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34 Thyroid andParathyroid Glands
381
34.2.5.5 Surgery
– A total thyroidectomy with bilateral neck dis-
section is the gold standard for treating medullary thyroid cancer.
– About 50% of patients have metastasis to
regional lymph nodes at the time of
diagnosis.
– In gene carriers: The timing of surgery
depends on the type of mutation present.
For those in the highest risk group, surgery
is recommended in the rst year of life. In
lower- risk cases, surgery may be delayed up
to the age of 10 years, the precise timing
depending on the mutation and other
factors.
Unlike other differentiated thyroid carcinoma,
there is no role for radioiodine treatment in
medullary- type disease [33].
34.2.5.6 Protein Kinase Inhibitors
Protein kinase inhibitors (vandetanib, cabozantinib) which block the abnormal kinase proteins
involved in the development and growth of medullary cancer cells, showed clear evidence of
response in 10–30% of patients for treatment of
late-stage (metastatic) medullary thyroid cancer
in adult patients who are ineligible for surgery
[34, 35].
34.2.5.7 Prognosis
– 5-year survival rate is 100% at stage I, 98% at
stage II, 81% at stage III, and 28% at stage IV
[36]. The prognosis of MTC is poorer than
that of follicular and papillary thyroid cancer
when it has metastasized (spread) beyond the
thyroid gland.
– The prognosis correlated with the rate at
which the postoperative calcitonin concentra-
tion doubles, termed the calcitonin doubling
time (CDT), rather than the pre- or postopera-
tive absolute calcitonin level.
– The calcitonin doubling time was a better pre-
dictor of MTC survival than CEA [21] but fol-
lowing both tests is recommended [37].
MEN1
(Werner’s
syndrome)
Parathyroid
adenoma or
hyperplasia
Pancreatic
Islet cell
tumors
(insulinoma,
gastrinoma)
Pituitary
adenoma
MEN2 (Sipple
syndrome) MEN2B
Medullary thyroid
carcinoma
Pheochromocytoma Pheochromocytoma
Parathyroid
hyperplasia
Medullary thyroid
carcinoma
Mucosal neuroma
Marfanoid habitus
34.2.5.8 Anaplastic Thyroid
Carcinoma
Two percent of all thyroid carcinomas, but
15–39% of all deaths. Tend to be older patients
(50–60s).
• Aggressive: rapidly growing inltrative thy-
roid mass, vocal cord paralysis.
• Metastasis possible to lungs, liver, bones
within weeks.
• FNA typically shows necrosis and
degeneration.
• Prognosis: survival rates low (20%) at 1year.
• Management: Aggressive multimodal therapy
in early stage: total thyroidectomy, intensitymodulated radiation therapy (IMRT), and
adjuvant chemotherapy [28, 38, 39].
• Palliative therapy: (tracheostomy controver-
sial due to poor prognosis) for advanced
lesions.
34.2.6 Thyroidectomy andIts
Complications
34.2.6.1 Thyroidectomy Types
(a) Hemithyroidectomy: It involves removal of
one lobe plus entire isthmus is removed. It is
performed in benign disease involving one
lobe (benign nodule or cyst).
(b) Subtotal thyroidectomy: Here about 8 g, or
tissue size of pulp of nger is retained on
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H. Haidar et al.
lower pole of thyroid on both sides, and rest
of gland is removed. Indications: Toxic thyroid, non-toxic multinodular goiter.
(c) Near-total thyroidectomy: Here both lobes
except less than 2g of thyroid tissue on the
lower pole, near to the recurrent laryngeal
nerve and parathyroid, are removed to retain
blood supply to parathyroid gland. Indication:
mostly done in papillary thyroid carcinoma.
(d) Total thyroidectomy: Here entire gland is
removed. Indication: thyroid cancer. Total
thyroidectomy provides the advantages of
eliminating the risk of recurrence and hence
an increasing number of total thyroidectomies are currently being performed for
benign cases.
34.2.6.2 Complications
(a) Hematoma: Hematoma can usually be differ-
entiated from seroma by the presence of skin
ecchymosis, rmness to palpation, or clotted
drain output. Two types of hematoma:
• Deep to deep fascia: A deep bleeding produces tension hematoma. Usually due to
slipping of the ligature of the superior thyroid artery, though it can also be from a
thyroid remnant or a thyroid vein. This
compresses on the airway and potentially
life threatening unlike the subcutaneous
bleeding. A tension hematoma requires
opening of the wound, evacuation of
hematoma, and ligature of the bleeding
vessels.
