Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_1382_Библиотеки_им_академика_М_И_Перельмана.pdf
X
- •Contents
- •1. Thyroid Embryology, Anatomy, and Physiology: A Review for the Surgeon
- •2. The Assessment of Thyroid Nodules
- •3. Thyroid: Fine-Needle Aspiration Biopsy
- •4. Thyroid Imaging
- •5. Multinodular Goiter
- •6. Thyrotoxicosis and Thyroiditis: Causes, Investigation, and Management
- •7. Molecular Biology of Thyroid Cancer
- •8. Well-Differentiated Thyroid Cancer: An Overview and the Chernobyl Effect
- •9. Poorly Differentiated and Undifferentiated Thyroid Cancer
- •10. Postoperative Management of Well-Differentiated Thyroid Cancer
- •11. Medullary Thyroid Cancer
- •12. Technique of Thyroidectomy
- •13. Lymph Node Dissection in Thyroid Cancer
- •14. Management of the Laryngeal Nerves and Voice
- •15. Embryology, Anatomy, and Physiology of the Parathyroid Glands
- •16. Presentation and Diagnosis of Primary Hyperparathyroidism
- •17. Parathyroid Localization and Imaging
- •18. Intraoperative PTH Monitoring
- •19. Focused Parathyroidectomy
- •20. Parathyroid: Bilateral Neck Exploration
- •21. Reoperative Parathyroid Surgery
- •22. Management of Secondary and Tertiary Hyperparathyroidism
- •23. Parathyroid Carcinoma
- •24. Adrenal Embryology, Anatomy, and Physiology
- •25. Adrenal Imaging
- •26. Adrenal Venous Sampling
- •27. Primary Hyperaldosteronism
- •29. Pheochromocytoma and Paraganglioma
- •30. Adrenocortical Carcinoma
- •31. Incidentaloma
- •32. Adrenal Metastases and Rare Adrenal Tumors
- •33. Technique of Open and Laparoscopic Adrenalectomy
- •34. Laparoscopic Retroperitoneal Adrenalectomy
- •35. Pancreas: Embryology, Anatomy, and Physiology
- •36. Pancreatic Imaging: The Value for Surgery of Neuroendocrine Pancreatic Tumors

350
ENDOCRINE SURGERY
resulting in a loss of signal intensity on out-ofphase images, while nonfunctioning tumors do
not generally have uniform signal loss on
out-of-phase images.
MRI Characteristics
of Pheochromocytoma
On MRI, pheochromocytomas are typically isointense to hypointense relative to the liver on
T1-weighted images and hyperintense on
T2-weighted images. The hypervascularity of
pheochromocytomas makes them appear characteristically bright, with a high signal intensity
on T2-weighted images and no signal loss on
opposed-phase images [24, 25]. Although pheochromocytomas may appear very bright, with a
‘‘light bulb’’ appearance, on T2-weighted
images, they are typically heterogeneous and
of moderately high signal intensity (Fig. 25.8)
[26]. T2-weighted images can clearly identify
chromaffin tissue; the T2-weighted adrenal
mass-to-liver ratio of pheochromocytomas or
paragangliomas is usually more than 3. This
ratio is much higher than that for adrenocortical
adenomas, ACCs, or metastases to the adrenal
gland. Thus, MRI may provide some functional
(biochemical) information.
Pheochromocytomas enhance after the intravenous administration of gadolinium. There
may be some heterogeneity in enhancement
due to cystic or necrotic areas. The enhancement may not be pronounced on immediate
contrast-enhanced images but may become
Fig. 25.8. T2-weighted MRI hyperintense pheochromocytoma.
progressively greater with time on later interstitial-phase images.
Our practice is to reserve MRI primarily for
patients with a biochemically proven pheochromocytoma but negative CT findings. MRI can
also be a valuable adjunct in evaluating patients
with extra-adrenal sites of pheochromocytoma.
MRI is considered slightly superior to CT in the
assessment of the relationship between the
tumor and the surrounding vessels, particularly
with regard to identifying vascular invasion [3].
The detailed anatomic and vascular information
can be used to determine resectability and plan
the operative approach.
