Cushing's Disease in Dachshunds — Management Guide

Comprehensive, practical guide to diagnosing and managing Cushing's disease (pituitary and adrenal forms) in Dachshunds, including testing cascade, trilostane use and monitoring.

Quick Overview

• What it is: Cushing's disease (hyperadrenocorticism, HAC) is excess cortisol production. In dogs the two main forms are pituitary-dependent (PDH) and adrenal-dependent (ADH).
• Who's at risk: Middle-aged to older dogs; Dachshunds are among small/medium breeds seen with HAC and appear over-represented in some clinic series. PDH is the most common form (~80–85% of cases in dogs).
• Prognosis: With appropriate treatment most Dachshunds have good clinical responses and improved quality of life. Long-term monitoring is needed; prognosis depends on cause, comorbidities (diabetes, infections), and response to therapy.

H2: Pathophysiology — simple explanation

Cortisol is a steroid hormone produced by the adrenal cortex. Normally its production is stimulated by ACTH (adrenocorticotropic hormone) from the pituitary and regulated by negative feedback. In Cushing's disease excess cortisol can come from:

• Pituitary-dependent hyperadrenocorticism (PDH): a pituitary corticotroph adenoma secretes excessive ACTH → bilateral adrenal hyperplasia → excess cortisol (most common).
• Adrenal-dependent hyperadrenocorticism (ADH): an adrenal tumor (benign adenoma or malignant carcinoma) autonomously secretes cortisol → suppressed pituitary ACTH.

H2: Breed-specific risk factors and prevalence in Dachshunds

• Dachshunds are commonly reported among small-breed dogs diagnosed with HAC. While PDH remains the dominant form in Dachshunds like other breeds, adrenal tumors can occur.
• Age: typical onset 6–12+ years.
• Sex/neuter status: no strong sex predisposition established; some studies report slightly higher rates in neutered animals.

H3: Common signs

• Progressive polyuria and polydipsia (often the first sign noticed)
• Polyphagia but muscle wasting and weight redistribution → pot-bellied appearance
• Bilateral symmetrical hair loss, thin fragile skin, recurrent skin/ear/urinary tract infections
• Panting, lethargy, poor exercise tolerance
• Hepatomegaly (enlarged liver) detectable on palpation or imaging
• Increased susceptibility to concurrent conditions: diabetes mellitus, hypertension, hypercoagulability

There is no universally accepted formal staging system used in first-opinion practice; severity is typically judged by clinical signs, biochemical abnormalities, comorbidities, and response to therapy. Dogs with systemic complications (severe diabetes, recurrent infections, thromboembolism) have a more guarded prognosis.

H2: Diagnostic approach — stepwise cascade

Aim: (1) Confirm hypercortisolism, (2) Determine PDH vs ADH, (3) Assess comorbidities.

H3: Step 1 — baseline screening tests

• CBC, serum biochemistry, urinalysis: look for increased liver enzymes, fasting hypercholesterolemia, dilute urine, concurrent UTI, elevated alkaline phosphatase (ALP).
• Urine cortisol:creatinine ratio (UCCR) — sensitive but not specific; a useful initial screen (high negative predictive value). If UCCR is normal, HAC is unlikely; if high, proceed to confirmatory testing.

Two commonly used tests:

• Low-dose dexamethasone suppression test (LDDST): sensitive and can help suggest PDH if there is suppression at 4 hours. More labor-intensive.
• ACTH stimulation test: widely used to monitor therapy; less sensitive for mild PDH but appropriate when clinical signs and screening tests are consistent.

H3: Step 3 — localize (PDH vs ADH)

• Measure endogenous plasma ACTH: high/normal in PDH; suppressed in ADH. Requires careful sample handling (EDTA, chilled, fast transport).
• Abdominal ultrasound: look for unilateral adrenal enlargement or mass (adrenal tumor) versus bilateral enlargement (PDH).
• Advanced imaging of the pituitary: MRI (preferred) or CT if pituitary tumor is suspected and if hypophysectomy or radiation is considered.

Refer to a board-certified veterinary internal medicine specialist or an endocrinology/surgery center when:

• Imaging suggests an adrenal mass (surgical options)
• Pituitary macroadenoma with neurologic signs (neurology/neurosurgery)
• Complex comorbidities (diabetes requiring insulin adjustments, refractory infections)

Choice depends on PDH vs ADH, clinical status, owner preferences, and availability of specialist services.

H3: Medical therapy — trilostane (Vetoryl) and mitotane (Lysodren)

1) Trilostane (most commonly used now)

• Mechanism: reversible inhibitor of 3β-hydroxysteroid dehydrogenase → reduces cortisol synthesis.
• Typical starting dose: 1–3 mg/kg orally once daily. Many clinicians begin at 1–2 mg/kg q24h and reassess. Some dogs do better with divided dosing (q12h) depending on clinical response and cortisol nadir.
• Monitoring: ACTH stimulation test (see below) 7–10 days after starting or dose change, then at 4–6 weeks, then every 3–6 months when stable. Adjust dose in small increments (e.g., 20–50% changes) based on clinical signs and ACTH stim results.
• Adverse effects: transient GI signs, lethargy, and most important — iatrogenic hypocortisolemia (Addisonian crisis). With appropriate monitoring, trilostane has good control rates; published clinical control rates are roughly 70–85% for PDH in many series (individual response varies).

• Mechanism: selective adrenocorticolytic agent causing necrosis of zona fasciculata/reticularis.
• Dosing (induction/maintenance): induction 50–60 mg/kg/day PO divided until clinical response or biochemical evidence of cortisol suppression (typically several days to weeks), then decrease to maintenance 2–3 times weekly. Protocols vary; close monitoring is essential.
• Adverse effects: higher risk of GI upset and oversuppression; requires careful monitoring. Use less commonly than trilostane in many regions.

