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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_808_Библиотеки_им_академика_М_И_Перельмана.pdf
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- •Preface
- •Contents
- •1.1 Introduction
- •1.2 Hypothyroidism
- •1.8 Thyroid Cancer
- •1.9 Non-thyroidal Illness (NTI)
- •1.10.1 Congenital Hypothyroidism
- •1.10.2 Consumptive Hypothyroidism
- •1.10.3 Juvenile Autoimmune Hypothyroidism
- •1.12 Post Thyroidectomy Considerations
- •References
- •2: Solitary Thyroid Nodule
- •2.1 Introduction
- •2.2 Clinical Evaluation
- •2.3 History
- •2.4 Physical Examination
- •1.3 Iodine Deficiency
- •1.4 Hyperthyroidism
- •1.5 Subclinical Thyroid Disease
- •1.6 Thyroiditis
- •1.7 Goitre
- •2.6 Serum Thyroglobulin
- •2.7 Serum Calcitonin
- •2.8 Radiological Evaluation
- •2.8.1 Thyroid Ultrasonography
- •2.8.2 Radioisotope Imaging
- •2.11 Cytological Evaluation
- •2.12 Molecular Assessment
- •2.14.1 Preparation
- •2.17 Summary
- •References
- •References
- •4.2 Ectopic Thyroid
- •4.3 Thyro-thymic Rests
- •4.5 The Nerves at Risk During Thyroidectomy
- •4.6 The Recurrent Laryngeal Nerve
- •4.9 Blood Supply
- •4.11 Parathyroid Glands
- •4.12 Lymphatic Drainage
- •4.13.2 Regulation
- •4.13.3 Actions
- •4.16 Actions
- •References
- •5: Pre-operative Counselling
- •6.1 Introduction
- •6.3 Immediate Post-operative Period
- •6.6 General Instructions
- •References
- •7: Central Compartment Lymph Node Dissection
- •Reference
- •8.1 Introduction
- •8.3 Postoperative Care
- •Reference
- •9: Trans-oral Endoscopic Thyroidectomy via Vestibular Approach (TOETVA)
- •9.1 Introduction
- •9.3 Preoperative Evaluation
- •9.5 Postoperative Care
- •9.6 Outcome
- •9.7 Operative Safety
- •9.8 Conclusion
- •References
- •10: Robotic Thyroidectomy
- •10.1 Introduction
- •10.3 Indications
- •10.4 Contraindications
- •10.4.1 Relative
- •10.4.2 Absolute
- •10.5.1 Retro-auricular approach—Robotic thyroidectomy
- •10.5.1.1 Surgical Equipment
- •10.5.2 Trans-axillary/Breast Approach
- •10.5.2.1 Surgical Equipment
- •10.5.3 Robotic trans-oral thyroidectomy
- •10.6.1 Postoperative Pain
- •10.6.2 Recurrent Laryngeal Nerve Injury
- •10.6.3 Brachial Plexus Injury
- •10.6.4 Hypoparathyroidism
- •10.6.5 Bleeding and Hematoma
- •10.6.6 Voice and Swallowing Function
- •10.6.7 Paraesthesia
- •10.6.8 Cosmetic Satisfaction
- •10.6.9 Complications Specific to Trans-Oral Approaches
- •10.7 Economic Parameters
- •10.7.1 Peri-Operative Time
- •10.7.2 Hospital Stay
- •10.7.3 Cost
- •10.8 Oncological Outcomes
- •10.8.1 Completeness of Resection
- •10.8.2 Lymph Node Retrieval
- •10.8.3 Survival and Recurrence
- •10.9.1 Visualisation
- •10.9.2 Dexterity
- •10.9.3 Retraction
- •References
- •11.1 Introduction
- •11.2 Hypocalcaemia
- •11.4 Wound Infection
- •11.4.2 Laryngotracheal Oedema
- •11.5 Oesophageal Injury
- •11.5.1 Thoracic Duct Injury
- •11.5.2 Thyroid Storm
- •11.6 Tracheomalacia
- •10.9.4 Precision
- •10.9.5 Surgeon Ergonomics
- •10.10.1 Cost
- •10.10.2 Learning curve
- •10.10.3 Lack of haptic feedback
- •10.10.4 Operative time
- •10.12 Conclusions
- •References
- •12.1 Introduction
- •12.2 Recurrent Laryngeal Nerve (RLN)
- •12.4 Unilateral Vocal Fold Paralysis
- •12.5 Bialteral Vocal Fold Palsy
- •12.8 Clinical Features
- •12.9 Treatment
- •References
- •13.1 Introduction
- •13.2 Post-operative Care
- •13.2.1 Immediate Post-operative Management
- •13.2.2 Post-operative Management
