Diagnostic ultrasound ( PDFDrive )

CHAPTER 11 The Adrenal Glands 419
A
B
C
D
FIG. 11.5 Adrenal Adenoma. (A) Sagittal and (B) transverse sonograms show a hyperechoic right adrenal mass (arrow) between the liver
and upper pole of the right kidney. (C) MRI demonstrates diffuse loss of signal on out-of-phase imaging conirming the presence of intravoxel
fat and the diagnosis of adenoma (arrow). See also Videos 11.2 and 11.3. (D) In another patient, sagittal sonogram shows a small solid right adrenal
mass.
Nonfunctioning adenomas are more common than functioning
adenomas and are oten larger in size by the time of diagnosis
as patients are asymptomatic. MRI evaluation to determine
intracellular lipid content or contrast-enhanced CT to ascertain
physiologic washout characteristics is helpful in characterizing
adenomas.
Although adenomas can grow, progressive or rapid interval
increase in size may suggest underlying malignancy or collision
tumor, where a malignant lesion arises within an adenoma. 14 In
this context, further imaging and possibly histologic evaluation
is warranted. 18-Fluorodeoxyglucose positron emission tomography
( 18 FDG-PET) CT has been found to be useful in diferentiating
a collision tumor from an adenoma. 15
Functioning adrenal adenomas are oten diagnosed earlier,
and with a smaller size, than nonfunctioning adenomas given
the clinical manifestations of the tumor. For example, Cushing
syndrome occurs with excessive glucocorticoid levels. Clinical
symptoms include increased weight gain, fat redistribution with
increased abdominal fat, characteristic bufalo hump and moon
facies, and decreased fat deposition in the extremities. Cushing
syndrome is most oten encountered secondarily in the setting
of chronic steroid use. Primary Cushing syndrome caused by
hyperfunctioning adrenal lesions account for about 15% to 20%
of cases, with adenomas, adenomas within a myelolipoma,
adenomas of uncertain malignant potential, and adrenal carcinomas
accounting for 92% of cases. 16 Unilateral disease is most common
and 70% of cases occur as a result of adrenal hyperplasia. 17 In
contradistinction, Cushing disease is hypercortisolism secondary
to a primary adrenocorticotropic hormone (ACTH)–producing
pituitary tumor. he two can be diferentiated via biochemical
analysis. An autonomously cortisol secreting adrenal lesion would
yield low serum ACTH as well as elevated plasma cortisol unsuppressed
by low dose dexamethasone test. 18
Conn syndrome results from oversecretion of aldosterone. 19
Primary aldosteronism can result from adrenal adenoma (70%),
adrenal hyperplasia (30%), and, in rare cases, adrenal carcinoma. 20
Clinical manifestations include hypertension and hypokalemia.
Patients with hyperaldosteronism from an adenoma typically
are female, whereas those with hyperaldosteronism from hyperplasia
are usually male. 21,22 hese tumors tend to be small (<2 cm).
Biochemically, elevated urine and serum aldosterone levels,
hypokalemia, hypernatremia, and elevated bicarbonate and low
plasma pH levels are found. A suppressed renin level indicates
primary hyperaldosteronism.
Adrenal vein sampling can be performed to determine
whether there is hypersecretion from the adrenal gland. Laparoscopic
adrenalectomy and radiofrequency ablation are the
treatments for hyperfunctioning adenomas. 23,24