1. Presentor: Dr Kusum
Pathania
Moderator: Dr Jyoti Arora
IMAGING OF ADRENAL MASSES

2. Adrenal Gland
 The adrenal gland is named for its location
adjacent to the kidneys: ad-renal
 Also known as suprarenal glands
 Characteristic inverted Y, V, or T shape
 Pair of important endocrine glands situated on the
posterior abdominal wall over the upper pole of
the kidneys behind the peritoneum.
 Each gland is enclosed in the perirenal fascia and
each have a body and two limbs -medial and
lateral.

5. HISTOLOGY
 ADRENAL CORTEX-90% of adrenal
three zones
1.Zona glomerulosa-outer most –10-15%
Secretes mineralocorticoids (aldosterone)
2.Zona fasciculata-80% - secretes cortisol
3.Zona reticulata-5-10% - secretes androgens

6. ADRENAL MEDULLA- 10% of adrenal
made up of chromaffin cells,
secretes-EPINEPHRINE or NOREPINEPHRINE
Partof sympathetic autonomic nervous system.

7. VASCULAR SUPPLY:
 Arterial supply :
inferior phrenic artery superiorly.
aorta medially .
renal artery inferiorlly
 Venous drainage :
Right side: drain to IVC .
Left side : drain to left adrenal vein or
directly to IVC.
 Lymphatics :
Para-aortic and paracaval lymph nodes.

8. Normal gland CT
 Right adrenal gland :
superior to right
kidney, medial to right
lobe of liver, lateral to
crus of right
hemidiaphragm,
posterior to IVC.
 Shape : elongated
comma lying in crease
between liver and
crus of diaphragm.

9. ngt

10. Normal gland CT
 Left adrenal gland :
superior to and
anterior to upper pole
of kidney in triangle
formed by left lateral
margin of aorta,
posterior surface of
body and tail of
pancreas and upper
pole of left kidney.

11. Normal CT measurements:
 Length - 4-6cm
 Width -2-3cm .
 Each limb normally measures ≤ 5mm in width and the
body should measure ≤ 8-10mm in width
 Criteria for Enlargement:
 Length >6cm
 AP diameter > 3cm
 Limb thickness > 6mm
 Thickness more than adjacent crus.

12. PURPOSE :
 Overview of adrenal disease and their imaging
appearance.
 Current concept of differentiating a benign from
malignant adrenal mass with particular attention
to CT and MRI.
 Present an imaging alogrithm for characterizing
an adrenal mass.

13. IMAGING MODALITIES :
 Ultrasound
 Computed tomography
 Magnetic resonance imaging
 Nuclear medicine imaging

14. ULTRASOUND :
 Primarily reserved for use in pediatric population
because of lack of ionising radiation and small
body habitus of children.
 Right adrenal best evaluated from midaxillary and
anterior axillary line . Liver provide acoustic
window.
 Left adrenal evaluated from posterior or mid
axillary approach. No suitable acoustic window for
left so completely evaluated in 80% of people.

15. CT
Routine CT protocol for adrenal
imaging
 NCCT abdomen
 CECT abdomen (70 secs delay)
 Delayed scan (after 15 minutes)
 Computed tomography (CT) is the imaging modality of
choice for evaluating adrenal glands morphology and masses
associated with it. High resolution CT of upper abdomen,
using 1-3mm thick slices to reduce the volume averaging, is
most accurate technique for indentifying adrenal lesions.
Contrast-enhanced CT and delayed images help in further
characterization of the lesions. 100-150ml of contrast is
injected at a rate of 3mlper second and images are aquired
at 70sec and 15 min after contrast injection.

