Dexavet

Contraindicated in pregnant animals due to causes abortion

Dexamethasone is a corticosteroid with anti-inflammatory and immunosuppressive effects that are approximately 30 times more potent than cortisol and 6–7 times more potent than prednisolone. Anti-inflammatory effects are complex but primarily occur via inhibition of inflammatory cells and suppression of expression of inflammatory mediators. The difference among formulations is that dexamethasone sodium phosphate is a water-soluble formulation that can be injected intravenously. Dexamethasone solution is in a polyethylene glycol vehicle that should not be administered rapidly intravenously.

Glucocorticoids have effects on virtually every cell type and system in mammals. An overview of the effects of these agents follows: 

Cardiovascular System: Glucocorticoids can reduce capillary permeability and enhance vasoconstriction. A relatively clinically insignificant positive inotropic effect can occur after glucocorticoid administration. Increased blood pressure can result from both the drugs’ vasoconstrictive properties and increased blood volume that may be produced.
Cells: Glucocorticoids inhibit fibroblast proliferation, macrophage response to migration inhibiting factor, sensitization of lymphocytes and the cellular response to mediators of inflammation. Glucocorticoids stabilize lysosomal membranes.
CNS/Autonomic Nervous System: Glucocorticoids can lower seizure threshold, alter mood and behavior, diminish the response to pyrogens, stimulate appetite and maintain alpha rhythm. Glucocorticoids are necessary for normal adrenergic receptor sensitivity. 

Endocrine System: When animals are not stressed, glucocorticoids will suppress the release of ACTH from the anterior pituitary, thereby reducing or preventing the release of endogenous corticosteroids. Stress factors (e.g., renal disease, liver disease, diabetes) may sometimes nullify the suppressing aspects of exogenously administered steroids. Release of thyroid-stimulating hormone (TSH), follicle-stimulating hormone (FSH), prolactin, and luteinizing hormone (LH) may all be reduced when glucocorticoids are administered at pharmacological doses. Conversion of thyroxine (T4) to triiodothyronine (T3) may be reduced by glucocorticoids; plasma levels of parathyroid hormone
increased. Glucocorticoids may inhibit osteoblast function. Vasopressin (ADH) activity is reduced at the renal tubules and diuresis may occur. Glucocorticoids inhibit insulin binding to insulin-receptors and the postreceptor effects of insulin.
Hematopoietic System: Glucocorticoids can increase the numbers of circulating platelets, neutrophils and red blood cells, but platelet aggregation is inhibited. Decreased amounts of lymphocytes (peripheral), monocytes and eosinophils are seen as glucocorticoids can sequester these cells into the lungs and spleen and prompt decreased release from the bone marrow. Removal of old red blood cells becomes diminished. Glucocorticoids can cause involution of lymphoid tissue.
GI Tract and Hepatic System: Glucocorticoids increase the secretion of gastric acid, pepsin, and trypsin. They alter the structure of mucin and decrease mucosal cell proliferation. Iron salts and calcium absorption are decreased while fat absorption is increased. Hepatic changes can include increased fat and glycogen deposits within hepatocytes, increased serum levels of alanine aminotransferase (ALT), and gamma-glutamyl transpeptidase (GGT). Significant increases can be seen in serum alkaline phosphatase levels. Glucocorticoids can cause minor increases in BSP (bromosulfophthalein) retention time.
Immune System (also see Cells and Hematopoietic System): Glucocorticoids can decrease circulating levels of T-lymphocytes; inhibit lymphokines; inhibit neutrophil, macrophage, and monocyte migration; reduce production of interferon; inhibit phagocytosis and chemotaxis; antigen processing; and diminish intracellular killing. Specific acquired immunity is affected less than nonspecific immune responses. Glucocorticoids can also antagonize the complement cascade and mask the clinical signs of infection.
Mast cells are decreased in number and histamine synthesis is suppressed. Many of these effects only occur at high or very high doses and there are species differences in response.
Metabolic effects: Glucocorticoids stimulate gluconeogenesis. Lipogenesis is enhanced in certain areas of the body (e.g., abdomen) and adipose tissue can be redistributed away from the extremities to the trunk. Fatty acids are mobilized from tissues and their oxidation is increased. Plasma levels of triglycerides, cholesterol, and glycerol are increased. Protein is mobilized from most areas of the body (not the liver).
Musculoskeletal: Glucocorticoids may cause muscular weakness (also caused if there is a lack of glucocorticoids), atrophy, and osteoporosis. Bone growth can be inhibited via growth hormone and somatomedin inhibition, increased calcium excretion and inhibition of vitamin D activation. Resorption of bone can be enhanced. Fibrocartilage growth is also inhibited.
Ophthalmic: Prolonged corticosteroid use (both systemic or topically to the eye) can cause increased intraocular pressure and glaucoma, cataracts, and exophthalmos. Renal, Fluid, & Electrolytes: Glucocorticoids can increase potassium and calcium excretion, sodium and chloride reabsorption, and extracellular fluid volume. Hypokalemia and/or hypocalcemia rarely occur. Diuresis may develop following glucocorticoid administration.
Skin: Thinning of dermal tissue and skin atrophy can be seen with glucocorticoid therapy. Hair follicles can become distended and alopecia may occur.

