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Dr. Samuel L.
1
ADRENAL MASS
Presenter: Dr. Samuel L. (GSRIII)
Moderator: Dr. Endale A.
Consultant General & Endocrine Surgeon
08/17/2025
Dr. Samuel L.
2 OUTLINE OF PRESENTATION
 Brief embryology, anatomy & physiology
 Hyperaldosteronism
 Cushing syndrome
 Pheochromocytoma
 Adrenocortical cancer
 Incidentaloma
 Miscellaneous adrenal masses
 Techniques of adrenalectomy
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Dr. Samuel L.
3 OBJECTIVES
After the end of this session, we will be able to know
 the differential diagnoses of adrenal masses
 different diagnostic & management algorithms to each disease entity
 techniques of adrenalectomy
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Dr. Samuel L.
4 EMBRYOLOGY
 The cortex originates around the 5th
week of gestation from mesodermal
tissue near the gonads
 The cortex differentiates further into a thin, definitive cortex and a thicker,
inner fetal cortex
 Zona reticularis is formed after birth at around 3 years of age
 Medulla is ectodermal in origin and arises from the neural crest cells
 During fetal development the migration of adrenocortical and medullary
cells can result in accessory or ectopic tissue
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Dr. Samuel L.
5
ANATOMY
 Paired retroperitoneal organs
 Weigh 4-5g each
 Arterial supply
 Superior adrenal aa- from inf phrenic aa
 Middle adrenal aa- from abd aorta
 Inferior adrenal aa- from renal aa
 Venous return
 Rt- short & drains directly to IVC
 Lt- into Lt renal vv
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6
PHYSIOLOGY
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7
Synthesis & metabolism of
catecholamines
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8 PRIMARY HYPERALDOSTERONISM
 Hypertension, hypokalemia, and alkalosis
 From a treatment standpoint, the subtypes of primary hyperaldosteronism
thus can be divided into two groups:
 Surgically manageable
 Medically treated
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Dr. Samuel L.
9 Epidemiology
 M:F- 1:2
 30-50 yrs
 5-13 % of hypertensive pts;
 20% in those with resistant HTN
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Dr. Samuel L.
10 Clinical & pathologic Features
Clinical features
 Hypertension with or without hypokalemia
 HTN is moderate to severe and resistant to medical mx
 Headache, fatigue, muscle weakness…
 Peripheral edema is rare due to ‘aldosterone escape’
 Significant cardiac and metabolic alterations
Pathologic features
 Solitary, unilateral , and small (<2cm)
 Characteristic golden yellow appearance
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11
Diagnosis
 Elevated aldosterone with suppressed renin levels
 Elevated PAC levels in combination with PAC:PRA ratio
 Saline suppression test
Failure to suppress PAC below 10 ng/ml and Urinary aldosterone
secretion greater than > 12 ug/24hr with urinary Na excretion more
than 200 mEq /24hr
PAC:PRA > 20-30 in the setting of PAC >15-20 ng/dl
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Dr. Samuel L.
12 Localization
 CT - a unilateral 1- to 2-cm hypo dense lesion with a normal contralateral
adrenal gland suggests aldosteronoma
 MRI
 NP-59 Scan
 Adrenal venous sampling
 First confirm proper cannulation
 Then compare aldosterone levels
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Dr. Samuel L.
13 TREATMENT
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14 TREATMENT
SURGICAL- laparoscopic Vs Open
 Pre-op rx with spironolactone reduces surgical risks
 Pre-op ARBs also reduce risk of postop hypoaldosteronism
Medical
 Also in poor surgical candidates
 Spironolactone, eplerenone
 Dexamethasone- for glucocorticoid suppressible
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Dr. Samuel L.
15 POST-OP OUTCOMES
 K levels normalizes in 95% pts immediately
 HTN improves in 75% within a month
 1/3 will no longer require medication
 2/3 require reduced dose
 There is association between increased age and longer duration of HTN
with persistent post-op HTN
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Dr. Samuel L.
16 Management Algorithm
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17
CUSHING SYNDROME
Cushing’s syndrome refers to a complex
of symptoms and signs resulting from
hypersecretion of cortisol regardless of
etiology.
Cushing’s disease refers to a pituitary
tumor, usually an adenoma, which
leads to bilateral adrenal hyperplasia
and hypercortisolism
• Rare disease (10/1mil)
• M:F ratio is 1:8
• Most are sporadic
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18 CLINICAL FEATURES
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19 LAB STUDIES
SCREENING
 Overnight dexamethasone suppression test
 48 hr./low-dose dexamethasone suppression test
 Late-night salivary cortisol measurement
 Urinary cortisol
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Dr. Samuel L.
