Head and neck Flashcards

1
Q
A
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2
Q

Classify the differential diagnoses of neck lumps according to the triangle/area they present.

A

Anywhere:

  • Epidermoid inclusion cyst, sebaceous cyst
  • Lipoma
  • Sarcoma

Midline:

  • Thyroid
  • Thyroglossal cyst
  • Dermoid cyst (does not move with swallowing/tongue protrusion)

Anterior triangle:

  • Lymph node
  • Thyroid nodule
  • Branchial cyst/fistula
  • Carotid body tumour
  • Carotid aneurysm
  • Cold abscess
  • Retropharyngeal abscess
  • Sternomastoid pseudotumour

Posterior triangle:

  • Lymph node
  • Zencker’s diverticulum
  • Cervical rib
  • Subclavian aneurysm
  • Cystic hygroma
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3
Q

What are the pharyngeal arches and pouches?

A

The pharyngeal arches appear in the 4th or 5th wk of development. Initially they consists of bars of mesenchymal tissue separated by deep clefts known as pharyngeal clefts on the external/ectodermal surface of the embryo (NB 5th arch rudimentary and only 4 clefts visible). Simultaneously a number of outpocketings, the phayrngeal pouches, appear along the lateral walls of the pharyngeal gut, the most cranial part of the foregut; these are on the endodermal side between the arches, opposite the clefts (4th and 5th pouches share a common opening into the lumen of the pharynx).

Each pharyngeal arch consists of a core of mesenchymal tissue covered on the outside by surface ectoderm and on the inside by epithelium of endodermal origin. In addition to the mesenchyme derived from paraxial and lateral plate mesoderm, the core of each arch receives substantial numbers of neural crest cells, which migrate into teh arches to contribute to skeletal components of the face. Original mesoderm of the arches gives rise to musculature of the face and neck. Thus, each pharyngeal arch is characterised by its own:

  • muscular components
  • the muscular components of each arch have their own cranial nerve, and wherever the muscle cells migrate, they carry their own nerve component with them
  • arterial component
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4
Q

What are the msucular contributions, skeletal contributions, nerve and artery associated with the 1st pharyngeal arch?

A
  • 1st pharyngeal arch also called ‘mandibular arch’
  • skeletal contributions
    • dorsal portion = maxillary process - gives rise to premaxilla, maxilla and zygomatic bone + part of temporal bone through membranous ossification
    • ventral portion = mandibular process
      • contains Meckel’s cartilage; during further development Meckel’s cartilage disappears except for 2 small portions at its distal end that form the incus and malleus
      • mandible is formed by membranous ossification of mesenchymal tissue surrounding Meckel’s cartilage
      • also sphenomandibular ligament
  • muscular contributions:
    • muscles of mastication (temporalis, masseter, pterygoids), anterior belly of digastric, mylohyoid, tensor tympani, tensor veli palatini
  • nerve supply to muscles of first arch: by mandibular branch of trigeminal nerve (?and maxillary branch)
  • since mesenchyme from first arch also contributes to dermis of face, sensory supply to skin of face is provided by ophthalmic, maxillary and mandibular branches of trigeminal nerve
  • artery: maxillary artery, external carotid artery
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5
Q

What are the components of the second pharyngeal arch?

A
  • aka hyoid arch
  • cartilage gives rise to: stapes, styloid process, stylohyoid ligament, lesser horn and upper part of body of hyoid
  • muscles = stapedius, stylohyoid, posterior belly of digastric, auricular, muscles of facial expression
  • facial nerve
  • stapedial artery, hyoid artery
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6
Q

What are the components of the third pharyngeal arch?

A
  • cartilage produces lower part of body and greater horn of hyoid bone
  • musculature: stylopharyngeus
  • glossopharyngeal nerve
  • artery: common carotid, internal carotid
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7
Q

What are the components of the fourth and sixth pharyngeal arches?

