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Fig. 24.6. H&E stain of adrenal gland, X 200. 1 ¼Connec-
tive tissue capsule. 2 ¼Zona glomerulosa. 3 ¼Zona fasciculate. 4 ¼Zona reticularis. 5 ¼Medulla. (Courtesy of Dr.
Sarah Johnson, Royal Victoria Infirmary, Newcastle Upon
Tyne, England; we are grateful to Mr Harry Elliot, School
of Applied Sciences, Northumbria University, England for
assisting with this figure).
para-aortic lymph nodes. Lymph from the
paraortic lymph nodes drain into the cisterna
chyli and then via the thoracic duct into the
confluence of the left internal jugular vein
and left subclavian vein.
The adrenal nerve plexus lies medial to the
gland and contains mostly preganglionic sympathetic fibers from the lower thoracic spinal
segments, this input travels via the coeliac
plexus and greater splanchnic nerve to the
adrenal nerve plexus. The neuroendocrine
cells within the adrenal medulla are chromaffin cells which are modified sympathetic ganglion cells that receive direct synaptic contacts
from preganglionic fibers from the eleventh
and twelfth thoracic segments. Chromaffin
cells secrete adrenaline, noradrenaline, and
enkephalin into the capillary bed around the
individual cells and as such play an important
role in the fight or flight response. These sympathetic fibers synapse with the large medullary chromaffin cells which can be considered
analogous to postganglionic sympathetic neurons [4].
340
ENDOCRINE SURGERY
Adrenal Physiology
Output from the adrenal gland from the two
functional components of the gland, the cortex, and the medulla is very distinct and different. The outer cortex represents 85% of the
gland and the medulla in the center 15%. The
cortex has three zones, an outer zone, the
zona glomerulosa which secretes aldosterone
and the zona fasciculata and the zona reticularis which are effectively a functional unit
producing cortisol and small amounts of sex
steroids.
Aldosterone
Aldosterone is released from the zona glomerulosa in response to a fall in blood volume or
an increase in serum potassium. Its function
is to contribute to blood pressure homeostasis. Aldosterone secretion is subject to circadian variation. Sympathetic nerves attached to
the adrenal gland, acting via BARO receptors
detect a fall in blood pressure, and also
induce secretion of aldosterone. In the kidney,
the juxtaglomerular apparatus contains cells
which synthesize renin, a hormone which is
secreted directly as a result of sympathetic
nerve stimulation and also in response to a
fall in renal artery perfusion pressure. Renin
induces the conversion of angiotensinogen to
angiotensin I, which in turn is converted to
angiotensin II via the angiotensin-converting
enzyme system, largely in the lung. Angiotensin II has a direct effect on the secretion of
aldosterone (Fig. 24.7).
Cortisol
Cortisol is secreted from the zona fasciculata,
principally under the control of ACTH. Multiple cofactors, however, also influence cortisol
secretion including vasopressin and physical
and emotional stress. ACTH is secreted from
the anterior pituitary in response to cortisolreleasing factor produced in the hypothalamus. The neurons in the hypothalamus
secrete small bursts of CRF into the pituitary
portal circulation which in turn stimulates the
release of ACTH, a 39-amino acid protein.
341
ADRENAL EMBRYOLOGY, ANATOMY, AND PHYSIOLOGY
Fig. 24.7. Pathway for the synthesis of aldosterone and cortisol.
This is subject to circadian variation. ACTH
acts directly on the adrenal gland to produce
cortisol. Cortisol is largely secreted to order
and is not stored and once in the circulation
95% of it is bound to protein. The active
component is free and unbound and only
5% of the total cortisol secreted. There is a
negative feedback loop which feeds back to
the hypothalamus and pituitary to regulate
and control the secretion of cortisol. The
plasma half-life of cortisol is 80–120 min. Its
function is part of the stress response, mobilizing substrate from stores, reducing inflammation, and raising blood pressure.
Sex Steroids
In the zona reticularis sex steroids are produced,
for example, dehydroepiandrosterone (DHEA).