16. MRI
 MRI of the adrenals is the modality of choice for
further characterization of adrenal lesions. MR
parameters should include T1-and T2-weighted
sequences along with chemical shift imaging.
 T1 weighted signal show normal adrenal as low signal
against high signal fat.
 Most tumor show high signal on T2W and low signal
on T1W image.
 Contrast enhanced dynamic MRI used in d/d of
adenoma, metastasis, granulomas and
pheochromocytoma
 Chemical shift MR used in d/d of adenoma and
metastasis: adenoma – high lipid content

17. (a)T1-weighted breath-hold. MR image
demonstrates a normal left adrenal gland
(arrow). (b)T2 weighted MR image.
Normal gland MRI

18. NUCLEAR MEDICINE IMAGING
 FDG PET.
 I-131MIBG
 In-111Octreotide

19. Adrenal masses
 A. Neoplasm B. Other mass lesion
1. Cortical 1. Granuloma
a. adenoma a. tuberculosis
b. carcinoma b. histoplasmosis
2. Medullary c. blastomycosis
a. pheochromocytoma 2. Bilateral hyperplasia
b. neuroblastoma 3. Cyst
c. ganglioneuroma a. endothelial (45%)
3. Stromal b pseudocyst (39%)
a. lipoma c. epithelial (9%)
b. myelolipoma d. parasitic (hydatid)
4. Metastasis 4. Hematoma

20. ADRENAL DISEASES
 GROUP I : Adrenal disease with normal
function.
 GROUP II : Adrenal Hyper-functional disease.
 GROUP III: Adrenal insufficiency.

21. GROUP I : ADRENAL DISEASE
WITH NORMAL FUNCTION:
 Most of these are incidentally detected as adrenal
masses.
 Include : nonfunctional adrenal adenoma or
carcinoma, metastasis , lymphoma , myelolipoma
, adrenal cyst.

22. INCIDENTALLY DISCOVERED
ADRENAL MASSES:
 Common incidental discoveries on CT, MRI, FDG-
PET.
 Adrenal incidentaloma – lesions <4cm or smaller ;
can be unilateral or bilateral.
 Whenever adrenal incidentaloma is discovered ,
two main concerns are :
1) hormonically active or inactive .
2) benign or malignant.

24. IS IT FUNCTIONAL?
 6% - 20% of adrenal incidentalomas have
hormonal abnormality.
 Hormonal hypersecretion is most likely in masses
that are at least 3 cm in diameter.

25.  85 percent of the masses : non fuctioning.
 9 percent secreted sufficient cortisol to produce
subclinical Cushing's syndrome .
 4 percent : pheochromocytomas (less than half
caused hypertension) .
 2 percent : aldosteronomas .

26. CHARACTERIZATION OF
ADRENAL MASSES: IS IT BENIGN
OR MALIGNANT
 Common site for both benign adenomas and
metastatic disease.
 Even though common site for metastasis , 70% of
adrenal masses in cancer patients are benign.
 Differentiation is essential in determining
treatment and prognosis.
 Benign- no further treatment.
 Metastasis – indicates advanced disease , not
amenable to surgical resection.

27.  Characterization depends upon :
leison morphology.
perfusion difference.
intracellular lipid concentration of mass.
metabolic activity of the mass.

28. INDICATORS SUGGESTING
POSSIBILITY OF MALIGNANCY:
 Masses > 4cm size tends to be metastasis or
primary adrenocortical carcinoma.
 Irregular shape.
 Heterogenous appearance.
 Growth of adrenal mass over time.

29. CT IN DIFFERENTIATING BENIGN
VS MALIGNANT:
 Two main CT criteria :
 1) : Intracellular lipid content represent anatomic
difference.
 2) : vascular enhancement pattern represent
physiologic difference.

30. Nonenhanced CT :
 Many adrenal adenomas can be characterized at CT
due to their abundant intracytoplasmic fat that tends
to lower the attenuation of these lesions (typically <10
HU) on a nonenhanced CT scan.
 NCCT DENSITY—
 <18 H.U.—considered adenoma
 <10 H.U.—96% specific , 79%sensitive
 <0 H.U.—100% specific, 47%sensitive
 At 10 HU specificity approaches 100% if size , shape
and change in lesion size is considered.

31.  Adenoma in patient
with lungcarcinoma.
LEFT: initial enhanced
CT (22HU). RIGHT:
unenhanced CT (-
19HU).
 On the unenhanced
CT the attenuation
value was -19HU
indicating the
presence of a lipid-
rich adenoma.
No further work up
was needed.

32.  A CT histogram determines number of pixels in
adrenal mass having negative HU .
 10% of pixels having negative HU have high
sensitivity and specificity for characterising
adrenal masses as benign.

