ATs, which are the most common endocrine tumours, may have a large variation with regard to ultrasonographic appearance. As a general rule, ultrasonography does not allow to differentiate between benign and malignant lesions nor can the type of tumour be specified. They may appear as focal increase in adrenal thickness (= nodule) or a diffuse increase in

thickness and/or length, resulting in various degrees of distortion of the normal shape (= adrenal mass). The parenchyma may be homogenous or heterogenous. The larger the tumour the more likely it is malignant; however, also small tumours may be malignant. Mineralization may occur in benign and malignant tumours, however, it may also be seen in hyperplastic adrenal glands and is therefore not a marker for AT. Anechoic lesions are preferably seen in large tumours, they are often part of a heterogenous or mixed pattern of echogenicity. They may represent foci of adrenal necrosis or hemorrhage and may be associated with fast tumour growth. Identification of vascular invasion (most often into the vena cava caudalis) is specific for a malignant tumour. Although ultrasonography in general is a fast and easy tool to detect vascular invasion it may not be possible to differentiate vascular involvement from compression or a blot clot in some cases.

A variety of other tumours (pheochromocytoma, aldosteronoma, sex-steroid-producing tumour, metastasis, myelolipoma, lipoma) or other lesions (cyst, hematoma, abscess, granulomatous disease) may occur in the adrenal glands and can not be differentiated from AT by means of ultrasonography. In a dog with an adrenal nodule/mass, a smaller than normal contralateral gland strongly supports the suspicion of an AT. However, in some dogs atrophy of the contralateral gland is not visible on ultrasonography. In this situation differential diagnosis are: unilateral AT without visible atrophy of the contralateral gland, AT and concurrent PDH, PDH and another adrenal tumour/lesion (as mentioned above), PDH with (irregular) nodular hyperplasia. Most AT are unilateral, however, bilateral tumours occur and may be impossible to differentiate from PDH with nodular hyperplasia. Endocrine tests may be helpful to make the exact diagnosis.

The second most common adrenal tumours are pheochromocytomas. Dogs with pheochromocytomas may be presented with various clinical signs; some of them are similar to those of HAC. Pheochromocytomas have a very wide range of size (mm-cm) and may reveal any of the ultrasonographic patterns described above, rendering differentiation from AT impossible. Mineralization within a pheochromocytoma seems to be a very rare finding; therefore, this finding would make pheochromocytoma less likely than AT.

Up till now information is scarce on the ultrasonographic appearance of the adrenal glands in cats with PDH or AT. So far, it appears that all statements made for the dog are also valid for the cat.

Ultrasonography of the adrenal glands may also be helpful in the workup of patients with hypoadrenocorticism. It is currently believed that most cases result from an autoimmune destruction of the adrenal cortices with bilateral atrophy of all three adrenal zones. It has been demonstrated that this atrophy is visible in the form of a bilateral, symmetrical reduction in size. In most dogs with hypoadrenocorticism adrenal gland thickness is less than 3 mm. However, due to their small size those adrenals are difficult to find and a high level of experience is required on the part of the operator. So far, no reports are available on the adrenal gland size in dogs with partial hypoadrenocorticism.

 
 
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