These small amounts of sex steroid are of
relatively little physiological significance except
for two situations. Firstly, in the postmenopausal
female when the ovaries cease to produce significant hormones the adrenal gland then becomes
the main source of sex steroids. This can be
exploited, for example, in the treatment of postmenopausal women in breast cancer [5–7]. Inhibition of the enzymes (aromatase), which convert
adrenal sex steroids into estrogen, largely in fat,
can be inhibited with drugs. The second incidence
where adrenal sex steroids become relevant is
when there are defects in the synthesis of enzymes
(most commonly 21 and 11 hydroxylase) responsible for the conversion of sex steroids in the
adrenal gland. In these circumstances at different
levels in the sex steroid pathway (Fig. 24.7)there
canbeabuildupofhormonallyactivesubstrate
which can on occasion lead to ambiguous gender
in an infant. Associated with this there is often
significant adrenal hyperplasia [5–7].
The mechanisms of action of adrenal cortical
steroids are all largely similar. The hormones
342
ENDOCRINE SURGERY
are fat soluble and they enter cells to bind to a
specific, usually nuclear, receptor. The ligand
receptor complex binds to DNA and induces
protein synthesis. Most hormones are metabolized in the liver to water-soluble products
which are then excreted in the urine.
Hormones and their metabolites can readily
be measured either directly in the plasma or in
the urine and in addition dynamic tests of the
negative feedback systems can be carried out to
assess the integrity and functionality of the
hypothalamic pituitary adrenal axis. Examples
of this include the dexamethasone suppression
test where exogenous corticosteroid (dexamethasone) is given to assessthe negative feedback and
suppression of ACTH production. Similarly, synthetic ACTH can be given to assess the resultant
expected cortisol secretion by the cortex.
The Adrenal Medulla
This small central core of the adrenal gland
produces catecholamines. These are synthesized in the medulla from tyrosine (Fig. 24.8).
The conversion from dopamine to noradrenaline and adrenaline occurs in a roughly 20%/
80% split, the majority being adrenaline. The
secretion of catecholamines is under direct
control from the sympathetic nervous system
and several stimuli will induce catecholamine
secretion including acidosis, hypovolemia,
hypoglycemia, hypoxia, cold, and fright. In
essence, this is a response to stress of any
type. Cortisol from the adrenal cortex also
influences the conversion of noradrenaline to
adrenaline. The enzyme phenylethanolamineN-methyltransferase converts norepinephrine
to epinephrine in the adrenal gland, but is
lacking in extra adrenalmedullarytissue.
Extra adrenal pheochromocytomas therefore
predominantly secrete norepinephrine. Catecholamines are broken down by the enzyme
monoamine oxidase and are excreted in the
urine where they can be readily measured both
as a breakdown product and as a free hormone.
Catecholamine presence in the circulation is
short lived so the measuring of plasma catecholamines is possible but difficult and expensive
due to their rapid breakdown in plasma.
Catecholamines have a large number of physiological effects, including rising heart rate and
blood pressure, as well as cardiac output,
increasing peripheral resistance, excitation of
the central nervous system, and sweating. Catecholamines also induce the breakdown of fat,
glycogen, and protein to produce substrate for
the ‘‘fight or flight’’ response. The actions of
catecholamines are mediated through and
receptors [5–7].
Fig. 24.8. Pathway for the synthesis of catecholamines.
References
1. Moore KL, Persaud TVN. Before we are born: essentialsof
embryology and birth defects. 6th ed. Philadelphia: Saunders; 2003. 243.
2. Abrahams PH, Marks SC, Hutchings RT. MCMinns color
atlas of human anatomy. London: Mosby; 2003. 261.
3. Wheater Pr, Burkitt HG, Daniels VG. Functional histol-
ogy: a text and color atlas. Edinburgh: Churchill Livingstone; 1979. 235.
4. Standring S, editor. Gray’s anatomy: anatomical basis of
clinical practice. 39th ed. Elsevier Churchill Livingstone;
2005. 1247.
5. Harrison TS, Gann DS, Edis AJ, Egdahl RH. Surgical
disorders of the adrenal gland: physiologic background
and treatment. Grune and Stratton, 1975. Chapter 2,
The adrenal cortex, and chapter 3, The adrenal
medulla.
