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NASAL AND SINUS MALIGNANCY
Nodal Failures
Radical neck dissection is considered the standard of care for management of nodal failures. e rationale for performing radical neck dissection instead of a lesser operation is that
there are usually multiple involved nodes, the incidence of extracapsular involvement is high
(< 70%), and further radiation may not be possible.
Further Reading
Hildesheim A, Wang C-P. Genetic predisposition factors and nasopharyngeal carcinoma risk: a
review of epidemiological a ssociation studies, 2000–2011: Rosetta Stone for NPC: genetics ,
viral infection, and other environmental factors. Semin Cancer Biol 2012; 22(2): 107–116.
Lee A, Sze W, Au J, et al. Treatment results for nasopharyngeal carcinoma in the modern era:
the Hong Kong experience. Int J Radiat Oncol Biol Phys 2005; 61(4): 1107–1116.
Tsang RK, Wei WI. Salvage surgery for nasopharyngeal cancer. World J Otorhinolaryngol
Head Neck Surg 2015; 1(1): 34–43. (open access)
66. NASAL AND SINUS MALIGNANCY
Sinonasal malignancies are an uncommon heterogeneous group of tumours. ey are oen
misdiagnosed as benign conditions. Extension of these tumours into the orbit, brain, and
infratemporal fossa causes profound symptoms, with signicant implications for morbidity
and prognosis. Surgery and radiotherapy remain the mainstays of treatment. e prognosis
is relatively poor compared with that for tumours at other head and neck subsites.
Epidemiology
Rare, with incidence of 0.5–1 per 100,000 per year.
•
0.2–0.8% of all malignancies.
•
<3% of upper aerodigestive tract neoplasms.
•
Predominately develop in the h and sixth decades of life.
•
Incidence in men is twice the incidence in women.
•
e misconception that certain races are more susceptible than others to sinus malig-
•
nancies is explicable by occupational exposure to carcinogens.
Incidence of Sinonasal Malignancy by Subsite
Maxillary sinus—the most common (55%)
•
Nasal cavities (35%)
•
Ethmoid sinuses (9%)
•
Fronta l si nu ses (1%)
•
Sphenoid sinuses (1%)
•
Aetiology
Multiple occupational exposures to carcinogenic compounds have been identied, including
(but not limited to):
Hard wood—adenocarcinoma
•
So wood—squamous cell carcinoma (SCC)
•
African mahogany
•
Nickel—SCC
•
Smoking
•
Chemicals (e.g. chromium, polycyclic hydrocarbons, aatoxin)
•
338 Head and Neck
NASAL AND SINUS MALIGNANCY
Primary
Frontal
sinus
Ethmoid
sinus
Maxillary
sinus
Sphenoid
sinus
Nasal
cavities
Figure 66.1 Patterns of local spread.
Anterior Posterior Medial Lateral Superior Inferior
Skin Ant. Cranial
Skin
Cheek, skin
Ethmoid
sinuses
Skin
fossa, frontal
Sphenoid
nasopharynx,
clivus, pituitary
Ptergopalatine,
infratemporal
fossae, mid.
Cranial fossa
pituitary gland,
posterior
cranial fossa
Sphenoid
nasopharynx
lobes
Clivus,
sinus,
Nasal cavities,
cribriform
plate
Nasal cavity
Orbit
Cheek, skin
Middle cranial
fossa,
cavernous
sinus
Maxillary sinus
Ant. Cranial
fossa, frontal
lobes
Orbit
Pituitary gland,
hypothalamus
Ant. Cranial
fossa, frontal
lobes
Ethmoid sinus,
nasal cavity
Nasal cavity
Palate
Nasopharynx
Palate
Local Extension
Sinonasal malignancies commonly spread by local invasion. Extension is possible into the
orbit due to proximity and the thin barrier of bone and intracranially due to olfactory nerve
bres extending into the nasal cavity. Periosteum, perichondrium, and dura appear to act as
temporary barriers and to resist tumour expansion to some extent. e anterior maxilla and
orbital oor are very thin and readily destroyed by tumour.
Patterns of local spread are summarised in Figure 66.1.
