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33 Pitfalls andPearls inEndoscopic Sinus Surgery
369
33.4.6 Frontal Sinus (Figs.33.11 and33.12)
The frontal recess dissection is always a challenge
to the surgeon [7–9] and it is considered as an
advanced step in sinus surgery. In order to achieve
the best outcome and avoid injury to the vital
structures in the region “orbit and skull base” the
surgeon has to be familiar with the frontal recess
anatomical variation. Recurrence of diseases in
the frontal sinus maybe due to either iatrogenic
Fig. 33.11 CT scan of paranasal sinuses showing the
frontal sinus (FS)
injury of the delicate frontal sinus pathway or
incomplete excentration of the disease itself. The
frontal recess is an hourglass shape pathway
bounded anteriorly by posterior wall of agger
nasi, posteriorly by bulla ethmoidalis, medially by
middle turbinate, and laterally by lamina papyracea. Before starting the dissection of frontal
recess, certain point should be accomplished
which is to keep a well-mucosalized frontal recess
to avoid postoperative scarring and neoosteogenesis. Angled instruments (like Hosemann, giraffe,
Bachert, and mushroom forceps) and endoscopes
are essential to success the surgery.
Frontal sinus surgery can be classied according to Wolfgang Draf’s into:
• draf 1: It comprises of anterior ethmoidectomy without touching the natural ostium.
• draf 2a: It is also called uncapping the egg. It
comprises of removal of all ethmoidal cells
that encroach the frontal recess like agger
nasal and the other fronto-ethmoidal cells
between the lamina papyracea laterally and
middle turbinate medially.
• draf 2b: It comprises of removal of the frontal
sinus oor between the lamina papyracea and
nasal septum.
• draf 3: It comprises of drainage of both side
through removal of the oor of frontal sinus
from orbit to orbit with removal of part of the
upper nasal septum (modied Lothrop
procedure).
Fig. 33.12 Endoscopic picture after dissecting the fron-
tal recess and the appearance of frontal sinus (FS)
Choosing between these depends on the
degree of disease extension. Approaching frontal
recess can be done either after completing uncinectomy, MMA, (anterior and posterior) ethmoidectomy and sphenoidotomy or from the
rst remove the uncinate and identify the recess,
then complete the remaining dissection. In the
rst approach, the aim is to identify the skull
base at the level of sphenoid sinus, then follow it
in post- ant direction till nding the anterior ethmoidal artery; this is done by using angled telescope (70° scope is highly useful in this step).
An important landmark to locate the artery is the
area of attachment of middle turbinate lamina to
the skull base once the anterior ethmoidal artery
370
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O. M. Bargas and A. AbuAlsoud
identied the frontal recess is immediately anterior to it, then an angled probe (Bolger–Kuhn
probe) is passed to the posterior frontal recess
and start fracturing the posterior wall of the
agger nasi cell and the other frontal recess cells
in antero-inferior direction. Removal of the bony
fragment and the mucosal pieces is better done
by using through- cutting forceps and microdebrider rather than using standard punch forceps
to avoid stripping of the mucosa. The movement
of the instrument in the region of the frontal
recess should be careful movement; it is better to
move from posterior to anterior direction (to
avoid the anterior ethmoidal artery, the skull
base and due to the presence of the beak which is
a thick bone anteriorly) and from medial to lateral direction (to be away from the lateral
lamella). The other approach to the frontal recess
is through what is called intact bulla technique in
which the uncinate process is removed and start
removing the agger nasi by passing above the
bulla medial to middle turbinate. Once the agger
posterior wall is removed, the anterior ethmoidal
artery is identied and hence the skull base then
the dissection continues the rest dissection.
Another method of intact bulla technique is like
what Wormald use in which a mucosal ap is
elevated just anterior to the middle turbinate
axilla and reected posteriorly, then dissect the
anterior wall of the agger nasi [10] to discover
the frontal recess.