- •13.2.3 Antibiotics
- •13.2.4 Pain Relief
- •13.2.5 Ice Pack Dressing
- •13.2.6 Head End Elevation
- •13.2.7 Drain
- •13.2.8 Hypocalcaemia
- •13.2.9 Levothyroxine Dose
- •13.2.11 Discharge Advice
- •13.2.12 Follow-Up
- •References
- •14.1 Historical Perspective
- •14.2 The Poorly Differentiated Thyroid Carcinoma (PDTC)
- •14.3 Undifferentiated Thyroid Cancer (UTC)
- •14.3.1 Risk Stratification
- •14.6 Tracheal Infiltration
- •14.6.2 Recurrent Laryngeal Nerve (RLN)
- •14.6.4 Locoregional Recurrence
- •14.7 Conclusion
- •References
- •15.1 Introduction
- •15.2 Aetiology
- •15.3 MEN 2B
- •15.3.1 RET Proto-Oncogene
- •15.4.1 Tumour Markers
- •15.4.2 Rearranged During Transfection (RET) Testing
- •15.4.4 Surgical Management
- •15.4.5 Postoperative Management
- •15.5 Conclusion
- •References
- •16.1.1 Radiopharmaceuticals [1]
- •16.1.3.3 18F Fluorodeoxyglucose, FDG
- •16.2 Thyroid Scintigraphy
- •16.2.2 Camera Method
- •16.2.2.2 Procedure
- •16.2.2.3 Interpretation
- •16.2.3 Amiodarone Induced Thyrotoxicosis (AIT)
- •16.2.6 Congenital organification Defect Evaluation—Perchlorate Discharge Test
- •16.3 Thyroid Nodule Evaluation
- •16.3.2 FDG PETCT Imaging
- •16.4.1 Indications
- •16.4.4 Complications
- •16.5.2 Patient Preparation
- •16.5.3 Scan Procedure
- •16.5.3.1 Interpretation
- •16.5.5 Radiation Safety Precautions
- •16.5.9.2 Carcinogenicity
- •16.5.9.3 Iodine Refractory Thyroid Cancer [18]
- •16.5.9.4 Martinique Principles
- •16.6.1 Introduction
- •16.6.3.1 Imaging Protocols
- •16.6.3.2 Patient Preparation
- •16.6.3.3 Procedure
- •16.6.3.4 Interpretation
- •16.6.7 Gamma Probe Guided Parathyroidectomy [22]
- •16.7 Conclusion
- •References
- •17.1 Introduction
- •17.2.1 Variations
- •17.3 Calcium Metabolism
- •17.4.1 Adenoma
- •17.4.2 Hyperplasia
- •17.4.3 Carcinoma
- •17.5 Hyperparathyroidism
- •17.5.1 Primary Hyperparathyroidism
- •17.5.2 Secondary Hyperparathyroidism
- •17.5.3 Tertiary Hyperparathyroidism
- •17.5.3.1 Primary Hyperparathyroidism
- •17.5.3.2 Neonatal Hyperparathyroidism
- •17.5.3.3 Familial Hypocalciuric Hypercalcemia
- •17.5.4 Familial Hyperparathyroidism
- •17.5.6 Hypoparathyroidism
- •17.5.7 Pseudohypoparathyroidism
- •17.6 Primary Hyperparathyroidism (PHPT)
- •17.6.1 Clinical Manifestations
- •17.6.1.2 Arterial Hypertension
- •17.6.1.3 Cardiovascular Disease
- •17.6.2.1 Biochemical
- •17.8 Localization Studies
- •17.8.1 Non-Invasive Localization
- •17.8.2 Scintigraphy
- •17.8.2.1 Technetium99 Sestamibi Scan
- •17.8.2.2 Positron Emission Tomography
- •17.8.3 Computed Tomography
- •17.8.4 Magnetic Resonance Imaging
- •17.8.5 Invasive Localization
- •17.8.6 Intraoperative Localization
- •17.8.6.1 Radio Guided Surgery
- •17.8.6.2 Intraoperative Ultrasound
- •17.8.6.3 Methylene Blue
- •References
- •18.1 Introduction
- •18.2 MEN 1
- •18.3 MEN 2
- •18.4 Conclusion
- •References
- •19.1 Secondary Hyperparathyroidism (SHPT)
- •19.3.1 Bricker’s Trade-off Hypothesis
- •19.3.3 Medical Treatment
- •19.4 Tertiary Hyperparathyroidism
- •19.5 Refractory Hyperparathyroidism
- •19.6.2 Preoperative Management
- •19.6.3 Post-operative Management
- •19.6.4 Hungry Bone Syndrome
- •19.7 Post-transplant Hyperparathyroidism
- •References
- •20.1 Introduction
- •20.2.1 Parathyroid Hormone Assay
- •20.2.2 Intra-Operative PTH Assay
- •20.2.3 Localization Studies
- •20.2.3.1 Radio-Guided Parathyroidectomy
- •References
- •21: Parathyroidectomy: Surgical Techniques