33. Does >10HU = Malignant? •
 Not necessarily! •
 Up to 30% of adenomas do not contain sufficient lipid
to have low attenuation at CT. (lipid poor adenoma)
 Adrenal masses with >10HU attenuation require
further workup
 This can be done via two modalities: – Contrast
“washout” on CT – Chemical Shift on MRI

35. CONTRAST ENHANCED CT :
 Dynamic contrast enhanced CT is usually
performed in portal venous phase of
enhancement (60-70s) and delayed 10 or 15 min
post contrast.
 Adenomas whether lipid rich or lipid poor shows
rapid contrast enhancement and subsequently
rapid washout of contrast. Metastasis also
enhance vigorously ; washout of contrast is more
prolonged.
 During the portal venous phase both adenoma
and metastasis enhance early so attenuation
values overlap. On delayed images washout of
the agent can be determined.

36.  Percentage of washout of contrast material is
useful parameter - attenuation of adrenal gland
at delayed CT is compared with its attenuation at
dynamic CT.
 Two specific measurements of washout
enhancement are :
1) relative percent washout .
2) absolute percent washout.

37. Lesions that demonstrate RPW < 40% (or
APW < 60%) on a 15-minute delayed scan are
almost always malignant.
Radiology 2008;249:756-775

38.  The enhancement washout = (43 - 22) : (43 - 9) =
62% indicating a fast washout characteristic of an
adenoma.

40. The discriminating
parameters on CT
based on
attenuation values
only apply to
homogenous
lesions.
Metastases may
have a relative
low HU due to

41. MRI IN DIFFERENTIATING BENIGN
VS MALIGNANT:
 Various MR parameters used are :
T1
T2
Enhancement pattern.
Chemical shift characteristics

42.  Significant overlap in T1 and T2 intensity between
adenoma and metastasis ; thus not reliably used
to distinguish.
 Generally metastasis and carcinomas contain
large amount of fluid – bright on T2.
 Adenomas contain lot of fat so bright on T1.
 Enhancement patterns are similar to CT :
adenomas rapidly enhance and show rapid
washout; metastasis enhance rapidly but exhibit
delayed washout.

43. Use of chemical shift imaging to
differentiate adenoma and metastasis
1. CHEMICAL
SHIFT IMAGING-
--
% loss of signal
on out-of-phase
images—due to
cancellation of
lipid & water
signals.

44. CHEMICAL SHIFT IMAGING
 Chemical shift imaging relies on the different
resonance frequency rates of protons in fat and
water molecules
 IN PHASE—signal of water and fat protons add
 OUT OF PHASE---signal of water and lipid protons
cancel out each other.
 Thus, tissues containing lipid and water have
signal loss (ie, appear darker) on out-of
phase images and amount of signal loss
depends on amount of lipid in tissue..

45.  Thus, on out-of phase images, adenomas appear
darker than on in-phase images,
 Metastases or carcinoma (because of lack of lipid
and presence of water) appear bright on both in-
phase and out-of-phase images.
 Moreover, it should be noted that even MRI
cannot be used to definitively characterize lipid-
poor adenomas.

46.  The loss of signal can be assessed virtually using
spleen as the internal control
 Liver should not be used as the internal reference
as it may also show signal loss on opposed
phase image when there is fatty infiltration of
liver.

47.  Two ratios have been described in CSI ;
 SI INDEX : > 16.5 & ADRENAL to SPLEEN
ratio<0.71 is suggestive of benign adrenal lesion.