The following drug interactions have either been reported or are theoretical in humans or animals receiving dexamethasone and may be of significance in veterinary patients:
AMPHOTERICIN B: Administered concomitantly with glucocorticoids may cause hypokalemia
ANTICHOLINESTERASE AGENTS (e.g., pyridostigmine, neostigmine, etc.): In patients with myasthenia gravis, concomitant glucocorticoid and anticholinesterase agent administration may lead to profound muscle weakness. If possible, discontinue anticholinesterase medication at least 24 hours prior to corticosteroid administration
ASPIRIN: Glucocorticoids may reduce salicylate blood levels
BARBITURATES: May increase the metabolism of glucocorticoids and decrease dexamethasone blood levels
CYCLOPHOSPHAMIDE: Glucocorticoids may also inhibit the hepatic metabolism of cyclophosphamide; dosage adjustments may be required
CYCLOSPORINE: Concomitant administration of glucocorticoids and cyclosporine may increase the blood levels of each, by mutually inhibiting the hepatic metabolism of each other; the clinical significance of this interaction is not clear
DIAZEPAM: Dexamethasone may decrease diazepam levels
DIURETICS, POTASSIUM-DEPLETING (e.g., spironolactone, triamterene): Administered concomitantly with glucocorticoids may cause hypokalemia
EPHEDRINE: May reduce dexamethasone blood levels and interfere with dexamethasone suppression tests
INDOMETHACIN: Can cause false negative test results in the dexamethasone suppression test
INSULIN: Insulin requirements may increase in patients receiving glucocorticoids
KETOCONAZOLE AND OTHER AZOLE ANTIFUNGALS: May decrease the metabolism of glucocorticoids and increase dexamethasone blood levels; ketoconazole may induce adrenal insufficiency when glucocorticoids are withdrawn by inhibiting adrenal corticosteroid synthesis
MACROLIDE ANTIBIOTICS (erythromycin, clarithromycin): May decrease the metabolism of glucocorticoids and increase dexamethasone blood levels
MITOTANE: May alter the metabolism of steroids; higher than usual doses of steroids may be necessary to treat mitotane-induced adrenal insufficiency
NSAIDS: Administration of ulcerogenic drugs with glucocorticoids may increase the risk of gastrointestinal ulceration
PHENYTOIN: May increase the metabolism of glucocorticoids and decrease dexamethasone blood levels
RIFAMPIN: May increase the metabolism of glucocorticoids and decrease dexamethasone blood levels
DEXAMETHASONE: In dogs, dexamethasone increased quinidine volume of distribution (49-78%) and elimination half-life (1.5-2.3X). (Zhang et al. 2006)
VACCINES: Patients receiving corticosteroids at immunosuppressive dosages should generally not receive live attenuated-virus vaccines as virus replication may be augmented; a diminished immune response may occur after vaccine, toxoid, or bacterin administration in patients receiving glucocorticoids

Side effects from corticosteroids are many and include polyphagia, polydipsia and polyuria, and hypothalamic–pituitary–adrenal (HPA) axis suppression. Adverse effects include GI ulceration, hepatopathy, increased risk of diabetes, hyperlipidemia, decreased thyroid hormone, decreased protein synthesis, delayed wound healing, and immunosuppression. Secondary infections can occur as a result of immunosuppression and include infections from Demodex spp., toxoplasmosis, fungal infections, and urinary tract infections (UTIs). High-dose glucocorticoids in animals with neurologic disease can lead to excitotoxic cell death and oxidative injury via increased excitatory amino acids. In horses, dexamethasone adverse effects have included risk of laminitis, although this effect is controversial and not supported by strong evidence.

Use cautiously in patients prone to ulcers or infection or in animals in which
wound healing is necessary. Use cautiously in animals with diabetes or renal
failure and in pregnant animals.