IMAGING OF ADRENAL

GLAND

IDA MIRIAM
 ADRENAL GLAND
• The adrenal gland is named for its location adjacent to the
kidneys: ad-renal
• Also known as suprarenal glands
• 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.
• The right adrenal gland is located in an area
just superior to the right kidney , medial to
the right lobe of the liver , lateral to the crus
of the right hemidiaphragm , and posterior to
the inferior vena cava.
• Its shape may resemble inverted letter V or
Y lying in the crease between the liver and
the crus.
• The lateral limb of the adrenal gland lies
close to the right lobe of the liver and can
sometimes be difficult to separate from the
surface of the liver
• The left adrenal gland is located
superior to and extends anterior to the
upper pole of the left kidney in a
triangle formed by the left lateral
margin of the aorta, the posterior
surface of the body and tail of the
pancreas, and the antero superior
medial surface of the upper pole of the
left kidney.
• It can be shaped like an inverted letter V
or Y , an inverted or reversed letter L, or
it may be triangular .
 NORMAL MEASUREMENTS

• Length : 3-5cm
• Width : 2-3cm
• Thickness : 5mm
• Weight : 3.5-5gm
• 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.
 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
ADRENAL MEDULLA - 10% of adrenal
• Made up of chromaffin cells
• Secretes-epinephrine or norepinephrine
• Part of sympathetic autonomic nervous system.
 VASCULAR SUPPLY
• Arterial supply :
-Superior adrenal artery (br. of inferior phrenic)
-Middle adrenal artery (arising from desc. aorta)
- Inferior adrenal artery (br. of renal artery)
• Venous drainage :
- right side: right adrenal vein drain into IVC .
- left side : left adrenal vein drain to left renal vein
• Lymphatics :
- para-aortic and paracaval lymph nodes.
 IMAGING MODALITIES

• Ultrasound
• Computed tomography
• Magnetic resonance imaging
• Nuclear medicine imaging
 ULTRASOUND

• Primarily reserved for use in paediatric 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 a good acoustic window.

• Left adrenal evaluated from posterior or mid axillary

approach. No suitable acoustic window for left.
Sagittal US scan demonstrates an enlarged right adrenal
gland (arrow) lying posterior to the right lobe of the liver
 COMPUTER TOMOGRAPHY

• NCCT abdomen
• CECT abdomen (after 60 secs & at 15 minutes)

CT is the imaging modality of choice for evaluating adrenal

glands morphology and masses associated with it.
CECT and delayed images help in further characterization of the
lesions. 100-150ml of low osmolarity nonionic contrast is
injected at a rate of 3ml per second and images are acquired at
60sec and 15 min after contrast injection.
• When studying the adrenal glands, the entire abdomen
through the aortic bifurcation is examined.

• This complete examination of the abdomen is helpful in

staging adrenal disease and evaluating possible ectopic
adrenal pathology that may occur in certain disease
processes.
 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

• T1W signal show normal adrenal as low signal against high

signal fat.

• Most tumor show high signal on T2W and low signal on T1W
image.
 Normal gland MRI

(a)T1-weighted breath-hold MR image demonstrates a normal

left adrenal gland (arrow)
(b)T2 weighted MR image.
 CHEMICAL SHIFT IMAGING

• The most important MRI protocol for the adrenal glands is

chemical shift imaging.

• It is performed with in-phase and opposed-phase T1-weighted

breath-hold 2D spoiled gradient-recalled echo (GRE) technique.

• These sequences allow for the detection of intracellular lipid

within an adrenal adenoma and play a critical role in
determining whether the lesion is benign or malignant.
 NUCLEAR MEDICINE IMAGING

• This technique is primarily used as a problem solving modality for

lesions not adequately characterized on CT and MR imaging.
• It provides functional imaging of the adrenal cortex and medulla.
• 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.
 ADRENAL PET/CT

