The adrenal glands are retroperitoneal organs immediately superior to the kidneys. These glands are slightly nodular with a firm texture and are surrounded by a layer of areolar connective tissue. Each gland weighs approximately 4 to 5 g in the adult and has a golden yellow-orange color distinct from the pale yellow retroperitoneal fat. The left adrenal gland is bordered inferiorly by the left kidney and left renal vein, superiorly and posteriorly by the diaphragm, anteriorly by the tail of the pancreas, and medially by the spleen and aorta. The right adrenal gland is bordered inferiorly by the right kidney; superiorly, posteriorly, and laterally by the diaphragm; anteriorly by the liver; and medially by the inferior vena cava (IVC; Fig. 1).

The arterial blood supply to the adrenal gland is derived mainly from the inferior phrenic and renal arteries as well as directly off the aorta. Occasionally, intercostal and ovarian vessels may contribute as well. Rather than one or two main arteries, the distribution is primarily one of multiple small branches that enter the superior, medial, and inferior aspects of the gland (Fig. 2). Venous drainage of the left adrenal is via the left adrenal vein, which arises from the inferomedial aspect of the gland and empties into the left renal vein. The inferior
phrenic vein usually joins the left adrenal vein above its entry into the renal vein. Blood from the right adrenal gland empties directly into the IVC via the short central adrenal vein that arises from the medial aspect of the gland. Accessory adrenal veins entering the vena cava or hepatic veins may be present on the right side. Lymphatic drainage from the adrenal gland is into adjacent pericaval and periaortic lymph nodes, which is important during resection of a malignant tumor.

The adrenal gland is divided into two distinct components: the cortex and the medulla. The adrenal cortex is the site of production of mineralocorticoids (aldosterone), glucocorticoids (cortisone), and sex steroids. The medulla contains chromaffin cells, which secrete the catecholamines epinephrine and norepinephrine and also dopamine.

Adrenal tumors may come to attention because of clinical signs and symptoms of hormone hypersecretion, because of local symptoms of pain due to a large mass, or as a lesion discovered incidentally during cross-sectional imaging done for other reasons. Appropriate diagnosis and localization are imperative for successful operative planning and treatment. The various indications for adrenalectomy are given in Table 1. Algorithms for biochemical testing as well as radiographic imaging are available for differentiating the various causes of adrenal lesions including aldosteronoma, Cushing syndrome, pheochromocytoma, adrenal cortical carcinoma, metastatic disease of the adrenal glands, and adrenal incidentaloma. A summary of the biochemical evaluation and preoperative preparation used for the treatment of these adrenal lesions is described in Table 2.

Primary hyperaldosteronism is the most common cause of secondary hypertension and has a much higher prevalence rate in the population than previously appreciated, occurring in 8% to 12% of hypertensive patients. Although the classic findings in primary hyperaldosteronism are hypertension and hypokalemia, many patients with this diagnosis have a normal serum potassium level. Therefore, any patient who has hypertension with an early age of onset that is difficult to control or refractory to medical management should be considered for this diagnosis, regardless of the serum potassium level. Because endogenous hyperaldosteronism suppresses renin secretion, biochemical screening entails simultaneous measurement of both plasma aldosterone and renin levels. A plasma aldosterone concentration (PAC)–to–plasma renin activity (PRA) ratio greater than 20:25 in the setting of an absolute PAC greater than 15 ng/dL is consistent with this diagnosis and should be evaluated further. Confirmatory testing consists of demonstrating elevated
24-hour urine aldosterone levels (>12 μg/24 h) while on a high-sodium diet or after intravenous saline loading. Other biochemical findings include an elevated urinary potassium excretion rate (>30 mEq/24 h).

The most common causes of primary hyperaldosteronism are aldosterone-producing adenoma (65%) and idiopathic cortical adrenal hyperplasia (35%). Aldosterone-secreting adrenal carcinomas are rare. Differentiation of these causes is critical in directing therapy since the preferred treatment of an aldosteronoma is adrenalectomy, whereas idiopathic hyperaldosteronism from cortical hyperplasia is treated medically with the aldosterone antagonist spironolactone. Adrenal cross-sectional imaging with thin-cut (3-mm image slices) computed tomography (CT) is indicated once primary aldosteronism has been confirmed biochemically. Younger patients (under age 40 to 50) with a discrete unilateral macroadenoma (>1 cm) and a normal contralateral adrenal may undergo adrenalectomy without further testing. All other patients should undergo adrenal vein sampling for cortisol and aldosterone to determine if there is a lateralizing source of increased aldosterone production.

Most aldosteronomas are small, less than or equal to 1 to 2 cm in size, with a golden orange color. These tumors are rarely malignant and are ideally suited for laparoscopic excision. Spironolactone may be given preoperatively to control hypertension but should not be administered until the biochemical evaluation, including adrenal vein sampling, is complete. Patients should also have potassium levels repleted and, in long-standing cases, assessment of cardiac function and renal insufficiency prior to surgery.

Prior to adrenalectomy, patients should have electrolyte abnormalities such as hypokalemia corrected. Hypertension should be controlled medically and patients with pheochromocytomas should receive 7 to 10 days of preoperative alpha-receptor blockade with phenoxybenzamine to avoid hypertensive exacerbations intraoperatively. Phenoxybenzamine is typically started in a dose of 10 mg twice daily and the dose is increased by 10 to 20 mg/d every 2 to 3 days until the blood pressure is well controlled and the patient is mildly orthostatic. Some patients with symptomatic pheochromocytomas in hypertensive crisis will need to be blocked while in the hospital, but for many patients the blockade can be managed on an outpatient basis. During this time, patients should be instructed to drink ample fluids to allow volume expansion as the alpha-blockade proceeds. Our practice has been to admit patients to the hospital the day before the scheduled adrenalectomy to increase the blockade and allow monitoring of orthostatic vital signs and urinary output. A total dose of phenoxybenzamine of 40 to 60 mg/d is sufficient to block most patients. Intraoperatively, patients with vasoactive pheochromocytomas should have continuous blood pressure monitoring via an arterial line. Intraoperative fluid resuscitation is crucial to avoid hypotension after the tumor has been removed.

Patients with Cushing syndrome should receive intravenous steroids perioperatively and will require maintenance doses of steroids for 6 months or longer postoperatively. Mechanical bowel cleansing is not routinely given prior to adrenalectomy.

The retroperitoneal location of the adrenals makes them accessible via a variety of surgical approaches: transabdominal, retroperitoneal, or through the flank, and using either laparoscopic or open techniques. The choice of surgical approach in a given patient depends on the size and functionality of the lesion, the degree of exposure needed, the likelihood that the tumor is malignant, and the surgeon’s experience (Table 3). For most patients with an adrenal tumor, laparoscopic adrenalectomy is appropriate and has become preferred over the various open approaches. This approach has been associated with less pain, a shorter hospitalization, faster return to unrestricted activities, and less morbidity than open adrenalectomy. Late complications such as incisional hernia and chronic incisional pain are also less common with the laparoscopic approach.