- •21.1.1 Preoperative Counselling
- •21.1.2 Desirable Additional Supports
- •21.4 Tertiary Hyperparathyroidism
- •21.4.1 Parathyroid Auto-transplantation
- •21.4.2 Intraoperative PTH Assay
- •21.4.3 Intraoperative Localization
- •21.4.4 Radio-guided Parathyroidectomy
- •21.4.5 Mini-parathyroidectomy
- •21.4.6 Postoperative Management
- •21.4.7 Hungry Bone Syndrome
- •21.5 Complications
- •References

218
Table 16.2 Scintigraphic uptake patterns in thyrotoxicosis (ndings are similar in Tc04 and
iodine scans)
Etiology Uptake patterns
Graves’ disease Diffuse increased uptake (homogenous) in both lobes of thyroid gland.
SG not seen/faintly seen. Uptake >4%
Toxic hot nodule (Autonomous) Increased uptake in nodule with suppression of
surrounding normal thyroid tissue. SG may be normally seen/reduced
uptake
Toxic MNG
(Multinodular
Goiter)
Nontoxic MNG Enlarged thyroid gland with multiple cold nodules, usually
Subacute thyroiditis The thyroid will be faintly visualized (depending on the duration/
Chronic thyroiditis
(Hashitoxicosis)
Factitious
thyrotoxicosis
(excess thyroxine
intake)
Secondary causes
(elevated TSG,
HCG)
Ectopic thyroid
tissue
SG Salivary gland
Multiple hot nodules are interspersed with cold nodules. SG faintly seen
nonfunctioning. In patients with additional thyroiditis (biochemically
detected hyperthyroidism), the gland may be faintly seen, and, nodules
if any, may not be apparent. In this situation, apart from the 99mTc04
scan, the I
Cold nodule in Tc scan and hot nodule in iodine scan, suspicious for
malignancy
severity of disease, i.e. nearly recovered case will show uptake close to
1% (normal 1–4%). Mimicking picture seen also with exogenous iodine
interference like homeopathic drugs/oral or iodinated contrast agents
Only serial imaging can differentiate this disease entity along with
biochemical evidence of waxing/waning thyrotoxicosis. Usually,
Hashimoto’s thyroiditis in hypothyroid status will show reduced uptake,
but in toxicosis, the phase will simulate the GD uptake pattern
Generalized reduced uptake (needs to be correlated with a history of
drug intake)
Increased uptake localized to ectopic sites such as pelvis/adnexa, etc.
Focal tracer uptake in lingual/sub hyoid or other ectopic sites. Uptake
may be focal normal or reduced. SG will be normally seen (Fig.16.2)
131
scan is also suggested to look for functioning nodules.
P. S. Sundaram et al.
Scintigraphy characterizes the exact cause of hyperthyroidism and helps to formulate the treatment protocol. There are however no differences in thyroid scintigraphic ndings in children compared to adults.
16.2.2.4 Scintigraphic Patterns inDifferent Thyroid Pathologies
(Table16.2)
1. Normal pattern: Structurally and functionally normal thyroid is known to have
as buttery-shaped appearance in the anterior neck at midline with homogenous
tracer distribution. Parotid uptake of
99m
Tco4 is at par with par with thyroid
uptake. Isthmus is a normally a thin bridging tissue and is occasionally visualized in scintigram. The pyramidal lobe may be seen in around 10% of patients.
The uptake is estimated by comparison with the degree of thyroid trapping with

16 The Role ofNuclear Medicine inThyroid andParathyroid Disorders
219
that in the salivary gland (NIS glycoprotein expression). The normal trapping
function is 1%–4%. Suprasternal notch is marked and the retrosternal extension
also is clearly seen in the imaging.
