UCD Student Manual / A Student Guide to Oto-Rhino-Laryngology 1

UCD STUDENT MANUAL

A STUDENT GUIDE TO

OTO-RHINO-LARYNGOLOGY

Compiled by :

Professor Aongus Curran

MB, BCh (NUI), FRCSI, FRCS (ORL-HNS), MD.

Professor of Otolaryngology
/ Head & Neck Surgery at UCD

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CONTENTS OF UNDERGRADUATE MANUAL.

Introduction.

Course Objectives.

Lecture Programme -refer to Teaching Programme booklet/noticeboard

Ear - Sensory Functions.

- Acute Suppurative Otitis Media.
- Chronic Suppurative Otitis Media.
- Central Perforation of Tympanic Membrane.
- Acute Mastoiditis.
- Labyrinthitis.
- Facial Nerve Paralysis.
- Petrositis.
- Brain Abscess.
- Otitis Media with Effusion - Glue Ear.
- Wax.
- Acute External Otitis.
- Furunclosis.
- Traumatic Perforation.
- Unilateral Sensorineural Hearing Loss.
- Sudden Onset Sensorineural Hearing Loss.
- Tinnitus.
- Menieres Disease.

Nose - Epistaxis.
- Sinusitus - Acute Sinusitus.
- Chronic Sinusitus.
- Allergic Rhinitis.
- Adenoids.
- Snoring Investigation.

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Pharynx - Tonsils
- Tonsillectomy.
- Hoarseness.
- Globus.
- Parotid Swelling.
- Vocal Cord Palsy.
- Facial Palsy.

Emergencies - Foreign bodies in the ear, nose and throat.

Tumours - Head and Neck Tumours.

- Thyroid Cancer, an update on its management.
Rarer Conditions.
- Angiofibroma.
- Acoustic Neuroma.
- Rare chronic inflammatory problems.

Recent Advancements - Laser

- Cochlear Implant.

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INTRODUCTION

Your rotation in Otolaryngology will be short and it is therefore essential that you utilise your
time to maximise your learning experience during your rotation. It is estimated that 40% of
general practice deals with patients presenting with Ears, Nose and Throat problems. It is
therefore essential that you have a good grasp of :

the range of diseases that present in the speciality.

how they should be managed .
a firm knowledge when to refer to an Otolaryngologist.

Otolaryngology is often referred to as ENT, although this description of the speciality does not
accurately describe the breadth of what this surgical sub-speciality covers. Whilst this is a
surgical discipline, a large portion of an Otolaryngologists work is in fact dedicated to
Outpatient Medicine. An Otolaryngologist may spend the morning in an Outpatients Clinic,
diagnosing anything from an Acoustic Neuroma to Acute Sinusitis. In the afternoon he/she may
perform a Neck Dissection or a Panendoscopy (to stage a head and neck cancer). Most
Otolaryngologists in Ireland now sub-specialise in one of the following areas, following
completion of a Fellowship, which is usually undertaken in the United States or in Australia.
The sub-specialities in Otolaryngology include:

Paediatric Otolaryngology.
Head and Neck Surgical Oncology.
Rhinology and Endoscopic Sinus Surgery.
Facial Plastics and Cosmetic Surgery.
Otology/Neurotology and Skull Base Surgery.

Whilst most Otolaryngologists in Ireland sub-specialise, the bulk of their work involves diseases
affecting an area, which overlaps with Respiratory Medicine, Paediatrics, Ophthalmology,
Neurology, General Medicine, General Surgery and General Practice. This speciality is unique,
in that it deals with an anatomical region rather than a specific organ system.

During your clinical rotation, which will be held at either the Mater / Temple Street Hospitals or
St Vincents University / Royal Victoria Eye and Ear Hospitals, you will observe Consultants
and non-Consultant Hospital Doctors during their Outpatient Clinics and at their surgical
sessions. After observing interaction with patients, it will be expected that you will be capable of
performing a thorough history and examination on your own. It is important that you question
and learn the necessary clinical skills during this time. I would suggest that you liaise closely
with the Senior Registrar or Registrar during rotation, who will continuously update you on
emergency admissions and the weekly schedule. This will ensure your learning experience is as
fruitful as possible. Since it is impossible to learn everything about Otolaryngology during your
rotation, it is worthwhile revising basic Anatomy, Pathology and Physiology of the area prior to
your attachment. Therefore this manual should be read thoroughly before you begin your
rotation. The ABC of Otolaryngology 3rd Edition by Harold Ludman is recommended.

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COURSE AIMS AND OBJECTIVES.

1. The objective of the course programme in Otolaryngology is that following the students
attachment, the student is capable of performing the following:-

- Otoscopy and Tuning Forks.

- Neck Palpation.
- Anterior Rhinoscopy
- Oral Cavity and Oral Pharyngeal Examination.

2. The student should be proficient in the concepts and principles of taking a full ORL
history, ie. ability to obtain and record in a verbal and written form, physical examination
and outline diagnosis.

3. Following completion of the course programme and the students attachment, the student
should be fully and thoroughly familiar with the contents of the UCD student booklet as
the MCQ examinations at the end of term will be based o n the contents of this booklet.

4. The student should be able to differentiate as to:-

- when a patient requires primary treatment of common ENT diseases.

- which conditions could be managed by a GP.
- which conditions require a specialist ENT opinion.
- which conditions require routine or urgent referral by the specialist.

5. To acquire a full understanding and knowledge of the basic management of common

diseases and of the pharmacology and toxicology of commonly prescribed drugs for ENT
diseases.

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SENSORY FUNCTIONS.

Hearing & Balance.

For purposes of communication with other human beings, hearing is the most important sense.
People spend a lot of time talking and listening, the ability to hear provides a fast and effective
way of receiving information. What we hear can also trigger strong emotional responses. Our
ears also provide a constant flow of information about the bodys orientation in space. This
input gives us our sense of balance, allowing us to stand and move without falling.

How we hear.

Molecules in the surrounding air are disturbed when an object moves and in turn hits adjacent
molecules, resulting in a sound wave. A movement such as turning the page in a book, causes a
slight air disturbance, whereas an aluminium pot falling on a hard surface causes a big sound
wave. The vibrations are sent as nerve impulses to the brain and interpreted as sound. The size
of a sound wave is measured in decibels (dB). The quietest sounds that can be detected are 10dB
eg. breathing. Sound levels of around 120dB and over, eg. loud nightclub music, can cause
permanent damage to the inner ear.

There are auditory areas in the brain that interpret sound on both sides of the brain. Speech is
mainly interpreted on the left side and music mainly on the right side.

How the Ear Processes Sounds.

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How the Ear Processes Sounds.

The ear contains sensory structures that detect sounds and information about our posture and
movement. This information is converted into nerve impulses and sent to the brain. Inside the
ear is a tube, the ear canal, at the end of which is a delicate fanlike membrane, the eardrum.
Sound waves pass down the ear canal which causes the eardrum to vibrate. Beyond the eardrum
is the middle ear, an air-filled space containing three tiny bones: the malleus, incus and stapes.
These bones pass on vibrations from the eardrum to a fluid-filled structure, the cochlea, in the
inner ear. The spiral-shaped cochlea contains the organ of Corti, the receptor for hearing, which
is filled with millions of sensory hair cells. When the fluid in the cochlea vibrates the hairs
move, stimulating nerves that carry sound messages to the brain in the form of electrical
impulses.

The Sense of Balance.

A number of structures in the inner ear, referred to collectively as the vestibular apparatus, help
us to stand upright and move without losing balance. This apparatus includes three fluid-filled
loops set at right angles to each other, the semicircular canals, at the base of which sensory hair
cells exist in small structures called cristae. The other structures that contribute to balance are
two chambers (the utricle and saccule) within a fluid-filled area called the vestibule. These
chambers both contain a macula, a sensory structure that is also full of hair cells. From the
semicircular canals and the maculae, information about the speed and direction of the heads
movement is transmitted by the hair cells to the brain in the form of nerve impulses.

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Vertigo.

If the delicate apparatus of the inner ear is disturbed the sense of balance can be affected. Being
off balance causes vertigo, a false sensation of movement or an unpleasant feeling that
everything around one is spinning. Causes of vertigo include an infection of the vestibular
apparatus, often following a viral infection such as a common cold or flu. Vertigo is also a
symptom of Menieres Disease, a disorder in which for unknown reasons excess fluid builds up
in the inner ear.

Vestibular Apparatus.

In the inner ear, the vestibule and the semicircular canals contain sensory areas (maculae and
cristae) that contribute to our sense of balance.

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Smell and Taste.

Smell.