20 EVALUATION OF THE UNDERLYING
CAUSES
 Plasma ACTH
 ACTH less than 2 pmol/l (10 pg/ml) indicate ACTH-independent Cushing’s
syndrome
 ACTH greater than 4 pmol/l (20 pg/ml)
 High dose dexamethasone suppression
 Pituitary MRI
 Bilateral petrosal vein sampling
 Chest and abdominal CT
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21
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22 Management
 MEDICAL
 For perioperative control of hypercortisolism or
 When surgery is not feasible
 Metyrapone, ketoconazole, and mitotane
 SURGERY
 Pituitary adenoma- TSS, *bilateral laparoscopic adrenalectomy
 Ectopic TSH secreting tumors-resection, *medical therapy or *bilateral
adrenalectomy
 Adrenal causes- adrenalectomy (unilateral or bilateral; open or laparoscopic)
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Dr. Samuel L.
23 PHEOCHROMOCYTOMA
 Arise from the cells of the adrenal medulla
 MEN2A, MEN2B, VHL disease, NF1
 10 percent tumor
 peak incidence in the fourth and fifth decades
 no gender predilection
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Dr. Samuel L.
24 Clinical Features
 Classic triad of headaches, palpitations, and extreme hypertension
 Paroxysmal spells
 In 0.1-0.2 % of hypertensive pts
 Myocardial ischemia
 Raynaud’s type phenomenon
 Other sxs : nausea, lassitude, heat intolerance, anxiety, abdominal pain,
pallor, fever, or glucose intolerance
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Dr. Samuel L.
25 Diagnosis
 Identification of the classic signs
 24 hr. urine metanephrines and fractionated catecholamines
 Plasma free metanephrines
 Localization
 CT of abdomen & Pelvis-heterogeneous, central necrosis
 MRI- hyper intense ‘bright white’ signal on T2
 MIBG scan-
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Dr. Samuel L.
26 Pre-op management
 Alpha blockage- phenoxybenzamine
 For a minimum of 1-3 wks
 Orthostatic hypotension & ‘stuffy nose’
 Ca2+ channel blockers- nicardipine
 Volume expansion- fluids, high salt diet
 Beta blocker- as needed
 Metyrosin - in refractory HTN/ Tachycardia
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Dr. Samuel L.
27 Intra-op mx
 The most volatile BP swings occur with induction of anesthesia
 With occlusion of the adrenal vein, the pt may rapidly vasodilate
 Excellent communication should be maintained b/n the surgeon &
anesthesiologist
 Physical manipulation of the tumor should be minimized
 RX- Adrenalectomy
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Dr. Samuel L.
28 Special populations
Pregnant
 Supine HTN
 MRI is the best imaging choice
 Follow with meds until safe GA for
delivery
 CS with tumor excision
Children
 HTN is more often sustained
 Tendency to be bilateral & extra-
adrenal
 Malignancy is less frequent
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Dr. Samuel L.
29 Malignant Pheochromocytoma
 There are no definitive histologic criteria defining malignant
pheochromocytomas
 Malignancy is usually diagnosed with evidence of invasion into surrounding
structures or distant metastases
 Mets: to bone, liver, regional lymph nodes, lung, and peritoneum
 Treatment
 Resection if feasible
 External-beam radiation for un resectable lesions
 Therapeutic 131 I-MIBG irradiation
 Chemotherapy
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Dr. Samuel L.
30 Adrenocortical cancer
 Rare neoplasms (2 per 1 million in the world)
 Bimodal age distribution
 The majority are sporadic
 ~ 50% of adrenocortical cancers are nonfunctioning
 Functional tumors secrete cortisol (30%), androgens (20%), estrogens (10%),
aldosterone (2%); or multiple hormones (35%)
 CF: rapid onset of Cushing’s syndrome accompanied by virilizing features
 Enlarging abdominal mass, pain
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31 Adrenocortical cancer
DIAGNOSTIC TESTS
 Lab tests
 CT/MRI:
 tumor heterogeneity, irregular margins, and the presence of hemorrhage and
adjacent LAP or liver metastases
 moderately bright signal intensity on T2-weighted images
 significant lesion enhancement, and slow contrast washout
 evidence of local invasion into adjacent structures
 CT of chest & pelvis: staging
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32
Adrenocortical cancer
Pathology : criteria to
predict malignancy
 nuclear grade III or IV;
 mitotic rate greater than 5 per 50 high-
power fields;
 atypical mitoses;
 clear cells comprising 25% or less of the
tumor;
 a diffuse architecture;
 microscopic necrosis;
 invasion of venous, sinusoidal, and capsular
structure
Tumors with four or more of these criteria were
likely to metastasize and/or recur
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33 Adrenocortical cancer
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34 Treatment
SURGERY
 Open adrenalectomy is the procedure of choice
 R0 resection must be the goal
 Enbloc resection with contiguous structures
 Surgical debulking
CHEMOTHERAPY
 Etoposide, cisplatin, doxorubicin, paclitaxel +_ mitotane
RADIOTHERAPY –incomplete resection, palliation of bone mets
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Dr. Samuel L.
