5. 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
6. SIZE OF MASS
• Size — The maximum diameter of the adrenal
mass is predictive of malignancy
• Adrenocortical carcinomas were significantly
associated with mass size, with 90 percent
being more than 4 cm in diameter when
discovered.
7. 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.
8. GROUP I : ADRENAL DISEASE WITH
NORMAL FUNCTION
• Adrenal incidentaloma (AI) is a term applied
to an accidentally discovered adrenal mass on
imaging performed for the investigation of an
unrelated complaint. Adrenal incidentalomas
(AIs) are a cluster of different pathologies, the
majority of which are benign and non-
functioning adrenal adenomas. However, mild
hormonal alterations as well as metabolic
abnormalities may be present in patients with
AIs.
Most of these are incidentally detected as adrenal masses.
Include : nonfunctional adrenal adenoma or carcinoma,
metastasis , lymphoma , myelolipoma , adrenal cyst.
9. Benign non-functioning adenomas
• The vast majority comprise non-functioning, benign
cortical adenomas or hypersecretory tumors (subclinical
Cushing’s syndrome, pheochromocytoma, aldosterone-
secreting adenoma), primary adrenocortical carcinoma,
myelolipomas, cysts and various rare benign tumors.
When they occur bilaterally, the most possible
diagnoses are metastatic disease, congenital adrenal
hyperplasia, bilateral cortical adenomas or infiltrative
disease
• 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 .
10. GROUP II : HYPERFUNCTIONING
ADRENAL NEOPLASM
• Adrenal medullary
neoplasm
• Pheochromocytoma
• Adrenal cortical
neoplasm
• Cushing syndrome.
• Hyperaldosteronism or
Conn sydrome.
• Hyperandrogenism .
11. Cortisol hypersecretory masses
• These lesions are characterized by autonomous
glucocorticoid production without specific signs
and symptoms of Cushing’s syndrome (CS), a
condition termed subclinical hypercortisolism
(SCS)& may be associated with a high prevalence
of arterial hypertension, obesity, impaired
glucose tolerance and dyslipidemia, clinical
features also shared by the metabolic syndrome.
This association is also supported by the fact that
these hormonal and clinical features were
improved in all patients after surgical treatment.
12. Pheochromocytoma (PHEO)
• PHEOs are rare, catecholamine-producing tumors arising from
the chromafin cells of the adrenal medulla. Their prevalence
in the general population is estimated at about 1 or 2 per
100,000 adults. The vast majority of PHEOs are sporadic
(about 86%), while the remainder (14%) are associated with
familial syndromes, such as neurofibromatosis type 1, von
Hippel-Lindau (VHL) syndrome, multiple endocrine neoplasia
type 1 (MEN1) and 2 (MEN2)
• Neoplasm of adrenal medulla.
• Usually unilateral and benign .
• C/F—paroxysmal headache, palpitation, tachycardia,
perspiration,
• HTN as tumor secretes catecholamines.
• Clinically suspected in younger patient with hypertension.
• Rule of 10 : bilateral in 10%
• malignant in 10%
• extraadrenal in 10%
• multicentric in 10%
• familial in 10%
13. • The main clinical feature is hypertension, which is
paroxysmal in 48% and persistent in 29%, while 13%
of the patients are normotensive. Besides
hypertension, a common triad of symptoms
comprises attacks of headaches (80%), palpitations
(64%) and diaphoresis. Other manifestations
frequently misdiagnosed are those related to
endocrine gland pathology (CS, hypercalcemia,
diabetes mellitus, thyroid carcinoma) or
cardiovascular episodes (such as shock, myocarditis,
dilated cardiomyopathy, cardiac arrhythmias)
14.
15. HYPERALDOSTERONISM
• Primary aldosteronism (PA) in its classical form manifests
with high aldosterone (ALD), low plasma renin activity
(PRA) and hypokalemia, although several reports indicate
that normokalemic PA constitutes the most common
presentation of the disease. Hypertension, mild or severe,
is the common finding in these patients and if
hypokalemia is present, nocturia, polyuria, muscle cramps,
palpitations or paralysis may occur.
• 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.
16. Primary adrenocortical carcinoma
• Primary adrenocortical carcinoma is rare.
can be functional or non-functional. The clinical
manifestation involves symptoms related to adrenal
hypersecretion, such as hypercortisolism (more
common), as well as high sex hormones or ALD
hypersecretion (presented with CS, hirsuitism, acne,
oligo- or amenorrhea, increased libido in the case of
androgens, gynecomastia in the case of estrogens,
hypokalemia-related symptoms, in the case of elevated
aldosterone)
17. Metastatic cancer
• Metastatic disease to the adrenal glands can
occur in a wide array of malignancies. The most
frequently reported primary cancers that
metastasize to the adrenals are lung (usually the
non-small cell type) and liver (hepatocellular
carcinoma)
18. Adrenal myelolipoma
• rare, benign usually hormonally inactive
neoplasm of the adrenal cortex and
consisting of mature adipose cells and
haematopoietic elements in varying
proportions.It is asymptomatic in most
cases, although, especially the large ones
can present with abdominal pain or
retroperitoneal bleeding. Adrenocortical
dysfunction occurs in 10% and may present
as Addison’s disease, Cushing’s disease,
hyperandrogenism or hypertension due to
catecholamine or aldosterone secretion
19. 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.)
20. Radiographic features
• Imaging plays a key role in assessing the vast number of incidental adrenal lesions, the
majority of which are adrenal adenomas. Correlation with previous imaging is often useful,
as a lesion which has not changed over some years is unlikely to be malignant.
• General
• They can be divided into those that have typical or atypical appearances.
• Typical adenomas are:
• small: <3 cm
• homogeneous and low density
• Atypical features include:
• haemorrhage
• calcification
• necrosis
• no fat
• large
• if >4 cm: 70% malignant (excluding adrenal myelolipomas which are easily recognised due
to fat, and pheochromocytomas which are usually recognised biochemically)
• if >6 cm: 85% malignant
21. 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.
25. The enhancement washout = (43 - 22)
: (43 - 9) = 62% indicating a fast
washout characteristic of an adenoma.
26. 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
27. MRI IN DIFFERENTIATING BENIGN VS
MALIGNANT:
• Various MR parameters used are :
• T1
• T2
• Enhancement pattern.
• Chemical shift characteristics
28. Use of chemical shift imaging to
differentiate adenoma and metastasis
CT scan
29.
30.
31. 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.