Page 40 - VetCPD Jnl Volume 7, Issue 4

Figure 4: Reproduced from Spencer et al., (2018), with permission of aucthor and BMJrib
Sub
ers
How often do I need at 0.5 – 1.0mg/kg every 12 – 24hours,
to reassess the patient? reducing to 0.5mg/kg every 12-24hours. KEY LEARNING POINTS Initially, we would be aiming to see that Regardless of the glucocorticoid used, • Hypoadrenocorticism can be
a patient has electrolytes within the refer- dose adjustments should be made no more primary or rarely secondary; it ence ranges on days 10 and 28 for at least than twice monthly, and doses should be can be typical or atypical (isolated two consecutive doses. Dogs should then hypocortisolaemia).
be reassessed every four to six months at the time of (or just before) injection.
s of
What is the difference between prednisolone and cortisone acetate? All dogs will require lifelong daily glucocorticoid treatment. Maintenance glucocorticoid therapy is started when the patient is stable, hydrated and eating and drinking normally. Physiological doses of prednisolone of 0.22mg/kg BID are ini- tially recommended (Klein and Peterson 2010b) before gradually being tapered, although some clinicians will initially
start with a slightly higher dose.The ‘final’ dose varies but is usually 0.05 – 0.1mg/ kg every 24 hours.These ‘physiological’ doses are much lower those used for
other therapeutic doses of corticosteroids. Overdosing is common therefore dogs should be monitored closely for signs of iatrogenic hyperadrenocorticism.
Some dogs develop glucocorticoid side effects despite very low prednisolone doses and in these patients cortisone acetate could be considered as an alterna- tive. Cortisone acetate has equipotent glucocorticoid and mineralocorticoid activity, and its shorter half-life and lower overall activity make it less likely to create iatrogenic hyperadrenocorticism with long-term administration. Cortisone acetate would typically be administered
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Summary/Conclusion:
the clinical signs and clinico- pathological abnormalities.
25-
50% of th
e previous
stress or illness doses could be increased
dose. A
t time
• The physiological roles of cortisol two to four-fold. and aldosterone can explain
Only
A good understanding of the HPA axis and
• The specificity of the Na:K ratio for diagnosing hypoadrenocorticism increases as the ratio decreases.
• Basal cortisol >55nmol/L can be used to exclude hypoadrenocorticism.
• Prior use of systemic or topical steroids can affect the results of an ACTH stimulation test, therefore results should be interpreted with caution.
• Careful attention should be given to initial fluid therapy
and management of electrolyte derangements in the acute setting.
• Dexamethasone or
hydrocortisone are both appropriate choices for glucocorticoid replacement in the acute setting. Prednisolone or cortisone acetate will be required indefinitely.
• ‘Zycortal’(Dechra,UK)is
the UK licensed product for mineralocorticoid replacement. Initial doses of 1.5 – 1.8mg/kg are now typically used.
the physiological effects of glucocorticoids
and mineralocorticoids helps in the
understanding of the diagnosis and
treatment of canine hypoadrenocorticism.
Many cases can be diagnosed and managed in general practice; however, because of the vague and sometimes intermittent signs cases are easy to ‘miss’. Specialist advice may be required in some situations, especially in cases of suspected isolated hypocortisolaemia or where prior use of corticosteroids hinders initial diagnosis. Although treatment is required life-long, dogs can often be managed successfully and have a normal life.With diligent owners the long-term prognosis is generally excellent.
References
For a full list of references please visit:
www.vetcpd.co.uk/references
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