Page 1038 - Cote clinical veterinary advisor dogs and cats 4th

Hypoadrenocorticism 513

• Nova Scotia duck tolling retrievers (NSDTR) suppresses normal ACTH production, or hypocholesterolemia. Some dogs have
only one clinicopathologic abnormality.
tend to be younger at time of diagnosis. resulting in adrenocortical atrophy; sudden • The diagnosis (typical or atypical) is con-
VetBooks.ir young/middle-aged, although any age may administration then produces signs of cortisol firmed with an ACTH stimulation test. Diseases and Disorders
cessation of exogenous glucocorticoid
• Rare in cats; affected cats are typically
An algorithmic approach to diagnosis and
deficiency.
be affected; no apparent sex predisposition
GENETICS, BREED PREDISPOSITION • Clinical signs and laboratory findings are management is outlined on p. 1429.
due to the absence of glucocorticoid and
• Increased risk: Great Danes, Portuguese water mineralocorticoid activity. Differential Diagnosis
dogs, West Highland white terriers, bearded • Hypoadrenocorticism with clinical signs of • Other causes of GI disease
collies, poodles, rottweilers, soft-coated glucocorticoid and mineralocorticoid defi- • Hyperkalemia and hyponatremia: acute
wheaten terriers, NSDTRs, and Leonbergers ciencies (typical hypoadrenocorticism; serum kidney injury/acute anuria, urinary tract
○ Autosomal recessive inheritance in stan- electrolyte concentrations are abnormal) is obstruction, trichuriasis, severe GI disease,
dard poodles, Portuguese water dogs, and much more common than hypoadrenocorti- peritoneal or thoracic effusion, diabetes
NSDTRs cism with signs of glucocorticoid deficiency mellitus, pregnancy
○ Highly heritable in bearded collies but only (atypical hypoadrenocorticism; electro- ○ Concurrent hyperkalemia, hyponatremia,
precise mechanism unknown lyte concentrations are normal). prerenal azotemia, and isosthenuria can
• Consequences of glucocorticoid deficiency make it difficult to distinguish between
Clinical Presentation ○ Weakness, lethargy hypoadrenocorticism and acute oliguric
DISEASE FORMS/SUBTYPES ○ Gastrointestinal (GI) signs (anorexia, or anuric kidney failure. Differentiation
• Typical hypoadrenocorticism: signs of glu- vomiting, diarrhea, abdominal pain, is important because hypoadrenocorticism
cocorticoid and mineralocorticoid deficiency melena, hematochezia, weight loss) carries an excellent long-term prognosis.
• Atypical hypoadrenocorticism: signs only of ○ Hypoglycemia Initial treatment for both is similar, and
glucocorticoid deficiency ○ Absence of a stress leukogram for an ill the disorders can be distinguished using
patient (failure of glucocorticoid-induced the ACTH stimulation test.
HISTORY, CHIEF COMPLAINT neutrophilia and lymphopenia), eosino- • Hyperkalemia (pp. 495 and 1235)
• Clinical signs are notoriously vague and often philia, mild anemia • Hyponatremia (pp. 518 and 1241)
wax and wane over weeks or months (some- • Consequences of mineralocorticoid • Hypercalcemia (pp. 491 and 1232)
times only apparent to owners in retrospect); (aldosterone) deficiency • Hypoglycemia (p. 552)
worsening in stressful situations (e.g., travel, ○ Decreased renal sodium, chloride (and • Hypoalbuminemia (p. 1239)
boarding) is possible. Severity of signs ranges consequently water) reabsorption, resulting
from a mild, progressive, intermittent course in hyponatremia (p. 518), hypochloremia, Initial Database
to an acute, life-threatening crisis. and volume depletion/dehydration • CBC, serum biochemical profile, urinalysis
• Dogs ○ Loss of free water and sodium results ○ Typical hypoadrenocorticism: common
○ Most common: generalized weakness, in hypovolemia, hypotension, decreased findings include normocytic, normochro-