When we breathe in substances that smell, the odour molecules that are created by the smell
come into contact with two regions of fatty tissue at the top of each nostril, behind the bridge of
the nose. In these areas, called the Olfactory regions, there are about 5 million nerve cells. The
cells carry cilia (tiny hairs) that project into the mucous layer of the nose and are stimulated by
specific odour molecules. The cells send electrical signals to a site at the base of the brain, the
olfactory bulb when stimulated by a smell. This bulb in turn transmits signals to other areas
deeper in the brain. One of these areas, the limbic system, is responsible for emotion, this is why
even a slight whiff of certain smells can provoke powerful memories and strong emotions.

Taste.

There are around 10,000 taste buds in the mouth. Taste buds are found primarily on the surface
of the tongue, but a few are scattered on the palate, throat and tonsils. Each bud is a cluster of
about 50 taste-detecting nerve cells contained within a pore. When food or drink is in the
process of being consumed in the mouth, it is dissolved by saliva and chemicals are released that
stimulate minute hairs on the taste cells. These cells transmit impulses along nerve fibres to the
brain. The tongue is divided into different types of taste regions. We taste:

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sweet things with the tip of the tongue.

salty foods are tasted mainly at the front of the tongue.
sour taste buds sit at the edges.
bitter tastes are at the back of the tongue.

Chemicals released during the breakdown of food and drink in the mouth enter pores in the
tongue and reach tiny hairs on the taste buds. These hairs respond to flavours by generating
nerve impulses which send messages to the taste area of the brain.

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ACUTE SUPPURATIVE OTITIS MEDIA.

What is Acute Suppurative Otitis Media?

Acute Inflammation of the middle-ear cavity.

Commonly bilateral.
Frequent in children.
Follows a U.R.T.I. either viral / bacterial.

Pathology.

Involves the entire middle ear cleft from Eustachian Tube to the most distal mastoid air cell.

Bacteria responsible:
Streptococcus pneumoniae 35%.
Haemophilus influenzae 25%.
Maraxella catarhalis 15%.
Group A Streptococcus or
Staphylococcus Aureus may also be responsible.

Inflammatory Steps:

Organisms invade mucous membrane.

Oedema closes the Eustachian Tube.
Pressure from pus rises, the drum bulges.
Local necrosis of the Tympanic Membrane Perforation.
Spontaneous drainage from the ear until infection resolves.

Symptoms:

Earache.
Deafness.
Signs.

Pyrexia.
and/or Tenderness of the Mastoid.
Tympanic Membrane appearance varies according to the stage of the inflammation
eg.
Grey, lack of lustre.
Radial injection of small drum vessels.
Redness and fullness of drum.
Bulging of drum, loss of landmarks.
Desquamation perforation.
Otorrhoea.

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Treatment.

Early - Antibiotics.
- Penicillin still drug of choice. Orally initially followed by I.V. if
necessary.
- Amoxycillin - for under 5 years old in view of
incidence of H. Influenza.
- Co-ammoxiclav in eg. Moraxella.
Swab if possible for C. & S.

Analgesics, nasal vasoconstrictors (0.5% ephedrine nasal drops).

Late - Bulging drum, failure to resolve with persistence of severe symptoms

frequently results in hospital admission for I.V. antibiotics followed by
myringotomy, specimen C. & S.

Discharging ear ie. persists after acute phase has passed. Specimen for
C. & S. followed by antibiotic of choice and / or ear drops eg. antibiotic / steroid
combination.

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Recurrent Acute Suppurative Otitis Media.

Suspect an underlying immunological defect eg. IgA deficiency of

Hypogammaglobulinaemia.

A grommet may break the sequence in a child with recurrent attacks eg. associated with
teething.

Further Management.

Treatment is complete when:

Symptoms have resolved.

Ear drum has returned to normal ie. Resolution has occurred.
Hearing is normal.

If resolution does not occur suspect:

Nose, sinus, adenoid, residual source of infection.

Choice of antibiotic.
Low-grade mastoid infection masked mastoiditis.

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CHRONIC SUPPURATIVE OTITIS MEDIA (C.S.O.M.)

If an attack of Acute Suppurative Otitis Media fails to resolve ie. with closure of the membrane
perforation, the stage is set for the development of C.S.O.M.

Types.

Mucosal type - tubotympanic safe variety.

Bony type - atticoantral - unsafe variety.

Predisposing factors:

Late treatment of Acute Otitis Media.

Inadequate or inappropriate antibiotic treatment.
Persistent upper respiratory sepsis.
Lowered resistance, malnutrition, immunological defect etc.
Particularly virulent infection eg. Measles.

MUCOSAL DISEASE (CSOM).

Features:

A perforation is present, usually centrally located with a well defined rim.

Recurrent infection occurs with otorrhoea, frequently triggered by upper respiratory
tract sepsis via the Eustachian Tube.
There may be period of quiescence, when the only problem is one of a hearing loss,
which over the years becomes progressive.
The perforation may spontaneously heal, but this is related to the size of the
perforation, large ones likely to remain permanent.

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Treatment of Mucosal Disease (CSOM).

Swab for Culture & Sensitivity (C&S) and antibiotic/treatment as indicated + topical
ear antibiotic / steroid ear drops.
Admission to hospital for aural toilet and I.V. treatment.
Surgery myringoplasty.

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BONY TYPE OF C.S.OM. ATTICOANTRAL DISEASE.

Position of the perforation is postero-marginal, postero-superior or into the attic part

of the ear through the pars flaccida, known as schrapnells membrane.
Granulations occur from the area of osteitis, which are bright red and bleed on
contact.
Aural polyps form from granulation tissue and may present as a cherry like growth at
the external ear canal opening.
Cholesteatoma a misnomer derived from the presence of cholesterol granules in
certain histological forms of chronic ear disease. It represents the progressive
invasion of the middle ear and mastoid by retracted tympanic membrane associated
with a perforation at its mouth and the production of squamous debris within its
depths and osteolytic enzyme activity at its periphery, if untreated it may be lethal.

Aural polyp

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Treatment.

Regular aural toilet in early cases may enable a small area of localised osteitis to be
aborted and progression prevented.
Microscopic debridement may permit evacuation of a small pocket of early
cholesteatoma development and enable stabilisation of the condition to be achieved.
Major surgical intervention if after a certain period of conservative treatment the
condition is failing to respond or is progressing.

Surgical Options.

Atticotomy
Combined approach tympanoplasty
Modified radical mastoidectomy.

Complications of Middle Ear Disease.

Intratemporal. Intracranial.

Acute Mastoiditis. Meningitis.

Labyrinthitis. Extradural abscess.
Facial nerve paralysis. Subdural abscess.
Petrositis (Gradenigos Syndrome) Brain abscess.
Lateral Sinus Thrombosis.

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CENTRAL PERFORATION of TYMPANIC MEMBRANE.

Grades of Perforation:
Dry (permanently)
Intermittent discharge.
Constant discharge.
A constant discharge with complication.

History:
Duration of symptoms.
Discharge - character, smell, periodicity.
Previous middle ear disease or surgery.
Hearing in the contralateral ear.
Other relevant disease.

Examination:
Wax and debris must be removed to give a good view of the tympanic membrane.
Tuning fork tests.

Investigation:
Pure tone audiometry.
A swab may sometimes be taken, especially if the ear continues to discharge or there
is a suspicion of fungal aetiology.

Treatment:
Discharge drops containing a combination of antibiotic and steroids may be used
and if the ear continues to discharge then system antibiotics should be given at least
for ten days.
When topical ear drops are prescribed the dose and length of time or usage
should be recorded. Topical eardrops should not be used for more than 10 days or
after otorrhoea ceases or if the patient complains of dizziness. Patients should be
reviewed every 10-14 days until the ear is dry, use repeat prescriptions of topical
eardrops with caution.

Indication for surgery.

Troublesome discharge.
Hearing loss.
Patient wishes to swim.
Hearing aid use.
Pain.
Other complications.

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CENTRAL PERFORATION of TYMPANIC MEMBRANE.

Surgery:
Avoid surgery for children under the age of 10 unless the discharge is persistent and
might damage the ossicular chain.
There is no point in doing a tympanoplasty to improve the hearing if the
operation will not reduce disability and improve the patients hearing.
Refer to Glasgow Benefit Plot.
Consider cortical mastoid as well as myringoplasty in the persistently
discharging ear that has not responded to treatment.

Length of Stay.
Usually patients go home on the first post-operative day after an
uncomplicated operation.

ACUTE MASTOIDITIS.

Extension of a middle ear infection into the mastoid air cell system with suppuration and bone
necrosis.

Symptoms.
Pain - persistent and severe.
Otorrhoea - smelly and profuse.
Increasing deafness.