2. Vascular status: Generally thyroid gland is highly vascular and is evidenced by
the increased trapping of the radiotracer. The vascularity of the gland in Graves’
disease is high and adds on to increased trapping ability of the follicular cells.
Thyrotoxicosis due to thyroiditis (viral or autoimmune) will display generalized
reduced vascularity.
3. Graves’ disease (GD): The scintigraphic appearance in Graves’ disease is char-
acterized by intense homogenous concentration in comparison with parotid
glands. The intensity of concentration is proportional to severity of the disease
and the trapping ability will always be more than 4%. The pyramidal lobe and
the isthmus are visible in the scintigram and if thyroid tissues are present in
thyroglossal tract shall be lighted in the scintigram. The trapping function is
blunted when patient is on antithyroid drugs and exogenous iodine
supplementation.
Graves’ disease with Marine Lenhart syndrome: The fundamental reason
of hyperactivity of follicular cells in Graves’ disease is stimulating TSH receptor
antibodies and the cells are no longer under control of TSH.The occasional presence of TSH-sensitive nodules coexisting in Graves’ disease was rst described
1911 by Marine and Lenhart. This rare association is known as Marine, Lenhart
syndrome and has a 2.7–4% incidence. Thyroid scan shows poorly functioning
or cold nodules scattered in bright areas. Presence of such nodules indicates
uncertain outcomes following radioiodine ablation. They are found to be slightly
resistant to
131
I therapy and need a larger dosage of
131
I when compared to GD
patients without nodules.
4. Toxic multinodular goiter (Plummer disease): The disease is characterized by
autonomous areas and nodules developing in nodular goiters. Thyroid scan
shows heterogeneous appearance with patchy areas of intense concentration and
cold areas. The overall trapping ability shall exceed 4%.
5. Nontoxic multinodular goiter: The scan shows a large volume goiter with scat-
tered areas with cold/warm nodules. Usually, thyroid uptake will not be more
than 4%.
6. Subacute (viral) thyroiditis: The initial clinical presentation is usually due to
symptoms related to thyrotoxicosis with local pain at the region of thyroid
gland. Dynamic imaging shows decreased vascularity and static image reveals
poor trapping of radiotracer. The pattern of tracer uptake depends upon the
phase of viral activity; acute phase, resolving phase, or chronic phase. Proper
clinical assessment is absolutely essential for arriving at a correct diagnosis.
Patients on iodine-containing drugs may also reveal a similar scintigraphic
picture.
7. Autonomous toxic nodule: The situation is characterized as autonomously
functioning thyroid nodule, the rest of the gland being suppressed. Unless the
nodule is large to cause cosmetic disgurement radioiodine ablation gives very
good response.

220
P. S. Sundaram et al.
16.2.3 Amiodarone Induced Thyrotoxicosis (AIT)
Amiodarone is a popular drug in the management patients with cardiac rhythm
abnormalities. The drug is rich in iodine and is inuence thyroid function due to
the high iodine load. Amiodarone contains about 37% iodine by weight and the
patient on daily dose of 200 mg, ingests 75mg of organic iodine. The drug undergoes further metabolic degradation releasing more iodine, approximately 6mg of
free circulating iodine. Ultimately the patient receives about 20–40 times higher
amount iodine daily. The clinical effects of amiodarone on thyroid function are
both related hypothyroidism and hyperthyroidism. Amiodarone-induced hypothyroidism (AIH) is common in iodine sufcient population [7]. AIT is prevalent in
iodine-decient populations; with Hashimoto’s thyroiditis being an important risk
factor. Type I AIT usually occurs in patient with subclinical autoimmune thyroid
disorder leading on to developing overt Graves’ disease. Type II is toxic manifestations due to cellular destruction induced by excess iodine and later becomes
hypothyroid. A combination of both types is not unusual (Type I, II, mixed).
Amiodarone induced thyrotoxicosis has to be properly diagnosed and treated
since thyrotoxicosis itself induces cardiac arrhythmias. Discontinuation of amiodarone with proper substitute is ideal and scintigram is good tool to make proper
diagnosis (Table16.3).
16.2.4 RAIU Studies: Radioactive Iodine Uptake Studies Using
Thyroid Uptake Probe
A miniature gamma camera with sodium iodide crystal otherwise called the Gamma
Probe is now in wide use. This cylindrical or conical shaped collimator mounted on
a stand and helps to calculate the uptake quantitatively and helps to calculate the
thyroid uptake in counts with the help of a computer software. There is no image
and the report is interpreted as counts per minute (cpm).
