Imaging of the adrenal glands

1. IMAGING OF THE ADRENAL GLANDS

2. ANATOMY
•Normal size: 2-4 cm CC,
smooth limbs without nodularity,
max thickness 10 mm.
•Inverted Y, V or L configuration.

3. Lambda-shaped body and 2 limbs.
Inverted Y-shaped body with 2
limbs that point posteriorly.
Normal CT appearance

4. NORMAL ADRENALNORMAL ADRENAL
Right
–Suprarenal
–Posterior to IVC
–Lateral to right crus
–Medial to right lobe of the liver
Left
–Lateral to left crus and aorta
–Posterior to pancreas and splenic vessels

5. II. Imaging characterization of
adrenal masses
II. Imaging characterization of
adrenal masses

6. The Hormonally Active Mass
Cortex:
•Functional adenomas (Cushing syndrome, Conn
syndrome, or hyperandrogenism).
•Carcinomas ( Majority Cushing’s syndrome).
Medulla:
•Pheochromocytomas (hypersecretes
cathecolamines)

7. The Hormonally Active Mass
•The work-up of a suspected hyperfunctioning
adrenal mass (pheochromocytoma and
aldosteronoma) should start with appropriate
biochemical screening tests followed by thin-
collimation computed tomography (CT).
•Unilateral mass Conn’s syndrome
(aldosterolonoma), Pheochromocytoma.
•Bilateral masses Hyperplasia (Cushing’s
diseasePituitary adenoma)

8. •CT has become the study of choice to differentiate
a benign adenoma from a metastasis in the
oncology patient.
The oncology patient with an
adrenal mass

9. NCCT
HU < 10
Benign
HU > 10
Delayed CECT (10 min)
Washout > 50%
HU < 30
Benign
Washout < 50%
HU > 30
Chemical Shift MRI
Signal drop-out
Benign
No signal drop-out
PET
Biopsy

10. Incidentalomas:
Two main concerns exist with incidentalomas:
• The first is whether it is hormonally active, and the
second is whether it is malignant.
•The treatment for a hormonally active adrenal tumor
is surgery.
•The treatment for a malignancy depends on the cell
type, spread, and location of the primary tumor.

11. From: eMedicine.com, Inc.

13. Adrenal mass characterization- MRI
•In phase and out of phase gradient echo MR sequences
are used to diagnose adrenal adenomas.
•The signal intensity of the adrenal adenoma decreases
on out of phase imaging.
•Precession frequencies of protons found in intracellular
fat and protons in water cancel out each other's signal at
the time the echo is acquired.
•The signal intensity of the adenoma follows that of the of
bone marrow, because bone marrow also contains small
amounts of adipose tissue.
•The spleen is used as organ of reference on OP images
for subjective evaluation.
***Lipid-poor adenomas if an adrenal mass fails to exhibit signal drop out on
out of phase imaging it could still be an adenoma.

14. Adrenal mass characterization
On the chemical shift imaging, signal intensity index, calculated as:
Signal intensity (SI) indexes (D)= [SI in-phase - SI opposed-phase] x 100
(SI in-phase)
A signal intensity index defined as D superior to 25% is
used as positive diagnosis criteria for adenoma.

15. 1.5 T
Chemical shift Imaging (CSI)
Schematic shows lipid and water protons precessing in and out of phase with respect to
each other over time at 1.5 T. The sine wave depicts the signal intensity within a voxel over
time as the water and lipid protons oscillate between in phase and out of phase after the
radio-frequency excitation pulse is delivered.

16. Adrenomedullary tumors :
•Pheochromocytoma
•Ganglioneuroblastoma
•Neuroblastoma
•Neuroendocrine
carcinoma
Adrenocortical carcinomas:
-Functional
-Nonfunctional
-Well differentiated
-Intermediate
-Poorly differentiated to
anaplastic
Adrenocortical adenomas:
-Functional- Cortisol, aldosterone,androgens
-Non-functional
Primary neoplasms

17. From: eMedicine.com, Inc.

18. Adenomas
•The prevalence of adrenal adenoma is age
related. 0.14%for patients aged 20–29 years and
7% in those older than 70 years
•The majority of lesions are not functioning
•the presence of contralateral adrenal atrophy
suggests that a lesion may be functioning,
because ACTH secretion is suppressed by
elevated cortisol levels

19. LIPID-RICH ADENOMA
•70 % are lipid-rich
–Clear cells have abundant intracytoplasmic fat
•CT
–Low attenuation on nonenhanced CT
–Threshold of < 10 HU is 71% sens, 98% spec [1]
–Spec approaches 100% when considering other
features (size, shape, stability)
–< 30 HU on delayed CECT also diagnostic
[1] Boland et al. AJR 1998; 171:201-4