Ohngren’s line runs from the medial canthus of the eye to the angle of the mandible. Tumour
position in relation to this line historically had implications for prognosis. Superiorly based
tumours tend to be more aggressive and poorly dierentiated, whereas tumours arising inferior
to the line are more amenable to treatment and, consequently, have a better prognosis. e advent
of craniofacial resection and radiation treatments has rendered this classication less relevant.
Lymphatic Drainage
e lymphatic drainage of the nose and paranasal sinuses predominantly splits into anterior
and posterior drainage.
e anteroinferior part of the nasal cavity and the skin of the nasal vestibule drain via the
•
anterior pathway to the rst-echelon facial, parotid, and submandibular lymph nodes.
e remainder drains via the posterior pathway into retropharyngeal nodes.
•
Both routes subsequently drain to the upper deep cervical chain. Lymphatic spread to
regional nodes becomes apparent in 25–35% of patients at some time during the course of
their disease. Nodal involvement at presentation is found in 10% of patients.
Distant metastases at the time of presentation are unusual; sites for metastases are bone,
brain, liver, lung, and skin.
Staging
For staging of nasal and paranasal sinus malignancy, please refer to Chapter 61.
Histopathological Subtypes
Squamous cell carcinoma (SCC)
Most common sinonasal malignancy.
•
Transformation of schneiderian membrane papillomas is a recognised risk.
•
Head and Neck 339
NASAL AND SINUS MALIGNANCY
Adenocarcinoma
•
Adenoid cystic carcinoma
•
Olfactory neuroblastoma
•
Arises from olfactory neuroepithelium, hence it is a neuroendocrine tumour with
•
paraneoplastic capabilities
Bimodal distribution, with peaks at 20 and 50 years of age
•
Classied by Kadish system
•
Sinonasal undierentiated carcinoma (SNUC)
•
Mucosal melanoma
•
Nasal cavity and the septum are usually the sites of origin
•
Haemangiopericytomas/glomangiopericytoma
•
Rare neoplasms of pericytes within the outer capillary wall
•
Biphenotypic sinonasal sarcoma
•
New addition to the WHO classication for head and neck tumours
•
A low-grade sarcoma with neural and myogenic phenotype
•
Clinical Features
Unilateral stuness/blockage
•
Bleeding or spotty nasal secretions
•
Nasal distortion (late sign)
•
Facial pain with or without progressive infraorbital nerve sensory change
•
Epiphora
•
Progressive trismus, mainly due to invasion of the pterygopalatine and infratemporal
•
fossae
Oral masses and teeth mobility
•
Proptosis and diplopia
•
A visible swelling of the cheek
•
Imaging
Dual modality with computed tomography (CT) and magnetic resonance imaging (MR I)
•
Allows accurate assessment/staging of bony and so tissue architecture, respec-
•
tively (Figure 66.2)
Biopsy
Ideally, biopsies are performed under general anaesthesia, to reduce the rate of non-diagnostic
samples and complications and to allow sampling from within the sinus itself.
Figure 66.2 MRI and CT scans are complementary and help distinguish between tumour,
retained secretions, and dural inltration. This patient had an extensive tumour that had spread
into the cavernous sinus and that had inltrated the dura of the temporal lobe (small arrows) and
the infratemporal fossa (large arrow). The spread was not apparent on the CT scan, which had
shown a relatively small tumour affecting the sphenoid.
340 Head and Neck
NASAL AND SINUS MALIGNANCY
Clinical Hx/Ex BiopsyImaging
MDT (Skull base expertise)
Curative intent
Stage I single modality otherwise
multimodality treatment
Surgery is often performed rst in multimodal treatment, however in large
volume disease initial treatment is often with (chemo)radiotherapy or
chemotherapy alone followed by chemoradiotherapy
Radiotherapy Chemotherapy
IMRTPhoton beam Platinum based
Post-op should initiate
within 6/52 delivering
60-65 Gy in 30 fractions
Dependant on
local availability
and expertise
ImplantsProstheticsOncologySurgery
Palliative intent
QoL/distant mets
Palliative
radiotherapy
Palliative surgery
Debulking
Figure 66.3 General principles of management of sinonasal tumours.