Signs.
Pyrexia
Patient is ill.
Tenderness of the mastoid on palpation.
Swelling of the post auricular region with obliteration of the sulcus, the pinna may be
pushed forward and downwards.
Sagging of the posterior canal wall on Otoscopy.
The drum may be bulging or discharging.

Occasional Presentations.
Subperiosteal abscess over the mastoid antrum.
Bezolds abscess presents in the neck as pus breaks through the mastoid tip.
Zygomatic mastoidits results in swelling over the zygoma due to extension of the
infection into the zygomatic air cells.

Treatment.
Admission to hospital, I.V. antibiotics (Amoxycillin, Metronidazole).
Cortical mastoidectomy - if there is a periosteal abscess or if the condition does not
settle rapidly on antibiotic treatment eg. 24 hours surgery entails drilling out the
mastoid air cell system in order to exenterate the disease.

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LABYRINTHITIS.

Cholesteatoma may erode the labyrinth eg. the lateral semicircular canal.

Clinical Features.
Vertigo.
Nausea.
Vomiting.
Nystagmus towards the diseased side.
Positive fistula sign.
Progressive sensorineural deafness.

Treatment.
Antibiotics.
Mastoid Exploration.
Occasionally labyrinth drainage.

FACIAL NERVE PARALYSIS.

Paralysis of the facial nerve may be caused by either of the following:

Acute Otitis Media.

Especially in children this may be associated with a facial paralysis due to dehiscence
in the fallopian canal within the middle ear.
Pressure phenomenon usually resolves spontaneously with resolution of the infection
sometimes assisted by myringotomy drainage of the ear.

Chronic Otitis Media.

Cholesteatoma may erode the facial nerve canal and produce granulations of the
facial nerve leading to paralysis.

Urgent exploration needed this should not be mistaken for Bells Palsy.

PETROSITIS.

Infection spreads from the petrous tip to involve the 5th cranial nerve.
Diplopia from lateral rectus palsy.
Trigeminal pain.
Evidence of middle ear infection.
Management involves C.T. Scanning, I.V. antibiotics.
Neurosurgical co-operation and exploration of the temporal bone as far as the apical
cells.

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BRAIN ABSCESS.

Temporal Lobe Cerebellum.

Modes of spread direct via bone or meninges septic thrombophlebitis.

Presentatation:

Systemic effects
o Malaise.
o Pyrexia.
Raised intracranial pressure such as:
o Headache.
o Drowsiness.
o Confusion.
o Papilloedema.
o Neck stiffness.
Localising signs.

Management:
Surgical
o Mastoidectomy.
o Neurosurgery.
IV Antibiotics

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OTITIS MEDIA with EFFUSION (OME) - GLUE EAR.

One third of all children at some time in their lives will be affected by OME more commonly
known as Glue Ear. It is most common in small children and may cause significant deafness. It
is important that this condition is recognised and treated at an early stage because its effects may
impair a childs development, academic potential and cause permanent middle ear damage. This
condition is caused by a build up of fluid, either serous or viscous within the middle ear cleft
which in turn results in conductive deafness.

Clinical Features.

Nasopharyngeal Obstruction - large adenoids or tumour resulting in Eustachian

Tube dysfunction.
Otitic Barotraumas - most commonly caused during descent in aircraft people
who have a cold are particularly susceptible. Lack of middle ear ventilation can
result in middle ear effusion.
Acute Otitis Media - if untreated can cause spontaneous perforation and drainage of
the middle ear. Can be prevented by treatment with an antibiotic if not treated
successfully middle ear effusion may occur.
Allergic Rhinitis - if missed in childhood may later predispose a patient to middle
ear effusions.
In many cases no cause is apparent.

Symptoms.

Deafness.
Discomfort in the ear - rarely severe.
Occasionally tinnitus or unsteadiness.

Signs.

Fluid in the middle ear.

Dull appearance with radial vessels visible on the tympanic membrane.
Tuning fork tests show conductive deafness.
Immobile drum on testing with pneumatic speculum.
Flat impedance curve.

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Glue ear with marked

drum change.

A Vesicle on the drum also

occurs in childrens glue ear.

Blue Ear Drum.

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Treatment.

Observation - many cases resolve without any intervention. Antihistamines and

mucolytics are sometimes helpful during this period.

Surgical treatment:
o Myringotomy and Grommets Insertion - under general anaesthetic if secretory
otitis media with poor hearing persists over 3 months. The tympanic membrane is
incised antero-inferiorly. The glue is aspirated and a grommet inserted. The
grommet is designed to ventilate the middle ear, post operatively it should be kept
dry. The grommet will extrude after a period of approximately 6 months.
o Adenoidectomy is usually performed if adenoid enlargement with post nasal
obstruction is present.

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WAX.

Wax in the ear is normal and healthy. Wax (cerumen) is produced by the ceruminous glands in
the outer meatus and migrates laterally along the meatus. Some people produce large amounts of
wax, but most cases of impacted wax are caused by the use of cotton wool buds in attempts to
clean the ears.

Impacted wax can cause some deafness or irritation of the meatal skin and is easily removed by
syringing. Ear syringing is a simple procedure which should be carried out carefully. Care
should be taken in the following situations:

Treatment.

Patient history - if the patient has had a discharging ear previously and there may
be a possibility of dry perforation, do not syringe.
Inspection - soften hard wax over a period of one week by using warm olive oil
drops nightly. Sodium bicarbonate ear drops (BPC) or a topical ceruminolytic
agent may be necessary where the olive oil drops have not been successful.
Use of sodium bicarbonate, 4-5g to 500ml. Or normal saline is ideal.
Temperature of the solution is very important, it should to 38 (100F) any
change to this could result in patient suffering vertigo.
Metal syringe or rubber syringes of the Bacon type can used. Make sure the
nozzle is firmly attached to the syringe and will not travel too far into the external
meatus - the adult meatus is about 1 inch long. Tympanic membranes have been
ruptured by deep penetrating nozzles.
Direct stream of solution along roof of auditory canal.
After removal of wax be sure to inspect the ear thoroughly to ensure no wax
remains.

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ACUTE EXTERNAL OTITIS.

Predisposing Factors:
Humidity.
Psoriasis.
Seborrhoea.
Trauma.
Swimming.

Aetiology:
Gram negative organisms.
Fungi.
Viruses.
Sensitivity to ear drops.

Diagnosis:
History of itching usually progressing to pain.
Serous Otorrhoea.
Diffuse erythema and oedema of the ear canal.
If a diabetic, consider the possibility of malignant external otitis.

Evaluation:
Careful history and examination.
Tuning fork tests rather than initial audiometry.
Careful cleaning under the microscope to exclude underlying middle ear conditions.

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Treatment:
Careful cleaning under the microscope.
If severe, a dressing - Pope wick or ribbon gauze in the ear canal with
Tri-adcortyl or Trimovate.
If mild, otosporin ear drops.
Appropriate analgesia consider admission if pain is severe and systemic antibiotics
if there is spreading cellulitis.
Unless very mild, re-clean and inspect in 2-7 days.
Advise the pateient to keep the ear dry and to resist the temptation to scratch the ears.

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FURUNCULOSIS of the EXTERNAL AUDITORY MEATUS.

Aetiology:

Staphylococcus infection of hair follicle.

Diagnosis:

Pain, especially on movement of the pinna or chewing.

Erythema and oedema of the ear canal.
Exclude mastoiditis.

Treatment:

Glycerine / Icthammol dressing.

Appropriate analgesics.
Systemic anti-staphylococcus antibiotics, probably Flucloxacillin.

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TRAUMATIC PERFORATION.

Diagnosis:

History of trauma.
Tympanic membrane perforation possibly with ragged edges.
Evidence of recent haemorrhage.

Aetiology:

The following may be implicated:

Foreign bodies (eg., cotton buds, hairclips, matchsticks).

Explosion.
Slap on the ear.
Fractured skull.
Welding sparks.
Barotrauma.
Syringing.
Water sports.

Evaluation:

History.
Careful examination of the ear, especially to exclude infection. Removal of blood
clot should not be performed. If the perforation is clearly seen, its size and shape
should be documented.
Audiogram if possible if not possible Tuning Fork Test and clinical assessment of
hearing.
If the patient has had head injury, it is important to record the function of the facial
nerve and to note if any CSF leakage is present.
Simple vestibular assessment if indicated.

Treatment:

Reassurance: explain to the patient that there is a good chance of spontaneous

resolution (unless due to a welding spark).
If the perforation is contaminated, consider either giving an oral antibiotic or an
antibiotic + antibiotic drops or drops alone.
Keep water out of the ears until the perforation has healed.
Review within 6 weeks but if the ear discharges, the patient should be advised to see
their general practitioner.
Consider surgery if the perforation persists for longer than two months.