A
  • cartilaginous components of these 2 arches fuse to form the thyroid, cricoid, arytenoid, corniculate and cuneiform cartilages of the larynx
    • other notes say 4th gives thyroid cartilage and epiglottic cartilage, while 6th gives cricoid, arytenoid, corniculate and cuneiform
  • muscles
    • 4th: cricothyroid, all intrinsic muscles of soft palate (including levator veli palatini) except tensor veli palatini
    • 6th: all intrinsic muscles of the larynx except cricothyroid
  • nerve
    • 4th: vagus nerve, superior laryngeal nerve
    • 6th: vagus nerve, recurrent laryngeal nerve
  • artery
    • 4th: right 4th aortic arch: subclavian artery, left 4th aortic arch: aortic arch
    • 6th: right 6th aortic arch: pulmonary artery and ductus arteriosus
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8
Q

What are the pharyngeal pouches?

A

The pharyngeal pouches are formed on the endodermal side of the primitive pharynx between the arches, opposite the clefts. The last of the 5 pharyngeal pouches is atypical and often considered part of the 4th.

First pouch - forms Eustachian tube and middle ear cavity; comes into contact with epithelial lining of first pharyngeal cleft, the future external auditory meatus

Second pouch - forms tonsillar fossa

Third pouch - 3rd and 4th pouches characterised at their distal extremity by a dorsal and a ventral wing. in 5th week, epithelium of dorsal wing of 3rd pouch differentiates into inf parathyroid gland, while ventral wing forms thymus. Both gland primordia lose their connection w the pharyngeal wall, and teh thymus then migrates in a caudal and medial direction, pulling inf parathyroid with it. Parathyroid tissue of third pouch finally comes to rest on dorsal surface of thyroid gland and forms inf parathyroid gland

Fourth pouch - epithelium of dorsal wing of 4th pouch forms superior parathyroid gland. When PT gland loses contact w wall of pharynx, it attaches itself to dorsal surface of teh caudally migrating thyroid as teh superior praathyroid

Fifth pouch - ultimobranchial body, which is later incorporated into thyroid gland; cells of ultimobranchial body give rise to the parafollicular or C cells, of thyroid gland (these cells secrete calcitonin, a hormone involved in regulation of the calcium level in the blood)

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9
Q

What is the consequence of a complete facial nerve injury?

What is the course of the facial nerve?

What are the most common sites of facial nerve injury?

A

LMN deficit involving all muscles of the ipsilateral face

Course of facial nerve:

  • arises in pons with a motor and sensory root
  • travels through int acoustic meatus & leaves skull via course through temporal bone (the facial canal)
  • exits facial canal via stylomastoid foramen just posterior to styloid process
  • turns superiorly to run just anterior to the ear
  • sensory branches come off early here (posterior auricular nerve)
  • main root continues anteriorly and inferiorly from here within the parotid gland dividing it into superficial and deep lobes
  • within the gland it branches into 5 main branches - temporal, zygomatic, buccal, marginal, mandibular, cervical

Most common sites of facial nerve injury:

  • intratemporal as a result of petrous temporal bone fractures (most common)
  • facial trauma - more likely to result in branch injury
  • parotidectomy - main branch or multiple branches
  • facial/anterior triangle surgery - most commonly injured is MM branch
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10
Q

What is Horner’s syndrome?

What are its common causes?

A

Horner’s syndrome = a combination of symptoms that arise when the sympathetic trunk is damaged. The signs and symptoms are ipsilateral to the lesion: miosis (constricted pupil), partial ptosis (a weak, droopy eyelid), apparent anhidrosis (decreased sweating), with or without enophthalmos (inset eyeball)

Can result from a lesion anywhere along a three-neuron sympathetic (adrenergic) pathway that originates in the hypothalamus

