Page 114 - Clinical Small Animal Internal Medicine

82 Section 2 Endocrine Disease

Epidemiology Less common clinical signs include generalized or
VetBooks.ir Hypoadrenocorticism affects approximately 1/2000 hindlimb muscle weakness, megaesophagus (ME), and
muscle cramping. The etiology of these abnormalities
dogs. Dogs with other immune‐mediated endocrinopa-
thies, such as hypothyroidism and diabetes mellitus, are is unclear, but is probably due to aberrant neuromuscu-
lar function caused by deranged electrolyte concentra-
at increased risk.
tions and/or hypocortisolemia. Muscle weakness can
be severe, and the patient may present for inability to
Signalment rise. Generalized debility could explain the weakness,
Young to middle‐aged female dogs are predisposed to but some of these dogs are specifically weaker in the
Addison disease, although dogs at any age may be affected, hindlimbs. Regurgitation due to ME is a rare presenta-
with some studies revealing a more equal distribution tion for hypoadrenocorticism, but since the ME usually
between sexes. Poodles of all sizes, West Highland white resolves with appropriate treatment, HOAC should be
terriers, Great Danes, bearded collies, Portuguese water ruled out in all cases of ME.
dogs, Leonbergers, and Nova Scotia duck‐tolling retriev- Hair loss or a change in hair coat color are observed
ers (NSDTRs) are predisposed. Notably, NSDTRs may occasionally in dogs with hypoadrenocorticism, but the
develop clinical signs at a very young age (as young as 2 cause is unknown. Hypothyroidism should be ruled out
months). Heritability has been proven in standard poo- in these patients following initial management of HOAC.
dles, bearded collies, and NSDTRs.
Approximately 30% of dogs with Addison disease pre-
sent in hypovolemic shock, or Addisonian crisis. In addi-
History and Clinical Signs tion to the aforementioned clinical signs, especially
vomiting, diarrhea, and GI bleeding, these dogs some-
The clinical manifestation of hypoadrenocorticism is times experience collapse and/or severe generalized
highly variable in presenting complaint, chronicity, and weakness. Classic signs of hypovolemic shock are usually
severity. Whereas some dogs present with chronic signs, present, including weak pulse, pale mucous membranes,
others present acutely, in an “Addisonian crisis.” The and prolonged capillary refill time. Some dogs are also
pathophysiology for chronic and acute hypoadrenocorti- hypothermic. Heart rate is variable. Whereas most hypo-
cism is the same, and these presentations represent a volemic non‐Addisonian dogs are tachycardic (>160
continuum of disease progression. If not diagnosed and bpm), patients in an Addisonian crisis often have a nor-
treated early in the course of disease, dogs with chronic mal to decreased heart rate. This is due to the effects of
signs may present in crisis. hyperkalemia on cardiac conduction. The presence of a
Addison’s disease often causes vague, nonspecific decreased or normal heart rate in a patient in hypov-
clinical signs that can be confused with other diseases, olemic shock (“relative bradycardia”) should raise suspi-
thus its nickname “The Great Pretender.” Nonspecific cion of hyperkalemia and hypoadrenocorticism. In
signs such as lethargy, inappetence, and weight loss patients with cardiac changes associated with hyper-
occur in most patients. A waxing and waning pat- kalemia, rapid treatment and correction are critical for
tern, with exacerbations following stressful events or the survival of the patient.
improvement following fluid or steroid administration, Gastrointestinal bleeding, including melena and hema-
is often noted. tochezia, is frequently seen during crisis. It may be
Gastrointestinal signs, including vomiting and diar- present initially or appear within 2–3 days of presenta-
rhea, are common and likely due to the loss of “trophic” tion. Progressively decreasing hematocrit during treat-
effects of cortisol on the gastrointestinal mucosa. Melena ment should increase suspicion of melena, and the
and/or hematochezia, and abdominal pain, may be possibility of GI bleeding should not be excluded despite
reported by the owners or found on rectal examination. the absence of melena or hematochezia on the initial
Exacerbation or onset of gastrointestinal (GI) signs fol- examination. Hospitalization is recommended until the
lowing a stressful event is often reported in dogs later hematocrit stabilizes or increases. GI blood loss is occa-
diagnosed with Addison disease, so HOAC should be sionally severe enough to require blood transfusion.
considered in patients with recurrent “stress colitis,” par-
ticularly if accompanied by other GI signs, lethargy, or
weakness. Diagnosis
Renal loss of sodium and water, and the resulting decreased Since dogs with HOAC often present with nonspecific
renal medullary concentration gradient due to hypona- signs, most of the diagnostics are performed early in the
tremia, sometimes lead to polyuria and polydipsia. Rarely, work‐up, prior to significant suspicion of hypoadreno-
seizures due to hypoglycemia occur, and HOAC should be corticism. A complete blood count, serum biochemistry
ruled out in all dogs with unexplained hypoglycemia. analysis, and urinalysis should be performed in each