• PET and PET/CT also have been shown to be valuable in the

differentiation of adrenal masses
• Adrenal glands are larger than the spatial resolution of PET
(about 5 mm), and, although rich in vascularity and
metabolically active, they are usually not visible on PET
alone.
• Combined PET/CT can assign adrenal tracer uptake to the
location of the adrenal gland when present
• With regard to standardized uptake value (SUV), the
average maximum and mean SUVs are recorded.
• Adrenal FDG uptake is considered to be of malignant origin
when intensity is higher than hepatic uptake
• The maximum SUV of normal adrenal glands range from
0.95 to 2.46, and given that normal liver tissue has an
average mean SUV between 1.5 and 2.0, physiologic
adrenal uptake might in some cases be in the range of
malignant lesions.
• Small adrenal lesions detected on CT, can be correctly diag-
nosed on the PET component by evaluating tracer uptake
Right adrenal adenoma. (A) contrast-enhanced CT scan demonstrates
a smooth-margin, low-attenuation right adrenal mass (arrow).
(B) FDG PET scan shows normal activity in the kidneys (arrows) but no
increasing activity in the right adrenal gland.
Right adrenal metastasis in a patient with lung carcinoma.
(A) NECT scan demonstrates a right adrenal mass (arrow).
(B) FDG-PET scan obtained at the same level shows increased activity in the
right adrenal gland (arrow), a finding diagnostic of a metastasis.
 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.
• Radiolabelled analogues of cholesterol, e.g. 75
selenomethyl norcholesterol, 59 NP beta iodomethyl–19-
norcholesterol can localize mass causing adrenal cortical
dysfunction, the latter one is particularly useful in the work
up for suspected aldosteronism

• Iodine-131 metaiodobenzylguanidine (MIBG) is

concentrated in sympatho adrenal tissue and is used for
imaging adrenal medullary lesion, especially to evaluate for
pheochromocytoma and to screen the whole body for extra-
adrenal pheochromocytoma
• When adrenal lesion cannot be accurately diagnosed on CT,
MRI and/or PET , adrenal biopsy should be considered to
establish definitive diagnosis.
 PERCUTANEOUS ADRENAL BIOPSY

• To establish a definitive diagnosis, biopsies are still performed

for adrenal lesions that remain indeterminate on imaging.
• Percutaneous biopsies carry a complication rate of 8 - 12.7%.
• Complications - bleeding, pancreatitis, pneumothorax, infection
and needle tract seeding.
• Biopsy of an unsuspected phaeochromocytoma carries the
potential risk of precipitating a catecholamine storm.
• Biochemical testing to exclude a possible phaeochromocytoma
is therefore advocated prior to undertaking any adrenal
biopsy.
 Adrenal Venous Sampling

• Adrenal venous sampling may be recommended in patients

with aldosteronism, for distinguishing unilateral from bilateral
disease and for localizing unilateral tumor.
• Bilateral adrenal vein samples are tested for aldosterone in
an attempt to localize the functional tumor to one adrenal
gland or the other.
• Each adrenal vein is cannulated with a catheter via either a
trans femoral or a trans jugular approach, and the catheter
position is verified under fluoroscopic guidance.
• The test is best performed under a continuous infusion of ACTH,
which acutely stimulates aldosterone release and accentuates
the difference in aldosterone secretion between the two
adrenal glands when an adrenal adenoma is present.

• Cortisol is also measured to prove that the blood samples were

taken from adrenal veins and not from other venous structures.

• Adrenal vein sampling is especially useful when there are no

apparent adrenal gland abnormalities on either CT or MRI in
a patient with suspected primary hyperaldosteronism.
 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
 ADRENAL DISEASES

• GROUP I : Adrenal disease with normal function.

• GROUP II : Adrenal hyper-functional disease.
• GROUP III: Adrenal insufficiency.
 GROUP I : ADRENAL DISEASE WITH
NORMAL FUNCTION

• Most of these are incidentally detected adrenal masses

• Include : nonfunctional adrenal adenoma or carcinoma,
metastasis , lymphoma , myelolipoma , adrenal cyst.
INCIDENTALLY DISCOVERED ADRENAL MASSES

• Adrenal incidentaloma – lesions <4cm or smaller ; can be

unilateral or bilateral.
• Whenever adrenal incidentaloma is discovered , two main
concerns are :
1) functinally active or inactive.
2) benign or malignant.
 IS IT FUNCTIONAL?