6. Obsley MH, Imms FJ, editors. Physiology in surgical
practice. Edward Arnold, 1992. Chapter 41, Tests of endocrine function.
7. Lynn J, Bloom SR, editors. Surgical endocrinology. But-
terworth Heinemann, 1993. Chapter 3, The physiology of
the endocrin
25
Adrenal Imaging
Elizabeth G. Grubbs, Rodolfo F. Nun˜ez, Revathy B. Iyer
and Nancy D. Perrier
Introduction
Adrenal imaging has historically been used for
localization and operative planning in patients
with biochemical evidence of adrenal disease.
However, with advances in imaging techniques,
it is now common for incidental adrenal masses
to be detected on abdominal imaging that was
performed for ‘‘nonendocrine’’ disease. Adrenal
imaging now has a role in determining the nature – functioning or nonfunctioning, benign or
malignant – of these incidentally discovered
adrenal lesions. In this chapter, we review adrenal imaging modalities and discuss their indications and limitations.
Adrenal Anatomy
A precise understanding of the adrenal anatomy
is necessary to interpret imaging studies of
these structures within the retroperitoneum.
Knowledge of the adrenal glands’ blood supply
and relationship to other organs is critical to
tumor localization and operative planning.
Each adrenal gland is composed of two physiologically distinct parts: the cortex and the
medulla. Histologically, both the medulla and
the cortex have a high lipid content; thus, they
cannot be differentiated by computed tomography (CT) or magnetic resonance imaging
(MRI).
In the medical literature, most measurements
of adrenal size refer to the body of the gland.
However, given the predominance of cortical tissue within the limbs of the gland, measurements
of these portions are important as well. The maximum width of the body measured perpendicular
to the long axis, at the junction of the adrenal
bodyandthelimbsis0.79cmfortheleftadrenal
and 0.6 cm for the right adrenal. The thickness of
the left adrenal limbs (0.13–0.52 cm) is slightly
greater than that of the right (0.14–0.49 cm). A
normal adrenal limb should not measure more
than 0.5 cm in length [1].
Computed Tomography
CT Overview
CT continues to be the initial imaging modality
of choice for the diagnosis and characterization
of adrenal tumors. High-quality CT with sections obtained through the abdomen and pelvis
has the advantages of moderate cost and high
sensitivity; the sensitivity of CT for detecting
adrenal lesions is in fact 93–100% [2, 3, 4].
The ideal protocol for detecting and characterizing adrenal lesions includes noncontrast-enhanced CT followed by intravenous
administration of iodinated contrast material
and then immediate and delayed contrastenhanced CT – all obtained with 2- to
5-mm thick collimation. With high-quality
J.G.H. Hubbard et al. (eds.), Endocrine Surgery, Springer Specialist Surgery Series,
DOI 10.1007/978-1-84628-881-4_25, Ó Springer-Verlag London Limited 2009
343
344
ENDOCRINE SURGERY
multidetector (multislice) CT, 95% of adrenal
masses larger than 6–8mmcanroutinelybe
detected.
Noncontrast-enhanced images and delayed
contrast-enhanced images can be used to distinguish benign adrenocortical adenomas from
adrenocortical carcinoma (ACC), pheochromocytoma, and metastatic disease. Using helical
nonenhanced CT imaging with delayed contrast-enhanced imaging at 1 and 10 min after
contrast injection, benign adenomas typically
have rapid washout of the contrast material and
pheochromocytomas have slower washout [5]. In
fact, the percentage of contrast enhancement
loss, both absolute and relative, at 10 min is
quite sensitive for characterizing benign tumors.
In a study by Pena et al., 99 of 101 lesions were
correctly characterized as benign or malignant
with a relative percentage washout threshold of
50% on delayed scans; benign lesions demonstrated more than 50% washout, and malignant
lesions, less than 50% washout [6].