48.  BENIGN
1. Size
 Small
 No change
2. Smooth margin
3. Homogenous
4. NCCT : HU < 10
5. CECT-----
 Mild & rapid
enhancement
 Quick wash-out
 MALIGNANT
1. Size
 >4cm
 Change in size
2. Irregular shape
3. Heterogenous
4. NCCT : HU > 10
5. CECT-----
 Heterogenous & vigorous
enhancement
 Prolonged wash-out

49. Criteria to diagnose adenoma and
malignancy:
Adenoma Malignancy
 CECT delayed : HU
<24 on 15 min
delayed or HU < 30
on 10 min delayed.
 Relative percentage
washout > 40%
 Absolute percentage
washout > 60%
 CSI : signal loss
 CECT delayed : HU
>24 on 15 min
delayed or HU >30 on
10 min delayed.
 Relative percentage
washout < 40%
 Absolute percentage
washout < 60%
 CSI : no signal loss

50. NUCLEAR MEDICINE IMAGING
 Highly accurate in differentiating malignant from
benign adrenal masses.
Sensitivity : 94.4%-100%
Specificity : 80-100%
 Malignancy : activity in adrenal mass is more
intense than that of liver.

51. Right adrenal adenoma. (a) Contrast-enhanced CT scan demonstrates a
smooth-margin, low-attenuationright adrenal mass (arrow).
(b) FDG PET scan shows normal activity in the kidneys (arrows) but no
increasing activity in the right adrenal gland.

52.  Right adrenal metastasis in a patient with lung carcinoma. (a) Nonenhanced
CT scan demonstrates a right adrenal mass (arrow). (b) FDG-PET SPECT
scan obtained at the same level shows increased activity in the right adrenal
gland (arrow), a finding diagnostic of a metastasis.

53. SCINTIGRAPHY:
 Demonstrate functional status of adrenal nodules.
 Assess function in contralateral gland.
 Detect extradrenal or ectopic site of hormone
production.
 Detect functioning metastasis in patient with
primary adrenal tumors.

54.  When adrenal lesion cannot be accurately
diagnosed on CT, MRI and/or PET , adrenal
biopsy should be considered to establish
definitive diagnosis.

56. ADRENAL ADENOMA
 Most common incidental finding.
 Prevalence of adrenal adenoma is age related.
 0.14% for patients aged 20–29 years and 7% in
those older than 70 years.
 Benign, with no malignant potential and mostly
nonfunctional.
 If non-functional, no need for intervention.

57. Benign adenoma
 Benign cortical adenoma
 Round & homogenous density
  < 4 cm, unilateral
 low unenhanced CT attenuate
values (<10HU)
 Rapid contrast washout
 Absolute contrast washout
>60%
 Isointensity with liver on both T-
1 & T-2 (MRI)
 Chemical shift : lipid on MRI so
loss of signal intensity.
As shown by Caoili et al in 2000 and 2002, regardless of lipid content , adenomas
typically demonstrate rapid washout, which is defined as an APW of more than 60%
and an RPW of more than 40% on delayed images.

60.  The majority of lesions are not functioning.
Although CT does not allow differentiation of
functioning from nonfunctioning masses, the
presence of contralateral adrenal atrophy
suggests that a lesion may be functioning,
because pituitary adrenocorticotropic hormone
secretion is suppressed by elevated cortisol
levels .

61. Indeterminate right adrenal mass found at CT in a 45-year-old woman
with breast cancer. (a) T1-weighted in-phase MR image demonstrates
a right adrenal mass (arrow). (b) T1-weighted out-of-phase MR image
shows signal drop-off in the adrenal gland (arrow), which is diagnostic
of an adenoma.

62. ADRENOCORTICAL
CARCINOMA
 Has a bimodal peak (1st and 4th decades);
however, this tumor is often identified earlier in
children because it tends to be hormonally
active .
 Invasion of the IVC is a well-known complication
of adrenocortical carcinoma

63. Adrenocortical carcinoma
 Irregular shape
 Inhomogenous density (central
necrosis)
 > 4 cm, unilateral, calcify
 High unenhanced CT (>20HU)
 Delayed contrast washout (10 min)
 Absolute contrast washout < 60 %
 Hypointensity compared with liver
T-1 and high to
intermidiateintensity T-2 MRI
 High standard uptake value (SUV)
on FDG-PET-CT study
 Evidence of local invasion or
metas.

