Download Glucocorticoids

Glucocorticoids:
Use and Misuse
Butch KuKanich, DVM, PhD, DACVCP
Kansas State University
Manhattan, KS
Glucocorticoids
Prednisone is a commonly used glucocorticoid. Prednisone is a pro-drug, therefore it must be metabolized to prednisolone to elicit its
pharmacologic effect. Cats are variable metabolizers of prednisone to prednisolone, so the effect will also be variable and less
predictable in cats.
Prednisolone is recommended for use in cats as it is pharmacologically active and does not need to undergo metabolism to be
effective. Prednisone/prednisolone has predominant glucocorticoid effects, but does have some mineralocorticoid effects as well. As
such fluid and sodium retention occurs which can result in pulmonary edema in patients even with subclinical and undiagnosed
cardiac dysfunction.
Dexamethasone is a glucocorticoid with essentially no mineralocorticoid effects, therefore the retention of fluid and sodium is
much less compared to prednisone/prednisolone. Dexamethasone is the glucocorticoid of choice in most patients with cardiac
dysfunction. Gastric adverse effects (vomiting, diarrhea, gastritis, erosions and ulcerations) appear to more frequent with
dexamethasone compared to prednisone/prednisolone. It is unclear if the increased risk is inherent to the drug or due to incorrect
dosages. Dexamethasone is approximately 10x more potent than prednisone/prednisolone, therefore an equivalent dose is 1/10.
Additionally, the duration of effect of dexamethasone is longer then prednisone/prednisolone, therefore it needs to be dosed less
frequently. For example, 2 mg of dexamethasone PO q 48 hours produces near equivalent glucocorticoid effects as 20 mg of
prednisone/prednisolone q 24 hours in dog/cats.
Injectable dexamethasone formulations are often confusing in their use in veterinary medicine. Dexamethasone solution is a 2
mg/mL solution of dexamethasone (free base) dissolved in polyethylene glycol due to the poor water solubility dexamethasone (free
base). Dexamethasone sodium phosphate is a water soluble formulation of dexamethasone solution in water. The onset of effect and
duration of effect for IV administration of either formulation will be near identical if equal doses are administered. IM or SC
administration of dexamethasone solution may have a slightly delayed absorption, but is unlikely to be clinically appreciated.
Repository formulations of glucocorticoids (methylprednisolone acetate, triamcinolone acetonide) should not be used systemically
in dogs and should only be used as a last resort in cats due to the increased risk and severity compared to oral glucocorticoids. Oral
glucocorticoids can be rapidly discontinued if adverse effects occur, but once a repository formulation is administered it cannot be
discontinued.
Glucocorticoid physiologic replacement therapy
Glucocorticoid physiologic replacement therapy is used when endogenous glucocorticoids are insufficient to maintain normal
processes. The primary indication is hypoadrenocorticism (Addison’s Disease). The recommended prednisone/prednisolone dose in
dogs is 0.2 mg/kg/d. An equivalent dexamethasone dose would be 0.02 mg/kg q 48 hours.
Anti-inflammatory therapy
Anti-inflammatory dosages are used for inflammatory conditions such as atopy. Anti-inflammatory dosages start at 1 mg/kg/d
(equivalent to 0.1 mg/kg q 48 for dexamethasone) and are decreased to every other day for chronic administration and titrated down to
the lowest effective dose for the shortest duration when needed.
Immunosuppressive therapy
Immunosuppressive dosages are used to control immune mediated diseases such as autoimmune hemolytic anemia and immune
mediate thrombocytopenia among others. Prednisone/prednisolone starting dose is 2 mg/kg/d (equivalent to 0.2 mg/kg q 48 for
dexamethasone) and may be titrated to every other day administration and or doses decreased. Immunosuppressive doses are
recommended for the treatment of anaphylactic shock and Addison’s crisis as well.
Shock therapy
A shock dose of glucocorticoids is only indicated for spinal trauma (methylprednisolone sodium succinate, 30 mg/kg IV) and data
suggest may only provide a benefit within the first 3-8 hours after the trauma. Other glucocorticoids have not demonstrated efficacy
for spinal trauma.
Current data suggest shock doses of glucocorticoids are detrimental for head trauma and increase death and disability in humans.
Current data do not indicate there is a benefit for shock doses of glucocorticoids for generalized trauma such as hit by car, sepsis or
endotoxemia, or heat stroke. Glucocorticoids may be detrimental in heat stroke due to the damage in the GI tract from the
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hyperthermia. Fluid therapy (isotonic crystalloids, hypertonic crystalloids, colloids) and analgesia (opioids are the treatments of choice
for shock due to trauma and pain) and fluid therapy for sepsis endotoxemia and heat stroke.
As stated in the immunosuppressive therapy section, immunosuppressive doses of glucocorticoids can be beneficial for
anaphylactic shock and Addison’s crisis, but not shock doses.
Disclaimer: The information is accurate to the best of the author’s knowledge. However recommendations change as new data
become available and errors are possible. The author recommends double checking the accuracy of all information including dosages.
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