CT Characteristics of Benign
Adenomas
Benign adrenocortical adenomas typically have a
high lipid content. When imaged using noncontrast-enhanced CT, the high lipid content imparts
low attenuation values, measured in Hounsfield
units (HU). An attenuation of >1,000 HU is usual
for bony structures, 1,000 HU for air, 0 HU for
water, and <0 HU for fat. Lesions with attenuation values 10 HU are virtually always lipid-rich
benign adenomas, whereas lesions with attenuation values >30 HU are consistently nonadenomatous tumors – ACCs, metastatic lesions, or
pheochromocytomas. Lesions with intermediate
attenuation values (between 10 and 30 HU)
may represent lipid-poor benign adenomas and
therefore must be evaluated carefully based on
other imaging characteristics such as contrast
enhancement and washout [2, 7]. Table 25.1 summarizes the CT characteristics of benign adrenal
lesions.
CT Characteristics of ACCs
Though rare (4–12 per 1,000,000 people), ACCs
have a poor prognosis. The overall 5-year survival rate is less than 50% [8]. Complete surgical
Table 25.1. CT Characteristics of benign adrenal lesions
Signal drop and intensity similar to liver
Low attenuation on noncontrast-enhanced CT
–20 to 0 HU = cyst
<10 HU = adenoma
–50 HU = myelolipoma
Homogeneous
Smooth borders
Smooth contour
Round or oval
<4 cm in greatest diameter
resection is the only chance of cure, and the
completeness of resection, tumor stage and
tumor grade are important predictors of survival [9]. Most ACCs are 10–12 cm in diameter at
diagnosis [9, 10]. Preoperative knowledge that a
tumor is ACC is critical to plan the correct
operative approach with the greatest likelihood
of eradicating all local disease.
CT detects 98% of ACCs [11]. Using a cut off of
>30 HU, contrast-enhanced CT has a positive
predictive value of 100% and a sensitivity of 95%
in determining malignant adrenal tumors [4].
ACCs often appear heterogeneous on contrastenhanced CT because of internal necrosis; are
usually large, exceeding 5 cm in diameter; are
irregular, with poorly defined margins; invade
the upper pole of the kidney or inferior vena
cava; and have associated adjacent nodal metastasis (Table 25.2). Calcifications or cystic degen-
eration is seen in about 30% of ACCs. Any
evidence of local invasion or nodal metastasis
supports the diagnosis of ACC. CT isin fact ideally
suited to image ACCs because it allows detection
Table 25.2. CT characteristics of malignant adrenal
lesions
High attenuation:
>30 HU is suspicious
Pheochromocytoma vs adrenocortical carcinoma
(>30 HU)
Heterogeneous
Irregular borders
Local/vascular invasion
Lymphadenopathy
Metastases
Large size (>6 cm)
345
ADRENAL IMAGING
Fig. 25.1. Adrenocortical carcinoma. A 13.3-cm heterogenous
mass with peripheral enhancement and central necrosis.
Hounsfield units of 78 and 15 min washout of 30%.
of metastatic disease in the regional lymph nodes,
liver, and lungs; enables staging of disease; and
aids with surgical planning. Figure 25.1 shows the
typical appearance of an ACC.
The use of intravenous contrast is important
for characterizing and staging ACCs. On contrast-enhanced images, ACCs typically show
peripheral enhancement of the mass with a central nonenhanced area of necrosis. The measurement of contrast washout is also valuable
in distinguishing benign adrenocortical adenomas from ACCs, which have slower washout.
Size is also an important criterion when evaluating an adrenal lesion with CT. The likelihood
of ACC is directly related to the size of the lesion:
only 2% of adrenal lesions 4 cm are ACCs; 6%
of lesions 4.1–6 cm are ACCs; and 25% of lesions
>6 cm are ACCs. A review by Kebebew et al. of
725 ACCs in the US National Cancer Institute’s
Surveillance, Epidemiology, and End Results
database [9] revealed a mean tumor size of
12 cm, with a range of 2–36 cm. Only 4.2% of
ACCs were <6 cm in greatest diameter.
