Nonfunctional Adrenal Masses
Nonfunctional adrenal masses are space-occupying lesions of the adrenal glands that have no hormonal activity. Symptoms, signs, and treatment depend on the nature and size of the mass.
(See also Overview of Adrenal Function.)
The most common nonfunctioning adrenal mass in adults is an adenoma (50%), followed by carcinomas and metastatic tumors. Cysts and lipomas make up most of the remainder. However, the precise proportions depend on the clinical presentation. Masses discovered on incidental screening are usually adenomas. Less commonly, in neonates, spontaneous adrenal hemorrhage may cause large adrenal masses, simulating neuroblastoma or Wilms tumor. In adults, bilateral massive adrenal hemorrhage may result from thromboembolic disease or coagulopathy.
Benign cysts are observed in elderly patients and may be due to cystic degeneration, vascular accidents, lymphomas, bacterial infections, fungal infections (eg, histoplasmosis), or parasitic infestations (eg, due to Echinococcus). Hematogenous spread of TB organisms may cause adrenal masses. A nonfunctional adrenal carcinoma causes a diffuse and infiltrating retroperitoneal process. Hemorrhage can occur, causing adrenal hematomas.
Most patients are asymptomatic. With any adrenal mass, adrenal insufficiency is rare unless both glands are involved.
The major signs of bilateral massive adrenal hemorrhage are abdominal pain, falling Hct, signs of acute adrenal failure, and suprarenal masses on CT or MRI. TB of the adrenals may cause calcification and Addison disease. Nonfunctional adrenal carcinoma usually manifests as invasive or metastatic disease.
Nonfunctional adrenal masses are usually found incidentally during tests such as CT or MRI conducted for other reasons. Nonfunctionality is established clinically and confirmed by adrenal hormonal measurements. (See also the ACR Appropriateness Criteria for Incidentally Discovered Adrenal Mass.)
Screening adrenal hormonal measurements include dexamethasone suppression testing and serum cortisol (to rule out Cushing syndrome), 24 hr urinary measure of fractionated metanephrines and catecholamines (to rule out pheochromocytoma) and plasma aldosterone and renin (to rule out primary aldosteronism).
If metastatic or infectious disease is possible, fine-needle biopsy can be diagnostic but is contraindicated if adrenal carcinoma or pheochromocytoma is strongly suspected.
Although new imaging modalities (eg, in-phase and out-of-phase MRI) may be diagnostic, if the tumor is solid, of adrenal origin, and > 4 cm, it should usually be excised unless the imaging characteristics are quite clearly benign.
Tumors 2 to 4 cm in diameter are a particularly difficult clinical problem. If scanning does not suggest cancer and hormonal function does not seem altered (eg, normal electrolytes and metanephrines, no evidence of Cushing syndrome), it is reasonable to reevaluate periodically with imaging studies, usually for 1 to 2 yr. If no progression is seen by then, further follow-up is unnecessary. However, many of these tumors secrete cortisol in quantities too small to cause symptoms, and whether they would eventually cause symptoms and morbidity if untreated is unclear. Most clinicians merely observe patients with these tumors, but clinicians should consider removal of these tumors if there is significant cortisol secretion.
Adrenal adenomas < 2 cm require no special treatment but should be observed for growth or development of secretory function (such as by looking for clinical signs and periodically measuring electrolytes).
Nonfunctional adrenal carcinoma that has metastasized is not amenable to surgery, though mitotane plus corticosteroids may help control symptoms of hypercortisolism.