An adrenal mass is any abnormal growth or lesion of the adrenal glands — the small paired hormone-producing glands that sit atop each kidney. The majority of adrenal masses are discovered incidentally on imaging performed for unrelated reasons (adrenal incidentalomas), which occur in approximately 5% of adults undergoing abdominal CT or MRI. Most are benign and non-functioning, but every adrenal mass requires evaluation to answer two critical questions: does it produce excess hormones, and is it benign or malignant?
Adrenal masses sit at the intersection of endocrinology, oncology, and imaging characterization. The adrenal glands sit directly atop the kidneys, and renal cell carcinoma is one of the most common primaries to metastasize to the adrenal — making adrenal evaluation a mandatory component of every renal cancer staging MRI. Malignant renal masses and primary adrenal malignancies share the retroperitoneum as their anatomic space, and distinguishing adrenal from renal origin for large upper abdominal masses is a core MRI task. Pheochromocytoma — a catecholamine-secreting adrenal tumor — is associated with several hereditary syndromes including VHL disease, which also causes clear cell renal cell carcinoma.
Causes
Non-functioning benign masses.
Non-functioning adrenal adenomas are by far the most common adrenal mass — present in approximately 2–3% of the general adult population and rising to over 10% in older adults. They arise from the zona fasciculata or zona reticularis of the adrenal cortex, are lipid-rich (reflecting their steroidogenic machinery), and produce no clinically significant hormone excess. Their intracellular lipid content is the basis for their characteristic MRI appearance — signal loss on opposed-phase chemical shift images. Myelolipomas are benign tumors containing mature adipose tissue and haematopoietic bone marrow elements — their macroscopic fat makes them immediately identifiable on MRI and requires no further workup. Adrenal cysts and adrenal hemorrhage (which can occur spontaneously in neonates, after severe physiologic stress, or as a complication of anticoagulation) are other benign causes of adrenal masses.
Functioning and malignant masses.
Pheochromocytomas arise from chromaffin cells of the adrenal medulla and produce catecholamines (epinephrine, norepinephrine, and dopamine) — causing paroxysmal or sustained hypertension, tachycardia, diaphoresis, and headache ("the rule of tens": 10% are bilateral, 10% are extra-adrenal paragangliomas, 10% are malignant — though hereditary cases have higher rates of each). Approximately 40% of pheochromocytomas are now recognized as hereditary, associated with VHL, RET (MEN2A/2B), NF1, SDHB/SDHD (hereditary paraganglioma-pheochromocytoma syndrome), and TMEM127 mutations. Aldosterone-producing adenomas (Conn syndrome) cause primary hyperaldosteronism — unilateral autonomous aldosterone secretion producing hypertension and hypokalemia that are often refractory to standard treatment. Cortisol-producing adenomas cause Cushing syndrome. Adrenocortical carcinoma (ACC) is a rare but aggressive malignancy — it is large at diagnosis (typically over 6 cm), often both functional (producing cortisol, androgens, or estrogens) and locally invasive. Adrenal metastases from lung, breast, renal cell, melanoma, and colon primaries are among the most common adrenal malignancies overall.
Symptoms
Most adrenal incidentalomas produce no symptoms — they are discovered when the patient has no adrenal-related complaint. When symptoms are present, they reflect the specific hormone or mass effect involved. Pheochromocytoma produces the classic paroxysmal triad of severe headache, diaphoresis, and palpitations — with episodic hypertensive crises that can cause stroke, myocardial infarction, or arrhythmia if unrecognized. The crises can be triggered by physical activity, emotional stress, anesthesia induction, contrast injection, or palpation of the tumor — making imaging characterization before any invasive procedure critical. Primary aldosteronism (Conn syndrome) presents with hypertension (often treatment-resistant), fatigue, muscle weakness, polyuria, and polydipsia from hypokalemia. Cushing syndrome presents with central obesity, facial plethora (moon face), dorsocervical fat pad ("buffalo hump"), purple striae, easy bruising, proximal muscle weakness, and new-onset diabetes or osteoporosis. Subclinical autonomous cortisol secretion — present in up to 30–40% of adrenal adenomas — produces none of the florid Cushing features but carries long-term cardiovascular, metabolic, and bone density consequences that justify identification and monitoring.
Diagnosis
Evaluation of every adrenal mass addresses two parallel questions: biochemical (does it produce hormones?) and imaging (is it benign or malignant?). Biochemical testing includes plasma or 24-hour urine fractionated metanephrines for pheochromocytoma (mandatory before any invasive procedure or surgery); overnight 1 mg dexamethasone suppression test for cortisol excess; and aldosterone-to-renin ratio for primary hyperaldosteronism in hypertensive patients. DHEAS and sex hormone levels are obtained when ACC is suspected.