Treatment—General Principles
In general, cases should be carefully discussed in a multidisciplinary forum with skull base
expertise to determine treatment approach and also to facilitate smooth and timely transfer
between specialties, thereby avoiding unnecessary delays in adjuvant therapy. Figure 66.3
outlines general principles of management, with the proviso that certain tumours require
more specic management strategies. Multimodality therapy (surgery, radiotherapy, and
chemotherapy) has generally been demonstrated to be the most eective approach in the
treatment of SCC and SNUC, whereas olfactory neuroblastoma is treated with surgery and
post-operative radiotherapy.
Other than the stage of disease, the patient’s wishes, and concurrent comorbidity, there are
relatively few contraindications to treatment. Local invasion of the anterior cranial fossa and
skull base are not necessarily contraindications given the development of modern surgical
techniques. Distant metastases confer a poor prognosis and by denition render the patient
incurable. Involvement of the facial skin is also not a contraindication to treatment. e
involved area is best excised and repaired with ap, which can be a rotational or a free ap.
Surgery for Maxillary Tumours
A variety of operations for maxillary tumours have been described, the choice of which
is determined by the extent of the tumour and amount of bone that needs to be removed.
Figure 66.4 gives an overview of surgical options for maxillary tumours.
Midface Approaches
In the midface, an appropriate so-tissue approach is required to facilitate bony resection,
and three are commonly described (Figure 66.5). e selection of the specic approach
depends on the pre-operative assessment of tumour location and anatomical considerations
for resection to allow for surgery with curative intent. e principles of surgery are so-tissue
approach, osteotomies, resection, and reconstruction.
Head and Neck 341
NASAL AND SINUS MALIGNANCY
Maxillectomy procedures
Partial maxillectomy
Two variants
PalatalMedial
Clearing medal wall
& ethmoid sinuses
Resection of affected palate
& adjacent alveolus
Reconstructive options include regional flaps, free
flaps, alloplastic implants and prosthetics
Figure 66.4 Maxillectomy procedures.
Surgical approaches for maxillary
Exposes nasal cavity, medial maxilla, ethmoids,
nasopharynx, sphenoid and ptergopalatine fossa
Total maxillectomy Extended maxillecto my
Complete maxillary removal,
ideally as a bony box
containing tumour
tumours via midface
Weber-FergusonLateral rhinotomy
Ideal access to
maxilla and orbit
Extension past a total maxillectomy,
if involvement of skull base then
termed a craniofacial resection
Midfacial degloving
Good access for maxilla, ptergopalatine
and nasal fossa, and central skull base
Demonstrating an extended
lateral rhinotomy incision to
include the lip
incision & right showing
palatal incision
Midface degloving exposureLeft demonstrating skin
Figure 66.5 Approaches to the midface.
Neck Dissection
e rate of occult metastasis is less than 10%, with no suggestion in retrospective reviews
that elective selective neck dissection contributes to an improved rate of neck control or
overall survival.
Reconstruction and Rehabilitation of the Midface
Patients requiring extensive ablative surgery will predominately need post-operative radiotherapy. Meticulous rehabilitation, be it biological or prosthetic, aims to ensure a good cosmetic and functional outcome with separation of the nasal and oral cavities. Low defects
not compromising the orbit adnexa can oen be treated eectively with obturators. Where a
dental obturator is used, healing of the bony cavity can be rapid, but it is benecial to apply
a split-thickness skin gra to the under surface of the facial skin ap. Aer the facial incision is closed, the cavity should be immediately tted with a temporary prosthesis to cover
342 Head and Neck
NASAL AND SINUS MALIGNANCY
Ethmoidal surgery approaches
Endoscopic
Many tumours that would have
previously been treated with a
craniofacial tranorbital route can
be accessed endoscopically
Requires endoscopic equipment,
drills, deriders, bipolar diathermy
& neuronavigation
Tumour debulking is normally
needed +/– septal resection for
Resection can continue to orbital
periosteum, dura, crista galli and
olfactory bulbs if needed
access
Involvement of nasal bones,
frontal sinus, dura lateral to
contraindications
Craniofacial transorbital
Extended medical maxillectomy
via lateral rhinotomy incision
Caraful inspection of anterior
nasal vaities with an operating
microscope and frozen section
control
Allows access to ethmoidal roof
and orbital periosteum
Used less nowadays due to
advances in endoscopic
approaches
Craniofacial window
craniotomy
Lateral rhinotomy approach used
for anterior access and a bicoronal
incision for a pericranial
ap to access the frontal bone
Small window craniotomy gives
access to the oor of the cranial
fossa and raise dura
Allows access to sphenoid
ptergopalatine fossa and
central skull base
Craniofacial with craniotomy
Combines transfacial approach
with a craniotomy
Performed with neurosurgical
colleague
Trend now to couple
neurosurgical osteotomy with
endoscopic techniques
Figure 66.6 Approaches to access and manage the ethmoid complex surgically.