Nuclear Medicine
Nuclear Medicine Overview
Scintigraphic imaging of the adrenal cortex and
medulla can provide useful information. Adrenocortical scintigraphy is not frequently performed owing to the widespread use of CT and
MRI. However, when CT and MRI are indeterminate, nuclear imaging studies may play a role
in assessing the functional status of adrenocortical lesions. Furthermore, scintigraphic imaging of the adrenal medulla and related tissues
is useful in providing a definitive diagnosis of
pheochromocytoma and paraganglioma.
Positron emission tomography (PET) is an
outstanding imaging modality in the evaluation
of many different types of malignant processes
and has grown in popularity and availability in
recent years. This growth has been in part
due to the exquisite sensitivity of PET with
18
[
F]fluorodeoxyglucose (FDG) in detecting
malignant lesions. FDG exploits the characteristically high glucose consumption of many tumor
cells. However, this modality has some limitations. FDG is not a specific tracer for a particular
type of cancer and therefore cannot differentiate
between types of malignant processes. Moreover,
infections and inflammatory conditions can
result in prominent FDG uptake, potentially
leading to false-positive interpretations of
PET studies. Nevertheless, PET and PET/CT
with FDG have proven to be extremely useful
for the detection of metastases. In addition,
FDG-PET has a higher sensitivity and resolution
than conventional scintigraphy, making PET an
attractive technique to image the adrenal glands.

351
ADRENAL IMAGING
Adrenocortical Scintigraphy
Radioiodinated NP-59 (
19-norcholesterol) is a radioiodinated cholesterol analogue that is bound to and transported
by low-density lipoproteins to specific receptors
on adrenocortical cells. Once NP-59 is taken
up by the cells, it is esterified and stored in
the adrenocortical cells without being further
metabolized. This allows imaging of the adrenal
cortex.
A drawback of scintigraphy with NP-59 is that
factors affecting cholesterol uptake into the adrenals also affect uptake of NP-59. Elevated serum
cholesterol levels reduce the percentage of radiocholesterol uptake, while an increase in ACTH
results in increased NP-59 uptake. In addition,
administration of drugs that may interfere with
scintigraphic studies must be interrupted: these
include glucocorticoids, diuretics, spironolactone,
beta and calcium channel blockers, and agents
that interfere with the hypothalamic axis and
renin–angiotensin–aldosterone system [27]. In
addition, NP-59 is not widely available, limiting
its widespread use as a routine diagnostic agent.
NP-59’s accumulation in the adrenal cortex
and background clearance occurs slowly over
several days. For routine studies, imaging is
usually performed 4–5 days after tracer injection.
NP-59 accumulation is greater in the normal
adrenalglandsthaninanyotherorganbutis
131
I – 6-ß-iodomethyl-
also noted in the liver, colon, and gallbladder. In
normal subjects, activity is usually more intense in
the right gland than in the left because of the
superimposed liver background activity and
decreased soft tissue attenuation on the right side.
Patients should be pretreated with iodine
[saturated solution of potassium iodide (SSKI),
1 drop/38 mg three times daily] for at least 1 day
before and 7 days after injection of NP-59. This
maneuver blocks the uptake of free radioiodine
by the thyroid that would otherwise occur. Dexamethasone suppression should be performed
in patients with hyperfunctioning of the zona
glomerulosa (hyperaldosteronism) or the zona
reticularis (hyperandrogenism) of the adrenal.
Without suppression of ACTH, the normal high
uptake of NP-59 by the zona fasciculata would
make interpretation of uptake by the other two
zones difficult.
In Cushing’s syndrome, the scintigraphic pattern depends on the etiology of hypercortisolism.
When a pituitary adenoma causes increased production of ACTH, bilateral early visualization of
the adrenal glands is found on scintigraphy.
When Cushing’s syndrome is due to a glucocorticoid-producing adrenal adenoma, typically
only the affected adrenal is visualized on
scintigraphy; the affected adrenal adenoma’s
production of cortisol shuts off pituitary ACTH
secretion and shuts off uptake of NP-59 by the
contralateral adrenal gland (Fig. 25.9). NP-59
Fig. 25.9. A denotes I-131 and NP-59 Static images and B represents the corresponding CT image in an adenoma of a patient with
Cushing’s syndrome.

352
ENDOCRINE SURGERY
scintigraphy is also useful in patients with
Cushing’s syndrome to detect postsurgical adrenal remnants that can cause recurrent disease.
