Corticosteroids depression with

Adrenal steroids chronic corticosteroid therapy with the equivalent of prednisolone 10 mg daily within the previous 3 months suppresses the hypothalamic-pituitary-adrenal system. Without steroid supplementation perioperatively the patient may fail to respond appropriately to the stress of surgery and become hypotensive (see Ch. 34). A single dose of etomidate depresses the hypothalamic-pituitary-adrenal axis for a few hours but this is not associated with an adverse outcome. 

Stroke induces an acute stress response—i.e., over-activation of the sympathetic nervous system and increased corticosteroid levels (with resultant neutrophiha and lymphocytopenia). This in turn leads to depressed immunity and altered immune responses during the acute phase of stroke and may predispose patients to infections, particularly pneumonia, which is the commonest cause of mortality after the first few days of stroke (Meisel et al., 2005). In the clinical setting, increased total white cell counts and neutrophilia, which correlate with infarct size, are independently associated with worse outcome after stroke. Recently a massive and early activation of the systemic immnne system has been shown to occur also in experimental stroke (Offner et al., 2006). 

Vaccinations containing live organisms are not administered within 3 months of immune globulin administration because antibodies in the globulin preparation may interfere with the immune response to the vaccination. Corticosteroids, antineoplastic dru, and radiation therapy depress the immune system to such a degree that insufficient numbers of antibodies are produced to prevent the disease. When the salicylates are administered with the varicella vaccination, there is an increased risk of Reye s syndrome developing. 

Prednisone -corticosteroid -leukocytosis -nausea and vomiting indigestion -anorexia or increased appetite -CNS effects (depression, anxiety, euphoria, insomnia, psychosis, confusion) -fluid retention -hyperglycemia -osteoporosis -acne -adrenal insufficiency with prolonged use... 

Adverse reactions of corticosteroids are frequent with the long-term immunosuppressive regimens which are often needed and include an increased risk of infections, Cushing-like symptoms, hypertension, hyperglycemia, osteoporosis, growth retardation in children and mental reactions such as dysphoria, psychosis and depression. 

Treatment with guanidine may produce clinical improvement within 3 to 4 days. Side effects include paresthesia, gastrointestinal distress, renal tubular necrosis, and hyperirritability. The most serious effect is bone marrow depression, which is dose-related and potentially fatal. Aminopyridines have been used in clinical studies with some positive results. Corticosteroids and plasmapheresis may also be of some benefit, whereas anticholinesterase agents are only marginally effective. 

Wada K, Suzuki H, Taira T, Akiyama K, Kuroda S. Successful use of intravenous clomipramine in depressive-catatonic state associated with corticosteroid treatment. Int J Psych Clin Pract 2004 8 131-3. 

Patten SB, Williams JV, Love EJ. Self-reported depressive symptoms following treatment with corticosteroids and sedative-hypnotics. Int J Psychiatry Med 1996 26(l) 15-24. 

Intralesional injection of steroid can lead to adrenal suppression. Infents and small children are especially susceptible, because a given amoimt of steroid is distributed in a smaller volume of fluid and tissue compartments. Infents injected with mixtiu es of triamcinolone acetonide and betamethasone or dexamethasone fiar periocular hemangiomas exhibited depressed serum cortisol and adrenocorticotropic hormone levels. The adrenal suppression can last up to 5 months and can result in weight loss and growth retardation. It is not known whether other corticosteroid preparations would produce similar effects or which other fectors might influence these results. In general, topical and periocular use of steroids produces minimal systemic effects. Withdrawal of topical or periocular steroids does not generally cause adrenal crisis. 

Medical surveillance may be indicated in persons with predisposing skin, liver, kidney, or respiratory conditions. General life-support should be maintained, symptoms treated and decontamination considered if necessary. Treatment is generally symptomatic and supportive. The patient should be monitored for delayed liver and kidney damage. If central nervous system depression occurs, EKG and vital signs should be monitored carefully. Patients who exhibit dermal hypersensitivity may require systemic or topical antihistamines or corticosteroids. 

Clinically, the animals do not show signs until 24-48 or more hours after ingestion of the bait. The affected animals are depressed, have reduced urine production, and the urine is of low specific gravity. Severely poisoned animals have hematemesis, azotemia, and cardiac arrhythmias. Animals with renal impairment are more susceptible to cholecalciferol poisoning than those with normal renal function. Cholecalciferol poisoning requires protracted treatment, which may require as long as 3 weeks in severe intoxications. Appropriate treatment consists of fluid therapy to assist the kidneys in removing the excess calcium, corticosteroids to minimize inflammation, and calcitonin to enhance calcium resorption into the bone. Pamidronate disodium is the new antidote for this poison. 

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