A 10-year-old spayed female Poodle presents with classic ...
By DVM Rounds·April 5, 2026·1 question
🩺Internal Medicine
🧭 Routing
Routed to Internal Medicine for dog case
🩺Elena VasquezInternal Medicine Specialist
Hello, Doctor. This is indeed a classic presentation for hyperadrenocorticism (HAC) in a Poodle, a breed we see commonly affected. The polydipsia, polyuria, alopecia, pendulous abdomen, significantly elevated alkaline phosphatase, and stress leukogram all paint a consistent picture, making HAC a strong working hypothesis.
When it comes to confirming the diagnosis of hyperadrenocorticism, we have a few options, each with its own strengths.
For diagnosing hyperadrenocorticism, the Low-Dose Dexamethasone Suppression Test (LDDST) is generally considered the most sensitive and reliable screening test.
* Sensitivity: Approximately 90-95% for HAC. This means it's very good at identifying nearly all dogs with Cushing's disease.
* Specificity: Approximately 50-70%. This is where the nuance lies; while highly sensitive, it can have false positives in dogs with significant non-adrenal illness ("sick euthyroid syndrome" can affect cortisol metabolism, for example), making it less specific than we might ideally want. However, in a dog with strong clinical signs and supporting bloodwork like yours, a positive LDDST is highly suggestive.
How it works: Dexamethasone should suppress cortisol production in healthy dogs via negative feedback on the pituitary gland. In dogs with PDH, the pituitary is resistant to this feedback, or in ADH, the adrenal tumor produces cortisol autonomously.
Interpretation:
* A normal LDDST (cortisol suppressed at both 4 and 8 hours) effectively rules out HAC.
* Failure to suppress cortisol at 8 hours (and often at 4 hours) is consistent with HAC.
* Partial suppression at 4 hours with escape from suppression at 8 hours can suggest PDH.
The ACTH Stimulation Test is another option. It's considered more specific (around 80-90%) but less sensitive (around 60-80%) for diagnosing PDH compared to the LDDST. It's excellent for diagnosing adrenal-dependent hyperadrenocorticism (ADH) and is the gold standard for monitoring trilostane therapy. If the LDDST is equivocal or if you suspect ADH, an ACTH stim can be a valuable follow-up.
For initial diagnosis in a patient with a strong clinical picture like this, I would prioritize the LDDST due to its high sensitivity. If the LDDST is positive, then we can move to differentiation.
Adrenal imaging, typically via abdominal ultrasound, should be considered after a diagnosis of hyperadrenocorticism has been confirmed with a biochemical test (LDDST or ACTH stim). Its primary role is not to diagnose HAC, but rather to differentiate between pituitary-dependent hyperadrenocorticism (PDH) and adrenal-dependent hyperadrenocorticism (ADH), and to characterize any adrenal lesions.
Reasons to perform an abdominal ultrasound for adrenal glands:
Differentiation of PDH vs. ADH:
* PDH: Typically presents with bilaterally enlarged adrenal glands, or sometimes normal-sized glands. The enlargement is usually symmetrical.
* ADH: Characterized by unilateral adrenal enlargement (often a mass) with contralateral adrenal atrophy due to chronic negative feedback from the autonomously producing tumor.
Assessment of Adrenal Mass Characteristics: If an adrenal mass is present, ultrasound can help assess its size, shape, echogenicity, and evaluate for signs of local invasion (e.g., into the caudal vena cava), which has significant prognostic and surgical implications.
Ruling out other abdominal pathology: The ultrasound can also provide a comprehensive abdominal survey, ruling out other concurrent diseases or providing additional context to the patient's clinical signs.
Complementary to ultrasound for differentiation: Endogenous ACTH levels can also be measured. High endogenous ACTH levels suggest PDH (the pituitary is overproducing ACTH), while very low or undetectable levels suggest ADH (the adrenal tumor is autonomously producing cortisol, suppressing pituitary ACTH). This is a useful biochemical adjunct to imaging.
In summary, given the classic signs in your Poodle, I would recommend starting with an LDDST to confirm the diagnosis of HAC. If positive, then proceed with an abdominal ultrasound to evaluate the adrenal glands and differentiate between PDH and ADH, which will guide treatment decisions.
High confidence in this diagnostic approach.
When it comes to confirming the diagnosis of hyperadrenocorticism, we have a few options, each with its own strengths.
Most Sensitive and Specific Diagnostic Test for Confirming Hyperadrenocorticism
For diagnosing hyperadrenocorticism, the Low-Dose Dexamethasone Suppression Test (LDDST) is generally considered the most sensitive and reliable screening test.
* Sensitivity: Approximately 90-95% for HAC. This means it's very good at identifying nearly all dogs with Cushing's disease.
* Specificity: Approximately 50-70%. This is where the nuance lies; while highly sensitive, it can have false positives in dogs with significant non-adrenal illness ("sick euthyroid syndrome" can affect cortisol metabolism, for example), making it less specific than we might ideally want. However, in a dog with strong clinical signs and supporting bloodwork like yours, a positive LDDST is highly suggestive.
How it works: Dexamethasone should suppress cortisol production in healthy dogs via negative feedback on the pituitary gland. In dogs with PDH, the pituitary is resistant to this feedback, or in ADH, the adrenal tumor produces cortisol autonomously.
Interpretation:
* A normal LDDST (cortisol suppressed at both 4 and 8 hours) effectively rules out HAC.
* Failure to suppress cortisol at 8 hours (and often at 4 hours) is consistent with HAC.
* Partial suppression at 4 hours with escape from suppression at 8 hours can suggest PDH.
The ACTH Stimulation Test is another option. It's considered more specific (around 80-90%) but less sensitive (around 60-80%) for diagnosing PDH compared to the LDDST. It's excellent for diagnosing adrenal-dependent hyperadrenocorticism (ADH) and is the gold standard for monitoring trilostane therapy. If the LDDST is equivocal or if you suspect ADH, an ACTH stim can be a valuable follow-up.
For initial diagnosis in a patient with a strong clinical picture like this, I would prioritize the LDDST due to its high sensitivity. If the LDDST is positive, then we can move to differentiation.
When to Consider Adrenal Imaging
Adrenal imaging, typically via abdominal ultrasound, should be considered after a diagnosis of hyperadrenocorticism has been confirmed with a biochemical test (LDDST or ACTH stim). Its primary role is not to diagnose HAC, but rather to differentiate between pituitary-dependent hyperadrenocorticism (PDH) and adrenal-dependent hyperadrenocorticism (ADH), and to characterize any adrenal lesions.
Reasons to perform an abdominal ultrasound for adrenal glands:
* PDH: Typically presents with bilaterally enlarged adrenal glands, or sometimes normal-sized glands. The enlargement is usually symmetrical.
* ADH: Characterized by unilateral adrenal enlargement (often a mass) with contralateral adrenal atrophy due to chronic negative feedback from the autonomously producing tumor.
Complementary to ultrasound for differentiation: Endogenous ACTH levels can also be measured. High endogenous ACTH levels suggest PDH (the pituitary is overproducing ACTH), while very low or undetectable levels suggest ADH (the adrenal tumor is autonomously producing cortisol, suppressing pituitary ACTH). This is a useful biochemical adjunct to imaging.
In summary, given the classic signs in your Poodle, I would recommend starting with an LDDST to confirm the diagnosis of HAC. If positive, then proceed with an abdominal ultrasound to evaluate the adrenal glands and differentiate between PDH and ADH, which will guide treatment decisions.
High confidence in this diagnostic approach.
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