  • first-order neuron descends caudally from hypothalamus to first synapse, which is located in cervical spianl cord (C8-T2)
  • second-order neuron travels from sympathetic trunk, through the brachial plexus, over the lung apex, then ascends to the superior cervical ganglion, located near the angle of the mandible and the bifurcation of the CCA (C3-4)
  • third-order neuron ascends within adventitia of internal carotid artery, through the cavernous sinus, where it is in close relation to the 6th cranial nerve
    • oculosympathetic pathway then joins the ophthalmic (V1) division of the trigeminal nerve; in the orbit and the eye, these oculosympathetic fibres innervate the iris dilator as well as a small smooth muscle in the eyelids responsible for a minor portion of the upper lid elevation and lower lid retraction
  • NB the sympathetic fibres responsible for facial sweating and vasodilation branch off at the SCG; remainder of the oculosympathetic pathway has only a few sudomotor fibres which supply a v small strip of skin along the forehead - thus anhidrosis isn’t a prominent feature of postganglionic or third-order lesions

Common causes

  • Central/first-order syndrome (anhidrosis of face, arm and trunk) - lesions of sympathetic tracts in brainstem or cervicothoracic spinal cord; usu assoc w other neuro signs and sx
    • syringomyelia
    • MS
    • encephalitis
    • brain tumours
    • lateral medullary syndrome
  • Preganglionic/second-order syndrome (anhidrosis of face) - can occur w trauma or surgery involving the spinal cord, thoracic outlet or lung apex; often have ipsilateral axllary or arm pain too
    • cervical rib traction on stellate ganglion
    • thyroid carcinoma
    • thyroidectomy
    • goiter
    • bronchogenic carcinoma of superior fissure (Pancoast tumour) on apex of lung
    • delivery-related trauma in babies to neck and shoulder, often assoc w Klumpke paralysis
    • trauma - base of neck, usu blunt trauma, sometimes surgery
  • Postganglionic/second-order syndrome (no anhidrosis) - often indicate lesions of ICA
    • cluster headache - combination termed Horton’s headache
    • carotid artery dissection/carotid artery aneurysm
      • acute Horner syndrome w neck or facial pain should be presumed to be caused by carotid dissection until proven otherwise; these pts at high risk for cerebral infarction
    • cavernous sinus thrombosis
      • often have abnormalities of eye movements epsec 6th nerve palsy
    • middle ear infection
    • sympathectomy
    • nerve blocks, such as cervical plexus block, stellate ganglion or interscalene block

How to localise the origin of Horner syndrome – associated neurologic symptoms and signs may be helpful

  • Brainstem signs (diplopia, vertigo, ataxia, lateralised weakness) suggest a brainstem location
  • Myelopathic features (bilateral or ipsilateral weakness, long tract signs, sensory level, bowel and bladder impairment) suggest involvement of the cervicothoracic cord
  • Arm pain and/or hand weakness typical of brachial plexus lesions suggest a lesion in the lung apex
  • Ipsilateral extraocular pareses, particularly a 6th nerve palsy, in the absence of other brainstem signs localise the lesion to the cavernous sinus
  • An isolated Horner syndrome accompanied by neck or head pain suggests an intenral carotid dissection
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11
Q

Describe the treatment of sialolithiasis

A
  1. Conservative
    • Warm compress
    • Analgesia
    • Sialogogues (e.g. sherbert)
  2. Obtain imaging (USS, CT, Sialography)
  3. Sialoendoscopy where available
  4. Surgery
    • Good for submandibular calculi
    • Parotid more complicated
      • Avoid surgery (especially difficult if chronic inflammation)
      • Can use ESWL.
    • Can surgically remove just the stone in the duct - uncommon to perform this procedure.
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12
Q

Describe your examination of a parotid mass.

A
  • Inspect the mass for site, size, symmetry skin changes
  • Assess for signs of inflammation
  • Palpate the gland
  • Palpate the duct
  • Palpate the masseter muscle with teeth clenched
  • Examine the FACIAL NERVE
  • Examine the mouth and tonsils for lesions
  • Examine the ductal orifice opposite second molar
  • Watch orifice and apply pressure to gland to check for pus in inflammtory conditions
  • Examine the neck
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13
Q

What are the complications specific to salivary gland surgery?

