How Vets Diagnose Cushing's in Dogs: Bloodwork & Tests

One of the defining challenges of canine Cushing’s syndrome (including Cushing’s disease) is how gradually it announces itself. Unlike a sudden illness, hyperadrenocorticism (HAC) develops over months — sometimes years — as cortisol slowly erodes normal physiology across multiple organ systems. By the time an owner seeks veterinary care, clinical signs have often been present for months — in one study of 66 dogs, the duration before diagnosis ranged from 1 to 36 months, with a median of 8 months. Understanding what to look for, and why, can meaningfully shorten that gap.

This post covers the clinical signs of HAC in detail: what owners observe at home, what clinicians find on physical examination, and what diagnostic screening typically reveals before formal endocrine testing begins. For a quick at-home checklist, see our symptoms of Cushing’s in dogs page; this post goes deeper into what your vet sees and tests for.

The Cardinal Signs of Cushing’s Syndrome in Dogs

Polyuria and Polydipsia (PU/PD)

Increased thirst and urination is the most common presenting complaint in dogs with Cushing’s, reported in the majority of affected animals. The mechanism is direct: excess cortisol antagonises (suppresses) the action of antidiuretic hormone (also called vasopressin or just “ADH”). In a normally functioning body, ADH is released by the pituitary gland in response to the body becoming dehydrated. In turn, the ADH acts on the kidneys and causes them to retain and re-circulate water as opposed to releasing it via urination. In a Cushing’s animal, this effect of ADH is effectively blocked or diminished, causing the kidneys to release urine regardless of how hydrated the animal is. The result is obligatory diuresis — the dog produces large volumes of dilute urine regardless of hydration status — followed by the animal’s efforts to offset the fluid loss by drinking ever more water (compensatory polydipsia).

Clinically, daily water intake above 100 ml/kg of bodyweight (or 45 ml/pound) is a recognised threshold for concern. Affected dogs may empty their water bowl repeatedly, seek water from unusual sources, and begin having accidents indoors — often the first behavioural change owners notice.

Polyphagia

Cortisol has direct appetite-stimulating effects on the central nervous system. Dogs with HAC are frequently ravenous — not just enthusiastic eaters, but genuinely driven by hunger in ways their owners describe as uncharacteristic. Food-seeking behaviour may intensify: counter-surfing, scavenging, vocalising around meal times.

This sign is sometimes dismissed as a normal variation in appetite, which contributes to diagnostic delay.

Pot-Bellied Abdomen

The pendulous, distended abdomen characteristic of Cushing’s results from the convergence of three processes. First, cortisol induces an enlargement of the liver (hepatomegaly) — in many cases dramatically so and observable on abdominal palpation (touching the animal’s abdomen to feel for abnormalities in size, shape, texture, etc.). Second, chronic glucocorticoid (cortisol) excess promotes redistribution of adipose (fat) tissue to the abdomen. Third, excess cortisol causes the breaking down of protein (protein catabolism). In a normal body, cortisol is usually only elevated in times of stress (“fight or flight”). In those situations, the body converts protein into sugar to give the body a burst of energy to survive the stress-causing situation (to fight or flee). In the Cushing’s animal, cortisol is always elevated and, thus, the body is always breaking down protein and converting it into sugar. This progressively weakens the abdominal wall musculature, reducing the structural support that normally contains abdominal contents.

The result is the classic pot-bellied silhouette, which owners often attribute to weight gain or bloat before a diagnosis is made.

Muscle Weakness and Exercise Intolerance

As discussed, cortisol promotes protein catabolism and inhibits protein synthesis, leading to progressive loss of lean muscle mass. This manifests as generalized muscle weakness — dogs struggle to rise from a lying position, hesitate at stairs, refuse to jump onto furniture they previously navigated easily, and tire quickly on walks. In advanced cases, muscle wasting is visible in the temporal muscles, limbs, and trunk.

A related finding is pseudomyotonia: an unusual stiffness and difficulty relaxing muscles after contraction, observed in a subset of Cushing’s cases and linked to cortisol’s effects on muscle membrane function.

Dermatological Signs

The skin in a dog with Cushing’s is profoundly affected by chronic glucocorticoid excess, and dermatological signs are among the most diagnostically useful findings.

Bilateral symmetric alopecia is a hallmark presentation: hair loss that develops symmetrically on both sides of the body, typically sparing the head, face, and extremities. The hair follicles enter a resting (telogen) phase and fail to cycle back into active growth. In many dogs, hair clipped for a procedure or surgery simply does not regrow.

Skin thinning is common — cortisol inhibits collagen synthesis and reduces dermal thickness, leaving the skin fragile and easily traumatised. Prominent superficial blood vessels (cutaneous vessel visibility), slow wound healing, and easy bruising may follow.

Comedones — follicular plugging (acne) — are frequently found along the ventral (belly-side) abdomen. Hyperpigmentation, a darkening of the skin, particularly in areas of alopecia, is also commonly observed.

Calcinosis cutis, the abnormal deposition of calcium salts in the skin, occurs in a subset of HAC cases. It presents as firm, chalky-white or yellowish plaques, most often along the dorsal (back) midline, inguinal (groin) region, and axillae (underarms). These lesions can ulcerate and become secondarily infected. Their presence is highly suggestive of hypercortisolaemia.

Persistent Panting

Inappropriate panting — at rest, in cool environments, without physical exertion — is reported in the majority of dogs with Cushing’s. The exact mechanism is not fully understood but likely involves cortisol’s effects on respiratory muscle function, altered thermoregulation, and possibly direct effects on central respiratory drive. It is frequently described by owners as one of the most disruptive signs, particularly at night.