65.  USG --
1. Size > 5cm (non-func > func.)
2. Lobulated, irreg.margins,
heterogenous,calcification
(30%-patchy/irreg/nodular)
3. Echogenic rim
4. hemorrhage/necrosis
5. spread—LN/liver mets/IVC
invasion

66. Adrenocortical carcinoma in woman with hypertension, virilization, and
an enlarging abdominal mass. Coronal arterial phase images show a
large left suprarenal mass with hypervascularity and necrosis on the

68. MRI

69.  Larger
lesions>4 cm
may appear
heterogenous
due to central
necrosis.
 High density
areas due to
h'ge can be
seen on NCCT.

70. Metastasis
 Irregular, inhomogenous
 Bilateral
 High attenuation CT (>20 HU)
 Enhancement with contrast
 Delayed contrast washout (10 min)
 Absolute contrast washout < 60%
 Isointensity or slightly less intense than liver T-1 , high to
intermediate intensity T-2 MRI (represent water increase)

72. Left adrenal metastases in a 74-year-old man with lung cancer. (a) T1-
weighted in-phase MR image demonstrates a left adrenal mass
(arrow). (b) T1-weighted out-of-phase MR image shows no significant
signal loss in the adrenal gland compared with that of the spleen. The
mass is either a metastasis or atypical adenoma, and biopsy was
recommended.

73. MYELOLIPOMA:
 Benign tumor of the cortex comprised of
both mature fat and hematopoeitic cells.
 AGE=5Th to 6Th decade
 SEX=M=F
 C/F----asymptomatic/mass effect
 Imaging appearance may vary acc to
histological component.

74.  USG-----
1.SIZE----<5cm
2.Predominantly
hyperechoic----fat
3.Iso/hypoechoic-----
myeloid tissue
4.Heterogenous----
h’ge

75.  CT-----
1. Well-defined ,
capsulated mass.
2. Fat density areas
(-30 to –115
H.U.).
3. Enhancement in
soft-tissue
component.
4. Calification in
30% ,often
punctate

76.  MRI :
 T1 – Hyperintense
 T1 FS : loss of signal intensity, if high signal
persist after FS images, hemorrhage should be
suspected.
 T1 +C : soft tissue element enhance.
 CSI : no signal dropout on opposed phase
because of insufficient water content.

78. LYMPHOMA :
 Unusual site for primary lymphoma.
 Involvement of adrenal gland occur in patient with
non hodgkin lymphoma.
 Bilateral in 70% .
 Most common presentation is diffuse bilateral
enlargement of adrenal glands.

79. CT :
 Solid homogenous mass of soft tissue density.
 CECT : mild enhancement.
 Calcifications can be present after radiation
therapy.

81. MRI :
 Nonspecific .
 T1 : low signal intensity
 T2 : moderate signal intensity.
 CSI : no signal loss on opposed phase as they
donot have intracellular lipid.

82. GROUP II : HYPERFUNCTIONING
ADRENAL NEOPLASM:
Adrenal medullary
neoplasm
Adrenal cortical
neoplasm
 Pheochromocytoma.  Cushing syndrome.
 Hyperaldosteronism
or Conn sydrome.
 Hyperandrogenism .

83. Pheochromocytoma :
 Neoplasm of adrenal medulla.
 Usually unilateral and benign .
 Rule of 10 : bilateral in 10%
malignant in 10%
extraadrenal in 10%
multicentric in 10%
familial in 10%
 C/F—paroxysmal headache, palpitation,
tachycardia, perspiration, HTN as tumor secretes
catecholamines.
 Clinically suspected in younger patient with
hypertension.

84. Syndromes associated with PCC
 Neurofibromatosis
 VHL
 MEN 2a (sipple syndrome)
 MEN 2b
 Struge weber syndrome
 Carney’s triad

85. Imaging in pheochromocytoma
 Typically solid intraadrenal masses , range in size
from 1cm to 20cm.
 90% intra abdominal at hilum of kidney and below
kidney. 1% in organ of zuckerkendl adjacent to carotid
bifurcation. Other site – wall of bladder, paravertebal
area.

86.  USG—
 well marginated.
 Hypoechoic
 Necrosis &
haemorrhage

87.  CT:
 Generally well defined oval or round mass and
occasionally have foci of calcification, necrosis or
cystic changes.
 Vascular lesions so enhance uniformly after
administration of contrast material.

