Tentative Diagnosis: The tentative diagnosis is Hyperadrenocorticism (HAC), or Cushing's Disease. The combination of the classic signalment, the insidious and progressive history of PU/PD, polyphagia, panting, and the hallmark physical exam findings (pot-belly, muscle atrophy, alopecia, thin skin) is strongly supported by the initial laboratory findings (especially the markedly elevated ALP and stress leukogram).
Further Diagnostic Test(s): The diagnostic plan involves a two-stage process: first, confirming the presence of hyperadrenocorticism, and second, differentiating between the pituitary-dependent (PDH) and adrenal-dependent (ADH) forms.
Confirmation Test: The Low-Dose Dexamethasone Suppression (LDDS) Test was performed. This is considered the screening test of choice.
Protocol: A baseline cortisol sample was taken, a low dose of dexamethasone was injected IV, and blood samples were collected at 4 and 8 hours post-injection.
Results:
Basal Cortisol: 5.2 µg/dL
4-hour Post-Dex Cortisol: 1.1 µg/dL (Suppression, as <1.4 µg/dL)
8-hour Post-Dex Cortisol: 4.8 µg/dL (Failure to suppress, as >1.4 µg/dL)
Interpretation: The failure of cortisol to remain suppressed at 8 hours confirms the diagnosis of Hyperadrenocorticism.
Differentiation Test: While the LDDS pattern (suppression at 4h, escape at 8h) is suggestive of PDH, an abdominal ultrasound was performed for more definitive localization.
Ultrasound Findings: Both adrenal glands were visualized and found to be symmetrically enlarged ("plump"), measuring 7.1 mm (left) and 6.9 mm (right) in width, with normal architecture. There was no evidence of a unilateral adrenal mass or atrophy of the contralateral gland.
Interpretation: This finding of bilateral adrenomegaly is consistent with constant stimulation from excess pituitary ACTH, confirming the pituitary-dependent form of the disease.
Definitive Diagnosis:
Pituitary-Dependent Hyperadrenocorticism (PDH), or Cushing's Disease. For more, see the
Treatment Plan: The treatment goal is to manage the clinical signs and improve quality of life by reducing the body's cortisol production.
Primary Medication: Daisy was started on Trilostane (Vetoryl®). This medication is a competitive inhibitor of the 3β-hydroxysteroid dehydrogenase enzyme, effectively blocking the production of cortisol in the adrenal glands.
Dosing: A starting dose of 30 mg was prescribed to be given once daily with a meal to enhance absorption.
Concurrent Disease Management:
Hypertension: Daisy was started on Amlodipine to manage her systemic hypertension and reduce the risk of end-organ damage.
Proteinuria/UTI: A urine sample was submitted for culture and sensitivity to guide antibiotic therapy for her subclinical bacteriuria. Treatment for proteinuria with an ACE inhibitor (e.g., benazepril) was planned pending blood pressure control.
Monitoring Protocol: This is a critical component of safe and effective management.
10-14 Day Recheck: Daisy is scheduled to return in 10 days for a re-evaluation. The owners will report on her thirst, appetite, and energy levels.
ACTH Stimulation Test: A precisely timed ACTH stimulation test will be performed 4-6 hours after she receives her morning dose of Trilostane. The goal is to see a post-stimulation cortisol level within the therapeutic range (typically 1.5–5.5 µg/dL), which indicates adequate control without over-suppression (which would risk an iatrogenic Addisonian crisis).
Long-Term: Once a stable dose is achieved, monitoring ACTH stimulation tests and biochemistry profiles will be performed at 1 month, 3 months, and then every 3-6 months thereafter for life.
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