In hyperaldosteronism, the distinction
between a unilateral adenoma and a bilateral
adrenal hyperplasia determines surgical versus
medical treatment. Aldosterone-secreting tumors
are often small and not easily diagnosed on CT
and MRI. While venous sampling has become an
attractive diagnostic test, NP-59 is also useful to
have in the armamentarium. Dexamethasone
suppression is required before scintigraphy.
Unilateral early activity on scintigraphy indicates
an aldosteronoma, while bilateral delayed activity
is more indicative of hyperplasia.
NP-59 scintigraphy provides functional
information that may complement the morphologic information provided by CT. Importantly,
up to 30% of adrenal tumors cannot be distinguished as benign versus malignant solely using
CT characteristics[28, 29]. The presence of concordant (unilateral) CT and NP-59 scans is
usually diagnostic of a benign adenoma. The
absence of discernible NP-59 uptake by an adrenal tumor strongly suggests either a destructive
process or a nonfunctioning lesion such as an
ACC or metastasis [30]. A study of 229 patients
with abnormal adrenal anatomy on CT found a
100% specificity and a 71% sensitivity of NP-59
scintigraphy in distinguishing benign versus
malignant unilateral adrenal masses [30]. The
lack of bilateral uptake with functioning ACC
may occur because the tumor is unable to incorporate enough tracer per gram of tissue to be
visualized, yet secretes sufficient cortisol to suppress ACTH and, thus, the contralateral adrenal
gland [31].
The poor tracer uptake by ACC may be due to
altered cholesterol metabolism or preferential de
novo synthesis of cholesterol by the carcinoma
[32]. However, there are several case reports of
ACCs (1.8–18 cm diameter) and their metastases
that were visualized with NP-59 scintigraphy.
In the presence of hormonal excess due to a
functioning ACC, unilateral visualization of an
adrenal tumor on NP-59 scintigraphy does not
always signify benign disease.
Adrenomedullary Scintigraphy
Nuclear medicine imaging is particularly useful
in patients with biochemical evidence of a
functioning adrenergic adrenal tumor that
has not been localized by CT or MRI and
in the follow-up evaluation of patients with
suspected or documented recurrent or metastatic disease. Scintigraphic studies of the adrenal medulla make use of the norepinephrine
analogue meta-iodobenzylguanidine (MIBG), a
tracer that is taken up and localized in the
storage vesicles of presynaptic adrenergic
nerves. In addition to being taken up by the
adrenal medulla, MIBG localizes to the heart
and spleen, two other organs with rich adrenergic innervation and to the liver, an organ that
processes catecholamines for excretion.
Certain drugs interfere with MIBG uptake
and must be stopped prior to scanning, some
of them for up to 21 days. These include sympathomimetics, reserpine, guanethidine, bretylium, calcium channel blockers, labetalol, ACE
inhibitors, tricyclic antidepressants, and
cocaine [8].
Radiotracers paired with MIBG include
131
I, the former affording a lower radiation
and
dose and the latter allowing delayed imaging.
123
I-MIBG is at present the principal tracer for
diagnostic purposes. The use of
131
I-MIBG for
123
diagnostic applications is largely outdated;
however, this radiopharmaceutical is used to
treat metastatic malignant pheochromocytoma,
paraganglioma, and neuroblastoma. A prerequisite to therapeutic
strated tracer uptake on a diagnostic study
123
using
I-MIBG.
131
I-MIBG is demon-
To prevent thyroid ablation, radiotracer
uptake by the thyroid must be blocked by
administering SSKI or potassium perchlorate
before and after administration of
131
or
I-MIBG. The usual intravenously administered dose of
surface and
imaging is usually performed between 4 and 6 h
after administration of
imaging is performed at 24 h. However, when
131
I-MIBG is used, optimal imaging is at
123
I-MIBG is 10 MCi/cm2body
131
I-MIBG is 0.5 mCi/1.7 cm2.Initial
123
I-MIBG; delayed
123
I-MIBG
48–72 h, and multiple scans may be needed
over 72 h to get the best possible image.
131
In
I-MIBG scintigraphy, faint visualization
of the normal bilateral adrenal medulla is seen
in only 10% of patients. In
123
I-MIBG imaging,
the normal adrenal medulla is visualized more
frequently. When pheochromocytoma is present, the characteristic appearance is a unilateral focus of uptake (Fig. 25.10).
