Christopher A. Adin and Richard W. Nelson

Anatomy

The paired adrenal glands are located in the retroperitoneal space, closely associated with the aorta and vena cava in the cranial abdomen (Figure 120-1).²⁰ The left adrenal gland is located medial to the cranial pole of the left kidney and is loosely adhered to fascia of the psoas minor muscle and transverse process of the second lumbar vertebra. The left adrenal gland is adjacent to the left side of the abdominal aorta medially, and its caudal aspect borders the left renal artery. The right adrenal, which is further cranial than the left, is located ventral to the thirteenth thoracic vertebra and is adhered to the right side of the vena cava. In many instances, the adrenal capsule is actually contiguous with vascular adventitia.²⁰ The right adrenal gland is covered by the caudal extension of the right lateral liver lobe; access to the region can be further complicated by hepatomegaly that accompanies hyperadrenocorticism. Both adrenal glands are also obscured by adipose tissue that accumulates in this region of the retroperitoneal space; however, they are easily identified by the beige appearance of the adrenal cortical tissue and by the phrenicoabdominal vein that crosses the ventral surface of each gland.

The microscopic anatomy of the adrenal glands reflects developmental origin and the physiologic function of this endocrine organ. The adrenal cortex is derived from a mass of mesodermal cells that arise near the genital ridges during embryonic development.²⁰ These cells differentiate into polygonal to columnar shapes, with varying lipid content.²⁰ The cortex takes on a laminar architecture adapted to serve specific endocrine functions, including regulation of renal fluid and electrolyte balance (aldosterone synthesis) and chronic stress adaptation and carbohydrate metabolism (steroid hormone synthesis). This mesodermal mass is later invaded by neural crest ectoderm, which migrates to the center of the gland and forms the adrenal medulla.²⁰ As indicated by its developmental origin, the adrenal medulla is essentially a sympathetic ganglion, consisting of postsynaptic neurons that are modified to release their neurotransmitters (epinephrine and norepinephrine) into the systemic circulation through the adrenal gland’s rich vasculature.

The arterial supply to the adrenal glands consists of 20 to 30 small branches arising from the phrenicoabdominal, renal, and cranial abdominal arteries and directly from the adjacent aorta.²⁰ These arteries form a plexus, which is visible through the thick adrenal capsule, and send penetrating branches into the cortex and medulla. Venous blood is collected in sinusoids and drains into a single adrenal vein. The right adrenal vein empties directly into the vena cava, and the left adrenal vein empties into the left renal vein.

Physiology9,18,31

The adrenal cortex is divided into three zones: the outer zona glomerulosa, which secretes mineralocorticoids, and the central zona fasciculata and inner zona reticularis, which secrete glucocorticoids and sex steroids. The majority of glucocorticoids are produced within the zona fasciculata. Adrenal corticoids are synthesized from cholesterol. Enzymatic cleavage of a carbon side chain within mitochondria produces the C-21 steroid pregnenolone. Within cells of the zona fasciculata and zona reticularis, pregnenolone is hydroxylated at C-17 to form the glucocorticoid molecule. Zona glomerulosa cells lack 17α-hydroxylase; absence of a hydroxyl group on C-17 is the major difference between aldosterone and cortisol.

Because steroid hormones are lipids, transport through blood relies on binding to plasma proteins. Corticosteroid-binding globulin, or transcortin, has a high affinity to cortisol. Consequently, 75% of cortisol in the plasma is bound to transcortin and 15% to albumin, with approximately 10% unbound. Transcortin transports only 10% of aldosterone; the majority is transported bound to albumin (50%) or remains in its free state (40%). Transcortin is affected by a variety of physiologic states, including pregnancy, which increases its hepatic synthesis, and liver dysfunction, which decreases it. Clearance half-lives of cortisol and aldosterone are 60 and 20 minutes, respectively. The liver is important for metabolism of these hormones into their less active states.

Identification of An Adrenal Mass

Adrenal masses are most commonly identified during ultrasound examination of the abdomen and less commonly with computed tomography (CT) or magnetic resonance imaging (MRI) (Figure 120-2). Clinical signs, findings on physical examination, results of routine blood and urine tests, or a combination of these may suggest adrenal disease (e.g., hyperadrenocorticism) and the need for diagnostic imaging. Alternatively, the adrenal mass may be an unexpected finding during abdominal ultrasonography that is performed for another reason (e.g., persistent vomiting). Regardless of how an adrenal mass is discovered, determining the functional status of the mass is critical to ensure appropriate perioperative management of the case and to improve the likelihood of a successful outcome after adrenalectomy.

Before proceeding with therapeutics, one of the first considerations is to confirm that an adrenal mass exists. Because of the subtlety of findings in ultrasound examination of the adrenal glands, the authors typically recommend repeating abdominal imaging to confirm that the mass is a repeatable finding and that therapy is warranted. Bulbous enlargement of the cranial or caudal pole of the adrenal gland is common in dogs with normal adrenal glands and can often be misinterpreted as an adrenal mass. The diagnosis of an adrenal mass is made when the maximum width of the adrenal gland exceeds 1.5 cm, the gland loses its typical “kidney-bean” shape, and the gland is asymmetric in shape and size compared with the contralateral adrenal gland.5,17

Adrenal asymmetry may represent a functional neoplasm; however, other differential diagnoses include hypertrophy of normal tissue, granuloma, cyst, hemorrhage, or an inflammatory nodule. Adrenalectomy is the treatment of choice if an adrenal mass is malignant and has not metastasized, but adrenalectomy may not be indicated if the mass is benign, small, and hormonally inactive and has not invaded surrounding structures. Unfortunately, it is not easy to determine if an adrenal mass is malignant or benign before surgical removal and histopathologic evaluation. Guidelines to suggest malignancy include mass size, invasion of the mass into surrounding tissues and blood vessels, and identification of additional mass lesions with abdominal ultrasonography and thoracic radiography. The bigger the mass, the more likely it is malignant and the more likely metastasis has occurred, regardless of findings on abdominal ultrasonography and thoracic radiography.

Diagnosis of Functional Adrenal Tumors

Adrenal tumors may secrete a hormone or may be nonfunctional. Excess secretion of cortisol, catecholamines, aldosterone, progesterone, and steroid hormone precursors have been documented in dogs and cats (Table 120-1). Clinical presentation and results of routine blood and urine tests often provide clues to the functional status of the adrenal tumor. The most common functional adrenal tumors in dogs secrete cortisol or catecholamines.

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