Indications:
1. This probe helps to iodine uptake in low dose
2. Probe helps to calculate the dosage of
131
3. As a diagnostic tool to differentiate Graves’ disease from subacute thyroiditis or
factitious hyperthyroidism.
The probe is also useful in management of differentiated thyroid carcinoma
(DTC) for assessment of regional and distant metastases. But the procedure can
be done with radioiodine (
125/131
I) given as 10-25 micro-Ci capsules, and no
images are obtained. The number of counts emanating from the thyroid gland is
recorded over a specied period of time to determine the functional status of the
gland. The uptake study gives information of percentage of administered
thyroid over a specied period.
131
I therapy in Graves’ disease.
I for low dose therapy.
131
I

16 The Role ofNuclear Medicine inThyroid andParathyroid Disorders
Table 16.3 Differentiation of Type I and II amiodarone induced thyrotoxicosis
Type I
Underlying thyroid
disease
Incidence 68% Remaining
Time after starting
amiodarone
Cause Sudden iodine load increases thyroid
24-h iodine uptake Low–normal (may be high in
USG ndings Diffuse may be nodular A normal or small gland
99m
TcO4
Scintigraphic
ndings–vascularity
99m
TcO4
Scintigraphic
ndings—static
images
T4/T3 ratio Usually, <4 Usually, >4
Tg AB/TPO ab/TSI Maybe present Usually, absent
Circulating
interleukin 6
99m
Tc MIBI ndings Goiter noted (GD/MNG) Outlines of gland delineated
Therapy Treat primary disease with low dose
Yes No
Short (median 3 months) Long (median 30 months)
hormone production in autonomous
thyroid tissue—Jod-Basedow
phenomenon
iodine-decient regions)
Increased Absent
The pattern of GD/MNG Gland not visualized
Normal to high Frequently markedly elevated
131
I
therapy
Type II
Direct toxic effect of the drug
on normal thyroid gland
resulting in subacute and
destructive thyroiditis
Low to suppressed
(even though no uptake on
99m
Tco4 scan)
Self-limiting on stoppage of
drug, supportive with NSAID,
steroids
221
16.2.5 Special Indications for
131
I Scintigraphy inBenign
Thyroid Diseases
1. The diagnosis of mediastinal primary goiter.
2. Diagnosis of functioning thyroid tissue in ectopic locations like Struma ovarai.
3. Congenital defect in organication of iodine.
16.2.6 Congenital organification Defect Evaluation—Perchlorate Discharge Test
Defect in organication of iodine is cause of congenital hypothyroidism and is evidenced in the rst few months of life. Laboratory studies show markedly elevated
TSH.The diagnosis is conrmed with perchlorate discharge test

222
Table 16.4 Camera method—scintigraphic uptake patterns in congenital organication defects
Diagnosis
Normal patient Homogenous tracer uptake Retained homogenous
Partial organication
defect
Complete
organication defect
Agenesis No uptake No uptake
(Table 16.4). Tracers used for this test are
tracer is
131
I.
Initial scan ndings
Homogenous/inhomogeneous tracer
uptake will be seen
Homogenous/inhomogeneous tracer
uptake will be seen
131
99m
I or
Tc04, but the recommended
P. S. Sundaram et al.
Delayed scan ndings
tracer uptake
>10% clearance of tracer
>90% clearance of tracer
(washout)
Perchlorate is a NIS inhibitor and in normally functioning thyrocytes, oral perchlorate (500–1000mg) challenge does not induce the clearance of tracer from the
thyroid gland. The is delayed when challenged with oral perchlorate a reduction in
thyroid tracer uptake by more than 10% in imaging after 1–2 h indicates a partial
defect. Iodine discharge more than 90% is considered total defect of iodide
organication.
But when
image at 60min are gathered. An additional
99m
TcO4 is used as tracer, an initial image at 10min and a delayed
99m
Tc MIBI thyroid scan may highlight
the presence or absence of native thyroid, uninuenced by thyroxine/presence of
stable iodine in the body pool.
16.3 Thyroid Nodule Evaluation
The challenge in routine evaluation of thyroid nodule is detection of neoplastic nodules. Thyroid scintigrams differentiate a functioning and nonfunctioning nodules and
functioning nodules are usually benign. Based on the scintigram the nodules which
fail to concentrate tracer are called cold and hot when the concentration is more than
surrounding area. A nodule with concentration of tracer similar to that of surrounding
area is called warm nodule. Nonfunction nodule has a higher risk for malignancy and
aspiration cytology is routinely done. Coupling with high resolution ultrasound imaging enhances the accuracy and also helps to take targeted cytology.