• 6% - 20% of adrenal incidentalomas have hormonal

abnormality.
• Hormonal hypersecretion is most likely seen in masses that are
at least 3 cm in diameter.
• If a hormonally functional adrenal mass is suspected, a
complete medical workup is warranted.
• 85 percent of the masses : nonfuctioning.
 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.
• Characterization depends upon :
Leison morphology.
Perfusion difference.
Intracellular lipid concentration of mass.
Metabolic activity of the mass.
 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.
CT IN DIFFERENTIATING BENIGN VS MALIGNANT:

Two main CT criteria :

• 1) intracellular lipid content represent anatomic difference.
• 2) vascular enhancement pattern represent physiologic
difference.
 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 HU — Considered adenoma
• <10 HU — 96% specific , 79%sensitive
• <0 HU —100% specific, 47%sensitive
• Adenoma in patient with lung
carcinoma. 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.
 HISTOGRAM ANALYSIS METHOD

• A CT histogram determines number of pixels in adrenal mass

having negative HU .
• A ROI cursor is drawn covering atleast 2/3rd of the adrenal mass
excluding areas of necrosis.
• The individual attenuation values of all the pixels in the ROI are
plotted against their frequency and the amount of lipid in the
mass is proportional to the number of negative pixels (less than 0
HU)
• 10% of pixels having negative HU have high sensitivity and
specificity for characterising adrenal masses as benign.
• No metastases have negative pixels.
• It may be a useful adjunct as the combination of CT
attenuation value <10 HU or >10% negative pixel content
would correctly identify 91% of adenomas compared with
66% using CT attenuation values alone
 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
 CONTRAST ENHANCED CT
• Dynamic CECT is usually performed in portal venous phase
of enhancement (60-70s) and delayed 10 or 15 min post
contrast.
• Characterisation of adrenal masses using CECT relies on the
unique physiological perfusion patterns of adenomas.
• Adenomas whether lipid rich or lipid poor enhance rapidly
after contrast medium administration and also demonstrate
a rapid washout of contrast medium—a phenomenon
termed contrast medium washout.
• Malignant lesions & pheochromocytoma also enhances
vigorously but washout of contrast is delayed.
• Measurements of the attenuation values of the mass before
injection of contrast medium, at 60 s following injection of
contrast medium and then again at 15 min, are made using
an electronic cursor that includes at least 2/3rd of the mass.

• These contrast medium enhancement washout values are only

applicable to relatively homogeneous masses without
large areas of necrosis or haemorrhage.

• Two specific measurements of washout enhancement are :

1) relative percent washout
2) absolute percent washout
Lesions that demonstrate RPW < 40% (or APW < 60%) on a
15-minute delayed scan are almost always malignant.
MRI IN DIFFERENTIATING BENIGN VS
MALIGNANT:

• Various MR parameters used are :

T1
T2
Enhancement pattern.
Chemical shift characteristics
• 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.
 USE OF CHEMICAL SHIFT IMAGING TO
DIFFERENTIATE ADENOMA AND METASTASIS

CHEMICAL SHIFT IMAGING—

% Loss of signal on out-of-phase images—due to cancellation of
lipid & water signals.
 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.
• 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.
• The loss of signal can be assessed virtually using spleen as
the internal reference

• 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.
The quantitative ways of assessing the degree of loss of signal
intensity are:
• adrenal-lesion-to-spleen ratio (ASR)
• signal intensity index (SII)
• To calculate ASR, ROIs are used to acquire the signal
intensity (SI) within the adrenal mass and the spleen from in-
phase and out-of-phase images.
• The ASR reflects the percentage signal drop-off within the
adrenal lesion compared with the spleen and it can be
calculated as:

• An ASR ratio of 70 or less has been shown to be 100%

specific for adenomas but only 78% sensitive
• Signal intensity index uses the same characteristics of the
adrenal mass on both in- and out-of-phase imaging and
can be calculated as:

• Adenomas characteristically have SII greater than 5%, whilst

metastases have indices lower than 5%
• BENIGN • MALIGNANT
1. Size 1. Size
• Small • >4cm
• No change • Change in size
2. Smooth margin 2. Irregular shape
3. Homogenous 3. Heterogenous
4. NCCT : HU < 10 4. NCCT : HU > 10
5. CECT : 5. CECT :
• Mild & rapid enhancement • Heterogenous & vigorous
• Quick wash-out enhancement
• Prolonged wash-out
CRITERIA TO DIAGNOSE ADENOMA AND MALIGNANCY