Various types of frontal cells are present which
is best described in modied Kuhn classication as following:
• Type 1—Single cell above the agger nasi cell.
• Type 2—Tier of cells above agger nasi cell.
• Type 3—Single large cell extending to <50%
of the vertical height of the frontal sinus.
• Type 4—Large cell extending to >50% of the
vertical height of the frontal sinus or isolated
cell within the sinus.
All these types of frontal cells should be removed
in the same manner of removing agger nasi cell.
Other types of frontoethmoidal cells include:
• Suprabullar cells which present above the
bulla and extend to skull base and may compress the frontal recess from behind.
• Supraorbital cell extends above the orbit and
opens behind the frontal recess and anterior to
anterior ethmoidal artery.
• interfrontal sinus septal cell a pneumatization
of the interfrontal sinus septum with variable
extension which may compress the frontal
recess from medial to lateral.
These cells should be well studied on CT scan
before working on the frontal sinus as it may
require special instrument or even require combined approach to completely manage the disease and open the frontal recess correctly.
Emerging of the navigation system in the endoscopic sinus surgery plays an important role in
revision cases and in presence of anatomical
variation especially in frontal recess region to
avoid injury to the nearby vital structure and to
achieve complete clearness of the recess.
Pitfall and Pearls of Frontal Sinus Surgery
• Endoscopic approach to frontal recess is
the golden way to treat chronic frontal
sinusitis.
• Good knowledge of the normal anatomy
and the normal anatomical variation is
vital for surgery success.
• Do the best in maintaining the mucosal
lining of the frontal recess.
• Try to avoid middle meatal collapse
postoperatively by maintaining middle
turbinate attachment, use of middle
meatal spacer, or even bolgerization.
• Postoperative care is crucial in endo-
scopic fontal surgery to maintain the
function and avoid closure of the recess
by blood clots and crust.
• CT scan coronal and sagittal cuts are nec-
essary to study the frontal recess region.
AL GRAWANY
33 Pitfalls andPearls inEndoscopic Sinus Surgery
Take Home Messages
If you can’t help don’t
Respect the tissues as
much as possible
371
harm
Don’t forget the aim of
FESS (remove the
disease and provide way
for topical medications)
Good preoperative
imaging study is vital
References
1. Wormald PJ, McDonogh M.The ‘swing-door’ technique for uncinectomy in endoscopic sinus surgery. J
Laryngol Otol. 1998;112(6):547–51.
2. Wormald P-J. Endoscopic sinus surgery, vol. 5.
Stuttgart: Thieme; 2013. p.28–44.
3. Stammberger H.Endoscopic surgery for mycotic and
chronic recurring sinusitis. Ann Otol Rhinol Laryngol.
1985;94(5_Suppl):1–11.
4. Yanagisawa E, Joe JK, Christmas DA. Where is the
ostium of the ethmoid bulla? Ear Nose Throat J.
1999;78(12):886.
5. Schlosser RJ, Harvey RJ. Endoscopic sinus surgery:
optimizing outcomes and avoiding failures. San
Diego: Plural Publishing; 2012.
follow the learning
curve of ESS
6. Kim H, Kim S, Kang SS, Chung IH, Lee J, Yoon
J.Surgical anatomy of the natural ostium of the sphenoid sinus. Laryngoscope. 2001;111(9):1599–602.
7. Levine HL. Endoscopic sinus surgery: reasons
for failure. Oper Tech Otolaryngol Neck Surg.
1995;6(3):176–9.
8. Kennedy DW, Senior BA. Endoscopic sinus surgery. A review. Otolaryngol Clin North Am.
1997;30(3):313–30.
9. Stammberger H, Kopp W, Dekornfeld TJ. Special
endoscopic anatomy. In: Functional Endoscopic
Sinus Surgery: The Messerklinger Technique.
Philadelphia: Decker Publication; 1991. p.61–90.
10. May M, Schaitkin B.Frontal sinus surgery: endonasal
drainage instead of an external osteoplastic approach.