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UCD Student Manual / A Student Guide to Oto-Rhino-Laryngology 31

UNILATERAL SENSORINEURAL HEARING LOSS.

History:

Onset (if sudden follow SNHL Protocol. If no hearing improvement after

treatment continue this protocol).

Tinnitus.

Vertigo / Imbalance.

Pain.

Discharge.

Head Injury.

Examination:

Exclude middle / external ear disease.

Investigations: Pure Tone Audiogram.

If < 5dB average difference 1 8 Khz review.

If > 5dB average 1 8 Khz MRI.

Also Unilateral Tinnitus < 10 years MRI.

+ subjective unilateral loss < 80 years old MRI.

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SUDDEN ONSET SENSORINEURAL HEARING LOSS.

History:

Otological.
Past medical history.
Drug history.
Systemic illnesses.

Examination:

General.
Otological.
Neurological.

Investigations.

Audiogram day of presentation if possible.

Haematological FBC, ESR
Glucose
Syphilis Serology
Rheumtoid factor.
ANCA.

Treatment.

If in Steroid Responsive Zone on audiogram, steroids dexamethasone 4 mg bd for

7 days as an outpatient, except if contra-indicated.
If not in the Steroid Responsive Zone, on audiogram, observe.

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TINNITUS.

History:

Duration of symptoms.
Site of tinnitus (unilateral, bilateral, central).
Intermittent / constant.
Synchronus with pulse.
Hearing difficulty.
Imbalance.
Effect on life.

Examination.

Examine Tympanic Membrane (TM).

Tuning Forks.
W. V. Testing.
Stethoscope for objective tinnitus.
CNS examination.

Investigation.

Audiogram. MRI Scan if unilateral.

Treatment.

If mild / intermittent explanation.

Treat conductive deafness / external ear disease.

Treat S/N deafness, eg. hearing aid.
If troublesome Tinnitus Clinic.
Masker / masker aid combination.
Relaxation tapes Hearing Therapist.
Self help - GP.

If severe - Clinical Psychologist.

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UCD Student Manual / A Student Guide to Oto-Rhino-Laryngology 34

MENIERES DISEASE.

History:

Episodic vertigo and/or nausea vomiting.

Tinnitus.
Fluctuating hearing.
Pressure / fullness in the ear.

Examination:

Normal TM or non-active CSOM.

Pure Tone Audiogram.
Electro Neurography (ENG).
MRI (if atypical ie. other unexplained symptoms).

Treatment:

Acute Attacks: Cinnarizine 30 mg TID

or
Prochlorperazine 20 mg
or
Buccal Prochlorperazine 1-2 tab.

Maintenance:

Serc 16 mg TID reducing to 8 mg TID as indicated.

Failed Medical Rx (time scale 6-12 months, sooner if v-debilitated)

Refer to Otologist for consideration of surgery.
Gentamicin ablation.
Endolymphatic sac surgery (70-80% success).
Labyrinthectomy if poor hearing (>50 dB) (99% success)
Vertibular Neurectomy if good hearing, fit (98% success)
Grommet insertion 50% success, no evidence to support efficacy.

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UCD Student Manual / A Student Guide to Oto-Rhino-Laryngology 35

THE NOSE.

The nose is for breathing. The design of its cavity results in cleaning, warming and moistening
the air on inhalation. The olfactory receptors are situated in the nose which allows us to smell
airborne odours. When a smell enters the nose it stimulates the cilia (tiny hairs) of nerve cells
causing signals to be sent to the brain. The floor of the nose is the hard palate and so chewing
can occur in the mouth without any interference in breathing capacity. The flap-valve of the soft
palate can shut off the mouth cavity from the airway through the oropharynx. Breathing is
arrested during swallowing, the soft palate is elevated and shuts off the nose (naso-pharynx)
from the foodway through the oro-pharynx. The oro-pharynx is the crossroads of airway and
foodway, clashes between air stream and food are avoided by the control mechanism of the soft
palate.

The nasal cavity extends from the external nostrils to the posterior end of the nasal septum, a
midline partition which divides the nasal cavity into two hales. Posteriorly it opens into the
naso-pharynx. The respiratory mucous membrane of the nasal cavity is very vascular and red in
colour. On the roof of the nose is the olfactory mucous membrane which is less vascular and
appears yellow in colour. The lateral wall of the nose is increased in area by the projection of the
nasal conch where the paranasal sinuses and the tear duct is found.

Respiratory mucous membrane lines the respiratory passages from the entrance of the nose to the
walls of the naso-pharynx including all the paranasal sinuses and from the lower larynx to
bronchioles of a diameter of 1mm. The mucous membrane is thick and loose-woven and
contains serous glands and mucous glands. The mucous glands have serous crescents and the
mucous membrane is surfaced by a single layer of ciliated columnar epithelium. The surface of
these ciliated columnar cells is self-cleansing. The watery secretion of the serous glands
evaporates to moisten the inspired air. In the nasal cavity the mucous membrane over the
inferior concha is redder and much more vascular than elsewhere.

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UCD Student Manual / A Student Guide to Oto-Rhino-Laryngology 36
EPISTAXIS.

Epistaxis (nose bleeding) is a nasal haemorrhage and a fairly common condition.

Between 10% to 15% of the population have at least one episode of nose bleeding and 4% have
recurring epistaxis requiring intervention therapy. Epistaxis in children is usually of venous
origin and in the older age group of the more severe arterial type.

The management of a nose bleed will depend on its severity. A good understanding of the
pathological factors producing epistaxis as well as a sound knowledge base of the anatomy of the
nasal cavity and its blood supply is essential.

Causes of Epistaxis.

Local. General.

Trauma. Congenital.
- Self-inflicted - Haemophilia.
- Nasal/Maxillo Facial Fracture. - Christmas Disease.
- Post surgical. - Von Willabrands disease.
- Foreign Bodies. - Haemorrhagic Telangiectasis.

Drying mucosal dessication due to septal Acquired blood disorders.

deviation. - Leukaemia.
- Aplastic Anaemia.
Nasal Septum Perforation. - Lymphoma.
- Thrombocytopenia.

Inflammatory Acquired Diseases.

- Allergy. - Liver.
- Seasonal Rhinitis. - Renal Disease.
- Perennial Rhinitis.
- Atrophic Rhinits. Vitamin.

Infective. Granulomatosis
- Acute Viral. (Sarcoid/Wegeners).
- Bacterial Infections.
- Fungal (Aids). Endocrine - Pregnancy.

Tumours Angiofibroma. Hypertension.

Anatomy / Pathophysiology.

Bleeding usually arises from the nasal septum, which is supplied by the following vessels:
Internal Carotid Artery - Anterior ethmoidal artery.
- Posterior-ethmoidal artery.
- Greater palatine.
External Carotid Artery - Sphenopalatine artery.
- Superior Labial artery.

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Two areas of the nose are frequently associated with epistaxis. Most anterior epistaxis originates
at Kiesselbachs plexus (or Littles area). Most posterior bleeding originates at Woodruffs
plexus, behind the middle turbinate at which the sphenopalatine artery enters the nose.

MANAGEMENT OF EPISTAXIS.

Nosebleed.

Controlled Profuse, not controlled with pressure

with
pressure.

Local mucosal Check vital signs. Obtain patient

therapy (eg. Co-phenylcaine) history. Rule out predisposing factors.
cautery, Full blood test, check
or observation coagulation, liver & renal profile.

Bleeding Bleeding
site site
identified. not
identified

Perform if bleeding not controlled following

cauterization cauterization, place anterior pack to control bleeding
- bleeding
controlled

Replace with
anterior / posterior
pack

Consider Endoscopic Consider

Spheno-palatine Artery Angiography
Ligation and/or and
Arterial Ligation Embolization

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Assessment of patient.

Obtain a full history from the patient - check for predisposing factors.
Assess blood pressure and pulse rate and signs of clinical shock.
Ascertain if possible the approximate amount of blood loss.
Patient should be sitting upright and leaning forward to lower blood pressure.
Pinch the nostrils tightly together.
Rule out the use of medications eg. non-steroidal anti-inflammatories or anti-coagulants
which may be predisposing to the bleed.
Carry out a physical examination to rule out obvious signs of telangiectasia.
General ecchymosis or bruising indicating systemic causes predisposing to the
haemorrhage.
Venous access.
Full blood count and haematocrit should be carried out, check coagulation screen, liver
function and renal profile.

Control of Bleeding.

Patient should be sitting upright and leaning forward.

