Bilateral subnormal adrenal glands in a German Shepherd
- enquiries16342
- May 2
- 3 min read
Updated: May 6
By Dr Maria Luz Aviles, April 2025
History:
In February 2025, the patient was presented at a clinic in Metropolitan Melbourne, Victoria, Australia due to a broken nail. A treatment with antibiotics was commenced. However, the owner reported that the dog later became more selective with food and displayed some urinary incontinence as well as polyuria. Bloodwork was performed and showed urea 14.74 (2.5-10), creatinine 143 (5-130), phosphorus 2.33 (0.8-2.1), sodium (Na) 140 (139-153), potassium (K) 5.8 (3.9-5.9), Na:K ratio 24 (26-35). An UA revealed USG 1020.
Given the clinical signs and lab results, an abdominal ultrasound was requested to assess the abdominal organs and rule out other potential conditions. An ultrasound was requested to find underlying causes of the symptoms and clinical signs.
Sonographic findings:
A complete abdominal ultrasound was performed with the patient in dorsal recumbency, under sedation of butorphanol, medetomidine and alfaxalone.
Sonographic findings were bilateral subnormal in size adrenal glands preserving adequate echogenicity and shape. Note: for 32.5 kg. dog, the thickness of the adrenal poles are expected to be around and up to 0.8 cm. In this case the left adrenal gland measured 0.27 cm in thickness at the caudal pole and 0.18 cm in thickness at the cranial pole, and the right adrenal gland measured 0.40 cm in thickness at the caudal pole. The cranial pole of the right adrenal gland was not visualised and subjectively small liver parenchyma was observed. The remainder of the abdominal organs were within normal limits and appearance.
Images:

Image 1 - left adrenal, subnormal in size and with flattened appearance

Image 2 - right adrenal subnormal in size with flattened appearance.
Outcome:
Although ultrasound is not a diagnostic test for Addison's disease, when the adrenal glands were observed subnormal in size there was some suspicious of this. An ACTH stimulation test was performed confirming hypoadrenocorticism and a treatment with Zycortal (desoxycorticosterone pivalate) was commenced.
Hypoadrenocorticism (HA, also known as Addison’s disease) occurs from deficiency of glucocorticoid and/or mineralocorticoid secretion by the adrenal glands. This disease is more common dogs and the median age is 3 to 4 years. Females may be at increased risk, and the breeds with increased risk include the Standard poodle, West Highland White Terrier, Soft-coated Wheaten terrier, Rottweiler, Great Dane, Bearded collie, Portuguese water dog, Labrador retriever, Great Pyrenees, Pomeranian, Cairn terrier, American cocker spaniel, English springer spaniel.
Primary HA is the most common type, and it results from adrenocortical destruction and failure of adrenal cortices to produce hormones, resulting in decreased production of both glucocorticoids and mineralocorticoids.
Atypical, primary HA refers to a condition of the adrenal cortex that results in hypocortisolemia while electrolytes concentrations remain normal.
Secondary HA occurs with failure of the pituitary gland from neoplasia, inflammation, infection, head trauma, infarction, or idiopathic causes. Iatrogenic HA, arising from rapid withdrawal of exogenous steroids or hypophysectomy.
Clinical signs:
HA can manifest as an acute crisis or a chronic, waxing and waning disorder. Most commonly they present with vague, nonspecific intermittent clinical signs like lethargy, anorexia, vomiting, weakness and diarrhea. Other clinical signs like polyuria, polydipsia, weight loss and melena can be also present. In an acute onset they may present hypovolemic shock displaying collapse, dehydration, weak pulses, bradycardia, diarrhea, vomiting, and hypothermia.
Diagnosis:
Bloodwork usually reveals lack of stress leukogram, as well as lymphocytosis and eosinophilia. Mild, nonregenerative anemia, hyponatremia, hypochloremia, and hyperkalemia may also be recorded. Urinalysis might show low specific gravity.
On radiographs, microcardia (from hypovolemia), microhepatica can be observed.
On ultrasound subnormal adrenal gland size can be observed but is not pathognomonic of the disease.
ACTH stimulation test is the gold standard for diagnosing HA. Endogenous plasma ACTH levels can differentiate primary from secondary HA and its measurement is indicated only if a patient has atypical HA. In dogs, basal cortisol levels can be used to rule out HA but cannot confirm the diagnosis.
Treatment:
Mineralocorticoid supplementation is needed for typical HA: fludrocortisone acetate (oral steroid with mineralocorticoid and glucocorticoid effects), desoxycorticosterone pivalate (DOCP - an alternative mineralocorticoid supplement).
Daily glucocorticoid supplementation is required in secondary HA, when there is primary disease treated with DOCP and in about 50% of patients treated with fludrocortisone: usually prednisone.
Prognosis:
Excellent with appropriate therapy and owner education.
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