Depo-Medrol z Lidokainą

MGPC (myristyl-gamma-picolinium chloride) formulation This medicinal product is for single use only. After the required dose has been administered, any remaining suspension must be discarded. Although crystals of adrenal steroids in the skin suppress inflammatory reactions, their presence may lead to disintegration of cellular elements and to physicochemical changes in the ground substance of connective tissue. The resulting, infrequent dermal and/or subdermal changes may produce depressions in the skin at the injection site. The degree of this reaction varies with the amount of adrenal steroid injected. Full regeneration usually occurs over several months or once all crystals of adrenal steroid have been absorbed. To minimise the incidence of dermal and subdermal atrophy, care must be taken not to exceed the recommended doses for injection. Whenever possible, multiple small injections into the lesion should be used. The technique of intrasynovial and intramuscular injection also requires care to avoid injection or leakage of material into the dermis. Because of the high incidence of subcutaneous atrophy, injection into the deltoid muscle should be avoided. DEPO-MEDROL must not be administered by any route other than those listed in section 4.1. It is essential that proper techniques be used for administration of DEPO-MEDROL in order for the drug to exert its intended action. Serious adverse events have been reported in association with the intrathecal/epidural route of administration (see section 4.8 Undesirable effects). Appropriate measures must be taken to avoid intravascular injection. Special warnings and precautions Intrasynovial injection of corticosteroids may produce systemic as well as local effects. The presence of microbes in the synovial fluid should be tested in order to exclude an infectious process. Marked joint pain, accompanied by swelling, restriction of motion, fever, and malaise is suggestive of septic arthritis. If these symptoms persist and septic arthritis is confirmed, appropriate antibiotic therapy should be initiated. Local injection of a steroid into an infected joint is to be avoided, as is injection into an unstable joint. Strict aseptic technique is mandatory to prevent contamination. It should be borne in mind that the active substance is absorbed more slowly following intramuscular administration. Immunosuppressant effects/increased susceptibility to infections Corticosteroids may increase susceptibility to infection, may mask some signs of infection, exacerbate existing infections, increase the risk of reactivation or exacerbation of latent infections, and new infections may emerge during their use. Decreased resistance and inability to localise infections may occur with corticosteroid use. Any type of viral, bacterial, fungal, or parasitic infection, at any site, may develop in patients treated with corticosteroids alone or in combination with other immunosuppressants affecting cellular or humoral immunity or neutrophil function. These infections may be mild but may also be severe and at times fatal. The rate of infectious complications increases with increasing corticosteroid doses. Monitor for the development of infection and, where appropriate, consider discontinuation of the corticosteroid or dose reduction. To achieve a local effect during an acute infection, administration into synovia, bursae, or tendons is not recommended. Persons receiving medicines that suppress the immune system are more susceptible to infection than healthy individuals. For example, chickenpox and measles may have a more serious or even fatal course in immunocompromised children or in adults taking corticosteroids. Administration of live or live-attenuated vaccines is contraindicated in patients receiving immunosuppressive doses of corticosteroids. Killed or inactivated vaccines may be administered to patients receiving immunosuppressive doses of corticosteroids; however, the response to such vaccines may be diminished. Indicated immunisation procedures may be undertaken in patients receiving non-immunosuppressive doses of corticosteroids. The use of corticosteroids in active tuberculosis should be restricted to cases of fulminating or disseminated tuberculosis in which corticosteroids are used in conjunction with an appropriate antituberculous regimen. If corticosteroids are indicated in patients with latent tuberculosis or tuberculin reactivity, close observation is necessary, as reactivation of disease may occur. During prolonged corticosteroid therapy, these patients should receive chemoprophylaxis. Kaposi's sarcoma has been reported in patients receiving corticosteroid therapy. Discontinuation of corticosteroids may result in clinical remission. The role of corticosteroids in septic shock has been controversial, with early studies reporting both beneficial and harmful effects. More recently, supplemental corticosteroids have been suggested to be beneficial in patients with persistent septic shock who exhibit adrenal insufficiency. However, their routine use in septic shock is not recommended. A systematic review of short-course, high-dose corticosteroids did not support their use. However, meta-analyses and reviews suggest that longer courses (5–11 days) of low-dose corticosteroids may reduce mortality, particularly in patients with vasopressor-dependent septic shock. Effects on the immune system Allergic reactions may occur. Because skin reactions and anaphylactic/anaphylactoid reactions have been reported on rare occasions in patients receiving corticosteroid therapy, appropriate precautions should be taken before administration, particularly when the patient has a history of allergy to any medicinal product. Effects on the endocrine system In patients receiving corticosteroid therapy who are subjected to unusual stress, increased doses of rapidly acting