Adrenal gland

Chapter 35

Adrenal gland

Adrenal gland problems in the cat are recognized with increasing frequency. They are most commonly identified in cats presenting for investigation of clinical signs attributed to excessive aldosterone, cortisol, or progesterone secretion. Surgery can be performed in selected cases of neoplasia, but first thorough investigation and stabilization are paramount. Adrenal surgery in cats is certainly not without risk, and is a technically challenging surgery that requires thorough planning, together with intensive perioperative care.

Surgical anatomy

The adrenal glands are found cranial to each kidney. They are cream colored as they are rich in lipids, and on ultrasound examination they have been reported to be 0.29–0.53 cm in size along their short axis.1 At surgery, the duodenal maneuver is used to identify the right side and the colonic maneuver the left.

The right adrenal gland is harder to visualize than the left gland, because it is situated more cranially and it sits slightly dorsal to the vena cava; the caudate lobe of the liver may also partly cover it. The phrenico-abdominal veins cross over both adrenal glands.

The arterial blood is supplied by branches of the renal artery, directly from the aorta and from the phrenico-abdominal and lumbar arteries. Venous drainage is into the vena cava, phrenico-abdominal or lumbar veins. Neoplastic disease will often disrupt this and make an understanding of this supply rather academic.

Disease of the adrenal gland may affect surrounding structures, including the vena cava medially (and possibly the aorta), the kidneys caudally, and the sublumbar musculature dorsally.

Diagnosis and general considerations

It is important for the surgeon to have knowledge of the disease processes involved, to ensure that surgical management is appropriate, and that the patient has been optimally stabilized preoperatively, with medical management where appropriate. Adrenal disorders predominantly affect older cats, and so concurrent disease may be common, and this is important to consider as it may significantly influence management. For the adrenal conditions reported there does not appear to be breed predisposition; most cases have been described in domestic short-hair cats. No sex predisposition exists; all reported cases have affected neutered animals, with roughly equal proportions of female and male cats.

Diagnostic imaging

Imaging is essential both for diagnostics and patient assessment before surgery. Currently, ultrasonography is the best imaging modality for detecting adrenal masses in dogs and cats. Inflated thoracic radiographs and/or computed tomography are used to rule out metastatic disease. Abdominal ultrasound, preferably combined with CT or MRI, should be performed to look for evidence of metastatic disease within the abdominal cavity (liver, spleen, lymph nodes), but also to assess local invasion or thrombosis within the vena cava. This information can make a great difference to surgical planning and treatment advice. Invasion into the adjacent vena cava, or renal vessels, renal or liver parenchyma is possible with more aggressive neoplasms and may be a contraindication for surgery if invasion is extensive. There are few reports in the literature about surgical management of caval invasion in the cat2 and so guidelines are not available for when surgery should be undertaken, but this may be largely dictated by surgeon experience.

Surgical diseases

Hyperaldosteronism (Conn syndrome)

Hyperaldosteronism or Conn syndrome is a condition caused by increased secretion of aldosterone from the adrenal glands. It has become increasingly recognized in cats, but whether this is due to an increased awareness and testing for the condition, or a true increase in frequency is not known.


Hyperaldosteronism may be of primary or secondary etiology. Secondary hyperaldosteronism occurs as a response to stimulation of the renin–angiotensin–aldosterone system (RAAS) and therefore may occur in any disease that stimulates the RAAS, such as dehydration, hypotension, reduced renal perfusion (most commonly secondary to renal disease), or sodium deficiency (reduced intake or increased loss). In primary hyperaldosteronism (PHA) there is an inappropriate increase in aldosterone secretion, independent of the RAAS. Unilateral adrenocortical neoplasia is the most commonly described cause of PHA in cats, with unilateral adrenal adenomas and carcinomas appearing to have approximately equal incidence. Although rare, bilateral adrenal neoplasms have also been described. Bilateral adrenal hyperplasia3 is also recognized, and in these cases medical management is advised.

Clinical features

The major clinical signs of primary hyperaldosteronism are similar, whether it results from adrenal adenoma, carcinoma or hyperplasia, and they can be divided into two main groups:

Additional clinical signs such as polyuria, polydipsia, and polyphagia have also been reported

Concurrent hyperaldosteronism and hyperprogesteronism has also been reported in some cases of adrenal neoplasia.4,5 In these cases the signs of hyperprogesteronism usually predominate, resulting in very similar clinical signs to those encountered with hypercortisolemia (Fig. 35-2).