A
  • Facial nerve palsy
    • 25% temporary
    • 1-5% permanent
    • Most commonly marginal mandibular
  • Frey’s syndrome (parotidectomy)
    • Up to 60%!
  • Salivary fistula
    • 1%
  • Lingual/hypoglossal nerve palsy
    • Submandibular gland surgery
    • ~1-3%
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14
Q

Discuss imaging in salivary gland masses.

A

Imaging of a salivary gland mass depends on the clinical indication, local availability, and expertise in imaging techniques and their interpretation.

Options include plain x-rays, sialography, USS, CT, MRI, and scintigraphy. Each has a place.

X-ray will pick up sialolithisis in the submandibular gland (90% stones opaque) but are less useful for parotid stones.

Sialography involves using a sialogogue first to stimulate saliva production to identify the duct, which is then cannulated & contrast injected under fluoroscopic control to ensure adeqaute filling; plain drays taken to identify filling defects, delays in emptying & extravasation. Digital subtraction sialography removes the pre-contrast image from post-contrast image to give improved identification of filling defects within the duct system.

Sialography is increasingly being replaced by USS and MRI for ductal pathology. USS is cheap, non-ionising, and excellent at imaging the superficial parotid and SMG. It allows for FNA. It is user dependent.

CT is distorted by dental artifact but is the modality of choice for bony involvement. MRI offers the best resolution for operative planning.

CT-PET is used to identify distant metastases.

The use of sialendoscopy is most applicable to pts who have sx of salivary galnd swelling on eating, indicative of a stone or stenosis; may distinguish between stones, stenosis, mucous plugs or debris within the duct, all of which may present in a similar manner

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15
Q

What are the causes of cervical lymphadenopathy?

A

L.I.S.T

Lymphoma

  • Usually NHL in the neck

Infection

  • Bacterial
  • Viral
  • Protozoal
  • Toxoplasmosis

Sarcoidosis

Tumour

  • Primary
    • Lymphoma, primary lesions masquerading as lymphadenopathy
  • Secondary
    • Nodal metastses from SCC, Melanoma, Upper GI, Lung, Thyroid
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16
Q

Describe the anatomy of branchial cleft fistulae/sinuses

A
  • 5 wk old embryo is characterised by the presence of 4 pharyngeal clefts, of which only 1 contributes to definite structure of embryo (dorsal part of 1st cleft penetrates underlying mesenchyme & gives rise to EAM)
  • active proliferation of mesenchymal tissue in 2nd arch cause it to overlap 3rd & 4th arches; finally buries 2nd, 3rd & 4th pharyngeal clefts
  • the clefts form a cavity lined w ectodermal epithelium, the cervical sinus, but w further development this sinus disappears
  • branchial fistulas occur when the 2nd pharyngeal arch fails to grow caudally over the 3rd & 4th arches, leaving remnants of the 2nd, 3rd and 4th clefts in contact w surface by a narrow canal
  • persistent complete communication between pharynx (in region of posteiror pillar of fauces) and skin (a complete branchial fistula) is rare, complex & may be assoc w various anatomical structures
  • more commonly, if the skin surface connections are lost, a branchial cyst develops
    • branchial cyst = congenital epithelial cyst, arises due to failure of obliteration of a (usu 2nd) branchial cleft - only its central portion remains
    • these cysts, remnants of cervical sinus = usu just below angle of jaw (though can be found anywhere along ant border of SCM); at least part is under anterior edge of upper 1/3 of SCM –> bulges forward into anterior triangle
  • branchial sinus = the cyst is assoc w a sinus tract to overlying skin (but has no communication w pharynx)
    • found on lateral aspect of neck directly anterior to SCM, usu at junction of middle and lower 1/3
  • internal branchial fistulas = rare; occur when cervical sinus is connected to lumen of pharynx by a small canal which opens in tonsil recess
    • usu results froma. rupture of the membrane between 2nd pharyngeal cleft & pouch at some time during development
  • if the origin is from the 1st branchial cleft, may give rise to a cyst in parotid region (indistinguishable from other parotid lumps) +/- may communicate as a sinus posteriorly w the EAM. or anteriorly w an opening of the skin of the mandibular region (or a complete fistula between the two)
17
Q

Classify the cervical spaces affected by soft tissue infection.