Oper Tech Otolaryngol Neck Surg. 1995;6(3):184–92.
Part IV
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Head and Neck
AL GRAWANY
Thyroid andParathyroid Glands
HassanHaidar, AbdelrahmanAlsaleh,
WaheedRahman, andHusseinEnezi
34
34.1 Introduction
Thyroid gland comprises two types of cells: follicular cells (or thyrocytes) which produce and
secrete thyroglobulin and thyroid hormones, and
parafollicular cells (or C cells), which secrete
calcitonin. Papillary Thyroid Carcinoma (PTC)
and Follicular Thyroid Carcinoma (FTC) are
tumors originating by thyrocytes and are referred
as Differentiated Thyroid Carcinomas (DTCs).
Anaplastic Thyroid Carcinoma (ATC) is the
undifferentiated tumor which may arise from
DTCs or may be undifferentiated to origin.
Medullary Thyroid Carcinoma (MTC) is the
tumor arising to C cell.
The four parathyroid glands, located posterior
to the thyroid gland, regulate calcium homeostasis through release of parathyroid hormone
(PTH). PTH increases serum calcium levels
through direct action on bone and the kidneys. It
stimulates osteoclasts to resorb bone and mobilize calcium into the blood.
34.2 Thyroid Gland
34.2.1 Embryology
The thyroid gland develops from three pharyngeal bodies: the median anlage and two lateral
bodies. Median anlage is derived as a ventral
diverticulum at the foramen cecum. During the
fourth to seventh week of gestation, the primitive
thyroid tissue descends along the thyroglossal
duct anterior to the hyoid bone and the laryngeal
cartilages to reach its nal position at the level of
the second and fourth tracheal rings [1, 2].
Calcitonin-secreting parafollicular C cells arise
within the ultimobranchial bodies from neural
crest cells of the fourth pharyngeal pouch [3, 4].
The entire gland may lie close to its point of
origin at the foramen cecum, giving rise to a lingual thyroid. About 70% of patients with lingual
thyroid glands have no thyroid tissue in the neck.
In many cases, the lingual thyroid does not function normally [3, 4].
The thyroglossal duct ultimately atrophies,
but any portion of it may persist to become the
site of a thyroglossal duct cyst.
H. Haidar (*)
Hamad Medical Corporation, Doha, Qatar
A. Alsaleh · W. Rahman · H. Enezi
ENT Department, Hamad Medical Corporation,
Doha, Qatar
e-mail: wrahman@hamad.qa; halenazi@hamad.qa
© Springer Nature Switzerland AG 2021
A. Al-Qahtani et al. (eds.), Textbook of Clinical Otolaryngology,
https://doi.org/10.1007/978-3-030-54088-3_34
34.2.2 Anatomy oftheThyroid Gland
The gland lies anterior to the second, third, and
fourth tracheal rings. Posterolaterally, the gland
overlaps the carotid sheath and its contents.
375
376
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H. Haidar et al.
A pyramidal lobe may be present in about
50% of patients [3, 4].
Arterial blood supply is derived from two
pairs of arteries.
1. The superior thyroid artery: the rst branch of
the external carotid artery.
2. The inferior thyroid artery: a branch of the
thyrocervical trunk of the subclavian artery. It
courses behind the common carotid artery to
enter the inferior thyroid pole.
3. The thyroid ima artery: inconsistently present
(7%). Because of its relation to the anterior
aspect of the trachea, the thyroid ima artery is
in danger of injury during a tracheotomy.
34.2.2.1 Lymphatic Drainage
oftheThyroid Gland
Dominant drainage to level VI known as precricoid, Delphian, paratracheal lymph node.
Anatomy oftheRecurrent Laryngeal Nerve
The right recurrent laryngeal nerve arises from
the vagus as this nerve crosses anterior to the
right subclavian artery. It then loops around the
artery and ascends in the tracheoesophageal
groove, posterior to the thyroid gland, to enter the
larynx behind the cricothyroid articulation [5].