16.3.1 Tracers Used forThyroid Nodule Evaluation
99m
1.
99m
2.
99m
3.
4. 18F FDG PET—18 Fluorodeoxyglucose
5. 68Ga DOTA PET—somatostatin (SST) analogs labeled with 68Gallium
6. 18F DOPA—Fluorine-18-dihydroxyphenylalanine
ever, it is used in US and European Union countries for evaluation of nodules >
10mm size regardless of TSH levels [8].
131I/123
Tc O4/
Tc MIBI (SestaMIBI)/
I
99m
Tc Tetrofosmin/
Tc DMSA (V)—dimercaptosuccinic acid
Generally,
99m
Tc4 thyroid scan is recommended when the TSH is low how-
201
Thallium

16 The Role ofNuclear Medicine inThyroid andParathyroid Disorders
223
Indications for MIBI thyroid scan in evaluation of thyroid nodule:
MIBI concentrates in metabolically active tissues and is used as a tracer in neo-
plastic thyroid nodules.
1. Thyroid scan with MIBI as tracer helps to locate the nodule in the hyper func-
tioning thyroid gland.
2. MIBI scan also helps to characterize USG detected suspicious thyroid nodule.
3. MIBI scan is also used as part of evaluation of amiodarone-induced thyrotoxico-
sis (AIT).
4. MIBI scan could be part of evaluation of nodules with indeterminate cytology
(Bethesda III and IV).
16.3.2 FDG PETCT Imaging
A uorodeoxyglucose positron emission tomography (FDG-PET) is now popular imaging used in assessment of extent of many malignancies. Now the imaging has applications in many elds other than malignancy. The imaging is usually performed using
vendor-specied simultaneous PET CT protocol. The image acquisition can be of the
whole body or region specic according to the need. Ideally the patient is fasting overnight and the blood sugar level <150mg/dL and serum creatinine levels within the normal ranges. The CT scan image acquisition precede the FDG administration.
FDG-PET imaging is not routinely performed as part of thyroid nodule evaluation.
But a nodule incidentally detected on PET scan done for other indications stand higher
chances of malignancy [9]. 18F FDG accumulates in neoplastic cells which use glucose as the source of energy source in proliferative activity. But FDG PET-CT is able
to identify and characterize with accuracy small thyroid nodules (i.e., ≥5mm) and
also cytological indeterminate thyroid nodule [10]. The 18F FDG PETCT scores over
the qualitative
FDG-PET is on regular use in assessment of advanced differentiated and poorly differentiated thyroid carcinoma especially when
distant metastases in the presence of elevated thyroglobulin levels.
Introduction of newer tracers like 18F-DOPA, 68Ga DOTATATE has widened the
scope of the evaluation of thyroid nodules with Medullary Thyroid Cancer (MTC).
However, neuroendocrine tumors (NETs), including MTC, have low proliferation
index and so has low 18F-FDG uptake. 68Ga-DOTATATE- PET-CT is useful in detection of recurrent MTC demonstrating a signicantly higher number of lesions.
99m
Tc MIBI scan in predicting risk of malignancy in thyroid nodules.
131
I scan fail to localize regional or
16.4 Low Dose
Conventionally, the term low dose
treat hyperthyroidism (dosage range 5–15mCi); while high dose
the use of
toxicosis management for over six decades. However, dosage of
131
I in dosage above 30mCi for DTC management.
Ablation using
131
I Therapy forHyperthyroidism
131
I therapy denotes oral administration of
131
I established economical, safe, and effective treatment thyro-
131
I therapy denotes
131
I for effective
131
I to
treatment of Graves’ disease remains controversial. Despite the wide spread usage

224
P. S. Sundaram et al.
of the radioactive iodine, few controversies exist in selection of patients, goal of
therapy, and dosage schedule.
16.4.1 Indications
1. Graves’ disease (GD)
2. Toxic multinodular goiter (TMNG)
3. Autonomously functioning toxic nodule/s (ATN)
16.4.2 The Goal ofLow Dose
131
I Therapy [11]
The debate over the aim of treatment was whether to make the patient euthyroid or
to make him hypothyroid. However, the wider accepted protocol is to administer a
dose of
131
I dosage to render patients euthyroid is not always possible and a higher
dose to render the patient hypothyroid is more practical.
