Adrenal imaging

General Approach

• Adrenal Mass Discovered Incidentally on Non-Contrast CT
  • HU < 10 benign
  • HU > 10 indeterminant
    • Contrast enhanced CT or MRI

• Adrenal Mass Discovered Incidentally on Contrast CT
  • Obtain Delayed Images (15 minutes), if HU < 24 benign
  • Calculate RPW, if >40% then benign, if above, consider biopsy or PET

Adrenal Lesion Characterization Calculator at www.chestxray.com.

Adrenal Lesions

Benign Adrenocortical Adenoma - round, sharp margins, can be lipid rich or lipid poor.

• CT - HU <10 (non contrast), rapid wash in and wash out, (non-adenomas have a more intense initial enhancement and a delayed washout.)
• MRI - chemical shift (signal dropout on out of phase imaging) because of intracellular lipid and water in same voxel compared to the in phase image.

In Phase

Out of Phase

T2

Adrenal Metastasis

• CT - HU>20, intense and persistent enhancement
• MRI - low T1 (or high if hemorrhagic), moderately hyperintense T2, delayed washout, no chemical shift

Adrenocortical Carcinoma - 10% clinically functional, large and aggressive

Myelolipoma - no malignant potential, macroscopic fat density lesions

Adrenal Hemorrhage

• CT - acute to subacute HU 50-90 with surrounding stranding
• MRI
  • Acute (<7 days) - iso or hypo T1, marked hypo T2, high intracellualr deoxyhemoglobin
  • Subacute (7 - 60 days) - hyperintense on T1 and T2, free methemoglobin (high T1)
  • Chronic (2- months) - bloom on GRE, hypointense rim on T1 and T2 (hemosiderin)

Adrenal Cysts - Fluid density, recc follow-up to exclude cystic neoplasm

Infection - fungal or TB

Hemangiomas, Ganlioneuromas, Angiosarcomas, Melanomas

Multiple Endocrime Neoplasia

• MEN Type I - cortical nodules or adenomas, rarely functional
  • Associated with: parathyroid hyperplasia, gastrinoma, insulinoma, vipoma and glucagonoma, anterior pituitary tumors (prolactinomas, growth hormone or ACTH), carcinoid tumors, lipomas and thyroid nodules.
• MEN Type IIA and IIB - pheochromocytomas in adrenal medulla
  • Associated with: medullary thyroid cancer, neuromas, ganglioneuromatosis, marfan like build

Patholiogic Conditions

Conn's Syndrome - aka primary hyperaldosteronism, clinical hypertension and hypokalemia

• Aldosterone secreting adenoma - 60%, less than 2cm, F>M, contains lipid laden cells, treated surgically
• Adrenal hyperplasia - 40%, nodular thickening, treated medically
• Functioning adrenocortical carcinomas - very rare

Cushing's Syndrome - chronic excess glucocorticoids, clinical obesity, plethora, bruising, striae, muscle wasting, osteoporosis, diabetes.

• ACTH Dependent - 80%, pituitary hypersecretin of ACTH (Cushing's Disease) or ectoptic ACTH secretion, causes adrenal hyperplasia
• ACTH Independent - 20%, adrenal adenoma and adrenocortical carcinoma

Adrenogenital Syndrome - excessive secretion of sex hormones with clinical symptoms reflecting time and hormone secreted.

Pheocromocytoma - tumor of the chromaffin cells in the medulla, release epi and norepi, clinical headaches, palpitations, sweating, tremor, anxiety, hypertension.

• Rule of Tens - 10% multicentric, bilateral, malignant, extra-adrenal
• CT - enhancing lesions, often with calcification and necrosis
• MRI - T1 isointense, T2 hyperintense, enhancing mass
• MIBG - analog of norepi, avid uptake

Addison's Disease - adrenal cortical hypofunction, clinical lethargy, fatigue, weakness, anorexia, weight loss, abdominal pain, hypotension

• Causes - autoimmune, infection, drugs, hemorrhage, mets, sarcoid, hemochromatosis, amyloid
• Small calcified adrenal glands

Pearls

• Cortisol producing adenomas suppress ACTH levels resulting in atrophy of the remaining gland.
• Adrenal Hyperplasia can be primary (Conn's) or response to ACTH (Cushing's).