the palate and restore normal facial contours. e temporary prosthesis is changed at 14-day
intervals until there is appropriate healing to allow tting the nal prosthesis. Larger defects
necessitate ap reconstruction, oen in the form of a free ap. Options for composite (bone
and muscle) aps include (but are not limited to):
Deep circumex iliac artery (DCIA) bone ap
•
Scapula tip ap
•
Surgery for Ethmoid Tumours
Figure 66.6 describes surgical approaches to the ethmoids. Surgical technique selection
depends on patient, tumour (location, extent), and surgical experience.
Management of the Orbit
Attempts to preserve the orbital contents and diminish mutilation oen result in orbital
recurrence. If the orbital muscles, globe, or orbital apex are involved, a lid-sparing exenteration is required. e lids provide good skin cover of the defect and can also be used to cover
osseointegrated implants, which can be placed at the time of the surgery. Orbital involvement despite exenteration signicantly aects survival.
Prognosis
e overall prognosis for sinonasal malignancy is directly related to the degree of local control. Prognosis varies very signicantly between dierent pathologies.
For olfactory neuroblastoma and adenoid cystic carcinoma, 5-year survival rates are
•
high, but patients may continue to develop relapses for several decades aer treatment.
SNUC and malignant melanoma have very poor 5-year survival rates.
•
KEY POINTS
• Sinonasal malignancies can be difcult to differentiate from non-neoplastic lesions.
• Sinonasal malignancies are uncommon, representing <1% of all malignancies and
<3% of all upper aerodigestive tract cancers.
• Sinonasal malignancies tend to present late.
• The main treatment modalities are surgery and radiotherapy.
• Olfactory neuroblastoma and adenoid cystic carcinoma may relapse after a decade;
therefore, patients should be followed up for at least 15 years.
Head and Neck 343
BENIGN AND MALIGNANT DISEASE OF THE ORAL CAVITY
Further Reading
Kak I, Perez-Ordoñex B. Sinonasal tract pathology: an updated review of select entities.
Diagnostic Histopatholgy 2019; 25(7): 2650273.
Paleri C, Rollands NJ. (Eds.) Head and Neck Cancer: United Kingdom National
Multidisciplinary Guidelines, 5
Sethi N, Pearson A, Bajaj Y. Key Clinical Topics in Otolaryngology, 2016.
67. BENIGN AND MALIGNANT DISEASE OF THE ORAL CAVITY
Common Disorders of Teeth and Periodontium
Dental Caries
Dynamic imba lance occu rs between demi neralisat ion and reminera lisation of enamel.
•
Bacteria in dental plaque generate acid environment.
•
Progression leads to cavitation and invasion of dentinal tubules.
•
Treatment is with restoration of integrity.
•
Tooth Wear
Non-plaque-mediated chemical dissolution of tooth tissue (erosion)
•
Non-masticatory tooth-to-tooth contact (attrition)
•
Friction of exogenous material against tooth surface (abrasion)
•
Dental Infections
Pulpitis: dental pulp inammation, usually secondary to caries. Treatment is root canal
•
or extraction rather than antibiotics.
Acute dentoalveolar abscess: pain, swelling, erythema, and suppuration usually adja-
•
cent to causative tooth. Treatment is root canal surgery or extraction with or without
systemic antibiotics.
Pericoronitis: acute localised infection around a partially erupted tooth.
•
Periodontal disease: plaque-related inammation of the gingival or periodontal tissues.
•
Gingival Abnormalities
Pigmentation: localised or generalised, with many causes, including melanoma, Kaposi’s
•
sarcoma, smoking, and Addison’s disease.
Redness: local or general, and can be attributed to lichen planus, allergies, or herpetic
•
stomatitis.
Swellings: can be local (epulides) or general, related to systemic causes.