In a review of 182 adults evaluated and treated for an adrenal tumor at The University of
Texas M. D. Anderson Cancer Center between
1971 and 2000, Barnett et al. found that only
5 (13%) of the 38 patients with ACCs had
tumors <5 cm at diagnosis [12]. For four of
these five tumors, radiographic criteria other
than size suggested malignancy: heterogeneity,
irregular shape, irregular margins, or hemorrhage. It is important to recognize that CT may
underestimate the true histologic size of a tumor
(as found in the surgical specimen) by up to
20%. In the review by Barnett et al., the mean
radiographic estimate for ACCs was 9.5 cm
(1.7–30 cm), but the mean pathologic measurement was 11.7 cm (3.0–30 cm). This difference
was significant (p = 0.001).
CT Characteristics of Functioning
Tumors
Pheochromocytoma
CT is accurate for detecting pheochromocytomas
because of its high spatial resolution. The overall
sensitivity ranges between 93and 100% [13]. CT is
less sensitive (60%) in evaluating patients with
metastatic or recurrent pheochromocytoma than
in those with primary tumors. Because pheochromocytomas may extend superiorly or inferiorly
from an otherwise normal-appearing adrenal
gland, contiguous thin sections of 5 mm are
recommended when a pheochromocytoma is suspected on the basis of biochemical findings. The
scans should include the diaphragm and extend
below the aortic bifurcation because of the possibility of extraadrenal sites of disease. The normal
contralateral adrenal gland should also be imaged.
Most pheochromocytomas are rounded, homogeneous masses with an attenuation similar to or
slightly less than that of liver tissue (Fig. 25.2).
Pheochromocytomas occasionally show hemorrhagic, cystic, or calcified areas.
Oral contrast enhancement of the bowel with
barium or an iodinated contrast agent is necessary to define the normal anatomy and prevent
confusion of unpacified bowel with a soft tissue
mass. Intravenous contrast enhancement
increases the sensitivity of lesion detection, but
there is a risk of precipitating an adrenergic
crisis if appropriate alpha and beta blockade
have not been instituted prior to injection of
the iodinated contrast agent. It is imperative
that volume expansion, hypertension control,
and some degree of orthostatic hypotension be
present prior to initiating the beta blockade.
Phenoxybenzamine (Dibenzyline, 10 mg twice
daily) for 5–7 days followed by propranolol
(Inderal, 10 mg three times daily) is an acceptable medical regimen. On contrast-enhanced
Fig. 25.2. CT of patient with pheochromocytoma (denoted by
thin arrow) of brown fat changes (denoted by thick arrows)
associated with pheochromocytoma.
CT scans, pheochromocytomas are irregular,
and the periphery of the tumor is often more
intense that the central portion.
Retroperitoneal Brown Fat
Patients with catecholamine excess may mobilize brown fat, resulting in changes in the
appearance of the retroperitoneal fat. This may
be seen on CT as infiltrative or vascular changes
346
ENDOCRINE SURGERY
in the retroperitoneal region. The changes are
diffuse and should be recognized as benign
reactive changes rather than locally invasive or
metastatic disease (Fig. 25.2) [14].
Aldosteronoma
The majority of patients with hyperaldosteronism have small, benign adrenal adenomas
producing aldosterone. A minority (25%),
however, have bilateral adrenal hyperplasia.
Determination of bilateral hyperplasia is critical in the workup as patients with bilateral
hyperplasia will not benefit from adrenalectomy. CT in a patient with biochemical findings suggesting hyperaldosteronism requires
0.3–0.5 cm thick contiguous slices in the adrenal region. Aldosteronomas are usually isodense and do not enhance with intravenous
contrast agent administration (Fig. 25.3).
Those most difficult to identify are in the
apex of the adrenal. The sensitivity of CT in
detecting aldosteronomas is only 85% – less
than that for other functioning lesions –
because of their small size [2]. Nuclear medicine studies and venous sampling are
frequently necessary to confirm the type of
disease (unilateral versus bilateral).
Cushing’s Syndrome
Most patients with cortisol excess have exogenous intake of corticosteroids. For patients with
ab
Fig. 25.3. (a) CT with intravenous contrast of a left-sided aldosteronoma denoted by arrow (b) corresponding pathology.
