and reduced physiological activity the dosage may have to be adjusted. These interactions may interfere with dexamethasone suppression tests which should be interpreted with caution during administration of these drugs.
False negative results in patients being treated with indomethacin have been reported.
The efficacy of coumarin anticoagulants may be changed by concurrent corticosteroid treatment. The prothrombin time should be checked frequently in patients who are receiving corticosteroids and coumarin anticoagulants at the same time in order to avoid spontaneous bleeding. The desired effects of hypoglycemic agents (including insulin), are antagonized by corticosteroids.
When corticosteroids are administered concomitantly with potassium-depleting diuretics, patients should be observed closely for development of hypokalemia.
Corticosteroids may affect the nitrobluetetrazolium test for bacterial infection and produce false-negative results.
Storage
Store at temperatures not exceeding 30°C. Protect from light.
Action
Pharmacology: Pharmacodynamics: Mechanism of Action: 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 inflammatory response, and suppression of humoral immune responses. Some of the net effects include reduction in edema or scar tissue and a general suppression in immune response. The 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.
Orally inhaled corticosteroid hormones are believed to reduce the immediate and late-phase allergic responses associated with chronic bronchial asthma. Proposed mechanisms of action include decreased IgE synthesis, increased number of beta-adrenergic receptors on leukocytes, and decreased arachidonic acid metabolism, which decreases the amount of prostaglandins and leukotrienes released. Chronic bronchial asthma is associated with increased peribronchial edema and mucus secretions, which can be decreased with corticosteroid therapy. During an immediate allergic reaction, allergens bridge the IgE antibodies on the surface of mast cells, which triggers these cells to release chemotactic substances. Mast cell influx and activation, therefore, is partially responsible for the inflammation and hyperirritability of the oral mucosa in asthmatic patients. This inflammation can be retarded by administration of adrenocorticoids.
Pharmacokinetics: Dexamethasone is administered via oral, intravenous, intramuscular, intra-articular, intravitreal, ophthalmic, otic, and topical routes. 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 1.8-3.5 hours whereas the biological half-life is 36-54 hours.
Affected cytochrome P450 isoenzymes and drug transporter: CYP3A4, P-gp.
Dexamethasone is an inducer of CYP3A4 and is a substrate for both P-glycoprotein (P-gp) and CYP3A4.
Orally inhaled corticosteroid hormones are believed to reduce the immediate and late-phase allergic responses associated with chronic bronchial asthma. Proposed mechanisms of action include decreased IgE synthesis, increased number of beta-adrenergic receptors on leukocytes, and decreased arachidonic acid metabolism, which decreases the amount of prostaglandins and leukotrienes released. Chronic bronchial asthma is associated with increased peribronchial edema and mucus secretions, which can be decreased with corticosteroid therapy. During an immediate allergic reaction, allergens bridge the IgE antibodies on the surface of mast cells, which triggers these cells to release chemotactic substances. Mast cell influx and activation, therefore, is partially responsible for the inflammation and hyperirritability of the oral mucosa in asthmatic patients. This inflammation can be retarded by administration of adrenocorticoids.
Pharmacokinetics: Dexamethasone is administered via oral, intravenous, intramuscular, intra-articular, intravitreal, ophthalmic, otic, and topical routes. 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 1.8-3.5 hours whereas the biological half-life is 36-54 hours.
Affected cytochrome P450 isoenzymes and drug transporter: CYP3A4, P-gp.
Dexamethasone is an inducer of CYP3A4 and is a substrate for both P-glycoprotein (P-gp) and CYP3A4.
MedsGo Class
Corticosteroid Hormones
Features
Dosage
4 mg / mL
Ingredients
- Dexamethasone
Packaging
Solution for Injection (I.M./I.V.) 2ml x 10's
Generic Name
Dexamethasone Sodium Phosphate
Registration Number
DR-XY17291
Classification
Prescription Drug (RX)
Product Questions
Questions