A
  1. Suprahyoid spaces
    • Masticator
    • Buccal
    • Parotid
    • Submandibular
      • below mylohyoid & deep to investing layer of fascia between hyoid bone & mandible
      • communicates around posterior border of mylohyoid with sublingual space
    • Sublingual
      • under mucous membrane of floor of mouth
      • Ludwig’s angina = rare but severe form of cellulitis that involves sublingual & submandibular space & spreads backwards into parapharyngeal space
    • Parapharyngeal
      • in lateral aspect of neck, shaped like inverted cone - base at skull & apex at hyoid bone
      • (upper part of this space is in infratemporal fossa, bounded laterally by pterygoid muscles & parotid sheath)
      • divided by styloid process & muscles into
        • anterior (nothing) compartment
        • posterior (CN IX, X, XI, XII) compartment
      • communicates medially with retropharyngeal space
  2. Infrahyoid spaces
    • Pre-tracheal
      • behind pre-tracheal fascia
  3. Spaces that involve the entire length of the neck
    • Retropharyngeal space
      • bound anteriorly by constrictor muscles of the neck & posteriorly by alar layer of deep cervical fascia
    • “Danger” space (alar-prevertebral space)
      • between alar and prevertebral fascia
      • potential space all the way down to mediastinum
    • Prevertebral space
      • infection in this space can track all the way down the spinal column
    • Carotid space
    • Superficial space
      • superficial to investing fascia
19
Q

How is facial nerve palsy/injury assessed?

A

Examination and classification according to the House-Brackman scale.

20
Q

Provide an overview of salivary gland lesions.

A
  • non-neoplastic
    • acute inflammatory conditions
      • acute bacterial infection - e.g. staph aureus, H influenza
      • acute viral inflammation - e.g. mumps
    • chronic inflammatory conditions
      • mycobacterium tuberculosis
      • atypical tuberculosis
      • cat-scratch disease
      • actinomycosis
      • sarcoidosis
      • Sjogren’s syndrome
      • HIV
  • non-inflammatory, non-neoplastic conditions
    • sialosis/sialodenosis
    • salivary gland cystst/mucoceles/ranulae
    • xerostomia post RTX
    • (sialolithiasis - not really a lesion)
  • neoplastic
    • benign epithelial lesions - 13 histo subtypes
      • Pleomorphic adenoma
      • Warthin’s
      • other e.g. basal cell adenoma, myoepeithelioma, oncocytoma
    • benign non-epithelial lesions
      • haemangiomas
      • lipomas
    • malignant epithelial lesions - 24 histo subtypes
      • mucoepidermoid carcinoma
      • adenoid cystic carcinoma
      • acinic cell carcinoma
      • polymorphous low grade adenocarcinoma
    • malignant non-epithelial neoplasms
      • lymphoma
      • metastatic cutaneous malignancy
21
Q

How are non-neoplastic diseases of the salivary glands classified? Provide details.