• Subcutaneous. A subcutaneous hematoma
is most likely due to slipping of the ligature of the anterior jugular vein and can be
aspirated.
(b) Recurrent Laryngeal Nerve Injury:
• Temporary dysfunction because of nerve
traction occurs in 2.5–5% of patients. —
Return of normal vocal cord function
occurs 6–12months after temporary RLN
injury occurs.
• The incidence of permanent RLN paralysis is approximately 1–1.5% for total thyroidectomy and less for near-total
procedures.
– Unilateral RLN paralysis: 1/3rd are
asymptomatic, 2/3 change in voice
which improves within 6months due
to compensation by the healthy cord.
—Concurrent injury of the SLN
results in a more laterally positioned
vocal cord and worsens voice quality
and glottic competence. Patients may
have difculty with aspiration and
pneumonia.
– Bilateral RLN paralysis: dyspnea and
biphasic stridor. Tracheostomy may
be needed. Posterior cordectomy
when bilateral nerve transaction was
certain or after 6months of injury.
(c) Superior Laryngeal Nerve Injury: Injury to
the SLN alters function of the cricothyroid
muscle. Often disturbance of SLN function
is temporary and unrecognized by the
patient and the surgeon. Patients may have
difculty shouting, and singers nd difculty with pitch variation, especially in the
higher frequencies. The external branch of
the SLN is not often visualized and lies near
the superior pole vessels. Safest approach is
to identify the branches of superior thyroid
artery and avoid ligating the main trunk as
in majority of cases superior laryngeal nerve
lies close to the main trunk. Adequate exposure of the superior thyroid pole and close
ligation of the superior thyroid artery close
to the superior pole of thyroid gland is considered safe.
(d) Hypoparathyroidism:
• Transient symptomatic hypocalcemia
after total thyroidectomy occurs in
approximately 7–25% of cases and may
be related to parathyroid gland trauma or
vascular compromise.
• Permanent hypocalcemia is less common
(1–3%). Due to removal of parathyroids
or the parathyroid end artery.
• Hypocalcemia: patients may experience
paresthesias, tetany, bronchospasm, mental status changes, seizures, laryngospasm, and cardiac arrhythmias. Chvostek
sign and Trousseau sign may develop with
increased neuromuscular irritability as
serum calcium levels drop.
• Treatment for hypocalcemia is typically
initiated if the patient is symptomatic or
AL GRAWANY
34 Thyroid andParathyroid Glands
383
serum calcium levels decrease to less than
7mg/dL.
(e) Postoperative infections: are very unusual
because of the abundant blood supply in the
thyroid bed.
34.3 Parathyroid Glands
34.3.1 Embryology andAnatomy
oftheParathyroid Glands
– Two pairs of glands: Superior and inferior.
– The inferior parathyroid glands arise from the
3rd pharyngeal pouch endoderm and have a
common origin and migration with the
thymus.
– They migrate inferiorly in a long course of
descent that can lead to a large area of possible
ectopic inferior parathyroid glands; can be
found anywhere from the level of the mandibular angle to the pericardium.
– The most common ectopic location for an
inferior gland is in the anterior mediastinum;
this is found in 5% of ectopic cases.
– Typically, inferior glands can be found ante-
rior to a plane drawn along the course of the
recurrent laryngeal nerve.
– The fourth pharyngeal pouch gives rise to the
superior parathyroid glands which has a
shorter embryologic descent than their inferior counterparts.
– Symmetry in the approximate location of the
glands when comparing right with left has
been reported at 80% for the superior and 70%
for the inferior glands [40, 41].
34.3.2 Primary Hyperparathyroidism
• Increased calcium levels with elevated PTH
levels.
• Might be spontaneous, familial, or associated
with multiple endocrine neoplasia (MEN)
syndromes.
• Caused by parathyroid adenoma in 80–85%,
by hyperplasia in all four glands in about 15%
of cases and very rarely by parathyroid cancer
[42, 43].
• Clinical manifestations: 80% asymptomatic;
20% symptomatic (fatigue, nephrolithiasis,
hypercalciuria, bony pain, muscle weakness).
34.3.2.1 Indications forTreatment
Indications for treatment (parathyroidectomy)
are:
• Symptomatic hyperparathyroidism.