20. LIPID-RICH ADENOMA
•MRI
–Chemical shift imaging is the most sensitive way to
differentiate adenoma
–Relies on the different resonance frequencies of
protons in fat and water molecules
–Use spleen as internal standard
–Look for signal drop-off (20%) on out-of-phase
images due to intra-voxel signal cancellation of the
lipid and water protons
–81-100% sens, 94-100% spec

21. LIPID-POOR ADENOMA
•30% are lipid-poor and do not have low
attenuation on CT
•Adenomas enhance rapidly and wash out
rapidly (independent of lipid content)
•Reflects physiologic differences in
perfusion between adenoma and other
lesions

22. The precontrast attenuation varies
according
to the presence or absence of lipid, with
mean attenuation in the range of
−2 to 16 HU in lipid-rich adenomas
20 to 25 HU in lipid-poor adenomas

23. ADENOMA
-3.0 HU

24. Adenomas
•Non-functioning adenomas (most common)
Incidentalomas.
•Functional adenomas
**15%-20% of all Cushing’s syndromes cases are
caused by adenomas or carcinomas .
** 80% of all Conn syndromes cases are caused by
small adenomas (the remaining 20% are caused
essentially by adrenal hyperplasia rarely by carcinomas).

25. ADENOMA
T1W OPT1W IP

26. ADENOMA
T2W
T1W IP
T1W OP

27. ADENOMA

28. The lipid-poor adenoma
•Although representing a minority of adrenal
adenomas (30%) the lipid-poor variety cannot
be accurately identified on unenhanced CT or
chemical shift MR imaging.
•“..lipid-poor adrenal adenomas show
enhancement and enhancement washout
features nearly identical to lipid-rich adenomas
and can be distinguished from nonadenomas on
the basis of a percentage washout threshold
value of 60% and a relative percentage washout
of 40%.”
AJR Am J Roentgenol. 2000 Nov;175(5):1411-5.

29. Percentage of enhancement washout

[E-D/E-U] x 100 = % ICM washout after 10 min.
E= enhanced attenuation value
U= Unenhanced attn value
D= Delayed enhanced value (15 min)
E= 90 HU
U= 40 HU
D= 50 HU
[90-50/90-40] x 100 = 80% washout

30. Relative % washout
If unenhanced CT has not been performed:
(E-D) / E x 100
Optimal threshold 40% washout (sens 96%,
Spec 100%)
•if threshold used is 50% then sens and spec=
100%

31. 40 HU
114 HU
65 HU
[114-65/114-40] x 100 = 49/74 x 100 = 66% washout
(>60 %)
Lipid poor adenoma
AJR:179, September 2002
[E-D/E-U] x 100
U
E
D

32. 32 HU
83 HU
57 HU
[83-57/83-32] x 100 = 26/51x 100 = 50% washout (<60 %)
Lung mets
AJR:179, September 2002
U
E
D
[E-D/E-U] x 100

33. Conn’s disease
Hypertension and hypokalemia
Causes: Adrenal adenoma 80%, adrenal hyperplasia 20%

34. Adrenal hyperplasia
Truncal obesity and elevated plasma Cortisol
**Hyperplasia- 70%
•Cushing’s disease- 90%
•Ectopic ACTH- 10%
**Adenoma 20%
**Carcinoma 10%
Cushing’s syndrome is caused by:

35. NCCT
HU < 10
Benign
HU > 10
Delayed CECT (10 min)
Washout > 50%
HU < 30
Benign
Washout < 50%
HU > 30
Chemical Shift MRI
Signal drop-out
Benign
No signal drop-out
PET
Biopsy

36. METASTASESMETASTASES
Common site for mets
Variable appearance
–Any size
–Round or lobulated
–Homogeneous or inhomogeneous
–Calcified
–Necrotic
Even in pt with known malignancy, 50% of
adrenal masses may be adenomas

37. METASTASESMETASTASES
Features that favor mets include:
–Size > 3 cm
–Poorly defined margins
–Thick, enhancing rim
–Inhomogeneous
–Invasion of adjacent structures
–Mets elsewhere

40. METASTASES
Metastatic adrenal tumors - Most common
potential primaries include the following:
•Lung
•Breast
•Melanoma
•Renal cell carcinoma
•Extra-adrenal lymphoma
•Leukemias
•Pancreatic carcinoma
•Colonic carcinoma
•Ovarian carcinoma