Pinch the nostrils tightly together on the lower nose this should compress the vessel on
the septum and arrest the bleeding.
Apply a plug of cotton wool soaked in cophenylcaine.
Cauterize the bleeding point with silver nitrate stick.
Electric cautery or diathermy can be performed under local anaesthetic in co-operative
adults or under general anaesthetic in children.
Nasal Packing - If simple measures fail to control the bleeding the nose will need to be
packed. A number of nasal packs are available. The simplest is a nasal tampon which
expands in the nasal cavity with moisture to apply pressure to the area. Insert along the
septum, remembering that the nasal cavity runs along the line of the palate. The insertion
of a nasal pack in the form of inch ribbon gauze coated with Vaseline or bismuth
iodoform paraffin paste (BIPP) has been the traditional method to control nasal
haemorrhage. It is important to remember that the length of the nasal cavity in adults is
approximately 6-7 cms. The packing should begin at the site of the bleeding and
gradually layered along the floor of the nose until control is achieved.
A vaseline gauze pack can be left in for 48 hours, a BIPP pack up to 3 weeks. There is a
significant morbidity associated with the use of nasal packs. A patient may require
admission to hospital for a period of anything from 48 hours to 2 weeks depending on the
severity of the bleed and underlying systemic causes. There is also a danger of using
bilateral nasal anterior nasal packing in the elderly patient, especially if they are on
respiratory depressants as obstructive sleep apnoea can be induced. The patient should be
put on careful observation in the ward, intravenous access established and only reversible
analgesic agents utilised.

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UCD Student Manual / A Student Guide to Oto-Rhino-Laryngology 39

Catheters - if packing fails nasal catheters can be used to control nasal haemorrhage.
They utilise proprietary double balloon catheters which may be inserted into the nasal
cavity with ease. One of the balloons is placed in the nasal cavity adjacent to the site of
the bleeding, the other balloon is inflated in the naso-pharynx to prevent the blood being
swallowed. The balloons are inflated to 5 to 8 ccs of air and can be left in position for
48 hours and deflated to assess if the haemorrhage has been controlled. The advantage of
using these catheters is that they are easy to insert and discomfort can be relieved by
simply deflating the catheter.

Refractory Epistaxis - if a haemorrhage is not controlled by the above means then more
active intervention is required. They may take the form of:

Insertion of a post nasal pack should be performed by an experienced

Otolaryngologist. These packs are made up of rolled gauze inserted into the naso-
pharynx by the use of Foley catheters passed through the nose and brought out
through the mouth. These patients require very careful observation.

Embolization. Under local anaesthesia a catheter is inserted percutaneously into the

femoral artery in the groin and advanced by fluoroscopic control to the external
carotid artery and into the bleeding vessel. In selected cases this is a very effective
method of controlling epistaxis with a success rate of 80-87%, but requires an
experienced Neuro-radiologist and highly sophisticated equipment which may not be
available in all centres.

Arterial ligation - ligation of the ethmoidal arteries via the medial orbit.

N. B. Epistaxis can be severe and may result in death for a patient in certain
circumstances. Circulatory resuscitation may be necessary before trying to arrest the
bleeding. An intravenous infusion if the patient has circulatory collapse and at the same
time blood should be analysed for cross-matching.

Be particularly vigilant in the care of a patient with post-traumatic epistaxis this can be
potentially fatal and often requires vessel ligation.

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UCD Student Manual / A Student Guide to Oto-Rhino-Laryngology 40

SINUSITIS.

Rhinosinusitis can be defined under two different categories:

Acute Rhinosinusitis - acute inflammation of the nasal and paranasal sinus mucosa.
Chronic Rhinosinusitis - chronic inflammation of the nasal and paranasal sinus mucosa
(symptoms present for more than 3 months).

Predisposing Factors:

Allergy - seasonal / perennial.

Structural - septal deviation abnormality of the osteomeatal complex.
Pathological - nasal polyps, hyptertrophic turbinates, tumour (benign or malignant).
Perennial non-allergic rhinitis or vasomotor rhinitis.
Mucociliary clearance abnormality (primary or secondary).
o Primary ciliary abnormality primary ciliary dyskinesia, Kartageners syndrome.
o Primary mucus abnormality - cystic fibrosis, Youngs syndrome.
o Secondary ciliary or mucus abnormality - viral or bacterial infection, smoking.
Immunodeficiency (local / systemic) IgA / IgG deficiency,
panhypogammaglobulinaemia
Medications - Aspirin, ACE inhibitors, OCP, Beta-blockers, rebound hyperaemia of
nasal mucosa following chronic vasoconstrictor use. Eg. ephedrine, otrivine.
Iatrogenic ie. post-surgery (secondary atrophic rhinitis)
Idiopathic.
Hormonal
o pregnancy, OCP (oestrogen),
o older men (testosterone).

Clinical Features.

Acute Rhinisinusitis usually involves more than one sinus. However the presentation depends on
which sinus is primarily involved.

Maxillary Sinusitis.

Symptoms .

infective nasal and post nasal discharge.

maxillary/dental pain.
nasal block cacosmia.
general malaise.
oedema of the upper eyelid may be present.

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Examination.
pyrexia.
tenderness over cheek and teeth.
mucopus in nose (from middle meatus).

N.B. Facial swelling is very unusual in maxillary sinusitis (consider dental

cause, tumour or a complication of sinusitis).

Frontal Sinusitis.

Symptoms.
infective nasal and post nasal discharge.
supraorbital pain.
nasal block.
cacosmia.
general malaise.

Examination.

Pyrexia.
Tenderness over forehead.
Mucopus in nose (from middle meatus). Swab for C&S.
Periorbital cellulitis.

Ethmoid Sinusitis.
May occur on its own, especially in children.

Symptoms.

Infective nasal and postnasal discharge.

Pain over medial canthus.
Nasal block.
Cacosmia.
General malaise.

Examination.

Pyrexia
Tenderness / Erythema of the medial canthus of the eye, swab for C&S.
Mucopus in nose (from middle meatus).
Periorbital cellulitis.

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Sphenoid Sinusitis.

Symptoms.
Infective nasal and postnasal discharge.
Severe headache over vertex or retro-orbital area.
Cacosmia.

Examination.
Pyrexia.
Mucopus in nose (above middle turbinate).
Nasal endoscopy (rigid or flexible endoscope LA).
FBC
Nasal swab.
Plain X-Rays of sinuses (occipito-frontal, occipito-mental, lateral)
CT Scan (coronal and axial bony windows).

Treatment of Acute Rhinosinusitis.

Medical.
Appropriate antibiotic x 10 days eg. amoxicillin, augmentin or vibramycin.
Decongestant nose drops / spray x 1/2 weeks eg. ephedrine, otrivine or steroids.
Analgesia.
Bed rest.
Consider admission to hospital for IV antibiotics, topical decongestants, CT scan if
unresponsive to above measures or in presence of complications.

Surgical (only if unresponsive to medical treatment or in presence of complications).

Antral washout (maxillary sinusitis).
Frontal trephine (frontal sinusitis).
Functional endoscopic sinus surgery (FESS) or external fronto-ethmoidectomy
(extensive fronto-ethmoid maxillary sinusitis.

Complications of Acute Rhinosinusitis.

Bacteraemia.
Septicaemia.

Respiratory Tract.
Adenotonsillitis.
Pharyngitis.
Laryngitis.
Tracheitis.
Bronchitis.
Lower Respiratory Tract Infection.

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Ear.
ASOM
Glue Ear (OME).
Eustachian Tube Dysfunction.

Orbit.
Periorbital cellulitis/abscess infection anterior to orbital septum.
Orbital cellulitis/abscess infection posterior to orbital septum. Suspect if visual
acuity (especially colour vision), diplopia (opthalmoplegia), proptosis
(exophthalmos), lateral displacement of eye, chemosis (conjunctival oedema).
Optic neuritis.

Treatment of Orbital complications.

IV antiobiotics / decongestants x 24 hours.
Urgent CT Scan.
Surgical drainage if extension into the orbit.

Treatment of Intracranial complications.

IV antitiotics/ decongestants x 24 hours.
Treatment of specific neurosurgical complication.
Surgical treatment of sinusitis.

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CHRONIC RHINOSINUSITIS.

Clinical Features.

Most cases of Acute Rhinosinusitis are resolved completely with appropriate treatment.
However Chronic Rhinosinusitis may develop especially if there are predisposing factors such
as:

Nasal Allergy.
Dental Infection.
Gross Septal Deformity.
65% of patients with nasal polyps have chronic sinusitis.

Symptoms.

Nasal Block.
Chronic rhinorrhoea (anterior & posterior intermittently infective).
Hyposmia.
Anosmia.
Facial pain.
Itch and sneezing (if underlying allergy).
Cachosmia may occur in infections of dental origin.

Examination.

Mucopus in the nose of nasopharynx.