A

Acute inflammatory conditions

  • Acute viral inflammation
    • Mumps (resurgence) causes parotitis; usually bilateral
  • Acute bacterial inflammation
    • Occurs in dehydrated (post-op) patients
    • Staph aureus most common aetiology
    • May be polymicrobial; cover anaerobes

Chronic inflammatory conditions

  • Mycobacterium tuberculosis
  • Atypical tuberculosis
    • MAC
    • May be treated with Abx or excision by paeds surgery.
  • Cat-scratch disease
    • Bartonella henselae. No Abx. Expectant.
  • Actinomycosis
    • Painless, hard masses in the neck
    • Long course Abx and debridement.
  • Sarcoidosis
    • Multisystem inflammatory disease
    • Non-caseating granulomas
    • Steroids and immune modulators.
  • Sjögren’s syndrome
    • Anti Ro and Anti La antibodies.
    • High risk of MALToma.
  • HIV

Non-inflammatory conditions

  • Sialosis
  • Salivary gland cysts / mucocoeles / ranulae
  • Post-radiotherapy xerostomia

Sialolithiasis

  • Submandibular >> Parotid (duct length, more mucin in former)
  • Diuretics and smoking are established RF
22
Q

How are neoplasms of the salivary glands classified?

Provide details in terms of histological diagnoses and relative frequency.

A

Benign epithelial neoplasms

  • ~7 per 100,000
  • 70% PA, 20% WT, 10% other
  • Heterogenous group
  • Classified histologically; 13 sub-types
    • Pleomorphic Adenoma
      • Most common, usually parotid
      • Slow growing painless mass
      • 1% per annum malignant transformation
    • Warthin’s tumour
      • aka adenolymphoma, papillary cystic lymphomatosum
      • Exclusively in Parotid
      • 10% bilateral, associated with smoking
      • Classically older men
    • Other e.g Basal Cell Adenoma, Myoepithelioma
  • Enucleation unacceptable now
  • Extracapsular dissection preserving nerve is standard of care.

Malignant epithelial neoplasms

  • 24 subtypes; the majority (70%) will have:
    • Mucoepidermoid carcinoma
    • Adenoid cystic carcinoma
    • Acinic cell carcnioma
    • Polymorphous low grade adenocarcinoma
  • MEC is most common; favourable outcome
  • ACC is next most common; poor outcome ~35% 5-year-survival
  • Management is dependent on grade and size
    • High-grade or large (>4cm) tumours require aggressive treatment - gland excision and selective neck dissection if node negative.
    • Node positive disease is treated with modified radical neck dissection.

Benign non-epithelial neoplasms

  • Haemangiomas most commonly affect the parotid gland in children.
  • Lipomas may also affect salivary glands.

Malignant non-epithelial neoplasms

  • Lymphoma most common non-epithelial primary
  • Metastatic cutaneous malignancy most common overall cause for malignant mass in parotid in NZ/AUS!!
23
Q

What are the anatomic sub-sets of Head and Neck cancer?

What is the major histopathological diagnosis?

A
  1. Oral Cavity
  2. Pharynx (naso-, oro-, hypo-)
  3. Larynx
  4. Nasal cavity and paranasal sinuses
  5. The major and minor salivary glands

>95% Squamous Cell Cancer

24
Q

What is Frey’s syndrome?

A

Frey’s syndrome is a pathophysiological phenomenon characterised by gustatory sweating - sweating, erythema or warmth over parotid bed area whilst eating.

It is thought to be due to PS nerve fibres from the auriculotemporal nerve re-anastamosing with sweat glands following parotidectomy.

The reported incidence is as high as 60%.

Botox may alleviate symptoms.

Several surgical methods to reduce it: SCM flap insertion, SMAS flap, dermal fillers and fat graft

25
Q

What is a plunging ranula?

A

Ranulae are a particular type of mucocoele; where obstruction of a sub-lingual gland has resulted in an extravasation mucocoele. It is termed “plunging” when it penetrates myelohyoid.

26
Q

What are the causes of cervical lymphadenopathy?