The nerve on the left arises from the vagus
where it crosses the arch of aorta. It then loops
around the aorta to ascend in the tracheoesophageal. The left recurrent nerve is generally more
closely applied to the trachea in the lower part of
its ascending course than is the right nerve.
As the recurrent laryngeal nerves ascend toward
the middle of the thyroid gland, they are intimately
associated with the inferior thyroid artery [5, 6].
Classically, the recurrent laryngeal nerve is
found intraoperatively in Simon’s triangle, which
is formed by the common carotid artery laterally,
the esophagus medially, and the inferior thyroid
artery superiorly. The nerve can also be reliably
found where it enters the larynx just behind the
inferior cornu of the thyroid cartilage.
Anatomy oftheSuperior Laryngeal Nerve
The superior laryngeal nerve originates at the
inferior ganglion of the vagus nerve near the jugular foramen.
It has two branches; the internal branch pierces
the thyrohyoid membrane and supplies sensation
to the supraglottic and pyriform sinus [7] and the
external branch which supplies the cricothyroid
muscle.
The nerve is variable in its relationship to the
highest point of the superior pole of the thyroid
gland and is at risk of injury during thyroid surgery [8].
34.2.3 Benign Thyroid Disease
34.2.3.1 Graves’ Disease
• Pathophysiology: Autoimmune, TSH receptor
antibody → stimulation→ goiter and elevated
levels of T3 and T4 secretion [9]. Associated
with exophthalmos and dermatopathy.
• Risk factors: exposure to radiation, females
more than males (adolescence or 30–40) and
genetic predisposition.
• Histopathology: Shows scattered lymphocytic
inltration.
• Investigations: Thyroid-stimulating immuno-
globulin levels (TSIs); Iodine-123 (I123)
scanning shows a diffuse increased gland
uptake [10].
• Radioactive Iodine (131I): the most common
therapy used.
• Subtotal Thyroidectomy: indicated when med-
ical therapy fails [11].
– Exophthalmos and optic neuropathy If
optic neuropathy persists despite medical
therapy, corticosteroids for 2 weeks; if no
improvement, then surgical decompression
is needed which includes trans-nasal endoscopic approaches to the medial and inferior orbital wall [12].
34.2.3.2 Toxic Nodular Goiter
No eye or skin ndings as in Graves’ disease.
Evolution of hyperfunctional regions, which
results in excess thyroid hormone that causes the
suppression of TSH resulting in the adjoining
normal gland becoming less active on I123 scans,
with hyperfunctional areas being hot [13].
Hyperthyroidism typically does not occur,
until the nodule is 3cm or larger or multiple toxic
nodules.
AL GRAWANY
34 Thyroid andParathyroid Glands
377
Treatment is either surgery or radioactive
iodine, antithyroid medications might be considered prior to more denitive surgical or radio
ablative treatment.
34.2.3.3 Hashimoto’s Thyroiditis
• Physiopathology: Antithyroglobulin antibody
→chronic lymphocytic inammation
→Transient hyperthyroidism followed by
hypothyroidism [14].
• Risk factors: More common in females in
third to fth decade, genetic susceptibility
(HLA- DR3). Can be associated with lym-
phoma, neoplasms, or other autoimmune dis-
ease such as SLE, Sjogren syndrome, and
scleroderma.
• Histopathology: Lymphocytic inltration with
germinal center formation.
• Investigations: Antithyroid peroxidase (anti-
TPO) [15].
• Treatment: thyroxin therapy; surgical excision
for compressive symptoms or suspicious
nodule.
• Complications: Rarely, progress into thyroid
lymphoma. A rapidly enlarging mass within a
Hashimoto’s gland should always raise con-
cern regarding lymphoma and warrants FNA
or biopsy.