corticosteroids are indicated before, during, and after the stressful situation. Pharmacological doses of corticosteroids administered over a prolonged period may result in suppression of the hypothalamic-pituitary-adrenal (HPA) axis (secondary adrenocortical insufficiency). The degree and duration of the resulting adrenocortical insufficiency vary among patients and depend on the dose, frequency, time of administration, and duration of glucocorticoid therapy. This effect may be minimised by use of alternate-day therapy. If glucocorticoids are withdrawn abruptly, acute adrenal insufficiency may develop, leading to a fatal outcome. Drug-induced secondary adrenal insufficiency may therefore be minimised by gradual dose reduction. This type of relative insufficiency may persist for several months after discontinuation of therapy; therefore, in any stressful situation occurring during this period, hormone therapy should be reinstituted. A "withdrawal syndrome" on steroid discontinuation, probably unrelated to adrenocortical insufficiency, includes symptoms such as: anorexia, nausea, vomiting, lethargy, headache, fever, joint pain, desquamation, muscle pain, weight loss, and/or hypotension. These effects are thought to be due to a sudden change in glucocorticoid concentration rather than to low corticosteroid levels. As glucocorticoids may worsen the condition of patients with Cushing's syndrome, the administration of glucocorticoids in these patients is not recommended. The effect of corticosteroids is enhanced in patients with hypothyroidism. Metabolism and nutrition disorders Corticosteroids, including methylprednisolone, may increase blood glucose levels, worsen pre-existing diabetes mellitus, and predispose patients on long-term corticosteroid therapy to diabetes mellitus. Psychiatric effects Psychiatric disturbances may occur during corticosteroid therapy, including euphoria, insomnia, mood swings, personality changes, severe depression, and psychotic manifestations. Pre-existing emotional instability or psychotic tendencies may also be aggravated. Potentially severe psychiatric adverse reactions may occur with systemic steroids. Symptoms typically emerge within a few days or weeks of starting treatment. Most reactions resolve after dose reduction or withdrawal, although specific treatment may be required. Psychological effects have been reported on withdrawal of corticosteroids; the frequency is not known. Patients/carers should be encouraged to seek medical advice if psychological symptoms develop in the patient, especially if depressed mood or suicidal ideation is suspected. Patients/carers should be alert to possible psychiatric disturbances that may occur either during or immediately after dose reduction/withdrawal of systemic steroids. Effects on the nervous system Corticosteroids should be used with caution in patients with seizure disorders. Corticosteroids should be used with caution in patients with myasthenia gravis (see also myopathy under Musculoskeletal effects). Cases of epidural lipomatosis have been reported in patients taking corticosteroids, typically with long-term use at high doses. Effects on the eye Visual disturbances may be reported with systemic and topical corticosteroid use. If a patient presents with symptoms such as blurred vision or other visual disturbances, the patient should be considered for referral to an ophthalmologist for evaluation of possible causes, which may include cataract, glaucoma, or rare diseases such as central serous chorioretinopathy (CSCR), which has been reported after the use of systemic and topical corticosteroids. Central serous chorioretinopathy may lead to retinal detachment. Prolonged use of corticosteroids may produce posterior subcapsular cataracts and nuclear cataracts (particularly in children), exophthalmos, or increased intraocular pressure, which may result in glaucoma with possible damage to the optic nerve. The establishment of secondary fungal and viral infections of the eye may also be enhanced in patients receiving glucocorticoids. In patients with ocular involvement in herpes simplex infection, corticosteroids should be used with caution because of the risk of corneal perforation. Effects on the cardiovascular system Adverse effects of glucocorticoids on the cardiovascular system, such as dyslipidaemia and hypertension, may predispose patients treated with these agents and with existing cardiovascular risk factors to further cardiovascular events when high doses are used over prolonged periods. Accordingly, corticosteroids should be used judiciously in such patients, with attention given to the modifiable risk and, if necessary, additional cardiac monitoring. Systemic corticosteroids should be used with caution, and only when strictly necessary, in cases of congestive heart failure. Effects on the vascular system Thrombosis, including venous thromboembolism, has been reported with corticosteroid use. As a result, corticosteroids should be used with caution in patients who have or may be predisposed to thromboembolic disorders. Corticosteroids should be used with caution in patients with hypertension. Effects on the gastrointestinal system High doses of corticosteroids may induce acute pancreatitis. There is no universal agreement as to whether corticosteroids per se are responsible for peptic ulcers occurring during therapy. Glucocorticoid therapy may mask the symptoms of peptic ulcer, so that perforation or haemorrhage may occur without significant pain. Glucocorticoid therapy may mask peritonitis or other signs or symptoms associated with gastrointestinal disorders such as perforation, obstruction, or pancreatitis. In combination with non-steroidal anti-inflammatory drugs (NSAIDs), the risk of developing gastrointestinal ulcers is increased. Corticosteroids should be used with caution in patients with non-specific ulcerative colitis