I

353
ADRENAL IMAGING
Fig. 25.10. (A) Anterior and posterior whole-body views of an
with pheochromocytoma. The MIBG avid tumor is visualized in the left adrenal gland. (B) Corresponding SPECT/CT of the abdomen,
clearly delineating the rim of increased
to tumor necrosis. No distant metastases are visualized.
We reserve
123
I-MIBG scanning for use in
123
I-MIBG activity to the large left adrenal mass. The center of the mass is not MIBG avid due
patients with biochemical evidence of pheochromocytoma in whom CT or MRI has failed to
identify the tumor or who have lesions greater
than 5 cm on CT or MRI because of the concern
for metastasis. It may also be helpful in patients
with distorted anatomy due to previous surgery
or with equivocal biochemical diagnoses.
131
I-MIBG scanning offers specificity ranging
from 95 to 100% but has lower sensitivity [45].
Despite recent optimization in acquisition and
processing protocols,
123
I-MIBG scintigraphy
interpretation remains challenging. False-positive
studies are normally due to artifactual findings.
False-negative scans have several possible causes,
123
I-MIBG scan done at 24 h after injection, in a middle age woman
such as size of the lesion, physiologic tracer
uptake masking a focus of disease, or decreased
uptake as a result of pharmaceutical interference
by other drugs. Therefore, MIBG scintigraphy is
often reviewed in conjunction with, and compared to, other imaging modalities such as CT
and MRI.
Over the past few decades, there have been
attempts to coregister nuclear medicine images
with images from conventional modalities such
as CT and MRI [33, 34]. However, the rather
cumbersome and time-consuming coregistration
algorithms have limitedthe use to research applications. Nevertheless, over the past few years,
single photon emission computed tomography

354
ENDOCRINE SURGERY
(SPECT)/CT scanners have entered the market,
providing the fusion of functional (MIBG) images
and anatomic (CT) images. Moreover, newer
SPECT/multislice CT scanners that have recently
become commercially available may overcome
some of the limitations of conventional wholebody planar CT and SPECT imaging.
SPECT/CT has been shown to improve the
delineation of physiologic diffuse intraluminal
bowel activity, the localization of tumor sites,
and the detection of bone and bone marrow
involvement. SPECT/CT can also optimize
the characterization of tumor recurrence
adjacent to organs with physiologic high
MIBG uptake, such as the heart, kidneys,
and liver [35]. The superb coregistration of
the fusion images that can be obtained with
today’s state-of-the-art SPECT/multislice CT
scanners can help avoid false-positive and
false-negative interpretations.
Positron Emission
Tomography
There is an increasing body of knowledge on
the use of PET and PET/CT for the noninvasive assessment and characterization of lesions
of the adrenal glands [31]. FDG is the only
commercially available PET tracer approved
by the US Food and Drug Administration
that can be used for the evaluation of the
adrenal glands. However, several other PET
tracers under investigation have provided
very encouraging results in the evaluation of
lesions of the adrenal cortex and medulla and
in the assessment of patients with an incidentally discovered adrenal mass [36].
PET or PET/CT with FDG is excellent at differentiating between benign and malignant
adrenal lesions, both primary ACCs and lesions
metastatic to the adrenal gland. FDG is a nonspecific tumor-imaging agent whose uptake in
tumor cells (measured as standard uptake
values, SUVs) is based on increased glucose
metabolism in malignant lesions (Fig. 25.11).
Over the past few years, the reported accuracy
of PET/CT for differentiating metastatic adrenal
lesions from benign adrenal lesions inoncologic
patients has ranged between 92 and 100%
[37, 38]. In distinguishing benign from
primary malignant adrenal lesions, many
studies describe 100% sensitivity and specificity
[39, 40]. In one of the largest studies, Metser
et al. used FDG-PET/CT to characterize adrenal
masses in 150 patients. With a cutoff SUV of 3.1
or higher to define malignant lesions, FDG-PET
alone had a sensitivity of 98.5% and a specificity
of 92% for characterizing lesions as benign or
malignant; the addition of CT to PET increased
the specificity to 98% [41].
FDG-PET and FDG-PET/CT have also been
used for the evaluation of patients with pheochromocytomas since this type of tumor usually
exhibits increased FDG uptake. Shulkin et al.
identified pheochromocytomas with FDG-PET
in 22 of 29 patients. In that study, pheochromocytomas that poorly concentrated MIBG were
depicted with FDG, and conversely, all tumors
that could not be imaged with FDG were
detected with MIBG [42].