lethargy, anorexia, vomiting cardiac output and poor tissue perfusion, mic nonregenerative anemia; absence of
○ Less common: hindlimb weakness, diarrhea solute diuresis and medullary solute stress leukogram (p. 1283), hyponatremia,
(possibly with melena or hematochezia), washout. Consequences include prerenal hypochloremia, hyperkalemia, metabolic
weight loss, trembling, polyuria/polydipsia azotemia, metabolic acidosis, weakness, acidosis, prerenal azotemia, and hypoalbu-
(PU/PD), regurgitation (due to mega- depression, decreased urine concentrating minemia. Hypoglycemia, hypercalcemia,
esophagus), and collapse. Rarely, seizures ability, and PU/PD. and isosthenuria are also possible. A
occur secondary to hypoglycemia. ○ Decreased renal potassium excretion decreased Na/K ratio (<27) is sugges-
• Cats: anorexia, weight loss, lethargy common; resulting in hyperkalemia (p. 495) tive of hypoadrenocorticism but is not
vomiting and PU/PD are uncommon. ○ Metabolic acidosis due to decreased renal pathognomonic and cannot be used to
hydrogen ion excretion and poor tissue make a definitive diagnosis.
PHYSICAL EXAM FINDINGS perfusion ○ The most common reason for a missed diag-
• As described (see History, Chief Complaint • Additional reported findings for which a nosis is failure to measure serum electrolyte
above) mechanism is not clearly defined include concentrations because hyperkalemia
• Abdominal pain and muscle cramping may hypercalcemia (total and/or ionized calcium), and hyponatremia are usually the first clues
be detected. hypoalbuminemia, hypocholesterolemia, and pointing toward hypoadrenocorticism.
• In crisis, signs may be severe. Mental depres- megaesophagus. ○ Atypical hypoadrenocorticism: similar
sion, bradycardia (from hyperkalemia), and to the typical form, with the excep-
hypovolemic shock are possible. DIAGNOSIS tion that electrolyte concentrations are
normal.
Etiology and Pathophysiology Diagnostic Overview • Electrocardiogram (p. 1096): changes con-
• Primary hypoadrenocorticism (typical and • Typical hypoadrenocorticism is suspected sistent with hyperkalemia possible, including
atypical): destruction of the adrenal cortices, based on compatible historical/clinical increased T-wave amplitude, decreased
usually due to idiopathic or immune-mediated findings in conjunction with hyponatremia P-wave amplitude, and bradycardia
processes. Other uncommon causes of adre- and hyperkalemia. Bradycardia (or relative • Thoracic radiographs: microcardia due
nocortical destruction are granulomatous bradycardia) in the face of hypovolemia to volume depletion common; signs of
disease (e.g., histoplasmosis, blastomycosis, and/or absence of a stress leukogram in an megaesophagus ± aspiration pneumonia
tuberculosis), infarction, neoplasia, and ill patient increases the likelihood of the possible
medications (e.g., mitotane, trilostane). diagnosis. • Abdominal ultrasound: adrenal glands may
• Secondary hypoadrenocorticism (spontane- • Atypical hypoadrenocorticism should be be normal or slender; whereas slender adrenal
ous): decreased secretion of ACTH from the considered in dogs with historical/clinical glands are supportive of hypoadrenocorti-
pituitary, rarely due to destructive lesions or signs of nonspecific illness (particularly GI cism, normal adrenal gland size does not
congenital defects. signs) and any compatible laboratory finding, rule out the diagnosis.
• Secondary hypoadrenocorticism (iatrogenic): including absence of a stress leukogram, • Basal serum cortisol level: if normal (>2 mcg/
administration of exogenous glucocorticoids anemia, hypoalbuminemia, hypoglycemia, dL [>55 nmol/L]), hypoadrenocorticism is

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