ADENOMA MALIGNANCY
• CECT DELAYED : HU <24 • CECT DELAYED : HU >24
on 15 min delayed or HU ON 15 min delayed or HU
< 30 on 10 min delayed. >30 on 10 min delayed.
• RELATIVE PERCENTAGE • RELATIVE PERCENTAGE
WASHOUT > 40% WASHOUT < 40%
• ABSOLUTE PERCENTAGE • ABSOLUTE PERCENTAGE
WASHOUT > 60% WASHOUT < 60%
• CSI : signal loss • CSI : no signal loss
Algorithm summarizes the work-up used to differentiate
benign from malignant adrenal masses :
 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.
BENIGN ADENOMA

• Round & homogenous density

• < 4 cm, unilateral
• Low unenhanced CT
attenuate values (<10HU)
• Rapid contrast washout
• Absolute contrast washout
>60%
• Rapid washout > 40%
• Isointense with liver on both T-1
& T-2
• Chemical shift : loss of signal
intensity.
• The majority of lesions are non 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 .
(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.
 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

• This hormonally active tumours, representing 30-40% of all

adult tumours, present with characteristic clinical manifestations :
• Cushing syndrome secondary to elevated cortisol (most common)
• Virilisation or feminisation secondary to elevated androgens
• Conn syndrome secondary to hyperaldosteronism (rare)
Associations
• Beckwith-wiedemann syndrome
• Li-fraumeni syndrome
• Carney complex
• Multiple endocrine neoplasia type 1
ADRENOCORTICAL CARCINOMA
• Irregular shape
• Inhomogenous density (central
necrosis)
• > 4 cm, unilateral, calcify
• CECT- rapid enhancement (>20HU)
• Delayed contrast washout (10 min)
• Absolute contrast washout < 60 %
• Hypointense compared with liver T-1
and high to intermediate intensity T-2
• High standard uptake value (SUV)
on FDG-PET-CT study
• Evidence of local invasion or mets.
USG

1. Well-defined mass
2. Size > 5cm
3.Lobulated, irregular margins,
heterogenous, calcification
4.Echogenic rim
5. Hemorrhage/necrosis
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 arterial phase
The mass exhibits heterogeneous low signal intensity on the T1-
weighted image and high signal intensity with a heterogeneous
pattern of contrast enhancement and areas of necrosis (arrow in b)
on the T2-weighted image
 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)
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.
 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 according to histological
component.
• USG
1.Size----<5cm
2.Appearances are varied depending on individual tumour
components
- Predominantly hyperechoic----fat
- Iso/hypoechoic-----myeloid tissue
- Heterogenous---h’ge
• CT
1. Well-defined ,
capsulated mass.
2. Fat density areas
(-30 to –115 HU).
3. Enhancement in
soft-tissue
component.
4. Calification in
30% ,often
punctate
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.
NUCLEAR MEDICINE:
• Adrenal myelolipomas typically do not demonstrate an avid
FDG uptake.
• It is generally lower than that of the liver background.
• However, in rare cases the adenomatous and hematopoietic
elements can show an increased FDG uptake
Differential diagnosis

General imaging differential considerations include:

•retroperitoneal liposarcoma

•fat containing adrenocortical carcinoma

•adrenal teratoma: extremely rare

•renal angiomyolipoma (AML)

• CT coronal reconstruction or MRI can help in
determining the kidney as the origin of the lesion
 LYMPHOMA

• Unusual site for primary lymphoma.