347
ADRENAL IMAGING
Fig. 25.4. CT of a cortisol-producing functional adenoma.
endogenous production, Cushing’s disease,
resulting from a pituitary tumor, accounts for
the majority of cases. Only 10% of cases have a
benign cortisol-secreting tumor of the adrenal
gland. CT is excellent (98% sensitivity) at detecting adrenal masses causing Cushing’s syndrome.
Adrenal lesions capable of producing enough
cortisol to become clinically apparent are usually
large enough (2–5 cm) to be seen with CT.
Cortisol-secreting adenomas rarely show contrast enhancement (Fig. 25.4). Visualization is
aided by the regional perinephric fat that is
usually present with this syndrome.
Ruling out adrenal macronodular hyperpla-
sia is critical. In such cases, the disease is
corticotropin (ACTH) dependent, and bilateral adrenal enlargement should be present
without a dominant nodule. The adrenal
parenchyma can be bilaterally thickened or
appear normal.
CT Characteristics of Nonfunctioning
Tumors
Cysts
Cystic lesions of the adrenal should be worked
up thoroughly as not all of them are benign. A
recent review by the Mayo Clinic revealed that
2% of ACCs present as cystic neoplasms [15].
Rim calcification may be observed on CT
(Fig. 25.5).
Myelolipoma
Myelolipomas have a characteristic CT
appearance because of the presence of fat
and myeloid elements. As a result, a definite
diagnosis can be rendered by CT. These
lesions have an attenuation of <0HU
because of the fat content (Fig. 25.6). Areas
of soft tissue attenuation are also seen and
correspond to the myeloid tissue. Borders
areusuallysmooth,withnoevidenceof
invasion. Myelolipomas may be inhomogeneous and contain blood products since larger lesions may bleed.
ab
Fig. 25.5. (a) Calcified left adrenal cyst 6 cm in maximum diameter. (b) Correlating path of benign calcified left adrenal cyst.
348
ENDOCRINE SURGERY
composed of fat and water. Chemical-shift
imaging takes advantage of differences in the
water-to-fat ratio of various adrenal lesions
and is performed with in-phase and out-ofphase gradient-recalled echo sequences.
Respiration-induced motion of the adrenal
gland may result in blurred, poor-quality MR
images. A breath-hold technique in conjunction with fast imaging is therefore essential to
decrease respiratory artifacts. T1- and T2weighted sequences (see below) and contrastenhanced imaging with gadolinium are also
often utilized for the characterization and
staging of known adrenal tumors.
Fig. 25.6. CT of myelolipoma with –23 HU on immediate
imaging. –23 HU on 15 min delayed imaging as well.
Magnetic Resonance Imaging
MRI Overview
For a number of years, CT has been the main
technique for characterizing adrenal lesions
because of its widespread availability and
speed, particularly with multislice CT. However,
MRI has proven to be of similar accuracy to CT
in characterizing adrenal masses and may in
fact have some advantages owing to its excellent
soft tissue contrast resolution [7]. MRI also has
the advantage of not exposing the patient to
ionizing radiation, which is particularly important in young patients or pregnant women.
The normal-sized adrenal gland is thin
and can easily be obscured on MRI by flowing blood, chemical shift misregistration, or
respiration. As a result, adrenal MRI requires
meticulous technique and a careful balance
of high spatial resolution and appropriate
signal-to-noise ratio [7]. The spatial resolution of MRI is adequate for the detection of
adrenal lesions that are 1 cm or greater in
diameter.
Technique of MRI
A protocol for imaging the adrenal glands
should include chemical-shift imaging in at
least two planes. Chemical-shift techniques
aresensitiveandspecificfortheidentification
of intracytoplasmic lipid in tissues that are
T1- Versus T2-Weighted Images
The signal intensity of a structure on an MR
image is dependent upon the proton density,
the longitudinal relaxation time (T1), the transverse relaxation time (T2), and flow. Proton
density is the concentration of protons in the
form of water and macromolecules (fat, protein,
etc.). The T1 and T2 relaxation times describe
the manner in which the protons revert to their
resting states after the initial radiofrequency
pulse.
Fat has a higher signal intensity and will
appear bright on T1-weighted MR images.