34.2.3.4 Subacute Granulomatous
(De Quervain’s) Thyroiditis
Typically, presents as enlarged, painful thyroid,
after upper respiratory tract infection, fever and
malaise are also common. Half of patients may
show hyperthyroidism, then patients will enter a
several-month hypothyroid period. Eventually,
most patients return to euthyroidism.
I123 scanning usually shows less than 2%
uptake.
It is a self-limiting disease that can be treated
with anti-inammatory drugs and rarely steroids
[16].
34.2.3.5 Riedel’s Thyroiditis
Fibrosis of thyroid gland of unknown cause that
manifests as “rock-hard” thyroid produces local
pressure and hypothyroidism. Histologically, it is
characterized by widespread brotic process.
34.2.4 Thyroid Nodules
– The prevalence of palpable nodules is only
4–7% while high resolution ultrasound can
detect 19–68% of individuals selected randomly with higher frequencies in women and
the elderly [17].
– Only 5–10% of nodules being malignant [18].
A single dominant or solitary nodule is more
likely to represent carcinoma than a single
nodule within a multinodular gland, with an
incidence of malignancy from 2.7 to 30% and
1.4 to 10%, respectively [19, 20].
– Important elements in patients’ history that
increase the likelihood of malignancy include
prior head and neck irradiation, reports of
rapid growth, dysphagia, dysphonia, male
gender, and presentation at extremes of age.
– Physical examination ndings that increase
the concern for malignancy include: nodules
larger than 4cm in size (19.3% risk of malignancy), rmness, xation to adjacent tissues,
cervical lymphadenopathy. Vocal cord immobility [21].
– Ultrasound imaging studies and FNA are the
main tools used to decide whether surgical
excision of a thyroid nodule is warranted.
– Molecular genetic biomarker analyses are
now being used to increase the accuracy of
FNAB.
34.2.4.1 Ultrasonography
Solid appearance (or hypoechogenicity);
increased vascularity; microcalcications; irregular margins; and the absence of a halo are features that have been consistently associated with
malignancy (Table34.1).
34.2.4.2 Radioisotope Imaging
About 80–85% of thyroid nodules are cold and
about 10% of these nodules represent a malignancy. While hot nodules account for 5% of all
nodules and the likelihood of malignancy is less
than 1% for these nodules.
Except for obviating the need to perform an
FNAB on a hyperfunctioning nodule in patients
who are thyrotoxic, the use of radioisotope scanning has been abandoned.
378
H. Haidar et al.
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Table 34.1 The sensitivity and specicity of various
sonographic characteristics
Sonographic characteristic
Sensitivity
(%)
Specicity
(%)
Microclassications 52 83
Absence of halo 66 54
Irregular margins 55 79
Hypoechoic 81 53
Increased intranodular ow 67 81
Data from Fish SA, Langer JE, Mandel SJ.Sonographic
imaging of thyroid nodules & cervical lymph nodes.
Endocrinol Metab Clin North Am 2008;37(2):401–17
34.2.4.3 Fine Needle Aspiration
Cytology
• Nodules 1 cm or larger or sonographically
suspicious sub-centimeter nodules warrant
cytologic analysis through FNAB to determine the risk for malignancy [22–24].
The pathology report from FNAB may be read as
benign, malignant, indeterminate, or nondiagnostic.
The only malignant pathology reliably diagnosed through FNA is papillary thyroid carcinoma because features, such as Orphan Annie
nuclei, nuclear grooves, intranuclear inclusions,
and psammoma bodies, can be sufcient for a
diagnosis.
Medullary carcinoma, anaplastic carcinoma,
lymphoma, poorly differentiated carcinoma, and
metastatic disease can also be classied on the
basis of cytology.
Benign and malignant follicular neoplasms
and oncocytic adenomas and carcinomas cannot
be distinguished on the basis of cytology alone,
because tissue architecture is required to make
the diagnosis of malignancy through observation
of capsular or angiolymphatic invasion. Patients
with lesions classied as follicular or oncocytic
neoplasm, or suspicious for malignancy should
be offered a diagnostic lobectomy.