•
Ulceration: most common causes neoplasm, aphthous ulcers, or bacterial infections.
•
Dental Trauma
Common especially in childhood. Avulsed permanent teeth need immediate reim-
•
plantation, avulsed deciduous teeth should be le out. Other dental trauma requires
dental practitioner follow-up. Be vigilant for non-accidental injury.
th
edition, 2016.
Infections of the Jaw
Alveolar osteitis (dry socket): localized inammation aer dental extraction.
•
Management is curettage of the socket to promote blood clot formation.
344 Head and Neck
BENIGN AND MALIGNANT DISEASE OF THE ORAL CAVITY
Osteomyelitis: acute or chronic. Treatment is with surgical debridement and systemic
•
antibiotics.
Osteonecrosis: secondary to medicat ion related osteoradionecrosis of the jaw (MRONJ)
•
or radiotherapy.
Cysts of the Jaw
Inammatory
Radicular cyst: most common inammatory cyst. Occurs around apex of non-vital
•
tooth. Diagnosis is with vitality testing. Treatment is with surgical enucleation.
Developmental
Dentigerous cyst: Develops around crown of unerupted tooth. Mostly unilocular.
•
Treatment is either enucleation or marsupialisation.
Non-Odontogenic Developmental Cysts
Nasopalatine duct cyst: embryological remnant of nasopalatine duct. Oen incidental
•
radiological nding.
Non-Epithelial Bone Cyst
Aneurysmal bone cyst: controversial because there is no cyst lining. Scalloped appear-
•
ance on radiography. Biopsy conrms no lining and healing then occurs.
Ameloblastoma: locally invasive odontogenic bone tumour. Appears uni- or multi-
•
cystic on x-ray. Histopathological diagnosis is mandatory.
Disorders affecting the Oral Mucosa
Benign Oral Mucosal Changes
Frictional keratosis: adaptation of oral mucosa to increased trauma.
•
Leukoedema and nicotinic stomatitis: generalised white change of the oral mucosa.
•
Most commonly seen in smokers. Sometimes red spots on white background when
openings of minor salivary glands are visible.
Fordyce spots: small yellow/white sebaceous spots commonly on the buccal mucosa
•
from developmental substitution of minor salivary for sebaceous glands.
Tongue coating: true coating of the tongue is rare. Occasional overgrowth and stain-
•
ing, ‘brown hairy tongue’, is rarely pathological.
Geographic tongue: synchronous turnover with thinning of the mucosa of the tongue
•
leads to red patches. Appearance moves across tongue. No curative treatment available.
Median rhomboid glossitis: red, depapillated, smooth, rhomboidal area on dorsum of
•
tongue. Mostly asymptomatic but occasionally associated with immunosuppression.
No treatment required.
Mucosal swellings: Fibroepithelial polyps, viral warts, and lipomas are common rea-
•
sons for referral.
Changes in Mucosa Colour
White: commonly with mucosal thickening by acanthosis or hyperkeratosis.
•
Established squamous cell carcinoma (SCC) can present as a white patch, but
dysplasia presents this way less frequently.
Red: reects thinning of the mucosa or increased vascularity (e.g. dysplasia or
•
malignancy).
Pigmentation: localised or generalised. Intraoral melanomas are rare.
•
Grey/blue: oen related to foreign bodies, such as dental amalgam or heavy metal poi-
•
soning. Dark blue lesions are mostly venous malformations.
Head and Neck 345
BENIGN AND MALIGNANT DISEASE OF THE ORAL CAVITY
Table 67.1 Clinical features of aphthous ulcers by type
Type of aphthous ulceration Clinical features
Minor Most common
Usually <10 mm in diameter
Last 2–3 weeks
Non-keratinised mucosa
Heal without scarring
Can be multiple, but fewer than 10
Major Diameter >10 mm
Can last up to 3 months
Non-keratinised or keratinised mucosa
Heals with or without scarring
Usually single, but maximum of 3
Herpetiform Least common
Diameter <5 mm
Last for up to 2 weeks
Heal without scarring
Large numbers—up to 100
Can coalesce into large groups
Oral Ulceration
Aphthous ulceration: immunological ulcers that are multifactorial in origin
•
(Table 67.1).