Pyrexia is usually present.
Tenderness over the antrum and on percussion of the upper teeth (swelling is
most commonly of dental origin).
Nasal endoscopy (rigid or flexible endoscope LA).
CT Scan (coronal and axial bony windows).
Allergy testing if history is suggestive skin prick test, RAST (allergen
specific IgE.

Treatment.

Antibiotics eradicate infection.

Long term topical steroids 3-6 months systemic side effects occur only if
higher than recommended doses are used.
Bed rest.
Restore mucociliary clearance aeration and drainage with topical steroids.
Surgery eg. functional endoscopic sinus surgery (FESS).
Intranasal ethmoidectomy.

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External frontoethmoidectomy.
Retain maximum normal anatomy as possible if surgery is performed.
Identify and treat any underlying cause eg.
o Correct septal deviation.
o Nasal polypectomy.
o Treat underlying allergy.
o Immunoglobulin therapy for immunodeficiency.
o Pregnancy avoid treatment if possible.
o Rhinitis medicamentosa: steroids, consider surgery.

Complications of Rhinosinusitis Surgery.

Nasal.

o Epistaxis.
o Infections.
o Mucosal adhesions.

Orbital.

o Haematoma (periorbtial / orbital).

o Optic nerve damage.
o Abscess / cellulitis (periorbital / orbital).

Intracranial.

o CSF Leak.
o Meningitis, abscess.
o Anosmia.

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ALLERGIC RHINITIS.

Allergic Rhinitis affects approximately 10% of the general population. A number of

pharmacologically active agents, including histamine and leukotrienes, cause variable degrees of
oedema and vasodilation (nasal blockage) increased mucus secretion (rhinorrhoea) and disturb
the autonomic regulation within the nose. Many patients develop a cellular infiltrate within the
nasal mucosa which accounts for reactivation of symptoms in response to minor stimuli, eg.
tobacco smoke.

Nasal allergy may be seasonal (hay fever) or perennial. Symptoms in both groups are similar,
although perennial allergic rhinitis tends to be associated with more discharge and with
diminished smell and taste.

Symptoms.
Sneezing.
Watery nasal discharge.
Nasal congestion.
Itchiness of the nose and eyes.

Symptoms result from a Type 1 hypersensitivity reaction to allergens mediation by 1gE

antibodies. Symptoms occur after a given period of time following exposure to an
allergen. The most common allergens include:

Pollens.
Animal danders.
House dust mites.
Foods and pollutants.

Examination.
Pale bluish, oedematous turbinates in the nose covered with a thin clear film of
mucus.
Children may have a crease across the lower part of the nose due to continuous
rubbing known as Allergic Salute.
Exclude polypi, septal deviation or tumour.

Treatment - Medical.
Avoidance of the offending allergen is most effective.
Antihistamines will reduce sneezing, pruritus and rhinorrhoea an intranasal
antihistamine, azelastine (Rhinolast) is available.
Short course of topical steroids such as beclomethasone (Beconase) fluticasone
(Flixonase) and flunisolide (Syntaris) are potent anti-inflammatory agents if clinically
warranted (cautions for proper use are important as side effects such as burning and
sneezing are not uncommon).
Combination of antihistamines and steroids provides good symptomatic relief.
Intranasal decongestants such as zylometazoline (Otrivine) constrict the blood supply
to the nasal mucosa use only for limited period.

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Treatment non Medical.

Remove bedroom carpeting.

Use foam pillows.
Enclose mattresses and box springs in plastic covers if allergy is due to dust mite.
Keep house windows closed and reduce indoor humidity by air-conditioning are
reported to be beneficial to those with pollen allergy.
Exclusion of dairy products from diet may alleviate symptoms.

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ADENOIDS.

Adenoids are a mass of lymphoid tissue shaped like a bunch of bananas, situated in gap of the
post-nasal space in children. If the adenoids are big nasal obstruction can occur. This can cause
snoring with purulent rhinnorrhoea if there is a secondary sinusitis. Epistaxis can also be a
consequence. Due to interference with the Eustachian tube aural symptoms can also occur, with
or without nasal symptoms. Hearing loss or earache can also occur. If a baby is experiencing
difficulty with nasal obstruction which affects feeding it may be necessary to remove the
adenoids. Usually a cautious approach is taken and it is only cases of significant nasal and aural
symptoms which will necessitate surgery.

The post-nasal space is very difficult to see in a child and a lateral X-ray will show the size of the
adenoids and degree of obstruction.

Adenoids normally regress before puberty, large adenoids in adults are rare. However, if an
adult has nasal obstruction due to post-nasal lymphoid tissue, the histology is essential to exclude
a lymphosarcoma.

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UCD Student Manual / A Student Guide to Oto-Rhino-Laryngology 49

THE PHARYNX.

The muscular walls of the pharynx and esophagus have distinctive subdivisions, but work
together. The pharynx is the fusiform organ at the back of the mouth that links the mouth and
nose to the trachea and oesophagus.

Pharyngitis and Tonsillitis.

In general most sore throats are caused by viruses and do not require antibiotics. Acute tonsillitis
and pharyngitis present with throat pain, that may radiate to the ears, and dysphagia. Fever is
more commonly associated with group A beta-hemolytic streptococci (Streptococcus pyogenes),
which accounts for about 15% of all cases. The proportion of pharyngitis and tonsillitis that is
caused by group A streptococci is related to the patient's age. In children aged 6 to 15 years of
age, approximately 50% of the pharyngitis that presents for care is caused by streptococci. The
primary reason to diagnose and treat strep throat is to decrease the underlying threat of acute
renal failure

Streptococcus Pyogenes.

Symptoms.
Sore throat.
Dysphagia,
Fever.
Malaise.
Headache.
Occasionally abdominal pain and vomiting.

Non-infectious causes of Pharyngitis.

include mouth-breathing secondary to nasal obstruction (as with a URI). Mouth breathing
classically presents as a sore throat that is worse in the morning and abates as the day
progresses. Consider adult epiglottitis in the febrile adult with severe sore throat, trouble
in swallowing and anterior neck tenderness. Also consider peritonsillar abscess.

Diagnosis. Rapid streptococcal tests demonstrate a sensitivity of

approximately 95%. Avoid false negatives with proper sampling technique
(i.e. vigorous samples of both tonsils and posterior pharynx while avoiding the
uvula and soft palate as they dilute the sample). The newer tests have a
concordance of 91% to 95% with those of a culture.

Treatment.

The central question in pharyngitis is deciding which patients require

antibiotics and doing so in a cost-effective manner keeping in mind antibiotic
resistance. The treatment and approach to pharyngitis is mired in controversy.

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TONSILS.

Acute Tonsillitis can occur at any age but is most prevalent in children under 9, the organism
which usually causes tonsillitis is streptococcus.

Clinical Features.

Symptoms.
Sore throat and dysphagia - small children will not necessarily complain of sore
throat but may refuse to eat.
Earache - referred otalgia.
Headache and malaise.

Signs.
Pyrexia is always present and may be high - can result in febrile convulsions is
some infants.
The tonsils are enlarged and hyperaemic and may exude pus from the crypts
follicular tonsillitis.
The pharyngeal mucosa is inflamed.
Foetor is present.
The cervical lymph nodes are enlarged and tender.

Treatment.
Bed rest.
Soluble aspirin or paracetamol held in the mouth for as long as possible then
swallowed will alleviate the discomfort.
Patient should drink as much as possible particularly small children who may be
susceptible to becoming dehydrated.
Antibiotics.

Complications.
Recurrent tonsillitis - some patients particularly children are prone to recurrent
bouts of tonsillitis. If such attacks are severe and frequent then a tonsillectomy
may be necessary.

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Acute Tonsillitis in an adult.

Acute Tonsillitis in a child

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PERITONSILLAR ABSCESS (Quinsy).

A Quinsy is a peritonsillar abscess (a collection of pus) which may form as a result of acute
tonsillitis. It is more common in adults and extremely rare in children. This can be severe with
absolute dysphagia with referred otalgia.

Clinical Features.

Symptoms.

Severe dysphagia with referred otalgia.

High temperature.
Swelling of the tonsillar lymph node.
Malaise.

Signs.

Similar to those of acute tonsillitis with medial displacement of the tonsil to the
midline.
Trismus (spasm of the pharyngeal muscles) the buccal mucosa is dirty and
foetor is present.
The anatomy of the buccopharyngeal isthmus is distorted by the quinsy.

Treatment.

Antibiotics high dose of intravenous antibiotic followed by a five day course of

oral antibiotics.
Draining the abscess may not always be necessary. If trismus is present and pus
suspected then drainage is required. A small incision is made midway between
the base of the uvula and the site of the upper wisdom tooth. The blades of a
sinus forceps are then inserted into the abscess cavity and opened. If the patient is
a child drainage should be carried out under anaesthetic.
Usually a tonsillectomy is carried out about six weeks after this procedure if there
is a history of recurrent tonsillitis or this is the 2nd episode of quinsy.