On serum biochemistry, hypokalemia is most often present; however, the degree is variable and normokalemia does not exclude the possibility of primary hyperaldosteronism. Serum sodium concentrations are usually normal or only mildly increased. Creatine kinase is usually elevated in cats with polymyopathy, with the degree of elevation being highly variable. Urea and creatinine may be elevated secondary to hyperaldosteronism, and so the presence of azotemia should not lead the clinician to conclude that hypokalemia and/or hypertension is a consequence of the renal disease itself.

Adrenal masses are rarely visible on radiographs, but if the mass is seen it is more likely to be an adrenocortical carcinoma than an adenoma. Pulmonary metastases can occur, albeit infrequently. In all reported feline cases of primary hyperaldosteronism in which adrenal ultrasonography was performed, unilateral adrenal enlargement with evidence of an adrenal mass was identified, ranging in size from 10–46 mm in diameter (Fig. 35-3). The contralateral adrenal gland may appear normal in appearance or may be unidentifiable. It is, however, vital that the contralateral gland be assessed, because bilateral adrenal neoplasms have been reported. Ultrasonography should also be used to identify the presence and degree of invasion of the caudal vena cava by the tumor or related thrombus, and the presence of metastasis to other organs. Close association of the tumor with the caudal vena cava is usually evident. Other imaging modalities, including MRI (Fig. 35-4), CT, and saphenous venography, have been used in a small number of cases in an attempt to establish the extent of the adrenal mass before undertaking surgery.

Confirmation of diagnosis relies mainly on demonstrating an elevated plasma aldosterone concentration. The assay is widely available at commercial endocrine laboratories and requirements for collection and handling of serum or plasma are routine. Ideally, plasma aldosterone concentration needs to be interpreted together with plasma renin activity, which would be expected to be elevated in cases of secondary hyperaldosteronism. There are difficulties with measuring plasma renin activity and as a consequence demonstration of the presence of adrenocortical neoplasia concurrently with a markedly elevated plasma aldosterone concentration is considered to be sufficient to make a diagnosis of aldosterone-secreting adrenocortical tumor in cats, especially in conjunction with persistent hypokalemia and hypertension. Histopathologic confirmation of the neoplasm together with resolution of clinical signs and plasma aldosterone measurements postoperatively assist in confirming the diagnosis.

If no adrenal mass is present, then non-neoplastic primary hyperaldosteronism should be considered, and this is more difficult to diagnose without assessment of plasma renin activity. Surgical treatment would not be indicated in these cases.

Hyperadrenocorticism (Cushing’s syndrome)

Hyperadrenocorticism or Cushing’s syndrome is rare in cats and usually associated with pituitary neoplasia rather than primary disease of the adrenal glands.


Hyperadrenocorticism results from chronic cortisol excess, and may occur secondary to iatrogenic cortisol administration, or with naturally occurring disease. Naturally occurring disease can be pituitary dependent, whereby a pituitary neoplasm secretes excessive ACTH with subsequent bilateral adrenocortical hyperplasia and increased cortisol secretion, or it may be adrenal dependent, as a result of a cortisol secreting adrenal neoplasm. Hyperadrenocorticism is rare in cats, but when it does occur the majority of cases (~80%) are pituitary dependent, most commonly as a result of a pituitary adenoma. About 50% are microadenomas (<3 mm diameter) and 50% are macroadenomas (>3 mm diameter). Pituitary carcinoma has only been rarely reported. In reported cases of adrenal-dependent disease, about 50% have been adrenocortical adenomas, and 50% adrenocortical carcinomas.

Clinical features

The major clinical signs are similar, whether hyperadrenocorticism results from adrenal adenoma, carcinoma or hyperplasia. Approximately 75% of cats with hyperadrenocorticism develop secondary diabetes mellitus, and the signs of uncontrolled diabetes mellitus usually predominate, namely polyuria, polydipsia, and polyphagia. Other clinical signs include lethargy, weight loss, an unkempt coat, and abdominal enlargement/pot belly appearance, although this is usually less appreciable than it is in dogs. Failure of hair regrowth, thin skin, and poor wound healing are common dermatologic features. Cushingoid cats may also exhibit severe skin fragility where the skin is so thin that it easily tears (Fig. 35-5). This is a serious complication as resultant wounds heal poorly, and it can also result in life-threatening sepsis.

Sep 6, 2016 | Posted by in SUGERY, ORTHOPEDICS & ANESTHESIA | Comments Off on Adrenal gland

Full access? Get Clinical Tree

Get Clinical Tree app for offline access