Other PET tracers are being developed to
evaluate the adrenal gland. However, for now,
these tracers are limited to the research arena.
Moreover, since several of these tracers are
labeled with the short-lived
11
C isotope, their
use is limited to a few institutions with on-site
cyclotrons and sophisticated radiosynthesis
facilities.
For functional imaging of the adrenal cortex,
11
C-metomidate (MTO) is currently being
investigated as a novel tracer. MTO binds specifically to 11b-hydroxylase, an enzyme that is
essential in the biosynthesis of cortisol and
aldosterone and is regulated by ACTH [31].
Minn et al., in a study of 16 patients with adrenal
masses, found that
11
C-MTO PET clearly separated 13 adrenocortical lesions (including both
nonfunctioning and functioning lesions: adrenocortical adenomas, ACC, and macronodular
hyperplasia) from three noncortical lesions
(benign and malignant pheochromocytoma
and metastasis to the adrenal) [43]. However,
11
C-MTO PET could not distinguish benign
adrenocortical tumors from ACC. In contrast,
FDG-PET separated all malignant lesions from
benign adrenal masses, showing a specificity,
sensitivity, and diagnostic accuracy of 100%
for the characterization of adrenal masses.
The number of PET tracers that target catecholamine synthesis or reuptake pathways continues
to increase and now includes
11
C-hydroxyephedrine,18F-fluorodopamine (18F-
FDA), and
18
(
F-DOPA).Theseagentstakeadvantageofthe
18
F-fluorodihydroxyphenylalanine
11
C-epinephrine,

355
ADRENAL IMAGING
Fig. 25.11. FDG PET/CT images of a young woman with metastatic recurrent right adrenal cortical carcinoma. Study requested for
restaging of disease. (A) Coronal view of the PET/CT scan, which shows the large and metabolically very active recurrent tumor in the
right adrenal bed of 16.5 12.3 cm (SUV = 43.6), and the metastatic lesion to the posterior mediastinum (SUV = 40.3). (B and C)Axial
images of the PET/CT scan at the level of the chest and upper abdomen, respectively, demonstrating the tumor lesions.
unique characteristics of catecholamine biosynthesis and metabolism in the adrenal medulla and
have high sensitivity and specificity for the localization of pheochromocytomas, neuroblastomas,
and related neoplasms. Somatostatin receptors
are widely distributed in neoplasms of the neural
crest, and based upon the earlier success of singlephoton-labeled somatostatin receptor-imaging
agents, numerous somatostatin antagonists
labeled with positron-emitting isotopes have
been developed [44].
18
F-FDA,18F-DOPA,11C-epinephrine, and
11
C-hydroxyephedrine have all been demonstrated to image pheochromocytomas and
related neoplasms. In a study using
11
C-hydroxyephedrine PET, rapid and early imaging –
approximately 10 min postinjection – was
reported in 9 of 10 patients with pheochromocytomas [45]. Mann et al. evaluated 14 patients,
8 of whom had proven pheochromocytoma,
11
using
CT, and
C-hydroxyephedrine PET, FDG-PET/
131
I-MIBG.11C-hydroxyephedrine
detected all sites of disease. FDG-PET/CT was
successful in depicting all sites of adrenal and
soft tissue metastatic disease, except metastases
to bone, whereas
firmed sites of disease in only four of eight
patients [46]. In a study of
16 patients with metastatic pheochromocytoma,
18
F-FDA correctly identified all sites of meta-
131
I-MIBG localized to con-
18
F-FDA-PET in
static pheochromocytoma, including some
metastatic lesions that were not detected with
131
I-MIBG scans [47].
For diagnosis of pheochromocytoma the
functional imaging test of choice today is
123
I-MIBG, if possible including SPECT/CT.
If the MIBG scan is negative, then PET using
a specific noradrenergic transporter system-

356
ENDOCRINE SURGERY
targeting agent such as18F-FDA or18F-DOPA
should be employed. If these studies are
negative, the tumor has likely undergone
dedifferentiation and is probably malignant.
Therefore, in these instances, imaging with
FDG-PET, FDG-PET/CT, or
111
In-pentetreotide
(Octreoscan) PET is recommended [48].
