Page 594 - Withrow and MacEwen's Small Animal Clinical Oncology, 6th Edition

572 PART IV Specific Malignancies in the Small Animal Patient

whether the lesions arise from the cortex or medulla, whether they PDH and ADH (these are described in detail elsewhere). 9,10 Simi-
are functional or nonfunctional, and whether they are benign or lar screening tests are used to confirm the diagnosis of HAC; how-
ever, the sensitivity of the ACTH stimulation test for the diagnosis
malignant. Functional adrenal tumors may secrete cortisol, cat-
VetBooks.ir echolamines, aldosterone, sex hormones, or steroid hormone of ADH is only approximately 60%. 141 Therefore the LDDST is
a better screening test when ADH is suspected. Dogs with ADH
precursors, and these may be associated with specific clinical and
laboratory findings. Hormonal testing and imaging techniques fail to show suppression on LDDST or HDDST, and differentia-
are central to the diagnostic evaluation of these patients, helping tion from PDH generally is determined by imaging studies, par-
ensure that the most appropriate course of therapy can be pur- ticularly abdominal ultrasound examination, and measurement of
sued. Large adrenal masses may be detected on abdominal radio- endogenous ACTH levels. Excessive secretion of glucocorticoids
graphs. 121–123 The presence of mineralization suggests an adrenal by a functional adrenocortical adenoma or adenocarcinoma occurs
tumor, but this finding is not highly specific, and it cannot be independently of pituitary control, with secondary atrophy of the
used to differentiate between benign and malignant masses. The normal adrenocortical cells in both the affected and contralateral
normal ultrasonographic appearance of canine adrenal glands has adrenal glands. Unfortunately, the functional atrophy of the con-
been described, 124,125 and many reports of the ultrasonographic tralateral adrenal gland is not always easily detected on abdominal
appearance of adrenal lesions in dogs are available, although no ultrasonography. This finding, termed equivocal adrenal asym-
16
particular ultrasound findings are pathognomonic for a specific metry, is also observed in some dogs with PDH and is associated
diagnosis. 126 Abdominal ultrasound examination frequently is with asymmetric hyperplasia of the glands. An ultrasound study
14
used to detect metastatic disease and to determine the local inva- of dogs with equivocal adrenal asymmetry suggested that a maxi-
siveness of adrenal tumors. Ultrasonography has been reported mal dorsoventral thickness of the smaller gland of less than 5.00
to be 80% to 100% sensitive and approximately 90% specific mm was consistent with a diagnosis of ADH. 17
for the detection of adrenal tumor invasion into the caudal vena Surgical adrenalectomy is the treatment of choice for dogs with
cava. 20,22,127 Contrast-enhanced ultrasonography may provide ADH. In one series of 144 dogs undergoing surgical removal of
additional information about tumor type and malignancy. 128,129 a functional adrenocortical tumor, the prognosis was described as
The CT appearance of both normal and abnormal canine adre- excellent for patients that survived 4 weeks postoperatively, and
nal glands has been described. 24,123,130–134 Contrast-enhanced CT the average life expectancy was 3 years. Nine of 144 dogs were
has been shown to provide accurate preoperative evaluation of euthanized at the time of surgery, and 29 dogs died during surgery
35
canine adrenal masses with 92% sensitivity and 100% specific- or immediately postoperatively. MSTs of 230 to 778 days have
ity for the detection of vascular invasion by adrenal tumors. 135,136 been reported for dogs undergoing adrenalectomy for adrenal car-
The MRI appearance of presumed normal canine adrenal glands cinomas, 19,116,117 compared to an MST of 688 days for dogs with
also has been described, 137 but as yet, few reports document the adenomas. 116
systematic use of MRI for evaluation of adrenal lesions in dogs SRT has been reported in a small number of dogs with adreno-
and cats. cortical tumors with vascular invasion. In the nine dogs evaluated,
of which six dogs had nonsecretory tumors, the MST was 1030
Canine Adrenocortical Tumors days, tumor size was reduced, and no dogs experienced severe
radiotoxicity. 142 However, more studies involving larger numbers
A review of case reports of functional adrenocortical tumors in are necessary to further evaluate this mode of therapy.
dogs suggests that carcinomas are slightly more common than Mitotane or trilostane therapy for ADH should be used when
adenomas, although this could reflect the fact that tumors with surgery is not a good option for the patient or client, or they may
features of malignancy are more likely to be removed surgically. be used before adrenalectomy in patients that are significantly
Adenomas typically are smaller; tumors larger than 2 cm are more debilitated by HAC. Treatment with mitotane as an alternative
likely to be carcinomas. 138 On histopathologic examination, ade- to surgical adrenalectomy uses the drug as a true cytotoxic agent.
nocarcinomas appear more likely to exhibit a trabecular growth Detailed protocols are readily available 9,143 ; clinicians should be
pattern, peripheral fibrosis, capsular invasion, necrosis, and/or aware that this approach typically requires higher doses of mito-
hemorrhage. 138 They are less likely to exhibit cytoplasmic vacuol- tane than those used in PDH, 144 and relapses are common. How-
ization, extramedullary hematopoiesis, or fibrin thrombi. ever, this treatment can be effective; a mean ST of 16.4 months
Approximately 20% of adrenocortical carcinomas invade into was reported in a series of 32 dogs, and dogs without evidence of
the phrenicoabdominal vein with extension into the renal vein and/ metastatic disease appeared to have a better response to mitotane
or caudal vena cava. 19,139 Intravascular invasion has the potential therapy. 145 Trilostane is not a cytotoxic drug, but it has been
to cause severe and life-threatening intraabdominal or retroperito- used successfully to manage patients with ADH, 42,146,147 includ-
neal hemorrhage. 22,140 Metastasis was identified in approximately ing a small number of dogs with metastatic disease. 148 In a ret-
50% of dogs with adrenocortical carcinomas. 138,139 Although rospective study comparing trilostane and mitotane in dogs with
involvement of the liver and lungs is most common, metastasis to ADH, the MSTs for dogs treated with trilostane and mitotane
the kidney, ovary, mesenteric lymph nodes, peritoneal cavity, and were 353 days and 102 days, respectively. These STs were not
thyroid gland also has been reported. In the absence of evidence significantly different; however, this study did further confirm
of tumor invasion or metastasis, no consistent clinical, biochemi- that STs are significantly reduced with metastatic disease. 149 The
cal, or imaging findings reliably distinguish between functional MSTs in a more recent study were 15.6 months and 14 months
adrenocortical adenomas and carcinomas. for dogs with ADH treated with mitotane or trilostane, respec-
Dogs with PDH and dogs with ADH are similar in age, but tively 150 ; thus either medication is a reasonable option for ADH
almost 50% of dogs with ADH weigh more than 20 kg compared if surgery is not feasible.
to approximately 25% of dogs with PDH. 121 The historic features, Aldosterone-secreting adrenocortical tumors have rarely
physical changes, clinical signs, and basic laboratory findings in been reported in dogs. 151–155 Clinical findings include lethargy,
canine Cushing’s syndrome essentially are the same in dogs with anorexia, polyuria/polydipsia, hypokalemia, metabolic alkalosis,