Page 114 - Cote clinical veterinary advisor dogs and cats 4th

36 Adrenocortical Neoplasia

Cushing’s syndrome, and diagnostics are ○ Invasion of the vena cava or kidney may pain, and shorter hospitalization time than
laparotomy.
directed toward confirming HAC. be visualized, but it is not apparent in • If the tumor is cortisol-secreting, glucocor-
VetBooks.ir signs consistent with both HAC and pheo- • Blood pressure: often mildly to moderately ticoids should be administered during and
• Occasionally, a patient presents with clinical
some cases even if present.
chromocytoma (e.g., polyuria/polydipsia
3-6 months after surgery.
increased with HAC; may be more severely
[PU/PD] and mild to moderate hyperten-
6 hours intraoperatively and then tapered
pheochromocytoma.
sion). Differentiating the two is necessary increased (>220 mm Hg) in dogs with a ○ Dexamethasone 0.1 mg/kg is given over
for appropriate treatment. to 0.05 mg/kg q 12h until prednisone is
• Alternatively, an adrenal mass may be identi- Advanced or Confirmatory Testing tolerated.
fied in a patient with no reported clinical • To confirm and differentiate the cause ○ Prednisone is started at 0.2-0.4 mg/kg q
signs. After careful questioning of the owner, of HAC, ACTH stimulation test, urine 12h and then tapered to 0.1 mg/kg SID
if clinical signs are not reported, additional cortisol/creatinine ratio, low-dose dexameth- over 3-6 months. Increase dose if lethargy
diagnostics may not be necessary depending asone suppression test, and/or endogenous or gastrointestinal signs noted.
on the size of the mass (p. 34). ACTH concentration can be performed ○ Prednisone can be discontinued when post
• Most cats with adrenocortical neoplasia have (p. 485). ACTH stimulation test cortisol concentra-
hyperaldosteronism, but some have HAC • To help screen for pheochromocytoma, tion (performed at least 12 hours after
or an incidentaloma causing no clinical signs. urine normetanephrine/creatinine ratio prednisone) is > 5 mcg/dL.
Clinical signs usually direct the appropriate (p. 785) • If bilateral adrenalectomy is performed,
diagnostic path. • CT or MRI of the abdomen (p. 1132) lifelong glucocorticoid and mineralo-
• The rest of the diagnostic and treatment ○ To confirm presence of the tumor and to corticoid supplementation is necessary
section covers cortisol- and sex hormone– assess invasion of adjacent structures (p. 512)
secreting adrenocortical neoplasia; see ○ Recommended before adrenalectomy Medical therapy
Hyperaldosteronism for more information • Histopathology is required after adrenalec- • Use only trilostane in cats.
on the diagnosis and treatment of tomy to differentiate mass type. • Mitotane (o,p′-DDD) can be used as when
aldosterone-secreting tumors. ○ Histopathology can help determine if treating PDH or at higher doses as a che-
adenoma or carcinoma, but differentiation motherapeutic agent to ablate all adrenocorti-
Differential Diagnosis can be difficult. Local tissue/blood vessel cal tissue (p. 485).
• Pheochromocytoma invasion and metastases are evidence of ○ Adrenocortical tumors are more resistant
• Nodular hyperplasia associated with pituitary- malignancy. to mitotane, and higher doses and longer
dependent HAC (PDH) ○ Functionality cannot be determined on induction periods are typically needed
• Metastatic neoplasia histopathology; appropriate testing pre- than when treating PDH.
• Granuloma operatively is required. ○ Some dogs cannot tolerate the high doses
required, especially when trying to ablate
Initial Database TREATMENT adrenocortical tissue.
• Complete blood count, serum biochemistry, • Trilostane 1-1.5 mg/kg q 12h or 2-3 mg/kg
urinalysis, urine culture Treatment Overview q 24h with food. Monitor and adjust dose
○ If functional, results depend on hormone • Adrenalectomy is the preferred and most as with PDH (p. 485).
being secreted; findings often consistent definitive treatment, but it has up to a 20% • Treatment with mitotane and trilostane yields
with HAC mortality rate and should be performed by similar survival times in dogs when mitotane
○ If nonfunctional, usually normal a specialist in a 24-hour facility for postopera- is not dosed for ablation.
• Thoracic radiographs tive monitoring.
○ Pulmonary metastasis may be seen. • Dogs with tumors larger than 5 cm and/or Drug Interactions
○ Pulmonary or hepatic metastasis occurs that invade the vena cava or kidney have a • Do not give trilostane concurrently
in about 10% of dogs with cortisol- worse prognosis. with ketoconazole because this can lead
producing adrenal adenocarcinoma. • Medical treatment with trilostane (dogs and to excessive cortisol suppression and
• Abdominal radiographs cats) or mitotane (dogs) is recommended hypoadrenocorticism.
○ If cortisol-secreting, may see hepatomegaly in nonsurgical candidates (patients with • Trilostane is more likely to cause hyperka-
○ Mass may be visible cranial to kidneys. metastasis, invasive tumors, comorbidities, lemia when given with angiotensin-converting
○ Mineralization of adrenal tumor occurs or unwilling owners) if it is a functional enzyme inhibitors; monitor electrolytes
in 50% of affected dogs; presence of tumor. closely.
mineralization does not help determine
if benign or malignant. Acute General Treatment Possible Complications
○ Adrenal mineralization can occur in cats Adrenalectomy Postoperative complications
without adrenal disease. • If a tumor is cortisol-secreting, stabilization • Hemorrhage
• Abdominal ultrasound with trilostane (1-1.5 mg/kg PO q 12h, with • Thromboembolism
○ Typically tumor is unilateral; bilateral food) is recommended for 3-4 weeks before • Pancreatitis
adrenal tumors (adrenocortical and/or surgery to decrease the risk of thromboem- • Acute kidney injury
pheochromocytoma) occur rarely (see bolism and dehiscence. Medical complications
Video). ○ An ACTH stimulation test should be • Hypoadrenocorticism
○ Patients with adrenal-dependent HAC performed 10-14 days into therapy
can have an enlarged, hypoechoic liver, (p. 1300). Goal is to have post-ACTH Recommended Monitoring
hepatic metastasis, and one large adrenal cortisol concentration between 2 and • After adrenalectomy, perform an ACTH
gland (>8 mm thickness) accompanied by 6 mcg/dL. stimulation test 2-4 weeks after the patient
an atrophied contralateral adrenal gland. is clinically normal on 0.1 mg/kg/day
If the contralateral gland is not atrophied Chronic Treatment of prednisone and monthly thereafter if
(<5 mm) in a patient with confirmed Adrenalectomy needed. Prednisone can be discontinued
HAC, consider the possibility that the • Laparoscopic adrenalectomy is associated after the post-stimulation cortisol is
mass is a hyperplastic nodule due to PDH. with fewer complications, less postoperative > 5 mcg/dL.

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