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17 Thyroid andParathyroid Diseases
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• Superior glands arise from fourth pouch
• Shorter descent→much less variability
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Anatomy
• Paired superior and inferior glands (4) → typically 70–80% are found to be
symmetric
• Typically weigh 35–40mg with average diameter of 3–8mm
• Variability of location
• Inferior: large area, from angle of mandible to pericardium
• Most common ectopic location anterior mediastinum
• Typically found with plane drawn along recurrent laryngeal nerve
• 1cm inferior, lateral or posterior to inferior pole of thyroid
• Superior: little variation in descent
• 85% can be found at posterior aspect of thyroid lobe in 1cm above crossing of
inferior thyroid artery and recurrent nerve
Epidemiology
• Adenoma prevalence in range of 0.1–0.4%, with highest incidence at 50–60 years
• 80–85% present with single adenomas, 10–15% with multi-gland disease, 5%
with double adenoma, and 1% with parathyroid cancer
• Higher frequency: women and history of neck irradiation
• Primary hyperparathyroidism most common cause of hypercalcemia in outpatient setting
Pathophysiology
• Parathyroid glands detect changes in serum calcium via calcium-sensing receptor
– Regulation of calcium levels via production of PTH
– PTH in turn acts on several receptors systemically up- or downregulating cal-
cium metabolism
• Primary hyperparathyroidism from an adenoma results in uninhibited production
of PTH→elevated serum calcium
• Must rule out other causes of hyperparathyroidism: chronic renal disease, thiazide diuretic use, lithium use, familial hypocalciuric hypercalcemia (FHH),
MEN I, MEN IIa, hyperparathyroidism–jaw tumor syndrome, neonatal severe
primary hyperparathyroidism, parathyroid cancer
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N. M. Phan et al.
Primary Hyperparathyroidism
Presentation
• Primary presenting sign: hypercalcemia with 80% asymptomatic or vague
symptoms
– Neurologic symptoms: fatigue, depression, memory loss, decreased concen-
tration, sleep changes
– Renal symptoms: nephrolithiasis (20%), hypercalciuria
– Bone symptoms: bony pain, osteitis, osteopenia, osteoporosis, fractures, mus-
cle weakness
Diagnosis/Work-Up
• Serum calcium levels, PTH levels, vitamin D, phosphorus, creatinine clearance,
24-h urine calcium
• Bone densitometry
• Neck imaging not indicated for diagnosis, but helpful for localization
• High-resolution ultrasound: inexpensive and allows concurrent study of the thyroid gland as 18% may have synchronous thyroid disease
• Sensitivity 72–85%
• Technetium 99 Sestamibi: avid uptake by adenomatous and hyperplastic parathyroid glands
• Sensitivity 76–88%
• Combination of techniques helps to increase sensitivity to 95%
Guidelines for surgical treatment of asymptomatic primary hyperparathyroidism
• Serum Ca >1 mg/dL above upper limit of normal
• CrCl <60mL/min
• Diminished bone density (T score <−2.5 or fragility fracture)
• Age <50 years
• Difcult follow-up
• Newer MRI and 4-D CT functional imaging has improved localization of adenomas especially for ectopic locations
• Multi-glandular disease difcult to image accurately
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Treatment
• Intraoperative parathyroid hormone assay: allows the determination of continued
disease and helps to prevent missed adenoma
• Utilize the Miami criteria: 50% or greater drop from highest PTH level to PTH
level measured 10min postgland excision
• Accuracy of 97%
• Minimally invasive parathyroid surgery: 2.5cm incision over anterior neck
• 97% success rate→preoperative localization is key
• Unilateral neck exploration if needed to explore and converted to bilateral if
gland cannot be located
• Complications
– Persistent hyperparathyroidism
– Recurrent laryngeal nerve injury
– Transient postoperative hypocalcemia
Parathyroid Carcinoma
• Frequency of 1% of patients with primary hyperparathyroidism, prevalence of
0.005% of all cancers, with typical age of onset 40–50s
• Majority of tumors are functional (secrete PTH), nonfunctional tumors present
as expanding neck mass with late diagnosis and typically have poorer prognosis
• Elevated calcium and PTH levels markedly elevated compared to adenomas
• Intraoperative appearance typically hard lobulated brous mass
• En bloc resection is key with resection of ipsilateral 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
Further Reading
1. Ahmad R, Hammond JM.Primary, secondary, and tertiary hyperparathyroidism. Otolaryngol
Clin North Am. 2004;37(4):701–13, vii–viii.