89.  As the tumors are
hypervascular they have the
propensity to undergo hmgic
necrosis thus having low
attenuation central area as
seen in large neoplasms.
 On contrast administration
they exhibit heterogenous
enhancement that is
indistinguishable from
carcinomas.
 So clinical correlation with
biochemical findings are
necessary.

91.  MRI:
 T1 : signal intensity similar or slightly lower
than solid abdominal organs.
 T2 : heterogenous with intermediate or high
signal intensity . Light bulb bright signal on T2
is neither specific nor sensitive.
 CHEMICAL SHIFT IMAGING: donot
demonstrate loss of SI due to lack of
intratumoral lipid.

93.  NUCLEAR MEDICINE IMAGING :
 I-131 MIBG : structural analogue of
norepinephrine, stored in neurosecretory
granules of adrenal medulla. Abdominal imaging
is performed 24-72hrs after administration of
agent . Any focal uptake in adrenal is abnormal.
sensitivity : 80-90% ; specificity : 90-100%.
useful to detect 10% of extraadrenal
pheochromocytoma metastatic disease and
residual tumour.

95.  In -111octreotide : synthetic octapeptide
analogue of somatostatin – shows uptake in
tumors that contain somatostatin receptors.
Sensitivity : 75-90%.
 Complementary role for In-111 octreotide and
I-131 MIBG. 25% seen only with I-131MIBG
nad 25% seen only with In-111 octreotide .
Remaining 50% visualized with both.

96. ADRENAL CORTICAL
NEOPLASM
CUSHING SYNDROME:
 Can be ACTH dependant or ACTH independant.
 ACTH dependant is secondary to cushings
disease or ectopic ACTH secretion.
 ACTH independant etiology include : adrenal
adenoma and adrenal carcinoma.

97.  Firstly imaging of pituitary gland is performed.
 Adrenal adenoma :2-4cm and located
eccentrically in the glands.
 Adrenocortical carcinoma : mixed density 10-
15cm occupying upper abdomen.
 Cortisol producing adenomas suppress ACTH
secretion resulting in atrophy of remaining
adrenal tissue.( if normal adrenal thickness is
observed adrenal mass may not responsible for
cushings.)

98.  Adrenal gland hyperplasia secondary to pituitary
and or ectopic cause can have several imaging
appearance: bilateral uniform adrenal
enlargement , irregular small nodule on surface,
multinodular gland with large dominant nodule.

99. HYPERALDOSTERONISM
 Characterized by hypertension and hypokalemia.
 Three main etiologies:
1) adrenal adenoma
2) adrenal hyperplasia
3) adrenocortical carcinoma
Adrenal adenomas are usually less than 2cm ,
solitary and eccentric within gland.
Adrenal hyperplasia : adrenal glands mildy
enlarged and have irregular surface.

101.  Adrenal cortical scintigraphy : NP-59 is
cholesterol analogue that bind to low density
lipoprotein receptor of adrenal cortex.
 A normal NP visualization of both adrenal gland
on day 5 after the injection or thereafter. Early
bilateral adrenal visualization before day 5
suggest adrenal gland hyperplasia.
 Unilateral adrenal visualization before day 5
suggest adrenal adenoma.

103. GROUP III : ADRENAL
HYPOFUNCTION ;
 No specific syndrome has been described.
 May be due to adrenal destruction or inadequate
pituitary stimulation.
 CAUSES : autoimmune disorders
infections – fungal and TB
Adrenal hemorrhage
Sarcoidosis
Drugs: inhibit cortisol synthesis(
ketoconazole , etomidate) , or increase cortisol
clearane (barbiturates and phenytoin.)

104. INFECTION :
 Most commonly fungal or tubercular.
 Involvement is bilateral ; often asymmetrical.
 Chronic cases may show gland atrophy and
calcification.