• Asymptomatic hyperparathyroidism with any
of the following:
– serum calcium >1mg/dl above upper limit
of normal
– objective evidence of renal involvement,
including silent nephrolithiasis, nephrocalcinosis, hypercalciuria with increased
stone risk, or impaired renal function
– osteoporosis
– People age<50
• For asymptomatic individuals who do not fulll the surgical criteria, serum calcium and
creatinine monitoring along with bone density
every year are recommended. If disease progression occurs, treatment is indicated.
34.3.2.2 Parathyroidectomy
Parathyroidectomy is the only denitive treatment of pHPT and it aims to remove the
adenoma(s).
• Preoperative localization studies: The best
imaging modality for preoperative localization of parathyroid adenomas is parathyroid
scintigraphy (Sestamibi scanning).
Technetium 99m methoxyisobutyl isonitrile
(Tc99MIBI) is rst absorbed by both thyroid
and parathyroids. The thyroid uptake is, however washed out over time while sestamibi is
retained by adenomatous parathyroid glands.
• Radioguided Parathyroidectomy: may be considered for an adenoma identied on a
Sestamibi scan; a tracer is injected 1.5–3hours
prior to surgery, then a gamma probe could be
utilized intraoperatively to identify abnormal
gland.
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H. Haidar et al.
• Obtaining intraoperative PTH before incision,
then to proceed by removing presumed pathologic gland, then PTH 10min later should be
checked for reduction >50% and/or into the
normal range. If persistently elevated, four
gland exploration with subtotal (three glands)
parathyroidectomy can be performed.
• Complications:
• Persistent hyperparathyroidism.
• Recurrent laryngeal nerve injury.
• Transient postoperative hypocalcemia.
34.3.2.3 Medical Treatment
A calcimimetic (such as cinacalcet) is a potential
therapy for patients who are unable to have surgery and whose primary indication for surgery is
symptomatic and/or severe hypercalcemia.
34.3.3 Secondary
Hyperparathyroidism
Secondary hyperparathyroidism is due to physi-
ological secretion of PTH by the parathyroid
glands in response to hypocalcemia. The most
common causes are vitamin D deciency and
chronic kidney failure.
In chronic kidney failure, there is a problem
converting vitamin D to its active form in the kidney. Lack of vitamin D leads to reduced calcium
absorption by the intestine leading to hypocalcemia and increased parathyroid hormone secretion. This increases bone resorption and leads to
renal osteodystrophy.
Treatment of secondary hyperparathyroidism
is with calcimimetic.
34.3.4 Tertiary Hyperparathyroidism
Tertiary hyperparathyroidism is seen in those
with long-term secondary hyperparathyroidism,
which eventually leads to hyperplasia of the parathyroid glands and a loss of response to serum
calcium levels. Parathyroid response becomes
autonomous and it persists even after correction
of the primary metabolic derangement with
increased PTH levels despite correction of
calcium.
This disorder is most often seen in patients
with end-stage kidney disease. Treatment is by
subtotal parathyroidectomy.
34.3.5 Parathyroid Carcinoma
• Parathyroid carcinoma occurs rarely and
accounts for approximately 1% of cases of
HPT.
• Elevated calcium and PTH levels markedly
elevated compared to adenomas.
• Intraoperative appearance is typically a hard
lobulated brous mass.
• En bloc resection is key with resection of ipsi-
lateral thyroid lobe with isthmus, and
paratracheal and central neck dissection, as
adjuvant therapy has been disappointing.
• Tendency for spread to local lymph nodes but
can also metastasize to lung, liver, and bone.
• 5- and 10-year survival is 85 and 50–75%,
respectively.
Take Home Messages
• The procedure of choice in the evaluation of thyroid nodules is FNAC which
is increasingly being performed with
ultrasound guidance to improve diagnostic outcomes.
• Management of well-differentiated thyroid carcinoma generally consists of
total thyroidectomy, excision of pathologic lymph nodes, and is followed by
radioactive iodine only in high-risk
patients.
• Thyroglobulin measurement is of great
value in the follow-up of patients with
differentiated thyroid cancer.
• Parathyroid adenoma accounts for
80–85% of primary
hyperparathyroidism.
• Localization of hyperfunctional parathyroid glands may be accomplished
using functional nuclear uptake studies
which allow a mini-invasive approach
for resection of the pathologic gland.