41. METASTASES

42. METASTASES
[E-D/E-U] x 100
33% washout

43. METASTASES

44. METASTASES
PET CT
FDG
FDG

45. METASTASES
Melanoma
T1W
T2W FS

46. ADRENAL CARCINOMAADRENAL CARCINOMA
Rare
Cortex
10% bilateral
50% functional
Usually large at
presentation (4-10 cm)

47. ADRENAL CARCINOMAADRENAL CARCINOMA
Heterogeneous,
irregular contour
Calcification in 30%
Large areas of internal
hemorrhage and
necrosis in most

48. ADRENAL CARCINOMAADRENAL CARCINOMA
Look for invasion of
adjacent organs and
veins

49. Adrenocortical carcinomas

50. Adrenocortical carcinomasAdrenocortical carcinomas
Left renal vein

51. Adrenocortical carcinoma
68-year-old woman with right upper quadrant palpable mass.

52. Precocious puberty in a child.
Adrenocortical
carcinoma

53. PHEOCHROMOCYTOMAPHEOCHROMOCYTOMA
Neoplasm of chromafin cells in medulla
(10% extra adrenal)
Capacity to store and release
catecholamines
0.1% of causes of HTN

54. PheochromocytomaPheochromocytoma
·"10-percent rule"
·10% bilateral
·10% malignant
·10% extra-adrenal
·associated syndromes:
·neurofibromatosis
·von-Hippel-Lindau
·multiple endrocine neoplasia: MEN-2 and MEN-
1
·extra-adrenal sites:
·detected with MIBG ( I 131-MIBG-NE analog)
· Organ of Zuckerkandl (most common)

55. PHEOCHROMOCYTOMAPHEOCHROMOCYTOMA
Size determines
imaging features
< 4 cm
–Well defined and
homogeneous
Larger tumors more
likely to have central
necrosis

56. PHEOCHROMOCYTOMAPHEOCHROMOCYTOMA
Classically
hyperintense on T2
Enhance avidly

58. Pheochromocytoma

59. Pheochromocytoma

60. Pheochromocytoma

61. Pheochromocytoma
T1W
T2W

62. T1W T2W
T1W POSTGAD
Pheochromocytoma

63. Paragangliomas
•Extra-adrenal paragangliomas, as the name implies,
can occur anywhere along the paraganglionic chain,
but are most commonly found in the superior para-
aortic region. between the diaphragm and the lower
poles of the kidneys.
•Patients often present with headaches, palpitations,
sweating, and hypertension.
•Clinical suspicion for extra-adrenal paraganglioma is
usually confirmed by elevated urinary catecholamines
and their metabolites.

65. Paraganglioma of the Organ of Zuckerkandl

66. Von-Hippel-Lindau
VHL- pheochromocytoma, carotid body tumor and islet cell tumor of the
pancreas.
T2W

67. MYELOLIPOMAMYELOLIPOMA
Rare benign tumor (0.2%)
Composed of myeloid, erythroid, fat
–Causes heterogeneous appearance
Occasionally calcify
Presence of pure fat on imaging is diagnostic
The primary complication-->retroperitoneal
hemorrhage
Clinically silent unless very large or
hemorrhage
 do not undergo malignant transformation

68. Adrenal myelolipoma

69. Adrenal myelolipoma

70. Adrenal myelolipoma

71. LYMPHOMALYMPHOMA
NHL more commonly than Hodgkin’s
–4% have adrenal involvement
Adrenal infiltration most often occurs with
retroperitoneal lymphoma
50% bilateral
Mass or diffuse enlargement of gland

73. ADRENAL HEMORRHAGEADRENAL HEMORRHAGE
Causes
–Trauma (80%)
–Systemic anticoagulant therapy
–Sepsis (Waterhouse-Friedrichson syndrome)
–Stress
–Neoplasm
20% bilateral
–Adrenal insufficiency rare

74. ADRENAL HEMORRHAGEADRENAL HEMORRHAGE
Acute
–Round or oval mass, 1-5 cm
–Increased attenuation or isodense to liver,
kidney, or muscle on NCCT
–Typical signal patterns of blood products on
MRI

76. Adrenal hemorrhage

77. ADRENAL HEMORRHAGEADRENAL HEMORRHAGE
Chronic
–Will shrink over 6 months
–“Ring pattern” on MRI
–Pseudocyst
–Residual calcification

79. s/p Adrenal hemorrhage
DDX:
•Neuroblastoma
•TB
•Carcinoma

80. Granulomatous (TB) disease
•Usually caused by hematogenous spread of systemic
infection, resulting in bilateral enlargement and
replacement of both the adrenal cortex and medulla by
caseous necrosis.
•This may cause adrenal failure by total or near-total
destruction of both glands.
•Calcification of the glands can be detected in about half
the cases.
•Imaging findings of adrenal tuberculosis are nonspecific
and consist often of normal or small size adrenal glands,
containing scattered calcifications. Findings are best
detected on CT.

