Steroid injection induced meningitis

Depending on timing, intra-tympanic steroid injection is also offered (dexamethasone 10-24mg/cc). Intra-typmpanic steroid injection is performed by inserting a needle through the eardrum and injecting about of highly concentrated steroids directly into the middle ear space. The patient is than instructed to keep the affected ear up for 30 minutes without swallowing, yawning, or popping the ear. After injection, the patient is allowed to immediately resume normal activities. This steroid injection has also been used to treat Meniere's Disease flare-ups.

The adverse effects of corticosteroids in pediatric patients are similar to those in adults (see ADVERSE REACTIONS ). Like adults, pediatric patients should be carefully observed with frequent measurements of blood pressure, weight, height, intraocular pressure, and clinical evaluation for the presence of infection, psychosocial disturbances, thromboembolism , peptic ulcers, cataracts, and osteoporosis. Pediatric patients who are treated with corticosteroids by any route, including systemically administered corticosteroids, may experience a decrease in their growth velocity. This negative impact of corticosteroids on growth has been observed at low systemic doses and in the absence of laboratory evidence of HPA axis suppression (., cosyntropin stimulation and basal cortisol plasma levels). Growth velocity may therefore be a more sensitive indicator of systemic corticosteroid exposure in pediatric patients than some commonly used tests of HPA axis function. The linear growth of pediatric patients treated with corticosteroids should be monitored, and the potential growth effects of prolonged treatment should be weighed against clinical benefits obtained and the availability of treatment alternatives. In order to minimize the potential growth effects of corticosteroids, pediatric patients should be titrated to the lowest effective dose.

An acute myopathy has been observed with the use of high doses of corticosteroids, most often occurring in patients with disorders of neuromuscular transmission (., myasthenia gravis ), or in patients receiving concomitant therapy with neuromuscular blocking drugs (., pancuronium). This acute myopathy is generalized, may involve ocular and respiratory muscles, and may result in quadriparesis . Elevations of creatine kinase may occur. Clinical improvement or recovery after stopping corticosteroids may require weeks to years.

Steroids should be used with caution in nonspecific ulcerative colitis, if there is a probability of impending perforation, abscess, or other pyogenic infection, also in diverticulitis, fresh intestinal anastomoses, active or latent peptic ulcer, renal insufficiency, hypertensions, osteoporosis, and myasthenia gravis. Signs of peritoneal irritation following gastrointestinal perforation in patients receiving large odses of corticosteroids may be minimal or absent. Fat embolism has been reported as a possible complication of hypercortisonism.

Glucocorticoid therapy is associated with an appreciable risk of bone loss, which is most pronounced in the first few months of use. In addition, glucocorticoids increase fracture risk, and fractures occur at higher bone mineral density (BMD) values than occur in postmenopausal osteoporosis. The increased risk of fracture has been reported with doses of prednisone or its equivalent as low as to mg daily [ 1 ]. Thus, glucocorticoid-induced bone loss should be treated aggressively, particularly in those already at high risk for fracture (older age, prior fragility fracture). In other individuals, clinical risk factor and bone density assessment may help guide therapy. The prevention and treatment of glucocorticoid-induced bone loss will be reviewed here. The clinical features are reviewed separately. (See "Clinical features and evaluation of glucocorticoid-induced osteoporosis" .)

Steroid injection induced meningitis

steroid injection induced meningitis

Steroids should be used with caution in nonspecific ulcerative colitis, if there is a probability of impending perforation, abscess, or other pyogenic infection, also in diverticulitis, fresh intestinal anastomoses, active or latent peptic ulcer, renal insufficiency, hypertensions, osteoporosis, and myasthenia gravis. Signs of peritoneal irritation following gastrointestinal perforation in patients receiving large odses of corticosteroids may be minimal or absent. Fat embolism has been reported as a possible complication of hypercortisonism.

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