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Complications.

Vascular fibrous tissue found lateral to the tonsil after a quinsy makes
tonsillectomy difficult.
Bleeding from a quinsy is an important and serious sign of complication due to
erosion by the peritonsillar pus of the internal carotid artery.

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HOARSENESS.

Hoarseness is a vague term best defined as an alteration in voice quality. Hoarseness is not a
diagnosis in itself, but a common symptom of many different conditions that can affect the
larynx. Diagnosis of the underlying cause of a patients hoarseness can often be difficult in a
primary care setting as the larynx is not readily accessible for examination. It is important in the
early stages of diagnosis to exclude hoarseness due to malignant disease, such as laryngeal
carcinoma.

Hoarseness can be categorised as follows:-

Acute - lasting less than 3 weeks

Chronic - more than 3 weeks.

Examination.

Take a careful history of the symptoms, pay particular attention to the following:-

Critical to check the duration of the symptoms.

Is the hoarseness constant or intermittent, worsening or static?
Have there been similar previous episodes?
A positive smoking and alcohol history suggest the possibility of malignant
disease.
Recent surgery, particulary on the thyroid gland may result in laryngeal nerve
damage which can cause vocal cord paralysis.

Ask the patient to cough. A unilateral vocal cord palsy gives the cough a
bovine quality as failure to appose the cords at the beginning of the cough
results in an inability to generate an explosive expiratory force.

The mouth and oropharynx should be inspected and the neck palpated with
specifc attention paid to any thyroid masses or cervical lymphadenopathy.

Further assessment of the hoarse patient requires review in an ENT outpatient

setting. Ideally this assessment should take place in a specialist voice clinic with
ENT surgeons and speech and language therapists in attendance and specific
equipment available for visualization of the larynx. Indeed laryngeal
visualization is the most important part of the examination of the hoarse patient
and may be performed in the following ways:

Indirect laryngoscopy.
Flexible fibreoptic nasendoscopy
Rigid endoscopy.
Direct laryngoscopy under general anaesthesia may be performed when
laryngeal visualisation is impossible.

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Indirect laryngoscopy, using a head mirror and light source can be difficult for the inexperienced
clinician and the patient with a strong gag reflex. Flexible nasendoscopy provides an excellent
view of the postnasal space, tongue base, vallecula, hypopharynx, larynx, vocal cords and their
movements. Further assessment of vocal cord movement can be perfomed by using a
stroboscopic light source and recording the images. This facilitates analysis and archiving of a
patients cord movements and has the added benefit of demonstrating the findings to the patient.

Where the need for biopsy to confirm pathology is identified or when laryngeal visualisation is
impossible, direct laryngoscopy under general anaesthesia may be performed.

Table 1. Hoarseness.
Acute (<3/52) Chronic (>3/52)

Traumatic Laryngitis eg. voice abuse, Chronic Laryngitis eg. voice abuse,
coughing, blunt trauma. smoke, reflux.
Infective laryngitis eg. viral, Nodules.
bacterial or fungal. Reinkes oedema.
Inflammatory laryngitis eg. tobacco Vocal cord polyps.
smoke. Vocal cord palsy.
Functional.
Laryngeal carcinoma.

Specific Conditions.

Acute Laryngitis.

Most people have suffered from this at some time or other. It commonly occurs as part of a
simple upper respiratory tract infection or acute excessive voice abuse. Treatment is
conservative. Steam inhalation may be helpful, voice rest is advised and the patient reassured.
Smoke inhalation, active or passive, should be avoided.

Chronic Laryngitis.

The mainstay of treatment is avoidance of precipitating factors eg. smoking, voice abuse and the
correction of underlying contributory conditions eg. GORD. It is estimated that up to 30% of
patients with GORD initially present with laryngeal complications. Where ongoing voice abuse
is an aetiologic factor, speech therapy can help re-educate the patient in correct voice use.

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Vocal Cord Nodules.

These are localized, small, benign nodules arising at the junction of the anterior and middle
thirds of the vocal cord. This is the maximum point of contact of the vocal cords during
vocalization and thus the point of maximal trauma. Usually they are bilateral and symmetrical.
Voice rest and speech therapy are usually successful in reversing early nodules but more
advanced ones may require microsurgical removal.

Vocal Cord Polyps.

Generally a single polyp occurs in the adult patient and is easily treated by surgical removal.

Reinkes oedema.

Reinkes space is a potential space beneath the epithelium of the vocal fold. An established
inflammatory process affecting the larynx can result in exudation of fluid into this space causing
bulkiness of the vocal fold and possible redundant mucosal folds. In the early stages speech
therapy and voice rest may suffice but more established cases may require surgical intervention
to improve voice quality.

Functional dysponia.

Reassurance that no organic pathology exists and that full, normal voice function will return is
vital when counselling these patients. Voice therapy may be useful and the appropriate
professional should deal with underlying emotional issues.

Table 2. Causes of Vocal Cord Palsy.

Benign. Malignant.

Trauma. Thyroid carcinoma.

Surgery. Oesophageal carcinoma.
Prolonged intubation. Lung carcinoma.
Cardiogenic (Ortners syndrome) Metastatic neck disease.
Idiopathic.

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Vocal Cord Paralysis.

In the same way as hoarseness is not a diagnosis, vocal cord palsy is not a diagnosis.
Management cannot be undertaken until an underlying cause is found. Vocal cord paralysis is
generally unilateral and is more often left sided due to the extended intrathoracis course of the
left recurrent laryngeal nerve. Causes may be malignant or benign (see Table 2). In up to 25%
of cases no cause is found. Recent thyroid, parathyroid or carotid surgery or prolonged
intubation suggests an iatrongenic cause. A chest x-ray is mandatory to exclude intrathoracis
pathology such as lung carcinoma, apical tuberculous scarring and cardiac anomalies.

Ortners syndrome describes the association of cardiovascular pathology and left recurrent
laryngeal nerve palsy. A CT scan from skull base to thorax, bronchoscopy, oesphagoscopy and
neuropathy screen may be required in order to elucidate a causative pathology.

Where causative pathology is identified, treatment is undertaken as appropriate. A period of

observation of the patient is then required, as most patients will experience some degree of
recovery of voice quality either due to nerve recovery or compensation of the contralateral cord.
Where recovery does not occur and voice quality is unacceptable to the patient, medialisation of
the affected cord can be achieved by cord injection or thryoplasty techniques.

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GLOBUS.

Globus is a common condition. A patient will complain of a sensation of a lump in the

throat (cricoid region) which will usually occur when swallowing saliva. It is a condition
which warrants investigation to rule out other possibilities. A barium swallow and meal
is carried out. `

Classical Globus
(with normal ENT + Explanation
Examination) & Reassurance

BARIUM SWALLOW

ABNORMAL NORMAL

HIGH RISK

ENDOSCOPY REASSURE,
ADVICE SHEET
& DISCHARGE

Treat Heartburn, Sinusitis etc.

as appropriate.

HIGH RISK = SMOKERS.

? . 50 years.
ALCOHOL.
ANAEMIA.

Unreassurable? - Endoscopy and immediate discharge if normal.

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INVESTIGATION of PAROTID SWELLING.

History:

Progressive lump.
Recurrent swelling / inflammation.
Acute inflammatory episode.

Examination:

Lump or diffuse swelling.

Size, edge, consistency, surface, other structures.
Draining lymph nodes, mouth, VII nerve.

Investigation - 1.

FNAC:
If diagnostic definitive treatment.
If ve repeat then imaging.

Imaging:
CT Scan.
MRI.

Treatment:
Elderly / unfit - if typical pleo leave.
if malignant treat surgically / chemoradiotherapy.

Operation:
Formal parotidectomy.

Investigation - 2.

Contrast CT Scan.

Treatment:
Surgery if recurrence persistent.

Investigation - 3.

Admit if severe.
IV antibiotics.
U/S if ? collection.

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VOCAL CORD PALSY.

Investigations: (in the absence of a known cause).

ENT Examination -
CXR.
CT or MRI skull base to aortic arch on the left - root of neck on the right
(if scan is abnormal treat as appropriate)
Panendoscopy, if scan normal.

Treatment:

Unilateral cord palsy - Main problems are poor voice quality and/or
aspiration.

If due to surgical trauma or tumour suggested treatments are:

Injection medialisation with fat or Teflon (Teflon to be used on a

named patient basis only) - on patients with a proven malignancy.
Thyroplasty.

Where recovery is possible & tumours are excluded suggested treatments are:

no treatment
wait 9 months with or without referral to Speech Therapy.