2. Akerstrom G, Malmaeus J, Bergstom R. Surgical anatomy of human parathyroid glands.
Surgery. 1984;95(1):14–21.
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3. Ball DW.American Thyroid Association guidelines for management of medullary thyroid cancer: an adult endocrinology perspective. Thyroid. 2009;19(6):547–50.
4. Bentrem DJ, etal. Is preoperative investigation of the thyroid justied in patients undergoing
parathyroidectomy for hyperparathyroidism? Thyroid. 2002;12(12):1109–12.
5. Bilezikian JP, Khan AA, Potts JT Jr. Guidelines for the management of asymptomatic primary hyperparathyroidism: summary statement from the third international workshop. J Clin
Endocrinol Metab. 2009;94(2):335–9.
6. Busaidy NL, et al. Parathyroid carcinoma: a 22-year experience. Head Neck.
2004;26(8):716–26.
7. Edge SB, Compton CC. The American Joint Committee on Cancer: the 7th edition of the
AJCC cancer staging manual and the future of TNM.Ann Surg Oncol. 2010;17(6):1471–4.
8. Fish SA, Langer JE, Mandel SJ.Sonographic imaging of thyroid nodules and cervical lymph
nodes. Endocrinol Metab Clin North Am. 2008;37(2):401–17, ix.
9. Fraser WD.Hyperparathyroidism. Lancet. 2009;374(9684):145–58.
10. Hoyes AD, Kershaw DR.Anatomy and development of the thyroid gland. Ear Nose Throat
J. 1985;64(7):318–33.
11. Hundahl SA, etal. A National Cancer Data Base report on 53,856 cases of thyroid carcinoma
treated in the U.S., 1985-1995 [see commetns]. Cancer. 1998;83(12):2638–48.
12. Hundahl SA, et al. Two hundred eighty-six cases of parathyroid carcinoma treated in the
U.S. between 1985-1995: a National Cancer Data Base Report. The American College of
Surgeons Commission on Cancer and the American Cancer Society. Cancer. 1999;86(3):538–44.
13. Irvin GL III, Solorzano CC, Carneiro DM.Quick intraoperative parathyroid hormone assay:
surgical adjunct to allow limited parathyroidectomy, improve success rate, and predict outcome. World J Surg. 2004;28(12):1287–92.
14. Johnson NA, Tublin ME, Ogilvie JB.Parathyroid imaging: technique and role in the preoperative evaluation of primary hyperparathyroidism. Am J Roentgenol. 2007;188(6):1706–15.
15. Kloos RT, etal. Medullary thyroid cancer: management guidelines of the American Thyroid
Association. Thyroid. 2009;19(6):565–612.
16. Lin JD, etal. Thyroid cancer in the thyroid nodules evaluated by ultrasonography and neneedle aspiration cytology. Thyroid. 2005;15(7):708–17.
17. Mack LA, Pasieka JL.Asymptomatic primary hyperparathyroidism: a surgical perspective.
Surg Clin North Am. 2004;84(3):803–16.
18. Pai SI, Tufano RP.Central compartment neck dissection for thyroid cancer. Technical considerations. ORL J Otorhinolaryngol Relat Spec. 2008;70(5):292–7.
19. Rodgers SE, Lew JI, Solorzano CC. Primary hyperparathyroidism. Curr Opin Oncol.
2008;20(1):52–8.
20. Ruda JM, Hollenbeak CS, Stack BC Jr. A systematic review of the diagnosis and treatment of primary hyperparathyroidism from 1995 to 2003. Otolaryngol Head Neck Surg.