if there is a probability of impending perforation, abscess, or other pyogenic infection, as well as in patients with diverticulitis, fresh intestinal anastomoses, or active or latent peptic ulcer. Hepatobiliary effects Hepatobiliary disorders have been reported, which in most cases were reversible after discontinuation of therapy. Appropriate monitoring is therefore required. Effects on the musculoskeletal system Acute myopathy has been reported with the use of high doses of corticosteroids, most often in patients with disorders of neuromuscular transmission (e.g. myasthenia gravis) or in patients receiving concomitant anticholinergic therapy, such as neuromuscular blocking agents (e.g. pancuronium). This acute myopathy is generalised, may involve ocular and respiratory muscles, and may result in quadriparesis. Elevation of creatine kinase may occur. Clinical improvement or recovery after discontinuation of corticosteroids may take weeks to months. Osteoporosis is a common but infrequently recognised adverse effect associated with long-term use of high-dose glucocorticoids. Effects on the liver and biliary system Drug-induced liver injury, including acute hepatitis or elevation of hepatic enzymes, may result from cyclical pulsed intravenous administration of methylprednisolone (usually at an initial dose ≥ 1 g/day). Rare cases of hepatotoxicity have been reported. The time to onset may be several weeks or longer. In most reported cases, the adverse reactions resolved after discontinuation of treatment. Patients should therefore be monitored appropriately. Renal and urinary disorders Caution is required in patients with systemic sclerosis because of an increased incidence of scleroderma renal crisis observed with corticosteroids, including methylprednisolone. Corticosteroids should be used with caution in patients with renal insufficiency. No dose adjustment is required in renal failure. Methylprednisolone is dialysable. Investigations Moderate and high doses of hydrocortisone or cortisone can cause elevation of blood pressure, sodium and water retention, and increased excretion of potassium. These effects are less likely to occur with synthetic glucocorticoid derivatives except when used in high doses. Dietary salt restriction and potassium supplementation may be necessary in patients receiving such treatment. All corticosteroids increase calcium excretion. Injury, poisoning and procedural complications Systemic corticosteroids are not indicated and therefore should not be used routinely in the treatment of traumatic brain injury. A multicentre study revealed an increase in mortality at 2 weeks and 6 months after injury in patients who received methylprednisolone sodium succinate compared with patients receiving placebo. A causal association with methylprednisolone sodium succinate treatment has not been established. Other Because complications of glucocorticoid therapy depend on the dose and duration of treatment, a risk/benefit decision must be made in each individual case as to the dose and duration of treatment and whether daily or intermittent therapy should be used. Concomitant treatment with CYP3A inhibitors, including cobicistat-containing products, is expected to increase the risk of systemic adverse effects. The combination should be avoided unless the benefit outweighs the increased risk of systemic corticosteroid adverse effects, in which case patients should be monitored for systemic corticosteroid adverse effects (see section 4.5). Acetylsalicylic acid and non-steroidal anti-inflammatory drugs should be used cautiously in conjunction with corticosteroids. Concomitant use of oral anticoagulants and methylprednisolone may increase the risk of bleeding. Diminished effects of oral anticoagulants have also been reported. Frequent monitoring of prothrombin time (INR) is recommended in patients receiving vitamin K antagonists, particularly during initiation of therapy or adjustment of the methylprednisolone dose (see section 4.5). Phaeochromocytoma crisis, which can be fatal, has been reported after administration of systemic corticosteroids. Corticosteroids should only be administered to patients with suspected or identified phaeochromocytoma after an appropriate risk/benefit evaluation. Tumour lysis syndrome (TLS) has been reported in the post-marketing setting in patients with malignancies, including haematological malignancies and solid tumours, following the use of systemic corticosteroids alone or in combination with other chemotherapeutic agents. Patients at high risk of TLS, such as patients with cancers that have a high proliferative rate, high tumour burden, and high sensitivity to cytotoxic agents, should be closely monitored and appropriate measures taken. Thyrotoxic periodic paralysis (TPP) may occur in patients with hyperthyroidism and methylprednisolone-induced hypokalaemia. TPP should be suspected in patients treated with methylprednisolone who exhibit signs or symptoms of muscle weakness, particularly in patients with hyperthyroidism. If TPP is suspected, blood potassium levels should be monitored immediately and corrected as appropriate to ensure restoration of normal blood potassium levels. Use in children Growth and development of children on prolonged corticosteroid therapy should be carefully monitored. Growth may be suppressed in children receiving long-term, daily divided-dose glucocorticoid therapy, and use of such a regimen should be restricted to the most urgent indications. Alternate-day glucocorticoid therapy usually avoids or minimises these adverse effects. Infants and children on prolonged corticosteroid therapy are at particular risk of increased intracranial pressure. High doses of corticosteroids may induce pancreatitis in children. Depo-Medrol contains less than 1 mmol (23 mg) of sodium per millilitre of suspension, that is to say, essentially "sodium-free".