105. ADRENAL HEMORRHAGE :
 Can be traumatic (80%) and nontraumatic.
 Bilateral in 20%.

106. Pathophysiology
Causes of adrenal haemorrhage:
 Coagulopathies: causing thrombosis in renal and
adrenal veins.
 Waterhouse-Friderichsen syndrome: in children
and young adults (occurring in 20% of meningitis
cases).
 Trauma: found in 28% of severe trauma cases
autopsy. (Sevitt, 1955)
 Asphyxia: in neonates – at birth the adrenal gland
is very large and vascular.
 Also associated with adrenal tumours. (Light, 2006)

107. Imaging: Computed tomography
CT scanning is the preferred method for
identifying adrenal haemorrhage in all patients
over 6 months old.
CT is rapid, widely available and accurate in
diagnosis.
 Useful for the identification of an underlying
neoplasm, tumour or large thrombosis.
 Allows examination of the adrenal glands in trauma
patients with other imaging indications.
Adrenal haemorrhage is detected as a round or oval
mass obliterating the normal chevron shape of the
adrenal gland. (Light, 2006)

108. Imaging: Computed tomography
CT of normal adrenals several
months before the onset of
haemorrhage.
CT two weeks after the onset of
an acute haemorrhage.
Images excerpted from: Rao et al. (1989)

109. Imaging: Magnetic Resonance
T1 weighted MRI displaying right adrenal infarction without
haemorrhage, in a 42-year-old man with anti phospholipid
syndrome. Image: Riddell and Khalili (2004)

110. MISCELLANEOUS DISEASES
AFFECTING ADRENAL GLAND:
 1) CYST
 2) INFECTION
 3) ADRENAL ABCESS
 4)SOLID LESIONS:
adrenal hemangiomas
ganglioneuroma
adrenal angiosarcoma
primary malignant melanoma.

111. CYSTS
Cysts
Endothelial
cysts (45%)
Lymphangiomatous /
Hemangiomatous
Pseudocysts
(39%)
H”ge in N gland H”ge in tumor
Epithelial(9%) Parasitic (7%)

112. IMAGING FINDINGS
 X-RAY----
curvilinear/peripheral
mural calcification(15%).
 USG ------
round/oval shape; thin
smooth wall; + internal
debris, septae/
hemorrhage /calcification

113.  CT-----
1. Hypoattenuating ,non
enhancing lesion ; Wall
enhancement may be
present.
2. Peripheral curvilinear
calcification.

114.  MRI-----
1. T-1----hypointense
2. T-2-----hyperintense
3. Signal intensity varies if
hemorrhage or proteinaceous
material is present.
 If simple –f/up imaging as cystic
pheochromocytomas or cystic
metastasis have similar
appearance.
 If sypmptomatic/ complex/
large aspiration /surgery( to
r/o malignancy )

115. HEMANGIOMA
 Incidence—rare ,cavernous > capillary
 AGE—50-70yrs
 SEX—F:M=2:1
 C/F—asymptomatic

116.  Most characteristic are phleboliths and presence of
vascular lakes.
 Centripetal enhancement is less characteristic than in
hepatic hemangioma

117. Imaging findings
 X-ray—calcifications
(64%)---similar to
phleboliths
 USG– no-specific app,
heterogenous lesion
often large>10cm is
seen.

118.  NCCT----well-
delienated
hypoattenuating
heterogenous mass +
necrotic areas
 CECT----periph. pools
of contrast (vasc.
lakes) fill-
in phenomenon
 less freq.-
necrosis/h’ge/
fibrosis

119.  MRI----
 T-1-heter. Low
signal,
 periph. persistent
enhancement in
delayed images.
 T-2-high signal.

120. Conclusion
 Most adrenal masses are incidentalomas and amongst them,
adenomas are most common, which can be functioning or non-
functioning.
 Some adrenal masses may have pathognomonic CT features such
as myelolipoma, cysts, lipid-rich adenomas and malignant masses
but most incidentalomas have nonspecific morphologic features.
 Most adrenal adenomas are lipid-rich and can be correctly diagnosed
on chemical-shift MR imaging or unenhanced CT.
 Most lipid-poor adenomas can be accurately characterized on
delayed enhanced CT.
 In patients with a primary extraadrenal neoplasm and no other
evidence of distant metastatic disease, noninvasive imaging can
reduce the necessity for percutaneous adrenal mass biopsy in most
patients by confirming presence of adenoma.
 Percutaneous biopsy can be limited to larger masses whose imaging
studies are not specific & do not indicate an adenoma.