• Involvement of adrenal gland occur in patient with NHL.
• Bilateral in 70% .
• Most common presentation is diffuse bilateral enlargement
of adrenal glands.
CT :
• Solid homogenous mass
of soft tissue density.
• CECT : Mild
enhancement.
• Calcifications can be
present after radiation
therapy.
MRI :
• Nonspecific .
• T1 : Low signal intensity
• T2 : Moderate signal intensity.
• CSI : No signal loss on opposed phase as they donot have
intracellular lipid.
 GROUP II : HYPERFUNCTIONING
ADRENAL NEOPLASM
ADRENAL MEDULLARY ADRENAL CORTICAL
NEOPLASM NEOPLASM
• Pheochromocytoma. • Cushing syndrome.
• Hyperaldosteronism or conn
sydrome.
• Hyperandrogenism .
 PHEOCHROMOCYTOMA
• Catecholamine producing tumors which arise from ganglion cells
anywhere in the autonomic nervous system.
• 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
• Clinically suspected in younger patient with hypertension.
 SYNDROMES ASSOCIATED WITH PCC

• Neurofibromatosis
• VHL
• MEN 2A (Sipple syndrome)
• MEN 2B
• Struge weber syndrome
• Carney’s triad
 IMAGING IN PHEOCHROMOCYTOMA

• Typically solid intraadrenal masses , range in size from 1cm

to 20cm.
• 90% originate in the adrenal medulla
• 10% are extra-adrenal, the common sites being: -
- paravertebral sympathetic ganglia
- organ of Zuckerkandl
- urinary bladder
- neck or mediastinum
USG:
• Well marginated.
• Variable appearance
ranging from solid to
mixed cystic and solid
to cystic
CT:
• Usually large, heterogeneous masses with areas of necrosis
and cystic change
• They typically enhance avidly
• May wash out similar to an adrenal adenoma, but they
tend to have a greater enhancement.
• Tend to enhance more on the portal venous phase than the
arterial phase
• 110 HU of enhancement on the arterial phase is
compatible with pheochromocytoma; hypervascular
metastases could be considered in an appropriate setting
• Up to 7% demonstrate areas of calcification
MRI:
• T1 : Isointense or hypointense
• T2 : extremely hyperintense.
light bulb bright signal on T2 is neither specific nor sensitive.

• Gadolinium–DTPA: Produces marked enhancement with slower

wash out of contrast as compared to adenoma

• Chemical shift imaging: Do not demonstrate loss of SI due to

lack of intra tumoral lipid.
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.
IN -111OCTREOTIDE :

• Synthetic octapeptide analogue of somatostatin – shows

uptake in tumors that contain somatostatin receptors.
• Sensitivity : 75-90%.
• 25% seen only with I-131MIBG and 25% seen only with in-
111 octreotide , remaining 50% visualized with both.
 ADRENAL CORTICAL NEOPLASM

CUSHING SYNDROME:

• Can be ACTH dependent (75%) or ACTH independent (25%)

• ACTH dependant is secondary to Cushing's disease or ectopic
ACTH secretion.
• ACTH independent is secondary to excess cortisol production
from adrenal adenoma or adrenal carcinoma.
• Ectopic ACTH producing nonendocrine tumors : bronchial
carcinoid tumor, islet cell tumor of the pancreas, medullary
carcinoma of thyroid, thymic carcinoid tumor and
pheochromocytoma

• The diagnosis of Cushing’s syndrome depends predominantly

on the clinical features and biochemical findings.

• The purpose of imaging is to identify the source of excess

ACTH either from a pituitary tumor or an ectopic source and
to detect or exclude adrenal mass.
• The adrenal appearances in Cushing’s syndrome depend on
the etiology.
• CT is the primary modality.
ACTH dependent Cushing’s syndrome:

• This results from pituitary cause in 85% and rest from ectopic
ACTH secretion.
• The adrenals show changes of hyperplasia in the form of
smooth thickened limbs or multiple small nodules of
varying size involving one or both limbs
• MRI SI in adrenal hyperplasia closely follows that of the normal
adrenal gland.
ACTH Independent Cushing’s Syndrome

• Adrenal adenoma : solitary, well-defined homogeneous

mass, usually around 2-3 cm & when large, it shows focal
areas of necrosis and hemorrhage.
Cortisol producing adenomas suppress ACTH secretion
resulting in atrophy of remaining adrenal tissue. contralateral
gland is normal but occasionally atrophic.

• Adrenocortical carcinoma : large mass ( >6.0 cm)

heterogeneous with areas of necrosis and calcification, with
features of local invasion, regional lymphadenopathy and
distant spread
• Primary pigmented nodular adrenal dysplasia (PPNAD):
- multiple tiny (2–5 mm) nodules seen bilaterally, with no
overall glandular enlargement and normal intervening
adrenal tissue.