Role of Nuclear Medicine
in Incidentalomas
The routine use of high-resolution imaging
techniques for the evaluation of many oncologic
and nononcologic disease processes has led to
the identification of an increasing number of
unsuspected adrenal lesions, or incidentalomas.
In this situation, the diagnostic algorithm
begins with biochemical evaluation to assess
for hormone hypersecretion, since hormonally
active adrenal masses require surgical resection.
Despite the excellent anatomic and structural
detail that CT and MRI provide, functional
adrenal imaging using targeted radionuclides,
such as NP-59, MIBG, and FDG, offers the best
diagnostic sensitivity and specificity for characterizing incidentalomas. These tracers target
entirely separate physiologic processes, and
they can be used selectively, based on clinical
setting and biochemical data, to identify different types of adrenal tumors. The role of
radionuclide imaging in the evaluation of
nonfunctioning incidentalomas has also been
unequivocally demonstrated.
In a study by Maure et al. of 54 patients with
incidentalomas, NP-59 imaging had a positive
predictive value of 89% for characterizing an
adrenal mass as an adenoma; the negative predictive value to rule out this type of tumor was
100%. The positive predictive value of
MIBG imaging for characterizing an adrenal
mass as a chromaffin tumor was 83%, and the
negative predictive value to rule out this type of
tumor was 100% [39].
In addition to the importance of wellestablished high-resolution imaging techniques,
there is increasing scientific documentation of
the benefits of functional adrenal imaging. The
availability of hybrid imaging techniques, including PET/CT and SPECT/CT, allows the simultaneous evaluation of adrenal function and anatomy. In addition, the recent introduction of
131
selective PET tracers that target specific biosynthetic pathways has created an impetus for the
development of novel approaches in adrenal
imaging.
References
1. Vincent JM, Morrison ID,Armstrong P,Reznek RH. The
size of normal adrenal glands on computed tomography. Clin Radiol. 1994;49:453–55.
2. Nwariaku FE, et al. Radiologic characterization of
adrenal masses: the role of computed tomography –
derived attenuation values. Surgery. 2001;130:1068–71.
3. Udelsman R, Fishman EK. Radiology of the adrenal.
Endocrinol Metab Clin North Am. 2000;29:27–42, viii.
4. Korobkin M, et al. CT time-attenuation washout
curves of adrenal adenomas and nonadenomas. AJR
Am J Roentgenol. 1998;170;747–52.
5. Dackiw AP, Lee JE, GagelRF, EvansDB. Adrenalcortical
carcinoma. World J Surg. 2001;25:914–26.
6. Pena CS, Boland GW, Hahn PF, Lee MJ. Mueller PR.
Characterization of indeterminate (lipid-poor) adrenal
masses: use of washout characteristics at contrastenhanced CT. Radiology. 2000;217:798–802.
7. Peppercorn PD, Reznek RH. State-of-the-art CT and
MRI of the adrenal gland. Eur Radiol. 1997;7:822–36.
8. Bombardieri E, et al. 131I/123I-metaiodobenzylguanidine (MIBG) scintigraphy: procedure guidelines for
tumour imaging. Eur J Nucl Med Mol Imaging.
2003;30:BP132–39.
9. Kebebew E, Reiff E, Duh QY, Clark OH, McMillan A.
Extent of disease at presentation and outcome for
adrenocortical carcinoma: have we made progress?
World J Surg. 2006;30:872–78.
10. Icard P, et al. Adrenocortical carcinomas: surgical
trends and results of a 253-patient series from the
French Association of Endocrine Surgeons study
group. World J Surg. 2001;25:891–97.
11. Fishman EK, et al. Primary adrenocortical carcinoma:
CT evaluation with clinical correlation. AJRAm J Roentgenol.1987;148:531–35.
12. Barnett CC, Jr., et al. Limitations of size as a criterion
in the evaluation of adrenal tumors. Surgery.2000;128:
973–82;discussion 982–73.
13. Quint LE, Glazer GM, Francis IR, Shapiro B, Chenevert
I-
TL. Pheochromocytoma and paraganglioma: comparison of MR imaging with CT and I-131 MIBG scintigraphy. Radiology. 1987;165:89–93.
14. Dundamadappa SK, et al. Imaging of brown fat associated
with adrenal pheochromocytoma. Acta Radiol. 2007;
48:468–72.