A

Infective

  • Viruses - EBV, HIV, viral tonsillitis
  • Mycobacteria - MAC, TB (cold)
  • Parasitic/Helminth - Toxoplasmosis, filarial
  • Bacterial - Chlamydia, Syphilis

Inflammatory

  • Sarcoidosis
  • Reactive

Neoplastic

  • Benign - Castleman’s disease
  • Primary
    • Reticulosis
    • Lymphoma
    • Lymphosarcoma
  • Secondary
    • Metastatic
      • Upper aerodigestive tract
      • Head and neck
      • Skin
      • Thyroid
      • Breast
      • Upper GI
27
Q

What are the important features of a salivary gland mass to note in the patient’s history?

A
  • How long has it been present?
  • Is pain a feature?
  • Does the lesion change with eating?
  • Is the whole gland affected?
  • Is more than one gland affected?
  • Is there a past medical history of chronic inflammatory disorders?
28
Q

What are the indications for adjuvant radiotherapy in salivary gland tumours?

Is there any role for chemotherapy?

A

Heterogenous group of histologically distinguishable tumours; 24 subtypes by WHO.

Generally speaking, radiotherapy improves local control but the impact on survival is unclear. T1/2 tumours (<4cm, not invading locally) do not require adjuvant RTx.

Radiotherapy is recommeded for large lesions, close margins, tumour spill, recurrence, and node positive disease.

There is no established role for chemotherapy.

29
Q

What is the aetiology/pathogenesis of sialolithiasis?

A
  • aren’t precipitated by metabolic disorders like renal stones
  • tend to be composed of calcium carbonates & phosphates along with glycoproteins adn mucopolysaccharids
  • theories for stone formation include
    • occurrence of intracellular microcalculi which form a nidus when excreted into the duct
    • or mucous plugs of sliva may act as the nidus
  • more common in smokers and those on diuretics
  • submandibular gland more commonly affected (60-70%)
    • longer duct, saliva more mucinous and flow is against gravity, predisposing to stone formation
  • vs salivary flow from parotid gland is aided by muscular squeeze of masseter muscle, saliva is more serous and some of drainage is in direction of gravity
30
Q

How do you investigate and treat sialolithiasis

A
  • chronic symptoms should be investigated with ultrasound, sialography or diagnostic sialendoscopy to determine stone location and ductal patency
  • acute intermittent episdoes can be managed w conservative measures: warm compress, massage, sialogogues, antibiotics if infection
  • small calculi may pass spontaneously
  • submandibular stones
    • sialendoscopy if local expertise allows (up to 4mm stones); but contraindicated in acute infection
    • stones in distal duct can be excised intraorally (complications = recurrent stones & scarring of duct –> further obstructive sx)
    • if stones at hilum or gland or if gland chronically fibrosed & symptomatic: excise gland
  • parotid duct stones
    • sialendoscopy when possible
    • extracorporeal shockwave lithotripsy - minimally invasive and painless w few side-effects
    • uses pressure to fragment stones, making them easier to be flushed out of gland in saliva, or can use sialendoscopy afterwards
    • combo of sialendoscopy & minimally invasive open surgery - incise directly over stone or pre-auricular incision
    • if chronic sialadenitis caused by stones or strictures, parotidectomy includes removal of all parotid tissue in affected gland (challenging due to chronic inflammation
    • or combination approach
31
Q

What are signs that suggest a tumour in the salivary gland is malignant?

A

Facial or hypoglossal nerve involvement, pain, a sudden increase in size of a pre-existing salivary gland tumour, associated cervical lymphadenopathy, history of H&N skin cancers

Increased risk with history of radiation/radioactive iodine

32
Q

T staging for major salivary glands (parotid, SM, SL)

A

T1 <2cm, T2 2-4cm, T3 >4cm and/or extraparenchymal extension; T4a invading skin, mandible, ear canal and/or facial nerve; T4b invading skull base, pterygoid plates and/or encasing carotid artery

(staging for minor salivary gland malignancy is based on staging sytsem of anatomic location of minor salivary gland; eg a salivary carcinoma of hard palate is staged using oral cavity cancer staging system)