2005;132(3):359–72.
21. Ruegemer JJ, etal. Distant metastases in differentiated thyroid carcinoma: a multivariate analysis of prognostic variables. J Clin Endocrinol Metab. 1988;67(3):501–8.
22. Skandalakis JE, Droulias C, Harlaftis N, et al. The recurrent laryngeal nerve. Am Surg.
1976;42(9):629–34.
23. Smallridge RC, Copland JA.Anaplastic thyroid carcinoma: pathogenesis and emerging therapies. Clin Oncol. 2010;22(6):486–97.
24. Wang C.The anatomic basis of parathyroid surgery. Ann Surg. 1976;183(3):271–5.
25. Wei CH, Harari A.Parathyroid carcinoma: update and guidelines for management. Curr Treat
Options Oncol. 2012;13(1):11–23.
26. Upile T, Jerjes W, Mahil J, Tailor H, Balakumar R, Rao A, etal. How to do it: the difcult
thyroid. Head Neck Oncol. 2011;3:54.
27. Cibas ES, Ali SZ.The 2017 Bethesda System for reporting thyroid cytopathology. Thyroid.
2017;27(11):1341–6.
N. M. Phan et al.
17 Thyroid andParathyroid Diseases
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28. Tuttle RM, Haugen B, Perrier ND, Tuttle M.The updated AJCC/TNM staging system for
differentiated and anaplastic thyroid cancer (8th edition): what changed and why? [cited 2020
Feb 16].
29. Lamki Busaidy N, Dickson P, Jude S, Duh Q-Y, Helen Diller Family U, Ehya H, etal. NCCN
Guidelines Version 2.2019 Thyroid Carcinoma NCCN Guidelines Panel Disclosures, 2019.
30. Tessler FN, Middleton WD, Grant EG, Hoang JK, Berland LL, Teefey SA, et al. ACR
Thyroid Imaging, Reporting and Data System (TI-RADS): white paper of the ACR TI-RADS
Committee. J Am Coll Radiol. 2017;14(5):587–95.
31. Ferris RL, Baloch Z, Bernet V, Chen A, Fahey TJ, Ganly I, etal. American Thyroid Association
statement on surgical application of molecular proling for thyroid nodules: current impact on
perioperative decision making. Thyroid. 2015;25(7):760–8.
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Chapter 18
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Salivary Gland Diseases
ZacharyG.Schwam andMohemmedKhan
Pearls
• Unlike many other head and neck neoplasms, histologic grade plays a signicant
role in tumor treatment and prognostication
• MRI is the imaging modality of choice for salivary neoplasms; however, there
are roles for CT and ultrasound
• As the glands get progressively smaller, the higher the likelihood that a mass is
malignant (sublingual>submandibular>parotid).
Saliva
• Approximately 1.5L of saliva is made daily, with two-third of basal saliva pro-
duced by the submandibular gland and two-third of stimulated saliva made by
the parotid.
• Saliva is 99.5% water and is slightly hypotonic/basic as compared to plasma.
Additional secretory components include salivary amylase, glycoproteins, IgA,
lysozymes, lactoferrin, and growth factors. Saliva lubricates and moistens food,
and protects mucosa.
• Saliva not only prevents dental plaque formation but also enhances tooth remin-
eralization, thereby preventing caries.
• The parotid gland secretes predominantly serous saliva, while the submandibular
and sublingual glands secrete progressively more mucinous saliva.
Z. G. Schwam (*) · M. Khan
Department of Otolaryngology - Head and Neck Surgery, Icahn School of Medicine at the
Mount Sinai Hospital, New York, NY, USA
e-mail: Zachary.schwam@mountsinai.org; mohemmed.khan@mountsinai.org
© Springer Nature Switzerland AG 2023
F. Y. Lin, Z. M. Patel (eds.), ENT Board Prep,
https://doi.org/10.1007/978-3-031-26048-3_18
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Z. G. Schwam and M. Khan
Microstructure oftheDuctal System
• Acinar cells clustered around a lumen, which ow into intercalated, striated, and
excretory ducts. Acini are surrounded by myoepithelial cells which aid in contraction and secretion.