15. Erickson LA, Lloyd RV, Hartman R, Thompson, G.
Cystic adrenal neoplasms. Cancer. 2004;101:1537–44.
16. Lockhart ME, Smith JK, Kenney PJ. Imaging of adrenal
masses. Eur J Radiol. 2002;41:95–112.
17. Renken NS, KrestinGP.Magnetic resonance imagingofthe
adrenal glands. Semin Ultrasound CT MR. 2005;26:162–71.
18. Mitchell DG, Crovello M, Matteucci T, Petersen RO,
Miettinen MM. Benign adrenocortical masses:
diagnosis with chemical shift MR imaging. Radiology.
1992;185:345–51.

357
ADRENAL IMAGING
19. Bilbey JH, et al. MR imaging of adrenal masses: value of
chemical-shift imaging for distinguishing adenomas from
other tumors. AJR Am J Roentgenol. 1995;164: 637–42.
20. Elsayes KM Adrenal masses: mr imaging features with
pathologic correlation. Radiographics. 2004;24(Suppl 1):
S73–86.
21. Semelka RC, et al. Evaluation of adrenal masses with
gadolinium enhancement and fat-suppressed MR imaging. J Magn Reson Imaging. 1993;3:337–43.
22. Sohaib SA, et al. Primary hyperaldosteronism (Conn syndrome): MR imaging findings. Radiology.2000;214:527–31.
23. Rossi GP Imaging of aldosterone-secreting adenomas: a
prospective comparison of computed tomography and
magnetic resonance imaging in 27 patients with suspected
primary aldosteronism. J Hum Hypertens. 1993;7:357–63.
24. Ichikawa T, Ohtomo K, Uchiyama G, Fujimoto H,
Nasu K. Contrast-enhanced dynamic MRI of adrenal
masses: classification of characteristic enhancement
patterns. Clin Radiol. 1995;50:295–300.
25. Mayo-Smith WW, et al. Characterization of adrenal
masses (< 5 cm) by use of chemical shift MR imaging:
observer performance versus quantitative measures.
AJR Am J Roentgenol. 1995;165:91–5.
26. Lee MJ, et al. State-of-the-art MR imaging of the adrenal
gland. Radiographics. 1994;14:1015–29; discussion 1029–32.
27. Heinz-Peer G, Memarsadeghi M, Niederle B. Imaging of
adrenal masses. Curr Opin Urol. 2007;17:32–8.
28. Dunnick NR. Hanson lecture. Adrenal imaging: current
status. AJR Am J Roentgenol. 1990;154:927–36.
29. Francis IR, Gross MD,Shapiro B,Korobkin M, QuintLE.
Integrated imaging of adrenal disease. Radiology.
1992;184:1–13.
30. Gross MD, et al. Scintigraphic evaluation of clinically
silent adrenal masses. J Nucl Med. 1994;35:1145–52.
31. Avram AM, Fig LM, Gross MD. Adrenal gland scintigraphy. Semin Nucl Med. 2006;36:212–27.
32. Fig LM, et al. Adrenal localization in the adrenocorticotropic hormone-independent Cushing syndrome. Ann
Intern Med. 1988;109:547–53.
33. Pietrzyk U, et al. An interactive technique forthree-dimensional image registration: validation for PET, SPECT, MRI
and CT brain studies. J Nucl Med. 1994;35:2011–18.
34. Dey D, Slomka PJ, Hahn LJ, Kloiber R. Automatic threedimensional multimodality registration using radionuclide transmission CT attenuation maps: a phantom
study. J Nucl Med. 1999;40:448–55.
35. Krausz Y, Israel O. Single-photon emission computed
tomography/computed tomography in endocrinology.
Semin Nucl Med. 2006;36:267–74.
36. Gross MD, et al. PET in the diagnostic evaluation of adrenal tumors. Q J Nucl Med Mol Imaging. 2007;51:272–83.
37. Chong S Integrated PET-CT for the characterization of
adrenal gland lesions in cancer patients: diagnostic
efficacy and interpretation pitfalls. Radiographics.
2006;26:1811–24; discussion 1824–16.
38. YunMetal.18F-FDGPETincharacterizingadrenallesions
detected on CT or MRI. J Nucl Med. 2001;42:1795–99.
39. Maurea S, Klain M, Mainolfi C, Ziviello M, Salvatore M.
The diagnostic role of radionuclide imaging in evaluation of patients with nonhypersecreting adrenal masses.