Conversely, water yields lower signal intensity
and appears dark on T1-weighted images. The
normal adrenal gland is homogeneously
hypointense compared to the liver and isodense
compared to striated muscle on T1-weighted
images [7, 16]. If a fat-suppression technique
is applied, the gland will appear isointense
relative to the liver on T1-weighted images.
T2-weighted imaging relies upon local
dephasing of spins following the application of
the transverse energy pulse. Fat has a shorter
T2 time than water, which means that protons
in fat relax or decay more readily than those
in water. Since the amount of transverse magnification in fat is small, fat generates less signal
intensity on a heavily T2-weighted image. Water
has a very high T2 constant and therefore has a
very high T2 signal intensity and appears bright
on a T2-weighted image. If a fat-suppression
technique is applied in T2-weighted MRI, the
normal adrenal gland appears slightly hyperintense relative to the liver. T2-weighted images
have a 70% overall accuracy for adrenal lesion
349
ADRENAL IMAGING
characterization, and their value compared to
chemical-shift images is limited, particularly for
lipid-containing lesions [17]. For nonlipid-containing masses, T2-weighted images may provide
additional information.
Gadolinium Enhancement
There is some evidence that gadoliniumenhanced dynamic MRI is better than
noncontrast-enhanced MRI for characterizing
adrenal tumors [7]. Adenomas demonstrate
mild enhancement with a rapid washout,
whereas ACCs and other nonadenomatous
lesions show strong enhancement with a slower
washout, similar to their CT enhancement characteristics. Gadolinium enhancement can also
be helpful in staging known adrenal tumors
and detecting metastatic disease.
MRI Characteristics of Benign
Tumors
With respect to MRI, the most important feature
of the adrenal adenoma is the presence of intracellular lipid. Chemical-shift MRI is the most
reliable technique for diagnosing this pathology
with most adenomas demonstrating a loss of
signal intensity on out-of-phase imaging [18].
A decrease in signal intensity on out-of-phase
imaging of greater than 20% is diagnostic of an
adenoma [19]. The accuracy of MRI in detecting
adenomas is 96–100% [20]. Adenomas tend to be
slightly hypointense on T1-weighted images and
slightly hyperintense on T2-weighted images
compared with liver tissue. Immediate contrastenhanced images show mild, uniform enhancement with quick washout of gadolinium from
these benign lesions [21].
MRI cannot differentiate a nonfunctioning
adenoma from a functioning adenoma [22].
Like all adenomas, an aldosterone-producing
adenoma is isointense to hypointense on
T1-weighted images and slightly hyperintense
on T2-weighted images compared with the
liver. MRI may have a slightly higher sensitivity
than CT for distinguishing between a unilateral
adenoma and a bilateral hyperplasia, which is
essential in determining the subtype of primary
hyperaldosteronism [23].
Fig. 25.7. T1 MRI with characteristic hyperintensity of a
myelolipoma.
The fatty component of a myelolipoma is
hyperintense on nonfat-suppressed T1-weighted
images (Fig. 25.7). Fat suppression helps to
confirm the diagnosis of myelolipoma by
demonstrating a loss of signal intensity within
the fatty component.
Simple cysts are hypointense on T1-weighted
images and hyperintense on T2-weighted
images, with no internal enhancement or soft
tissue component.
MRI Characteristics of ACC
On T1-weighted images, ACCs are typically
hypointense relative to the liver, whereas on
T2-weighted images, ACCs are hyperintense
relative to the liver. However, ACCs may appear
heterogeneous on both T1- and T2-weighted
images owing to internal hemorrhage and
necrosis. Blood products in areas of hemorrhage appear bright on T1-weighted images.
An advantage of MRI is its ability to demonstrate flow within blood vessels, which allows
visualization of the invasion of ACC into surrounding structures, particularly the inferior
vena cava. Of note, right-sided ACCs have a
propensity to form venous tumor emboli, and
vascular invasion and thrombus can be seen
with flow-sensitive MRI sequences [7].
Enhancement after contrast agent administration is usually pronounced around the periphery of ACCs in nonnecrotic areas, and the
washout is often prolonged. Functioning ACCs
can contain foci of intracytoplasmic lipid,