• ACTH-independent macronodular adrenal hyperplasia

(AIMAH):
- glands are grossly enlarged with nodules up to 3 cm in
diameter.
HYPERALDOSTERONISM
• Conn’s syndrome is associated with excess of mineralocorticoids.
• c/f: hypertension, muscle weakness, polyuria, polydipsia and
persistent hypokalemia.
• Three main etiologies:
1) adrenal adenoma
2) adrenal hyperplasia
3) adrenocortical carcinoma
Adrenal adenomas : small (1.6-1.8 cm) and may have
central low attenuation due to high lipid content
Adrenal hyperplasia : adrenal glands mildly enlarged and have
irregular surface.
ADRENAL CORTICAL SCINTIGRAPHY :
• If CT examination is inconclusive, adrenal cortical scintigraphy
with NP-59 can be done.
• NP-59 is cholesterol analogue that bind to low density
lipoprotein receptor of adrenal cortex.
• Both adrenals are normally visualized on 5th day or later
following injection.
• Early bilateral adrenal visualization before day 5 suggest
adrenal gland hyperplasia.
• Unilateral adrenal visualization before day 5 suggest
adrenal adenoma.
ANDROGENITAL SYNDROME

• It is a consequence of excessive secretion of sex hormones.

• It causes virilization, feminization or precocious puberty

depending upon the age and sex of the patient.

• The adrenal causes of androgen excess include congenital

adrenal hyperplasia in children and virilizing tumors
(adenoma or carcinoma) in adults.
• MRI is preferred to CT to image adrenals as well as ovaries
particularly in children to detect tumors because of MRI
being non-ionising.
• CT is however often the initial and only modality performed
in evaluation of suspected CAH, due to easy availability.
• The tumors are usually more than 2.0 cm in size and show
bilateral nodular adrenal hyperplasia
• Occasionally adrenal and gonadal venous sampling may be
necessary to locate the source of excessive androgens
 GROUP III : ADRENAL HYPOFUNCTION

• It is classified as primary or secondary.

• Primary form is due to destruction of the adrenal cortex, while

the secondary form results from pituitary causes.

• Usually 85-90 percent of the adrenal cortex must be destroyed

before the clinical syndrome manifests.
Primary adrenal insufficiency or Addison’s disease :

• presents with weakness, hypotension, weight loss with or

without pigmentation.
• causes are idiopathic atrophy, chronic granulomatous
infections, e.g. TB, histoplasmosis, blastomycosis and adrenal
haemorrhage, autoimmune diseases and drugs.
• In patients with idiopathic atrophy, the glands are often too
small to be Identified.
• In TB there may be B/L asymmetrical adrenal enlargement
with or without calcification or necrosis, small gland with
calcification involving one or both adrenals, or small gland
with no calcification.
• In histoplasmosis, adrenals may show B/L asymmetrical
enlargement but often normal configuration and usually no
calcification are seen
NCCT scan of patient with Addison’s disease showing bilateral
atrophic adrenal glands
Axial CECT and coronal MPR image of a patient with Addisons’s
disease reveal bilateral, calcified adrenal glands, suggesting
granulomatous involvement
 ADRENAL HEMORRHAGE

• Can be traumatic (80%) and nontraumatic.

• Bilateral in 20%.
• Bilateral adrenal haemorrhage is usually associated with
anticoagulant therapy or with stress caused by surgery,
sepsis or hypotension.
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.

• Asphyxia: in neonates – at birth the adrenal gland is very

large and vascular.
• Also associated with adrenal tumours.
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.
CT of normal adrenals several
months before the onset of
haemorrhage.