Selection Criteria:
1. Ensuring iodine avidity by a
99m
TcO4 thyroid scan or RAIU study is
recommended.
99m
2. A
TcO4 thyroid scan or RAIU study will exclude the other forms of thyrotoxi-
cosis such as viral thyroiditis and factitious thyrotoxicosis.
The low dose
131
I therapy as a primary treatment for hyperthyroidism was found
more effective than following anti-thyroid drugs (ATD) failure [12] probably due to
drug induced impairment of follicular cell activity. Propyl Thiouracils have lasting
effects on the cells even after the drug is withdrawn for 15 days. Generally, antithyroid drugs are withdrawn at least 5–7 days before low dose
131
I therapy (a minimum of 5 days for methimazole and 3 days for propylthiouracil) and are restarted 7
days after treatment.
The success rate of one sitting of low dose
131
I therapy for hyperthyroidism management is 93% in our institute with adequate patient preparation. A second or third
doses are required in high volume glands and those with orid Graves’ disease
evidenced by a high technetium trapping function. Hypothyroidism sets in due
course of time and levothyroxine supplementation is essential.
Patients with Graves’ ophthalmopathy may worsen following
131
I therapy. It is not
unusual to develop ophthalmic complications following ablation. When Graves’ ophthalmopathy is suspected a proper ophthalmology assessment to assess the clinical
activity score is mandatory before scheduling for low dose
in a dose 0.5mg to 1mg/kg body weight started a week before low dose
131
I therapy. Systemic steroid
131
I therapy and
is continued for 3–4 weeks as a prophylaxis against worsening of ophthalmopathy.

16 The Role ofNuclear Medicine inThyroid andParathyroid Disorders
225
16.4.3 Methods ofCalculating
131
I Therapy
1. The dosage of
131
I calculated based on volume of the thyroid gland calculated by
131
I Dosage forLow Dose
ultrasound imaging.
2. Otherwise, a xed empirical dosage is given.
There is no signicance evidence supporting dosage calculated has superiority
over the xed dose regimen. Majority of patients receiving low dose therapy ends
up in hypothyroid state irrespective of the dosage schedule adopted and a xed dose
regimen is convenient to follow.
Ideally, 150–300Gy (gray) radiation absorbed dose needs to be delivered to
thyroid tissue for exerting cytotoxicity and get successful ablation in hyperthyroidism. The
131
I dosage necessary to deliver the above radiation effect is ideally 160
microCi per gram of thyroid tissue. The routine practice followed in our Institution
a xed dosage protocol as noted below.
Graves’ disease: 8–10mCi
Toxic MNG: 10–15mCi
Autonomous toxic nodule: 15–20mCi
The radiopharmaceutical is administered orally as a single dose and the patient
report after overnight fasting. The procedure is conducted as a day procedure and
the patient is instructed to restart the antithyroid medications a week after. The
patient is reviewed after 6–8 weeks later and thyroid function is estimated after
discontinuing antithyroid medications for a week. In case of resolution of hyperthyroid state and hypothyroidism has set in levothyroxine supplementation is started.
Those who show persistence of hyperthyroid state need additional doses of
131
which is planned 8–12 weeks after the initial ablation.
I
16.4.3.1 Factors Affecting theClinical Outcome
Patient characteristics such as gender and age, disease severity, and goiter volume
are the common features inuencing the outcome. Discontinuing antithyroid medications for a minimum period one helps to achieve a better outcome.
16.4.3.2 Low Dose
Generally, the use of
few centers have treated children with radioiodine. The dosage of
131
I Therapy inChildren
131
I is not recommended in children with Graves’ disease but a
131
I has to be
adjusted with reference to the clinical and biochemical severity, and body mass
index. Hypothyroidism almost always sets in with a dose more than 200–250Gy
(220–275microCi/g). The size of the gland is a signicant predictor of predictor
with large volume goiter>80g. Usually,
131
I therapy is avoided in children <5 years.

226
16.4.4 Complications
P. S. Sundaram et al.
The common side effects include nausea, neck pain.
Side effects of low dose
131
I therapy are transient and include nausea, mild neck
pain lasting for few days. Thyroid storm had been reported rarely 1–14 days post-
131
I administration in patients with severe, uncontrolled hyperthyroidism and very
large goiters. Worsening of ophthalmopathy has been reported in a small percentage
of adults who have received
131
I, but now is controlled by prophylactic steroid.
