Page 116 - Clinical Small Animal Internal Medicine

84 Section 2 Endocrine Disease

often reveal nonspecific signs of hypovolemia, including due to long‐term administration of glucocorticoids,
VetBooks.ir microcardia. Megaesophagus is seen infrequently. should be identified based on historical findings.
Administration of glucocorticoids prior to an ACTH
Electrocardiogram
decreased response to the test. Most synthetic glucocor-
Additional diagnostics for patients that present in hypo- stimulation test can interfere with and/or cause
volemic shock include blood pressure measurement and ticoids, including prednisone and methylprednisolone,
electrocardiography. ECG abnormalities are caused by cross‐react with the cortisol assay, which can result in
hyperkalemia. Although rigid criteria associating spe- falsely increased cortisol concentrations. Dexamethasone
cific ECG findings with specific potassium concentra- and triamcinolone do not. Thus, if a steroid is given just
tions do not exist, cardiac effects are rarely seen when prior to the test, dexamethasone is recommended. Other
K+ <7.0 mEq/L, and frequently observed when K+ short‐acting glucocorticoids (such as prednisone) should
>9 mEq/L (and may be fatal). With increasing severity of be withheld for 12–24 hours prior to the test. Longer‐
hyperkalemia, ECG changes may include increased acting glucocorticoids, such as methylprednisolone ace-
T‐wave amplitude (“spiked” T wave), shortened Q‐T inter- tate, should be withheld for at least four weeks prior to
val, decreased P‐wave amplitude, prolonged P‐R inter- the test to avoid cross‐reactivity.
val, absent P‐wave, severe bradycardia, and asystole. Administration of glucocorticoids decreases endoge-
Bizarre QRS complexes, including ventricular tachycar- nous ACTH concentrations, which causes atrophy of the
dia and ventricular fibrillation, may also occur. Patients adrenal cortex (fasciculata and reticularis). A blunted
with ECG abnormalities require immediate interven- cortisol response during the ACTH stimulation test is
tions to prevent progression to a fatal arrhythmia. expected in patients that have received glucocorticoids
(oral, parenteral, or topical) within a month of the test, or
Endocrine Diagnostics longer if longer‐acting glucocorticoids (such as methyl-
The ACTH stimulation test is required for defini- prednisolone acetate) have been administered. A post-
tive diagnosis of hypoadrenocorticism. A baseline stimulation cortisol between 2 μg/dL and 5 μg/dL is often
cortisol concentration alone can help rule out the the result of recent steroid administration and not
diagnosis of HOAC, but cannot be used to definitely hypoadrenocorticism.
diagnose it. One way to save money with ACTH stimulation
During an ACTH stimulation test, a supraphysiologic tests is to freeze the unused portion of a vial of cosyn-
dose of ACTH is administered, and the cortisol concen- tropin. Cosyntropin can be frozen in plastic syringes
tration is measured 1–2 hours later. In a dog with nor- (not glass, as it binds to ACTH) for up to six months.
mally functioning adrenal glands, ACTH should cause a The use of a frost‐free freezer is not recommended, as
significant increase in cortisol concentration. In HOAC the effect of the freeze/thaw cycles on the ACTH is
dogs, minimal to no increase in cortisol will occur. unknown.
To perform an ACTH stimulation test, a baseline A baseline cortisol concentration is a less expensive
serum sample is first obtained. Then, 1 μg/kg (up to way to rule out hypoadrenocorticism. Since the cortisol
250 μg/dog) of synthetic ACTH (cosyntropin or tetracos- concentration in almost any patient with HOAC is <2 μg/
actrin) is administered intravenously. One hour later, dL, a baseline cortisol concentration of >2 μg/dL rules
another serum sample is obtained. Cortisol concentra- out the diagnosis in most dogs. However, if the patient
tion is then measured in both pre‐ and post‐ACTH has a baseline cortisol concentration <2 μg/dL, an ACTH
serum samples. stimulation test is required for definitive diagnosis of
Protocols for the ACTH stimulation test vary when HOAC.
testing for HOAC or hyperadrenocorticism. The use of For the definitive diagnosis of primary hypoadreno-
compounded ACTH gel is not recommended for the corticism, a potential alternative to the ACTH stimula-
diagnosis of hypoadrenocorticism, due to inconsistent tion test is the cortisol‐to‐ACTH ratio (CAR). Since
results. Additionally, since dogs with HOAC are often dogs with HOAC have low cortisol concentrations and
hypovolemic, intramuscular administration of ACTH is high ACTH concentrations (due to lack of negative
not recommended. feedback), the CAR is significantly lower in patients
The diagnosis of HOAC requires a post‐ACTH corti- with hypoadrenocorticism than in normal dogs or dogs
sol concentration <2 μg/dL (55 nmol/L), with a post‐ with nonadrenal illness (Lathan et al, 2014, JVIM).
ACTH cortisol concentration >2 μg/dL ruling out the Unfortunately, there is some overlap between dogs with
diagnosis. Rarely, dogs with HOAC have a post-stimula- Addison’s and dogs with non-adrenal illness (Boretti
tion cortisol between 2 and 3 µg/dL. Note that this test et al, JVIM, 2015). Thus, at this time, the CAR cannot be
does not differentiate between primary, secondary, and recommended for definitive diagnosis of HOAC when
iatrogenic Addison disease. However, iatrogenic HOAC, synthetic cosyntropin is available.