Ct two weeks after the onset of

an acute haemorrhage.
• T1 weighted MRI displaying right adrenal infarction without
haemorrhage, in a 42-year-old man with anti phospholipid
syndrome.
MISCELLANEOUS DISEASES AFFECTING
ADRENAL GLAND:

• Cyst
• infection
• adrenal abscess
• solid lesions:
Adrenal hemangiomas
Ganglioneuroma
Adrenal angiosarcoma
Primary malignant melanoma.
 CYSTS

Cysts

Endothelial Pseudocysts
Epithelial(9%) Parasitic (7%)
cysts (45%) (39%)

Lymphangiomatous /
H”ge in N gland H”ge in tumor
Hemangiomatous
 IMAGING FINDINGS

• USG -
Round/oval shape; thin
smooth wall; + internal
debris, septae/ hemorrhage
/calcification
CT
• Well-defined round low
attenuating lesion suggesting
fluid with rim enhancement
• Rim calcification may be
noted
• The attenuation values may
be mixed in the presence of
debris or hemorrhage.
MRI-
• T-1 - Hypointense
• T-2 - Hyperintense
• 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 )
 MULTIPLE ENDOCRINE NEOPLASIA

• MEN com prises a group of disorders in which tumor or

hyperplasia develops in two or more endocrine organs in a
single patient.
• It exists as three main types: MEN I , MEN II A , and MEN II B.
• Autosomal dominant Inheritance occurs in all three types.
 MEN Type I

• MEN I primarily affects the adrenal cortex by the

formation of either nodules or adenomas.
• Rarely do functional adrenocortical adenomas occur; if they
do, they present as either hyperaldosteronism or Cushing' s
syndrome.
• The other endocrine abnormalities involved with MEN I
include parathyroid hyperplasia or adenoma, gastrinoma,
insulinoma, vipoma, and glucagonoma of the pancreatic islet
cells.
• The anterior pituitary gland can be involved with adenomas
that secrete prolactin, growth hormone, or ACTH.
• Carcinoid tumors can also occur , as can multiple lipomas
and thyroid nodules
 MEN Types II A and II B

• MEN II A is characterized by pheochromocytoma, medullary thyroid

carcinoma and parathyroid hyperplasia or adenomas
• MEN II B is characterized by pheochromocytomas, medullary thyroid
carcinoma, soft tissue neuromas and ganglioneuromatosis of the
intestine with Marfan-like anatomic build.
• The pheochromocytomas that occur in this are often smaller than
isolated intra-adrenal pheochromocytomas and more frequently
bilateral.
• An increased incidence of extra-adrenal pheochromocytomas or
paragangliomas also occurs
 Carney' s Syndrome

• It is a disorder characterized by the presence of gastric

leiomyogenic neoplasms, extra-adrenal pheochromocytomas
or paragangliomas, and pulmonary chondromas

• Accurate imaging to define the extra-adrenal

pheochromocytomas or paragangliomas, which are often
functional, is important for preoperative localization.

• The combination of MIBG scanning with MRI or CT has been

successful.
A 40-year-old female with Carney' s triad.
MR images demonstrate a left adrenal paraganglioma (large arrow
in A) as well as a gastric sarcoma (small arrow in A) and pulmonary
chondromas (arrows in B)
 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 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.
• 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.
 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.
• Five percent of adrenal abnormalities interpreted as positive at PET are
false-positive for malignancy.
• This is secondary to inflammatory lesions (sarcoidosis, tuberculosis [44]),
Hemor-rhage and necrosis adrenal endothelial cysts, some adrenal
adenomas, and periadrenal abnor-mality and adrenal cortical hyperplasia
may all mimic metastases because they have been associated with increased
FDG uptake.
• Metastasis detection at PET/CT, however, depends on the primary tumor,
metastasis size, and differentiation. PET scanners have a spatial resolution of
about 5 mm.
• Metastases from primary carcinomas that are non-FDG avid have been
found to be false-negative on PET, including carci-noid (neuroendocrine
tumors) and pulmo-nary carcinoma of the bronchioloalveolar type [46–48].
FDG PET cannot differenti-ate among malignant lesions, for example, among
metastases, ACC, malignant pheo-chromocytoma, and lymphoma.
• (PET) PLAYS AN INCREASINGLY PIVOTAL ROLE IN FUNCTIONAL IMAGING, GOVERNED BY THE METABOLIC ACTIVITY OF THE ADRENAL LESION. LIKE MOST OTHER NON-BENIGN LESIONS, MALIGNANT
ADRENAL NEOPLASMS SHOW INCREASED 18F-FLUORO-DEOXYGLUCOSE (18FDG) ACTIVITY OWING TO INCREASED GLUCOSE UTILISATION. THE STRENGTH OF PET LIES IN ITS ACCURATE ABILITY TO
ASSESS PHYSIOLOGICAL CHANGE, WHICH OFTEN PRECEDES GROSS ANATOMICAL CHANGES THAT ARE DETECTED MUCH LATER. EXCELLENT RESULTS OBSERVED BY BOLAND ET AL.13 IN A META-
ANALYSIS, REPORTED A 97% SENSITIVITY AND 91% SPECIFICITY IN DISTINGUISHING BENIGN FROM MALIGNANT LESIONS. THE USE OF HYBRID PET-CT HAS IMPROVED THE DIAGNOSTIC YIELD THROUGH
INCLUDING CT DENSITOMETRY, MORPHOLOGICAL FEATURES AND ACCURATE LOCALISATION. QUALITATIVE PET ANALYSIS USING VISUAL COMPARISON WITH LIVER UPTAKE IS USED MORE
COMMONLY. QUANTITATIVE SUV ANALYSIS IS OF LIMITED DIAGNOSTIC USE.