Recurrent Infections

Chronic cortisol excess is profoundly immunosuppressive. Affected dogs show impaired neutrophil (an immune system cell) function despite a stress leukogram (changes in white blood cell counts) that appears to indicate adequate numbers, and cell-mediated immunity (adaptive immunity that does not depend on antibodies, for example, T-cells) is broadly suppressed. The practical consequence is a predisposition to infections that are either unusually frequent, unusually persistent, or caused by pathogens that would not normally establish disease.

Urinary tract infections are among the most common, occurring in an estimated 40–50% of dogs with HAC at the time of diagnosis. Many are subclinical — the dog shows no obvious signs of dysuria — which is why urine culture (not just urinalysis) is recommended as part of the diagnostic workup. Recurrent pyoderma (pus-containing skin condition), otitis (ear inflammation or infection), and poor response to standard treatment courses are also characteristic.

Reproductive Changes

Cortisol inhibits hypothalamic release of gonadotropin-releasing hormone (GnRH) (a sex hormone regulator) and suppresses the HPG (hypothalamic-pituitary-gonadal) axis. In intact females, this commonly produces anoestrus or irregular cycles. In intact males, testicular atrophy and reduced libido are observed. In rare cases, clitoral enlargement has been reported, related to adrenal androgen excess.

Neurological Signs

In most cases of pituitary-dependent HAC (PDH), the causative adenoma (tumor) is a microadenoma — small enough to produce no direct neurological effect. However, in a clinically important subset (estimated 10–25% of PDH cases), a macroadenoma is present, large enough to compress or invade adjacent brain structures.

Signs of a pituitary macroadenoma may include behavioural changes, obtundation (lack of alertness), circling, ataxia (loss of muscle control and coordination), and vision loss. These neurological signs may precede, accompany, or develop after diagnosis of HAC, and their presence significantly influences treatment options and prognosis. Advanced imaging (MRI or CT) is indicated in any dog with PDH that develops neurological signs.

Bloodwork and Urinalysis Findings

Before formal endocrine testing, routine diagnostic screening often provides important corroborating evidence.

Complete blood count: The classic stress leukogram — mature versions of the white-blood cell diseases neutrophilia, lymphopenia, eosinopenia, and monocytosis — is present in the majority of HAC cases. It reflects cortisol’s direct effects on immune cell trafficking and is a useful, if non-specific, indicator.

Serum biochemistry: Alkaline phosphatase (ALP), which is an enzyme that indicates liver or bone disorders, is elevated in approximately 85–90% of dogs with HAC, often markedly so. This elevation is driven partly by hepatic glycogen (glucose stored in the liver) accumulation (Cushing’s hepatopathy) and partly by cortisol-induced upregulation of a specific corticosteroid-induced isoenzyme of ALP. A markedly elevated ALP in a middle-aged to older dog with PU/PD is a strong signal warranting endocrine investigation. Alanine aminotransferase (ALT) is also frequently elevated, though less dramatically. (ALT is an enzyme normally found in the liver. Thus, elevated amounts of ALT in the blood indicate leakage from the liver and associated diseases.) Hypercholesterolemia (high cholesterol) and hypertriglyceridemia (high triglyceride levels) are common findings. Blood glucose may be mildly elevated; frank hyperglycemia (obvious (vs borderline or ambiguous) diabetes) and concurrent diabetes mellitus occur in an estimated 10% of cases.

Urinalysis: Urine specific gravity is typically low — often below 1.020, and in many cases below 1.008 — reflecting impaired concentrating ability. Proteinuria (protein in the urine) is common and has prognostic relevance; glomerular hypertension (high blood pressure in tiny blood vessels inside the kidney) driven by systemic hypertension and cortisol’s effects on how the blood circulates through blood vessels leads to protein loss across the glomerular filtration barrier (the sieve in the kidney that filters blood to create urine). The urine cortisol:creatinine ratio (UCCR), performed on a first-morning sample collected at home, serves as a useful screening test — a normal result effectively rules out HAC.

Abdominal ultrasound: Not a diagnostic test in itself, but a valuable part of the workup. Bilateral adrenal enlargement supports PDH (in pituitary-dependent Cushing’s, the adrenal glands should be affected equally); a unilateral adrenal mass with contralateral atrophy suggests ADH (in adrenal-dependent Cushing’s, the problem-causing adrenal gland (and part of the adrenal gland) should look different than the other (and rest of the) gland). Hepatomegaly (enlarged liver) is nearly universal. The presence of a unilateral adrenal mass also raises the question of malignancy, which influences both treatment planning and prognosis.

Why Diagnosis Is Often Delayed

The signs described above overlap with those of many other conditions. For example, polyuria (excessive urination), polydipsia (excessive drinking) and muscle weakness are associated with many conditions. Alopecia can reflect allergy, hypothyroidism, or dermatological disease. Polyphagia (over-eating) is common. Panting is attributed to pain, anxiety, or heat. The pot-bellied appearance is assumed to reflect obesity.

What distinguishes HAC is the accumulation of these signs in combination, developing gradually over time, in a middle-aged to older dog — particularly one of the breeds with documented predisposition. Recognising that pattern is the foundation of an early diagnosis.

In the next post, we examine those breeds in detail: which dogs are most at risk, and what the epidemiological data tell us about age, sex, and tumor type predisposition.

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The information on this site is educational and not a substitute for veterinary diagnosis or treatment. Always work with a licensed veterinarian for your dog’s care.

Recognising Cushing’s Syndrome (including Cushing’s Disease) in Dogs: Clinical Signs, Bloodwork, and Why Diagnosis Is Often Delayed