AL GRAWANY
34 Thyroid andParathyroid Glands
385
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AL GRAWANY
Diseases oftheSalivary Glands
HassanHaidar, AbhishekMenon,
andEmadAl Duhirat
35
35.1 Introduction
There are essentially three-paired salivary glands:
the parotid glands, submandibular glands, and
the sublingual glands. In addition, the minor salivary glands, or accessory glands are present in
the oral cavity. They can be split into three main
categories: the anterolingual glands, the serous
glands of Von Ebner, the lingual buccolabial and
palatal glands.
35.1.1 Saliva
– Lubricates and moistens food.
– Protects mucosa from desiccation and chemi-
cal irritation.
– It has antibacterial action via secretory IgA,
lactoferrin, salivary peroxidase, and lysozymes. Prevention of dental caries.
H. Haidar (*)
Hamad Medical Corporation, Doha, Qatar
A. Menon · E. Al Duhirat
Otolaryngology-Head and Neck Surgery Division,
Department of Surgery, Hamad Medical Corporation,
Doha, Qatar
35.1.2 Saliva Secretion
– 1–1.5L in 24h, contains electrolytes.
– Non-stimulated ow primarily from subman-
dibular gland.
Mixed serous and mucinous saliva.
– Parotid gland supplies the majority of stimu-
lated salivary ow.
Serous saliva.
35.2 Anatomy
35.2.1 Parotid Gland
– Derived from rst pharyngeal pouch.
– Situated between the external auditory canal,
mastoid tip, and the ramus of the mandible.
Anteriorly, it lies above the masseter muscle
and sternocleidomastoid muscle posteriorly.
– The supercial layer of the deep cervical fas-
cia forms the parotid gland fascia which
incompletely surrounds the gland.
– The facial nerve divides the gland into a deep
lobe and a supercial lobe.
– Lymphoid tissue makes up the gland.
Histologically, it consists of basophilic and
serous cells.
– Stensen’s duct runs 1 cm inferior to the
zygoma and opens opposite to the upper second molar.
© 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_35
387
388
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H. Haidar et al.
– Stylomandibular ligament, separates the
parotid gland from the submandibular gland.
– Parasympathetics innervation: Mediate secre-
tion of saliva. Inferior salivatory nucleus in
brain stem→CN IX, Jacobsen’s nerve→lesser
supercial petrosal nerve → Otic
Ganglion→auriculotemporal nerve (V3).
– Blood Supply: Posterior auricular and super-
cial temporal arteries, branch of external
carotid Artery.
35.2.2 Submandibular Gland
– Second largest salivary gland, lies in the sub-
mandibular triangle.
– Enveloped by the supercial layer of the deep
cervical fascia which contains the marginal
mandibular nerve.
– The facial artery hooks over the posterior
belly of the digastric to enter the gland. It runs
medial to the digastric muscle.
– Hypoglossal nerve runs deep to the digastric
tendon and medial to the deep layer of the
deep cervical fascia,
– CN XII runs deep into the digastric tendon
and the mylohyoid along the hyoglossus.
– Consists of serous and mucinous cells
(mixed).
– Histologic cell type: mixed cells (serous and
mucinous).
– Wharton’s duct: opens lateral to frenulum in
the anterior portion of the oor of mouth,
behind the incisors.
– Parasympathetics innervation: superior saliva-
tory nucleus → nervus intermedius → chorda
tympani → submandibular ganglion→ lingual
nerve.
35.2.3 Sublingual Gland
– Mucinous cell type.
– Opens into ducts of Rivinus.
Fever, Sicca, arthralgia
And systemic symptoms
Sjogren Syndrome, Lymphoma,
Fungal or mycobacterial pathology
Viral Infections
• Observation
• Supportive Care
History & Physical
Acute
Sialadenitis
(pain, fever,
swelling)
Bacterial Infections
• Needle
Aspiration
• C&S
• Sialagogues
• Antibiotics
• Supportive
care
Obstructive Causes
• Dialation
• Sialodochoplasty
• Gland Excision
• Antibiotics
• Supportive care
Localised Symptoms
Recurrent/Chro
nic Sialadenitis
(Recurrent,
firm swelling)
X-ray, Sialogram,
CT
(Duct Evaluation)
Non Obstructive Causes
• Salivary Gland
biopsy
• Rheumatoid
Serologies
• Salivary analysis
• Needle biopsy
AL GRAWANY
35 Diseases oftheSalivary Glands
389
35.3 Salivary Gland Inammatory
Process
35.3.1 Acute Sialadenitis
35.3.1.1 Viral
– Mumps virus is the most common cause of
acute parotid enlargement. Other causes
include HIV, coxsackie, and inuenza.