• PET-CT, ALTHOUGH A SUPREME DIAGNOSTIC TOOL, IS NOT WITHOUT LIMITATIONS:

• • IT IS LESS SENSITIVE IN DETECTING AND CHARACTERISING SMALL LESIONS, PARTICULARLY THOSE LESS THAN 1 CM.

• • A SMALL PERCENTAGE OF ADENOMAS AND INFECTIVE LESIONS ARE MILDLY FDG AVID.

• • FALSE NEGATIVES MAY BE ENCOUNTERED IN ADRENAL METASTASES FROM PRIMARY MALIGNANCIES THAT ARE NON-FDG AVID, E.G. BRONCHOALVEOLAR CARCINOMA, CARCINOID TUMOURS.

• OTHER PRIMARY AGENTS (F-FLUORO-DOPAMINE, 11C-HDROXYEPHEDRINE, F-DOPA,) ARE ALSO IN USE, PARTICULARLY FOR THE DIAGNOSIS OF PHAEOCHROMOCYTOMAS.

• D. ADRENAL SCINTIGRAPHY

• SCINTIGRAPHY PROVIDES FUNCTIONAL CHARACTERISATION OF THE ADRENAL GLAND BASED ON THE UPTAKE AND ACCUMULATION OF RADIOTRACER. ADRENOMEDULLARY AGENTS (E.G. META-IODO-
BENZYLGUANIDINE (MIBG)) AND ADRENOCORTICAL AGENTS (E.G. NP59 (IODOMETHYLNORCHOLESTEROL)) ARE THE TWO MAJOR CATEGORIES OF RADIOPHARMACEUTICALS IN USE. MIBG IS A
STRUCTURAL AND FUNCTIONAL ANALOGUE OF NOREPHEDRINE, TAKEN UP BY ADRENERGIC NEOPLASMS INCLUDING PHAEOCHROMOCYTOMAS, NEUROBLASTOMAS AND PARAGANGLIOMAS WHOLE-
BODY IMAGING ALLOWS THE DETECTION OF MULTIFOCAL DISEASE, EXTRA-ADRENAL PHAEOCHROMOCYTOMAS (PARA-GANGLIOMAS), METASTATIC DISEASE AND RESIDUAL/RECURRENT TUMOUR.
OCTREOTIDE (A SOMATOSTATIN ANALOGUE) IS OCCASIONALLY USED FOR THE EVALUATION OF MEDULLARY DISORDERS, BUT CARRIES A LOWER SENSITIVITY OF APPROXIMATELY 30% IN THE
DETECTION OF PHAEOCHROMOCYTOMAS.6 N59 IS THE MAIN RADIO-ISOTOPE EMPLOYED IN ADRENAL CORTICAL SCINTIGRAPHY. IT IS A CHOLESTEROL ANALOGUE THAT BINDS TO LIPOPROTEIN
RECEPTORS OF ADRENAL CORTICAL CELLS. ADENOMAS, WITH INTACT STEROIDOGENESIS, SHOW UPTAKE OF NP59, WHEREAS MALIGNANT AND NON-ADENOMATOUS LESIONS DO NOT