81. Adrenal histoplasmosis

82. Adrenal histoplasmosis

83. Adrenal TB

84. ADRENAL CYSTADRENAL CYST
True cyst (45%)
–Epithelial lining
–Looks like a simple cyst
Pseudocyst (39%)
–Results from old hemorrhage
–May see a calcified rim
Parasitic (< 10%)
–Echinococcosus

87. Lung carcinoma necrotic mets
Cysts?
Irregular thick wall

88. SUMMARY
•Adrenal Embryology , Anatomy and Histology.
•Physiology of the Adrenal Gland (endocrine gland).
•Clinical importance of adrenal masses characterization.
•Imaging Techniques (CT, MRI).
•Non-hyperfunctioning Lesions of the Adrenal Cortex
(incidentaloma) and their clinical significance for the
oncology patience.
•Hyperfunctioning Lesions of the Adrenal Cortex and
endocrinologic clinical presentations.
•Neoplasms of the adrenal cortex.
•Neoplasms of the Adrenal Medulla -pheochromocytoma
•Metastatic Neoplasms to the Adrenal Glands.
Miscellaneous Conditions of the Adrenals (infection,
trauma, cyst)

89. CT Scan - DDx By appearance:
·Diameter less than 2 cm: consider Conn’s syndrome
(recommend thinner cuts to better visualize)
·Diameter greater than 5 cm: consider carcinoma
·Bilateral: consider metastasis, infection, hyperplasia
·Calcifications: consider pheochromocytoma, carcinoma, cyst
(peripheral), infection, myelolipoma, hemangioma,
ganglioneuroma
·Heterogeneous appearance: consider adenoma, myelolipoma,
hemangioma
·Central area of necrosis: consider pheochromocytoma,
carcinoma, granulomatous infection
·Nodularity:, metastasis

90. By Attenuation:
·-115 to -30 HU: consider myelolipoma (lower than
adenoma)
·Less than 10 HU: consider adenoma
·50 to 90 HU: consider acute to subacute
hematoma

91. By enhancement and contrast washout
characteristics
•If the attenuation of the adrenal gland is
over 10 HU on nonenhanced CT, contrast
material–enhanced CT should be performed
and washout calculated.
•Over 50%-60% washout of contrast material
on a 15-minute delayed CT scan is
diagnostic of an adenoma.

92. thanku

93. •Fat-containing adrenal masses can be
classified into two main types: those that
contain intracellularfat (eg, adenoma) and
those with macroscopicfat (eg,
myelolipoma). Adrenal masses that
contain intracellular fat have been shown
to lose signal intensity on chemical shift
out-of-phase images compared with in-
phase images owing to the presence of
intracellular lipid. Adrenal lesions that
contain macroscopic fat demonstrate a
loss of signal intensity on fat-saturated
images.

94. For patients in whom a pheochromocytoma is
suspected and an adrenal mass is not identified at
CT or MR imaging, nuclear medicine imaging
can be used. I-131 MIBG and In-111 octreotide
are the two radiopharmaceuticals used to evaluate
for a pheochromocytoma. I-131 MIBG is a structural
analog of norepinephrine, which is stored in
neurosecretory granules of the adrenal medulla.
Abdominal imaging is performed 24–72 hours
after administration of the agent, and whole-body
imaging should be performed to detect extraadrenal
lesions. If there is a high clinical suspicion of a
perivesicular paraganglioma, bladder catheterization
may be necessary as the agent is excreted
in the urine. When pheochromocytoma is suspected,

95. any focal uptake of I-131 MIBG in the
adrenal gland is abnormal (Fig 6). The reported
sensitivity of I-131 MIBG for detection of a pheochromocytoma
is 80%–90%, with a specificity of
90%–100% (7–9). I-131 MIBG scintigraphy is
useful to detect the 10% of pheochromocytomas
that are extraadrenal and to document metastatic
disease or residual tumor after surgery.
In-111 octreotide, the second agent used to
detect pheochromocytomas, is a synthetic octapeptide
analog of somatostatin that shows uptake
in a variety of tumors that contain somatostatin
receptors. A total of 5 mCi (185 MBq) of
In-111 octreotide is administered intravenously,
and whole-body imaging is performed at 4 and 24
hours after injection. In-111 octreotide has a sensitivity
of 75%–90% for detection of pheochro

96. There is a complementary role
for In-111 octreotide and I-131 MIBG, since
25% of pheochromocytomas are seen only
with
I-131 MIBG and another 25% are seen only
with
In-111 octreotide. The remaining 50% of
pheochromocytomas
are visualized with both agents