– Peak incidence at 4–6years.
– Associated sudden sensorineural hearing loss,
pancreatitis, meningitis, and orchitis.
– Secondary to salivary obstruction or stasis.
– Symptoms include trismus, warmth, erythema
and tenderness over gland, purulence at ductal
orice, auricle may protrude (parotitis).
– Treatment similar to bacterial except for the
use of antibiotics.
35.3.1.2 Bacterial
– Ascendant ductal infection.
– Dehydration, diabetes, renal diseases, wrong
dental hygiene.
– S. aureus most common bacterial cause.
Followed by Streptococcus viridans, H. inu-
enzae, S. pyogenes, and E. coli.
– Diagnosed by clinical history and examina-
tion, cultures (FNA usually not required).
– Parotid most commonly infected due to stasis
in serous secretions which are less.
– Bacteriostatic than mucinous secretion.
– Treatment: rehydration, warm compresses,
antibiotics, sialogogues. If no resolution after
2–3days, then consider CT or U/S to evaluate
for abscess (may require I&D).
– Complications include deep neck space inva-
sion (Ludwig’s angina), ductal stula (cutane-
ous), abscess (toxemia).
35.3.2 Sialolithiasis (Figs.35.1 and35.2)
– More common in submandibular gland (high
mucin content, high PH, long duct with small
orice, and antigravity ow).
– 90% of submandibular calculi are radiopaque.
– 90% of parotid calculi are radiolucent.
– Symptoms include swelling and recurrent
pain, worse with meals (salivary colic).
– Recurrent painful swelling at mealtime.
– Diagnosed by palpating the stone, sialogra-
phy, CT, US.
– Treatment—gland massage, gland excision,
sialoendoscopy.
– Complications include stula, acute suppura-
tive sialadenitis, ductal stricture.
Fig. 35.1 Left submandibular gland stone (yellow arrow)
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Fig. 35.2 Right parotid duct stone
H. Haidar et al.
35.3.5 Sjogren’s Syndrome
– Triad of symptoms: xerostomia, keratocon-
junctivitis sicca, and a connective tissue
disorder (rheumatoid arthritis in over 50% of
the cases).
– Women are affected by Sjogren’s syndrome
more frequently than men.
– The parotid glands generally are enlarged
bilaterally and the patient may have noticed a
chronic progressive enlargement.
– Major histopathologic features are atrophy and
loss of acinar tissue, with distortion of lobular
architecture. Lymphoid inltration occurs.
35.3.6 Recurrent Parotitis
Secondary to sialectasis, autoimmune disease
(Mikulicz’s disease, Sjogren’s) or nonautoimmune (Mikulicz’s syndrome—recurrent sialoadenitis, sialosis, multi-nodular gland).
35.3.3 Uveoparotid Fever
(Heerfordt’s Disease)
– Variant of sarcoidosis (seen in third to fourth
decade).
– More common among women.
– Symptoms include parotitis, uveitis, CN VII
paralysis in 50% of patients, sensorineural
hearing loss, fever.
– Diagnosis conrmed with ACE levels.
– Treatment—steroids and ocular care.
35.3.4 Kuttner’s Tumor (Chronic
Sclerosing Sialadenitis)
– Autoimmune disease.
– Symptoms include rm, enlargement of the
submandibular gland (can be mistaken as a
malignancy), may be painful.
– Diagnosed on biopsy.
– Histopathology shows chronic inammatory
changes with destruction of acinar cells, scle-
rosis, and “cirrhotic” changes.
– Treatment is submandibular excision for diag-
nosis and treatment.
35.3.7 Benign Lymphoepithelial
Cysts
– Associated with HIV.
– Differential diagnosis—branchial cleft cyst,
epidermoid cyst, dermoid cyst, mucocele,
sialocele (pseudocyst).
– Treatment: aspiration or excision.
35.3.8 Necrotizing Sialometaplasia
– Inammatory process that mimics malignancy.
– Presents as ulceration or nodular lesion of the
minor salivary glands.
– Easy to mistake as malignancy histopatholog-
ically (pseudoepitheliomatous hyperplasia).
– Treatment: self-resolution.
35.4 Salivary Gland Neoplasms
Less than 2% are malignant.
Most neoplasms are in parotid 75%, most of
them are benign.
AL GRAWANY
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