35 INCIDENTALOMA
 These are adrenal lesions discovered during imaging performed for
unrelated reasons
 Frequency: 5.9% of autopsies & 4.3 % from images
 Although non-functional by definition , most of them may be sub clinically
functioning
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36
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37 Screening for subclinical disease
 Subclinical Cushing’s Syndrome
 Ranges from slightly attenuated diurnal cortisol rhythm to atrophy of the
contralateral gland
 Do dexamethasone suppression test
 Subclinical Pheochromocytoma
 Refers to totally asymptomatic adrenal incidentaloma that histologically proves
to be pheochromocytoma
 24 hr urine metanephrine & VMA, or fractionated urinary catecholamine
 Subclinical Primary Aldosteronism
 Pt with adrenaloma who is normotensive or hypertensive with normokalemia
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Dr. Samuel L.
38 Screening for subclinical disease
 Screening for adrenal Ca
 4-25 % harbor Ca
 Imaging findings
 CT-ragged tumor with stippled calcifications and with areas of necrosis; enlarged LN or
local invasion
 MRI-heterogeneously increased, early T2-weighted signal, weak and late enhancement
after gadolinium
 FNAB has limited role
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Dr. Samuel L.
39 Management: Surgery Vs Follow-up
• Surgery
Lab evidence for sub
clinically functioning
tumor
Associated metabolic
features
Evidence of primary
or solitary metastatic ca
• Follow-up: yearly for 5-10
yrs.
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Dr. Samuel L.
40
Miscellaneous adrenal masses
ADRENAL METASTASES
 From the lung , melanoma, breast, kidney, and GI neoplasms
 ~50% are functional
 Appropriate biochemical evaluation prior to further imaging, bx or rx
 Imaging: CT with contrast, MRI
 The definitive dx of malignancy requires percutaneous bx or surgical
pathology
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Dr. Samuel L.
41 Management of adrenal metastases
Appropriate mx
depends on:
Type & extent of
primary malignancy
DFI
Patient comorbidity
Resection of isolated
adrenal metastases
may offer a survival
benefit.
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Dr. Samuel L.
42 Miscellaneous adrenal masses
ADRENAL HEMORRHAGE
Causes
 trauma, surgery, anticoagulant rx,
septicemia or tumor
 Increased ACTH
 Adrenal medullar venous
thrombosis
ADRENAL CYSTS
 Benign or malignant(7%)
 Endothelial cysts, epithelial cysts
 Pseudocysts can arise from
hemorrhage
 Small, asymptomatic or non-
functioning- can be followed
 Size >6cm, symptomatic,
functioning or suspected
malignancy- surgery
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Dr. Samuel L.
43 Miscellaneous adrenal masses
 Lymphangioma
 Pseudocysts
 Paracytic infections
 Myolipoma
Surgery
 Symptomatic
 Suspicion of malignancy
 Hydatid cyst
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Dr. Samuel L.
44 Techniques of adrenalectomy
 OPEN Vs LAPAROSCOPIC
 OPEN ADRENALECTOMY
Anterior approach
Posterior approach
Lateral approach
Thoraco -abdominal approach
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45
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46 ANTERIOR APPROACH
• Midline incision or bilateral subcostal Incision
• Access to Rt adrenal
• Mobilize the liver medially; reflect hepatic
flexure of the colon
• Kocher maneuver & exposure of RP
• Gerota’s fascia is incised
• Mobilize the sup & lat surfaces first
• Divide the adrenal vein
• Access to Lt adrenal
• Medial visceral rotation
• Via lesser sac by division of the gastrocolic
ligament
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Dr. Samuel L.
47 Complications of adrenalectomy
 Infection
 Bleeding
 Hemodynamic instability
 Adrenal insufficiency
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48 Postoperative care
 Depends on the operative approach, extent of resection, and functional or nonfunctional nature of the
tumor
 Pheochromocytoma
 ICU for a minimum of 4 hrs
 a-blockers: discontinue
 B-blockers- if started pre-op, it should be continued & weaned post-op
 Aldosteronoma
 DC all antihypertensive meds except b-blockers
 DC spironolactone
 Check serum K the next morning
 Follow BP as an outpatient
 Cushing’s syndrome
 Continue glucocorticoids with subsequent dose tapering
 Mineralocorticoid supplementation after bilateral adrenalectomy
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Dr. Samuel L.
49 REFERENCES