FNAB specimens read as unsatisfactory
should be sent for a repeat biopsy while samples
read as follicular lesions with unknown signicance or “FLUS”. FLUS are generally sent for
repeat FNAB, as the risk for malignancy is only
5–10%. FNA that showed follicular neoplasm or
suspicious for follicular neoplasm has a 15–30%
risk of malignancy and diagnostic thyroidectomy
should be discussed with the patient vs. radiological surveillance (see algorithm).
High Suspicion
Pattern
Nondiagnostic
Repeat FNA
FNA ≥ 1 cm
Benign
No Surgery
Intermediate
Suspicion
Pattern
AUS/FLUS
Suspected thyroid nodule
TSH normal or elevated
Thyroid/Neck US
Low Suspicion
Pattern
FNA ≥ 1.5 cm
Cytopathology
Bethesda
system
FN/FSN
Radiological surveillance
or diagnostic surgery
Very Low
Suspicion
Pattern
FNA ≥ 2 cm
Suspicious
No nodule or nodule not
meeting FNA size cutoff
Benign
Pattern
FNA Not
required
Malignant
Surgery
AL GRAWANY
34 Thyroid andParathyroid Glands
379
AUS/FLUS: Atypia of undetermined signi-
cance or follicular lesion of undetermined.
FN/FSN: Follicular neoplasm or suspicious
for a follicular neoplasm [25].
34.2.5 Malignant Thyroid Disease
34.2.5.1 Papillary Thyroid Carcinoma
The most common type of thyroid cancer represents 75–85% of all thyroid cancer cases. More
frequently in women and presents in the 20–55
years of age [26].
Features include:
• Characteristics: Orphan Annie eye nucleus
and psammoma bodies on light microscopy.
• Lymphatic spread is more common than
hematogenous spread.
• Multifocality is common.
• The so-called “Lateral Aberrant Thyroid” is
actually a lymph node metastasis from papillary thyroid carcinoma.
• Papillary microcarcinoma is a subset of papillary thyroid cancer dened as measuring less
than or equal to 1 cm and the management
strategies for incidental papillary microcarcinoma on ultrasound (and conrmed on FNAB)
range from total thyroidectomy with radioactive iodine ablation to observation alone.
Staging (AJCC staging)
• T1: ≤2 cm tumor conned to thyroid
(T1a≤1cm tumor, T1b>1cm but ≤2cm).
• T2: >2cm but ≤4cm tumor limited to thyroid
gland.
• T3: >4 cm tumor or gross extrathyroidal
extension invading strap muscles only
(T3a > 4 cm tumor limited to thyroid, T3b
gross extrathyroidal extension invading only
strap muscles of any size).
• T4: includes gross extrathyroidal extension
(T4a invades subcutaneous soft tissue, larynx,
trachea, esophagus, or recurrent laryngeal
nerve; T4b invades prevertebral fascia or
encasing carotid or mediastinal vessels).
Management
– Thyroid lobectomy alone may be sufcient
treatment for small (<1cm), low-risk, unifocal, intrathyroidal papillary carcinomas.
– Gross disease (diameter over 1.0 cm)—total
thyroidectomy, and central compartment
lymph node removal is the therapy of choice.
– Central compartment neck dissection for
patients with nodal disease or in high-risk
patients (advanced papillary thyroid carcinoma (T3–T4).
– Lateral neck dissection is indicated for biopsy-
proven metastatic lateral neck nodes.
Postoperative management
• For low-risk Well-Differentiated Thyroid
Carcinoma (WDTC), radioactive iodine adjuvant therapy is not routinely recommended
after thyroidectomy but should be considered
in intermediate- and low-risk WDTC with
other risk factors.
• Radioactive iodine adjuvant therapy is usually
recommended after total thyroidectomy for
high-risk WDTC.
Patient is considered high risk if any of the
following present [27]:
• Macroscopic tumor invasion.