33
Q

Management of malignant salivary gland neoplasms

A
  • following appropriate staging, treatment f= surgeyr with complete tumour resection; some controversy re extent of parotidectomy that should be done; at a minimum want gross total tumour resection
  • deep lobe parotid malignancy: total parotidectomy (superficial and deep lobe) including removal of all parotid LNs & mobilisation of facial nerve branches
  • for superficial either total superficial or total parathyroidectomy (both have been advocated)
  • if possible, facial nerve & its branches should be preserved except if gross tumour invasion
  • radical parotidectomy or extended radical parotidectomy to include resection of skin, facial nerve or temporal bone, may be required for gross total tumour extirpation
  • for submandibular, sublingual and minor salivary gland tumours, gross total tumour resection w neg margins
    • major nerves whose sacrifice would cause functional deficits (lingual, hypoglossal marginal mandibular branch of facial etc) should be spared unless tumour can’t be completely removed w/o removal of nerves
  • neck dissection usu recommended for clinically node positive necks, high-grade primary tumours & T3-4 tumours
  • for incompletely resected tumours or those w gross residual disease, surgical re-resection should be offered if possible
  • adjucant radiotherapy typically recommended for gross residual disease and/or adverse features eg intermediate or high-grade, close or positive margins, neural/perineural invasion, LN mets, LVI and T3/4 tumours
  • rad therapy typically recommended following removal of adenoid cystic carcinomas w rad fields extended to cover adjacent or involved nerves due to its high propensity for perineural invasion & spread
  • role of systemic therpay in salivary malignancy less studied but can be considered for cases of gross residual disease or adverse pathologic features
34
Q

Drainage and associated primary malignancies of lymph node levels of the neck

A
  • level Ia
    • drains: skin of mental region/chin, mid lower lip, anterior portion of oral tongue, floor of mouth
    • malignancies: lower lip, floor of mouth, anterior oral tongue, mandibular alveolar ridge
  • level Ib
    • drains: efferent lymphatics from Ia, lower nasal cavity, hard and soft palates, maxillary and mandibular alveolar ridges, skin and mucosa of cheek, both upper and lower lips, floor of mouth, anterior oral tongue
    • malignancies: oral cavity, anterior nasal cavity, soft tissues of midface, submandibular gland
  • level IIb
    • drains: efferent drainage of level Ia & Ib, lymphatics of face, parotid gland, retropharyngeal nodes
    • directly drains: nasal cavity, pharynx, larynx, external auditory canal, middle ear, sublingual and submandibular glands
    • malignancies: nasal and oral cavities, nasopharynx, oropharynx, hypopharynx, larynx, major salivary glands (most commonly involved level)
  • level III
    • drains: efferent lymphatics from II & V and partially form retropharyngeal, pretracheal, recurrent laryngeal nodes
    • direct drainage from base of tongue, tonsils, larynx, hypopharynx, thyroid
    • malignancies: oral cavity, nasopharynx, oropharynx, hypopharynx, larynx
  • level IV
    • drains: efferent lymphatics from III and V and partially from retropharyngeal, pretracheal and recurrent laryngeal nodes
    • direct drainage from larynx, hypopharynx, thyroid, trachea, oesophagus
    • malignancies: hypophyarnx, larynx, trachea, cervical oesophagus, thyroid
  • level V:
    • drains: efferent lymphatics from occipital, retro-auricular, parietal scalp nodes
    • direct drainage from skin of lat & post neck and shoulder, nasopharynx, oropharynx, thyroid gland
    • malignancies: nasopharynx, oropharynx, thyroid, skin of post scalp and neck
  • level VI:
    • drains: lower face, anterior neck, anterior floor of mouth, tip of tongue, lower lip, thyroid, glottic, supragottic larynx, hypophyarnx, cervical oesophagus
    • malignancies: lower lip, chin, tip of tongue, anterior floor of mouth, thyroid, larynx, hypopharynx, oesophagus