Erythema multiforme: immunological hypersensitivity reaction that can aect an
•
individual system or multiple systems (Stevens-Johnson syndrome). Intraorally, it
presents as widespread oral ulceration leading to tissue damage and swollen, crusted
lips. Multiple drug triggers. Treated with high-dose systemic steroids.
Systemic Diseases and the Mouth
Skin Diseases
Pemphigus and pemphigoid: autoimmune disorders driven by immunoglobulins,
•
resulting in separation of epithelial cells (pemphigus) or of basement membrane
(pemphigoid). Signicant variability in skin lesion presentation. All patients should
have ophthalmological assessment due to conjunctival scarring.
Lichen planus: very common T-cell-mediated attack on basement membrane. Can be
•
white (acanthosis), red (atrophy/ulceration), or mixed. Lesions tend to be intermittent
and recurring. Diagnosis is via incisional biopsy. Treatment is usually symptomatic,
with topical steroids.
Scleroderma: either in isolation or as part of CREST. May signicantly aect mouth
•
opening.
Gastrointestinal Disorders
Ulcerative colitis: aphthous ulceration during periods of disease activity.
•
Crohn’s disease: can present early in disease process with swelling, angular cheilitis,
•
mucosal tagging, cobblestone appearance of mucosa, linear ulceration, or gingival
inammation.
Orofacial granulomatosis: features of Crohn’s disease but no GI disorder. Likely
•
immunological. Exclusion diet initially (e.g. benzoate, sorbate, cinnamon, and chocolate). Systemic immunotherapy occasionally required.
346 Head and Neck
BENIGN AND MALIGNANT DISEASE OF THE ORAL CAVITY
Viral Diseases
Herpes simplex virus (HSV): HSV 1 or 2 can cause primary herpetic stomatitis.
•
Recurrent lesion can present as persistent ulceration on palate.
Herpes zoster virus (HZV): multiple oral vesicles, which may be neuropathic.
•
Epstein–Barr virus (EBV): neck swellings, hairy leukoplakia, and nasopharyngeal
•
cancer.
Human herpesvirus 8 (HHV8): Kaposi’s sarcoma.
•
Human immunodeciency virus (HIV): rarely associated with oral lesions following to
•
highly active antiretroviral therapy (HAART).
Fungal Infections
Types of candidiasis Predisposing factors
Acute pseudomembranous candidiasis (thrush) Local or systemic immunosuppression
Acute atrophic candidiasis Broad-spectrum antibiotics
Erythematous candidiasis None, ageing
Chronic atrophic candidiasis Denture wearing, esp. at night
Chronic hyperplastic candidiasis Tobacco smoking
Median rhomboid glossitis Tobacco smoking, local immunosuppression
Angular cheilitis Denture wearing, diabetes
Chronic mucocutaneous candidiasis Immune deciency
Orofacial Pain
Trigeminal neuralgia: Unknown origin; classically, electric shooting pain with a trig-
•
ger zone on face. Single branch of trigeminal nerve oen aected. Carbamazepine is
rst-line management.
Cluster headaches: unilateral pain with ptosis, facial erythema/swelling, lacrimation,
•
and nasal discharge. Inhaled oxygen or triptan benecial.
Atypical odontalgia: intense toothache with no dental pathology.
•
Oral dysesthesia: Altered sensation, such as feeling of dryness, burning, numbness,
•
or change in taste. No underlying pathology. Occasional haematinic deciency.
Reassurance oen helpful.
Temporomandibular disorder: common.
•
Malignant Tumours of the Oral Cavity
Introduction
The oral cavity is lined by stratified squamous epithelium of varying degrees of keratinisation. Primary tumours can be derived from mucosa, salivary glands, neurovascular tissues, bone, or dental tissues. Over 90% of tumours are squamous cell carcinoma
(SCC). There has been an increase of over 20% of oral cancer in patients under the age of
65, with HPV-associated oropharyngeal carcinoma playing an increasing role. Globally,
tobacco and alcohol remain the main aetiological factors. Five-year survival rates are
80% if the cancer is confined to the mucosa, 40% for those with regional spread, and
20% with distant disease.
History
orough symptom history, including for metastatic disease
•
Medical history
•
Social history
•
Possible site-specic history (e.g. claudication)
•
Head and Neck 347
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