• Incomplete tumor resection with gross residual disease.
• Distant metastases.
• Postoperative serum thyroglobulin suggestive
of distant metastases.
• Pathologic N1 with any metastatic lymph
node ≥3cm in largest dimension.
• Follicular thyroid cancer with extensive vascular invasion (>4 foci of vascular invasion).
• Follow-up: thyroglobulin measurement and
diagnostic radioactive iodine scanning 2–8
days after radioiodine treatment.
– Radioiodine scan is usually repeated
6–12months after treatment with 131-I in
moderate- to high-risk patients and in
lower-risk patients who have detectable Tg
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H. Haidar et al.
levels during follow-up that are not
declining.
• Prognosis: 95% 5-year survival; poor prognostic indicators include tumors >1.5 cm or
extracapsular spread (cervical metastases have
increased cervical recurrence rates without
affecting survival).
34.2.5.2 Follicular Carcinoma
The second most common thyroid carcinoma
representing about 10% of thyroid cancers [28].
It is more common in female with median age
around the sixth decade.
Twenty to 50% spread hematogenously with
distant metastasis (lymphatic spread is rare).
• Diagnosis: Requires open biopsy in order to
distinguish adenoma from carcinoma.
• Histopathology: It has a sub-stational morphologic overlap with the benign follicular
adenoma. Typically, it shows unifocal neoplastic follicular cells that is less distinct
from malignant papillary cells; malignancy
can be determined if extracapsular spread is
noted.
• Staging: is similar to that of PTC.
• Treatment: Total thyroidectomy ± neck dis-
section. Radioactive iodine adjuvant therapy
is usually recommended after total thyroidectomy for high-risk WDTC (see papillary thy-
roid cancer).
• Prognosis: 70–85% 5-year survival and
reaches to about 20% with distant metastasis.
Angioinvasion, extracapsular spread denotes
worse prognosis.
34.2.5.3 Hurthle Cell Carcinoma
Occurs mostly in older patients (60s).
Can be considered a variant of follicular carci-
noma, oxyphilic cells noted.
Believed to be more aggressive in nature,
spread can occur via lymphatic or hematogenous
pathways.
Distant metastasis can reach up to 30%, with
40% bone followed by 30% lung.
Management: While the staging is similar to
•
that of the PTC, radiouptake is poor in such
cancers; aggressive surgery is the mainstay in
treatment.
• Prognosis: about 50% 5-year survivals [29, 30].
34.2.5.4 Medullary Thyroid
Carcinoma
The third most common of all thyroid cancers
(3%), it originates from the parafollicular cells (C
cells), which produce the hormone calcitonin
[31, 32].
• 25% of medullary thyroid cancer cases are
genetic in nature, caused by a mutation in the
RET proto-oncogene and inherited as an auto-
somal dominant trait. This form is identied
as familial medullary thyroid cancer (FMTC).
When it coexists with tumors of the parathyroid gland and medullary component of the
adrenal glands (pheochromocytoma), it is
called multiple endocrine neoplasia type 2
(MEN2).
• Surgical removal of the thyroid in children
who carry the mutant gene is curative if the
entire thyroid gland is removed at an early
age, before there is spread of the tumor.
• The parathyroid tumors and pheochromocytomas are removed when they cause clinical
symptomatology.
• 75% of medullary thyroid carcinoma occurs in
“sporadic” fashion.
Markers: Calcitonin is useful as a marker
which can be tested in blood for detecting the
presence of a tumor, and is an indicator of tumor
mass.
Treatment: A plasma level of metanephrines
should be checked before surgical thyroidectomy
to evaluate for the presence of pheochromocy-
toma as 25% of people found to have medullary
thyroid cancer and have the inherited form of the
MEN2A syndrome. Undiagnosed pheochromo-
cytoma leads to a very high intraoperative risk of
hypertensive crisis and, potentially, death.
AL GRAWANY
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