• Each acinar cell is highly specialized, with the apical side of each cell facing the
lumen of the acinus and functioning in an excretory capacity.
Anatomy
Parotid Gland
• The parotid is the largest of the salivary glands and is responsible for approxi-
mately two-third of stimulated saliva production. It is derived from the rst pharyngeal pouch.
• The parotid gland is bordered posteriorly by the external auditory canal, superi-
orly by the zygomatic arch, anteriorly by the buccinator muscle, and overlies the
masseter and mandible. It is attached to the sternocleidomastoid muscle.
Overlying the parotid is the parotidomasseteric fascia, which is a continuation of
the supercial musculoaponeurotic system (SMAS), temporoparietal fascia
superiorly, and platysma inferiorly.
• The parotid has a supercial and deep lobe separated by the plane of the facial
nerve. Deep lobe parotid tumors may enter the parapharyngeal space via the
stylomandibular tunnel. Stensen’s duct is approximately 1 cm inferior to the
zygomatic arch and empties into the oral cavity via a papilla in the buccal mucosa
found opposite the maxillary second molar.
• Accessory parotid tissue is commonly found anterior to the main gland and emp-
ties into the main ductal system. This is in contrast to ectopic salivary tissue,
which is typically found in the neck and not connected to the rest of the ductal system.
• The retromandibular vein runs through the substance of the gland and serves as
a landmark for the approximate depth of the facial nerve. It empties into the
external jugular vein as well as the internal jugular system.
• Innervation
– Parasympathetic pathway: Inferior salivatory nucleus (medulla) → glosso-
pharyngeal nerve→ tympanic plexus (Jacobson’s nerve)→ lesser petrosal
nerve → otic ganglion (synapse) → auriculotemporal nerve (branch of
V3)→parotid gland
– Sympathetic pathway: Intermediolateral horn of the spinal cord→superior
cervical ganglion → branches following the external carotid system→parotid gland.
• The parotid gland is the only one with intraglandular lymph nodes.
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Submandibular Gland
• The submandibular gland (SMG) is located within the submandibular triangle
between the anterior and posterior bellies of the digastric muscle and supercial
to the mylohyoid.
• Overlying the SMG is the supercial layer of the deep cervical fascia. Within this
fascia is the marginal mandibular branch of the facial nerve. The facial artery
runs through the substance of the gland, and the posterior facial vein over the
posterior aspect.
• The SMG wraps around the posterior aspect of the mylohyoid, giving off
Wharton’s duct, which travels in the oor of mouth in close proximity to the
lingual nerve, to exit sublingually adjacent to the sublingual ducts of Rivinus.
The course of this duct is slightly antigravity.
• Parasympathetic innervation: superior salivatory nucleus → chorda tympani,
which joins the lingual nerve→submandibular ganglion (synapse)→SMG
• Sympathetic innervation: Same as parotid gland.
Sublingual Gland
• Smallest named glands. Located in the sublingual space and open into the ducts
of Rivinus.
Diagnostics
• Sialography
– Previously, this required cannulation of the ductal systems with injection of
radiopaque material. More recently, non-invasive techniques such as MRsialography are not only more convenient, but can be used in chronic and
acute settings. Strictures and anatomy are easily visualized. Traditional sialography should not be performed in cases of acute sialadenitis or in those
with allergies to iodinated contrast material.
• Sialendoscopy
– The papillae of the ducts are rst dilated with lacrimal-type probes, then the
ducts are cannulated with very small endoscopes (1.1 mm is the smallest
working-channel scope available), and the ductal system can be visualized.
Through a working channel, debris can be ushed, the system can be irrigated
with steroid, and small sialoliths <5mm may be removed with a variety of
instruments.
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• CT
– Excellent for delineating gross anatomy, disruption of fat planes, identifying
sialoliths, and looking for nodal disease. CT is also the preferred modality for
evaluating bony erosion in extensive disease.