1) Adrenalectomy (for adrenal tumors)

• Indicated when an adrenal tumor is identified and dog is a surgical candidate.
• Requires experienced surgeon and perioperative endocrine/critical care. Success rates for adrenalectomy in cases of benign adenoma are good; carcinomas have variable outcomes and metastatic risk.
• Preoperative stabilization often includes medical adrenal suppression (trilostane or mitotane) and management of hypertension and coagulation status.

• Curative for many PDH cases when performed at specialized centers with experienced teams. Availability is limited to a few referral centers worldwide.
• Alternative options when surgery not available: medical therapy and radiation therapy for large pituitary macroadenomas causing neurologic signs.

• Radiation therapy: palliative or adjunctive for pituitary macroadenomas causing neurologic signs; reduces tumor size/progression.
• Address concurrent infections, skin care, weight management, and control of concurrent diabetes mellitus.

• Baseline sampling: take a baseline blood cortisol (pre-pill if possible), then administer trilostane and perform ACTH stimulation 2–4 hours after trilostane in many protocols for peak effect; timing should be consistent for each test.
• First recheck: 7–10 days after starting or changing dose. Then at 4–6 weeks, then every 3–6 months when stable or when clinical signs change.
• Target post-ACTH cortisol: many clinicians aim for a post-ACTH cortisol approximately 1.5–5.0 µg/dL (41–138 nmol/L) with clinical improvement and absence of hypocortisolemia signs. Avoid post-ACTH cortisol <1.5 µg/dL, which suggests over-suppression.
• Clinical assessment is as important as numbers: improvement in drinking/urination, skin, energy, and appetite guides therapy.
• Emergency monitoring: if signs of hypoadrenocorticism (weakness, vomiting, collapse), stop trilostane and see vet immediately; may require IV fluids and corticosteroid replacement.

• Diabetes mellitus: HAC frequently induces insulin resistance. Starting HAC therapy can change insulin needs — monitor blood glucose closely and adjust insulin safely with veterinary guidance. Tricky cases benefit from specialist involvement.
• Recurrent infections (UTIs, skin): culture and sensitivity guide antibiotics; treat underlying HAC to reduce recurrence.
• Hypertension: measure blood pressure and treat if persistent (e.g., ACE inhibitors, amlodipine) as indicated.
• Hypercoagulability: consider risk for thromboembolism if additional risk factors exist; address immobility, obesity and treat underlying disease.
• Dermatologic care: medicated shampoos, topical therapy, treat secondary infections promptly.

• Regular rechecks: clinical exam and ACTH stimulation or appropriate endocrine tests as described. Frequency: rechecks at 1–2 months after therapy changes, then every 3–6 months when stable.
• Routine lab monitoring: CBC, biochemistry (liver enzymes, electrolytes), urinalysis every 3–6 months or sooner for concerns.
• Owner logs: track water intake, urine frequency, appetite, energy, panting, and any new infections — very helpful for dose decisions.
• Adjust therapy slowly: small dose changes and close follow-up limit abrupt swings into hypoadrenocorticism.

• With medical therapy many dogs have marked improvement in clinical signs and quality of life. Average survival times reported vary with cause and comorbidities — PDH managed medically often live 2–3+ years or longer, sometimes several years; dogs with adrenal carcinoma or severe comorbidities may have shorter survival.
• Dogs with uncontrolled comorbidities (severe diabetes, recurrent sepsis, thromboembolism) have more guarded outcomes.
• Early identification and management of complications improves long-term comfort and function.

• Medication consistency: give trilostane or other drugs at the same time(s) each day; keep a pill calendar.
• Record keeping: maintain a log of water intake, urination, appetite, energy, skin problems, and any vomiting/diarrhea.
• Skin and ear care: regular grooming, watch for recurrent infections; get cultures when infections recur.
• Weight and muscle: encourage controlled exercise and a balanced diet to limit obesity and muscle loss; discuss targeted nutrition with your vet.
• Dental care: poor dental health worsens systemic inflammation — keep teeth clean.
• Travel/boarding: inform caretakers about the disease and medications; include vet contact and emergency instructions.

Seek immediate veterinary care if your Dachshund on HAC treatment has:

• Collapse, severe weakness, pale gums
• Repeated vomiting or severe diarrhea
• Refusal to eat for >24 hours
• Severe lethargy and shaking
• Signs suggestive of adrenal insufficiency after trilostane/mitotane (weakness, vomiting, severe lethargy)

H2: Key takeaways

• Cushing's disease is common in middle-aged to older Dachshunds; PDH is most frequent.
• Confirm diagnosis using a stepwise approach (screening UCCR, endocrine testing, imaging, ACTH and adrenal ultrasound, pituitary MRI when indicated).
• Trilostane is now the most commonly used medical therapy — start at a conservative dose (often 1–3 mg/kg/day), monitor with ACTH stimulation tests and clinical assessment, and adjust carefully.
• Adrenal tumors may be cured by adrenalectomy; pituitary surgery is curative in specialized centers.
• Manage comorbidities (diabetes, infections, hypertension) aggressively to preserve quality of life.

Sources and further reading

• Merck Veterinary Manual: Cushing's Disease (Hyperadrenocorticism) in Dogs. https://www.merckvetmanual.com/endocrine-system/thyroid-and-adrenal-glands/adrenal-gland-hyperfunction-cushings-disease-in-dogs
• ACVIM consensus guidance and veterinary endocrinology textbooks (e.g., Feldman & Nelson; Plumb's Veterinary Drug Handbook) for diagnostic strategies and drug dosing recommendations.

Frequently Asked Questions