Symptoms of hyperthyroidism if any in the interval period can be readily controlled
with adequate use of beta-blockers (usually oral metoprolol 20–40mg per day).
16.5 High Dose
131
I Therapy inDifferentiated
Thyroid Carcinoma
Since the DTC cells retain iodine avidity to certain extent
vant in the management of these cancers following thyroidectomy. The term high
131
dose
I ablation aims to destroy locoregional residual tissues and high dose therapy
aims at locoregional or distant metastases. Distant metastases from DTC at any
location can be treated with high dose therapy.
16.5.1
131
I Therapy Indications inDTC [13]
1. Gross extrathyroidal extension or incomplete tumor resection regardless the size
of the tumor.
2. Primary tumor size more than 4cm regardless of age.
3. When distant or regional metastases are conrmed irrespective of the size of
primary tumor.
4. DTC patients of age more than 45 years.
5. Presence of tumor invasion to the perithyroidal soft tissues.
6. Papillary tumor with aggressive histological subtypes.
7. Patients with
131
I concentrating distant metastases (lymph node, pulmonary, and
skeletal).
8. Patients who has inoperable residual disease.
131
I is widely used adju-
16.5.2 Patient Preparation
The uptake of
are starving. Serum TSH level≥30μIU/L enhances uptake of iodine by an increased
NIS expression and the hypothyroid state is achieved in 3 weeks after thyroidectomy. If the patient is on levothyroxine (LT4) discontinuation for 3–4 weeks is necessary. Such severe hypothyroid state is intolerable to a few patients and in those
patients Recombinant human TSH (rhTSH) is an alternative. Recombinant human
131
I depends upon the TSH and low serum iodine where by the cells

16 The Role ofNuclear Medicine inThyroid andParathyroid Disorders
227
TSH (rhTSH) is a genetically engineered molecule containing thyrotropin Alfa
(0.9mg in each vial) (Thyrogen by Genzyme). The molecule is commercially available vials containing 1.1mg of thyrotropin Alfa, 36mg Mannitol, 5.1mg sodium
phosphate, and 2.4mg sodium chloride. The drug is reconstituted prior to use with
1.2 mL of sterile water to deliver 1 mL injection from each vial. One milliliter
reconstituted medication is injected intramuscularly in the gluteal region followed
by the second injection 24 h later. There are no major side effects except for an
occasional mild u-like symptoms. The common recommendations for rhTSH
include for those patients intolerable to hypothyroid state, other major illness preventing a hypothyroid state and extensive functioning metastases [14].
16.5.3 Scan Procedure
Pre-therapy scan indicates a preliminary scan done after administering 2–3 mCi of
131
I which shall expose the disease status. Images of anterior neck and whole body
are collected. The argument against this procedure is possibility of stunning of follicular cells when the actual ablative dose of
dose of ablation is administered a smaller dose of 2–3 mCi of
131
I is administered. Before the full
131
I given and images
are acquired and the procedure is called pre-therapy scan. The chances of stunning
are minimalized by the dose not exceeding 5 mCi.
16.5.3.1 Interpretation
There is physiological uptake of iodine in extra-thyroidal regions such as salivary
glands, breasts, and stomach. The absorbed iodine is metabolized in liver and
excreted through the urinary system and so liver and urinary tract are also visible in
whole body scan. When the pre-therapy scan shows no signicant residual tissue
and the serum thyroglobulin levels are also low the patient may there is no need for
ablation. False-positive
131
I uptake may be encountered in inammatory, cystic,
non-thyroid neoplastic disorders, for example, pleural or pericardial effusions;
aspergilloma, arthritis; ovarian or breast cysts (Figs.16.3 and 16.4).
Usually,
131
I uptake in nasopharynx, esophagus, smearing of urine in pelvis/any
other sites of contamination is recognized easily by experienced specialists, and
repeat imaging after decontamination claries the case. Stunning is the phenomenon of low or absent uptake of
131
I by residual or metastatic tissue due to previous
iodine loading.
16.5.4 Nuclear Medicine Algorithm ofManagement ofDTC
[15, 16]
Conventionally, 3–4 weeks after total thyroidectomy, a residual thyroid and whole
body (low dose)
thyroid tissue. In presence of residual thyroid tissue, as per risk stratication,
patients undergo
131
I scintigraphy is performed to assess the presence of residual
131
I residual thyroid ablation/therapy. Two important determinants
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