• MRI
– MRI is the preferred imaging modality for salivary neoplasms. It provides
excellent delineation between normal and abnormal soft tissue with more
granularity and nuance as compared to CT.
• Ultrasound ± FNA
– A very cost-effective, simple test for evaluating cystic and solid pathology
and for guiding ne-needle aspiration (FNA). Abnormal lymph nodes can
also be distinguished in parotid pathology by loss of their fatty hila.
Z. G. Schwam and M. Khan
Salivary Gland Diseases
• Acute Sialadenitis
– Secondary to salivary obstruction or stasis. The parotid is most commonly
affected as serous secretions are less bacteriostatic than mucinous material in
the smaller glands. Stasis may be due to inammation and dehydration while
obstruction is typically due to stones or strictures.
– Treatment consists of antibiotics, sialogogues, warm compresses, and
rehydration.
• Sialolithiasis
– Sialoliths are more common in the submandibular gland due to the antigravity
trajectory of the duct and more mucinous saliva. Submandibular sialoliths are
more commonly found in the duct, while parotid stones are frequently in the
hila of the gland.
– Stones can be retrieved via sialendoscopy if ≤5mm in diameter in either
gland. Submandibular stones that can be palpated in the oor of mouth may
be cut down on and extracted. Gland extraction is a last resort.
• Sjogren’s disease
– More common in HLA-B8 and HLA-Dr3 genotypes. Characterized by dry
eyes and dry mouth, anti-Ro (SSA) and anti-La (SSB) antibodies, and
enlarged salivary glands. Minor salivary gland biopsy may show lymphocytic inltration and increase in the number of myoepithelial islands.
There is a higher rate of Hodgkin lymphoma from prolonged B-cell
stimulation.
– Treatment is with articial saliva, pilocarpine, and good oral care.
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• Sarcoidosis/Heerfordt syndrome
– “Uveoparotid fever” with uveitis and parotitis, facial nerve palsy. A variant of
sarcoidosis
• Infectious
– S. aureus, strep. viridans
– Atypical mycobacteria: may have a violaceous hue to the overlying skin
– Actinomycosis: Gram positive, anaerobic. Characterized by sulfur granules,
sinus tracts, and multiloculated abscesses. Treatment: Penicillin G IV followed by PO erythromycin or clindamycin.
– Bartonella (catscratch): May be seen in the parotid lymphatics. Diagnosed
with serology/PCR as well as Warthin Starry staining. Treatment: Azithromycin
– Toxoplasmosis: Protozoan from undercooked meat or exposure to infected cat
feces. Treatment is with pyrimethamine and sulfadiazine.
– Mumps: A viral cause of parotitis, which may be unilateral but is classically
bilateral. May get sensorineural hearing loss, pancreatitis, orchitis, and meningitis. Diagnosis is typically with RT-PCR for mumps virus or with IgM for
mumps antigens.
• Sialorrhea/ptyalism
– Can be treated with scopolamine, botox, or glycol. Duct ligation will cause
sialadenitis and stulization
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• Xerostomia
– When radiation-induced (effects typically seen >25Gy of external beam or
with radioactive iodine), due to acinar cell loss.
– Amifostine can be used as a radioprotector and assists in DNA repair.
– Stenosis and mucus plugging secondary to radioactive iodine can be addressed
with sialendoscopy.
Salivary Gland Tumors
• Benign lesions
– Pleomorphic adenoma: the most common salivary lesion in adults. Incomplete
brous capsule, epithelial, and stromal components. Enucleation has unac-
ceptably high rates of recurrence. Complete resection with small cuff of sur-
rounding tissue recommended. On MRI, T1 dark, T2 bright. They are often
polylobular/bosselated in shape. No enhancement PET+ and Technetium-99+.
– Warthin tumor (papillary cystadenoma lymphomatosum): double layers of
epithelium over a lymphoid stroma with germinal centers. May be bilateral
and often associated with male smokers. MRI: T1 dark with bright cholesterol
cysts, T2: variable. FDG-PET+.
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