An MRI of the abdomen is the most accurate noninvasive imaging test for adrenal mass characterization. The cornerstone technique is chemical shift imaging: on opposed-phase T1-weighted images, intracellular lipid-rich adenomas lose signal relative to in-phase images — this signal dropout confirms lipid-rich adenoma with high specificity and no radiation. The adrenal-to-spleen ratio on opposed-phase vs. in-phase images provides a quantitative signal intensity index — a drop exceeding 16.5% (using the adrenal signal intensity index, ASI) is highly specific for adenoma. Pheochromocytomas have a characteristic MRI appearance: markedly T2-hyperintense ("light bulb" T2 brightness), heterogeneous with central necrosis in larger tumors, and intense enhancement. This T2 brightness is the single most distinctive imaging feature of pheochromocytoma and should be recognized on every adrenal MRI. Adrenocortical carcinoma appears as a large, heterogeneous mass with necrosis, calcification, and invasion of adjacent structures — venous invasion of the renal vein or IVC requires MR venography for precise characterization. Adrenal metastases are typically T2-hyperintense without signal dropout on chemical shift imaging, with restricted diffusion on DWI. For lateralization of aldosterone-producing adenomas before adrenalectomy, adrenal vein sampling (AVS) remains the gold standard, as adenomas may be too small to detect on any imaging modality.
Classification
Adrenal masses are classified by whether they produce hormones and by their tissue of origin.
- Non-functioning adrenal adenoma: Most common adrenal mass (~80% of incidentalomas). Lipid-rich; chemical shift signal dropout on MRI is diagnostic. No hormone excess. Observe if <4 cm with classic imaging features; repeat MRI at 12 months to confirm stability.
- Subclinical autonomous cortisol secretion: Adenoma producing mild cortisol excess without florid Cushing syndrome. Present in 30–40% of adenomas. Associated with hypertension, diabetes, dyslipidemia, and bone loss. Adrenalectomy may improve metabolic parameters.
- Pheochromocytoma: Markedly T2-bright on MRI; intense enhancement; often with central necrosis. Biochemical diagnosis with plasma metanephrines. Surgical resection after alpha-blockade preparation. 40% hereditary — genetic testing recommended.
- Aldosterone-producing adenoma (Conn syndrome): Often small (<2 cm); may not be visible on MRI. Biochemical diagnosis with aldosterone-to-renin ratio; lateralization by adrenal vein sampling. Laparoscopic adrenalectomy is curative.
- Myelolipoma: Macroscopic fat on MRI = pathognomonic. No malignant potential. Observe unless symptomatic or >10 cm (rupture risk).
- Adrenocortical carcinoma (ACC): Large, heterogeneous, invasive. Often hormonally active. MRI evaluates venous invasion. Complete surgical resection + mitotane adjuvant therapy. 5-year survival approximately 30–40% after complete resection; poor for stage IV.
- Adrenal metastasis: Common in patients with known primary malignancy. No chemical shift dropout; restricted diffusion on DWI. Management per primary cancer. Isolated metastasectomy in selected patients with controlled primary disease.
Treatments
Treatment is guided by hormonal function, imaging characteristics, size, and the presence of malignancy.
Observation: Incidentally discovered non-functioning adrenal masses with classic lipid-rich adenoma features on MRI and less than 4 cm in size are followed with repeat MRI at 12 months to confirm stability, then discharged from imaging follow-up if stable. Masses with indeterminate imaging features are followed more closely. Annual biochemical testing for hormone excess is continued for 4–5 years given the small risk of developing hormonal activity over time.
Adrenalectomy.
Laparoscopic or robotic adrenalectomy is the standard surgical approach for functioning tumors of any size, any mass greater than 4–6 cm regardless of function, masses growing on surveillance imaging, and any mass with imaging features concerning for malignancy. For pheochromocytoma, alpha-adrenergic blockade (phenoxybenzamine or doxazosin) must be established for at least 10–14 days before surgery to prevent intraoperative hypertensive crisis — followed by volume loading and optional beta-blockade. Surgery without adequate alpha-blockade risks fatal hypertensive crises from catecholamine release during tumor manipulation.
Treatment of adrenocortical carcinoma.
Complete surgical resection with wide margins is the only potentially curative treatment — ACC is highly aggressive with a propensity for local recurrence and early metastasis. Adjuvant mitotane (an adrenocortical cytotoxic agent) is standard after resection of high-risk ACC. EDP-M (etoposide, doxorubicin, cisplatin plus mitotane) is used for advanced disease. Five-year survival is approximately 30–40% after complete resection and less than 15% for stage IV. Care is best provided at high-volume endocrine surgery centers.
Management of adrenal metastases.
Adrenal metastases in patients with a known primary cancer are managed per the primary cancer's treatment plan. In patients with isolated adrenal metastasis and controlled primary disease — particularly from renal cell carcinoma, lung, or colorectal primaries — surgical adrenalectomy or ablation may achieve prolonged disease-free survival. Stereotactic body radiation therapy (SBRT) is an increasingly used non-surgical option for adrenal metastases in patients with limited systemic disease.
Long-term monitoring.
Patients with subclinical autonomous cortisol secretion who do not undergo adrenalectomy require ongoing monitoring of bone density (DEXA scan annually), blood pressure, glucose, and lipids — as even subclinical hypercortisolism accelerates cardiovascular and metabolic risk. Patients who undergo bilateral adrenalectomy for any indication require lifelong glucocorticoid and mineralocorticoid replacement and carry a lifelong risk of adrenal crisis during physiologic stress.
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