J Nucl Med. 2001;42:884–92.
40. Blake MA, et al. Adrenal lesions: characterization with
fused PET/CT image in patients with proved or suspected malignancy – initial experience. Radiology.
2006;238:970–7.
41. Metser U, et al. 18F-FDG PET/CT in the evaluation of
adrenal masses. J Nucl Med. 2006;47:32–7.
42. Shulkin BL, Thompson NW, Shapiro B, Francis IR, Sisson
JC. Pheochromocytomas: imaging with 2-fluorine-18fluoro2-deoxy-D-glucose PET. Radiology. 1999;212:35–41.
43. Minn H, et al. Imaging of adrenal incidentalomas with
PET using (11)C-metomidate and (18)F-FDG. J Nucl
Med. 2004;45:972–9.
44. Maecke HR, Hofmann M, Haberkorn U. (68)Ga-labeled
peptides in tumor imaging. J Nucl Med. 2005;46(Suppl
1):172S–8S.
45. Shulkin BL, et al. PET scanning with hydroxyephedrine:
an approach to the localization of pheochromocytoma.
J Nucl Med. 1992;33:1125–31.
46. Mann GN, et al. [11C]metahydroxyephedrine and
[18F]fluorodeoxyglucose positron emission tomography improve clinical decision making in suspected
pheochromocytoma. Ann Surg Oncol. 2006;13:187–97.
47. Ilias I, et al. Superiority of 6-[18F]-fluorodopamine
positron emission tomography versus [131I]-metaiodobenzylguanidine scintigraphy in the localization of
metastatic pheochromocytoma. J Clin Endocrinol
Metab. 2003;88:4083–87.
48. Ilias I, Pacak K. Current approaches and recommended algorithm for the diagnostic localization of
pheochromocytoma. J Clin Endocrinol Metab.
2004;89:479–91.

“This page left intentionally blank.”

26
Adrenal Venous Sampling
Radu Mihai and Gregory P. Sadler
Introduction
Interventional radiology has become a
major tool in the localization of endocrine
tumours. Inferior petrosal sinus sampling
for patients with Cushing’s disease, selective parathyroid venous sampling for
patients with persistent hyperparathyroidism, hepatic venous sampling with arterial
stimulation for patients with pancreatic
neuroendocrine tumours and adrenal
venous sampling (AVS) for Conn’s tumors
are currently used in all tertiary endocrine
centers [1].
In the adrenal disease, cross-sectional
anatomical imaging using computer tomography (CT) and magnetic resonance imaging (MRI) can lateralize the side of adrenal tumors in patients with Cushing’s
syndrome, pheochromocytoma or adrenal
cancer. The vast majority of these patients
have tumors located in one adrenal gland
with sufficient size to be identified by the
above scans. The contralateral gland is
usually atrophic or of normal size. In contrast, patients with primary hyperaldosteronism (PHA) have small tumors, frequently
less than 20 mm, that can be difficult both
to demonstrate and to differentiate from
other nonfunctioning benign adrenal adenomas.
Anatomy of Adrenal Venous
Drainage
Adrenal glands receive arterial supply from
numerous small branches from the phrenic
artery, renal artery, and aorta. These branches
create a plexus of capillaries under the adrenal
capsule from which blood drains through the
adrenal cortex into small venous branches collecting finally into a single central adrenal vein.
On the right side, a short adrenal vein drains
directly into the vena cava. Additional small
branches can sometime be present. On the left
side, the adrenal vein drains into the renal vein.
Indications for AVS
The most common indication for AVS is the
need to demonstrate unilateral excessive aldosterone secretion in patients with PHA, thus
localizing the tumor. Rarely AVS may be used
in patients with biochemical diagnosis of
phaeochromocytoma in whom conventional
radiology demonstrates bilateral micro or
macro modularity. In a minority of such
patients only one adrenal gland is the source of
excessive catecholamine secretion and they can
be potentially spared having to undergo a bilateral adrenalectomy if unilateral hypersecretion
can be demonstrated.
J.G.H. Hubbard et al. (eds.), Endocrine Surgery, Springer Specialist Surgery Series,
DOI 10.1007/978-1-84628-881-4_26, Ó Springer-Verlag London Limited 2009
359
Соседние файлы в папке Библиотека им академика М.И. Перельмана