If symptoms unacceptable then use either:

Injection Medialisation Techniques:

Internal and external GA or LA
Teflon (for patients with malignancy) or
Fat Injection as appropriate (GA or LA)

or

Laryngeal Framework Surgery:

Type 1 Thyroplasty.
Arytenoid adduction procedures.

Bilateral Cord Palsy.

No treatment.
Laser Cordotomy.
Laser Arytenoidectomy.
Tracheostomy.

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LOWER MOTOR NEURONE FACIAL PALSY.

History.

Onset, duration, progression, pain & eye symptoms.

Examination.

Ears, mouth + oropharynx.

Parotid, salivary glands, eyes and neck.
Association Neurology.
House-Brackman grading of CN VII

Preliminary Investigations.

PTAs.
EnoG at 110 days for complete facial palsies as prognostic indicator
(no management value).
Patient seen at Day 1 with Incomplete Palsy review at Day 3 to see if it
becomes Complete.

Immediate Management.

Non idiopathic eg. parotid, middle ear disease, head injury treat as
appropriate.
Idiopathic - complete oral steroid and anti-viral therapy.
Simple advice regarding eye care, patching not taping at night and use of drops
and ointments.
Advise patient to attend Eye Casualty if suggestion of Corneal Ulcer.
Analgesia as appropriate.

Review.

6 weeks, if still complete proceed to scanning of parotid temporal bone and CPA.

Management of Incomplete Facial Palsy.

Simple eye care and watch for progression to completion.

Long Term Management.

If no recovery at one year consider re-examination techniques with management

as appropriate by ENT, Opthalmology and Plastics.

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EMERGENCIES.

Foreign Bodies in the Ear, Nose, Throat and Oesophagus.

Foreign bodies are of major importance when looking at otolaryngology emergencies because of
the physiologic importance of the upper airway and the tendency for children to lodge objects in
the various orifices and cavities of the head. The most common cause of accidental death in the
home in children under the age of six is the inhalation of a foreign body. The incidence of
foreign bodies is higher in older people such as a food bolus which may become lodged in the
oesophagus.

Clinical presentation of a foreign body varies depending on the:

Anatomic site involved.

Age of the patient.
Size, shape and type of material involved.
Degree of obstruction or inflammation caused by the object.

Severity of symptoms range from minimal to life-threatening. It is important to obtain a precise

description of the foreign body ingested. A knowledge of the shape, size and type of object is
critical in planning its removal. Many plastic objects are not visible on plain radiographs. The
possibility of a foreign body in the tracheobronchial tree in a child with an atypical presentation
such as asthma should be considered.

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EMERGENCIES.

Foreign Bodies in the Ear.

Beads, pips, popcorn, tiny pebbles and other objects are often put into the ear by small children.
Attempts to clean the ear by an adult may compound the problem and result in the item
becoming stuck.

Symptoms.
Severe discomfort may occur - especially from live insects.
Often discovered when routine otoscopy is performed with asymptomatic patient.
Secondary Otitis Externa is likely to develop with vegetative material.
Occluded hearing loss can occur if the canal is blocked.

Examination.
Otoscopy.

Treatment.
Syringing.
Organic material should not be syringed since it will swell and impact the ear
canal.
Insects can be killed with alcohol or chloroform water.
Children usually require a general anaesthetic to allow safe removal.

Complications.
Attempts to remove objects by inexperienced personnel may result in injury to the
tympanic membrane or ossicular chain.
The main danger of a foreign body in the ear lies in its careless removal.
Perseverance in the removal of a foreign body, particularly in a child, can result in
perforation of the ear drum.

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EMERGENCIES.

Foreign Bodies in the Nose.

The nose is a common site of foreign bodies usually in children or patients with intellectual
disabilities. Attempted removal of foreign bodies by untrained personnel in the accident and
emergency department may result in epistaxis, displacement of the foreign body and/or ingestion
or inhalation.

Symptoms.
Unilateral rhinorrhoea a foul smelling yellow/green discharge.
Nasal obstruction.
Occasionally a blood tinged discharge.
Button batteries fit easily into a childs nose and rapidly cause severe burns with
subsequent septal perforation.
Orbital or intracranial infection may develop if undetected.
Vestibulitis affecting one nostril is almost always a sign of a foreign body.

Examination.
Anterior Rhinoscopy a good light and suction are required because secretions
may obscure the foreign body.
Radiographs are of limited value since most objects are radiolucent.
The other nostril must be examined to exclude a second foreign body.

Treatment.
Atraumatic removal in a controlled manner if the child is co-operative.
Anaesthesia may be required if this is not successful.
Rigid nasal endoscopes are useful to visualise the object and facilitate atraumatic
extraction.
If the patient is a child attempts at removal may cause distress. An adult may
need to restrain a young child by wrapping the child in a blanket in order to
restrain its limbs and the childs head is held steady. This may be necessary as
unsuccessful attempts may push the object back further with an increased risk of
inhalation or traumatic haemorrhage. In some instances a general anaesthetic may
be required.

Complications.
Attempted removal of foreign bodies by untrained personnel may result in
epistaxis, displacement of the foreign body and/or ingestion or inhalation.

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EMERGENCIES.

Foreign Bodies in the Throat.

Foreign bodies such as fish, poultry and other bones are often swallowed inadvertently. Usually
they will scratch or tear the pharyngeal mucosa before passing down into the stomach, they may
on occasions lodge in the hypopharynx or oesophagus. This may result in perforation,
mediastinitis or abscess or even fatal perforation of the aorta.

Symptoms.
Odynophagia pain on swelling is usually the presenting symptom.
Otalgia referred ear pain.
Dysphagia or drooling are present with larger objects.
Stridor on inspiration will occur if the airway is obstructed.
If complete airway obstruction occurs death may result from hypoxia.
Young children may present with subtle symptoms such as intermittent wheezing
our coughing.
Hoarseness and varying degrees of dyspnoea.

Diagnosis.
X-ray examination however may fail to show small fish bones.
Mirror examination (indirect laryngoscopy) or fibreoptic examination of the
hypopharynx are necessary to visualise the hypopharynx.

Treatment.
Emergency treatment may be necessary if obstruction of the airway is complete to
save the patient. The Heimlich manoeuvre should be applied when a foreign body
has been aspirated.
In a co-operative adult removal with a forceps may be undertaken under topical
anaesthetic.
Most children should have foreign bodies under general anaesthesia.
Laryngoscopy may be required to remove the object.

Complications.
Airway Obstruction.
Perforating objects may lead to deep neck space infections such as
parapharyngeal or retropharyngeal abscess.

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EMERGENCIES.

Foreign bodies in the Oesophagus.

Symptoms.
Dysphagia, drooling and/or stridor.
Chest pain and regurgitation or vomiting occur with impacted oesophageal
foreign bodies.
Secondary oedema can occur with chronic foreign bodies and may compromise
the tracheal airway.
Coins often become lodged at the postcricoid area or cricopharyngeal region.
Some patients with carcinoma of the oesophagus may present with an
oesophageal foreign body and adequate visualisation of the oesophageal mucosa
is mandatory at the time of therapeutic endoscopy.

Diagnosis.
Plain radiographs posteroanterior (PA) and lateral chest views are mandatory.
Barium swallow is not recommended in a patient with complete oesophageal
obstruction as aspiration may ensue.

Treatment.
Removal using a rigid endoscope under general anaesthesia.
Small, disc shaped batteries contain KOH or NaOH are capable of causing caustic
burns with possible oesophageal perforation and should be removed as an
emergency.
The use of papain (enzymatic tenderizer) should be avoided as an impacted sharp
bony object may cause further ulceration and/or oesophageal perforation.
Fogarty Balloon Catheters are not recommended deaths have occurred
previously from attempted extractions using this method.
Flexible endoscope should be avoided as irregular edges may tear the oesophageal
mucosa. This can be avoided by drawing the object into the lumen of a rigid
endoscope.

Complications.
Patients must be monitored post-operatively for oesophageal perforation and have
a chest x-ray prior to their discharge.
Severe chest pain radiating to the back suggest oesophageal perforation.
Pneumothorax and pneumomediastinum indicates penetration of the oesophageal
wall has occurred and the patient is at risk of developing potentially fatal
mediastinitis.

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EMERGENCIES.

Foreign bodies in the Larynx, Trachea and Bronchi.

Symptoms.
Young children may present with subtle symptoms such as intermittent wheezing
or cough.
Hoarseness and varying degrees of dyspnoea.
Inspiratory stridor is typical of foreign bodies lodged in the supraglottic or glottic
region. Inspiratory and expiratory stridor indicates tracheal or subglottic
impaction.
Any patient with a history of choking or gagging, in particular an infant with a
history of having something in its mouth, should be investigated thoroughly.
Some patients may have diminished breath sounds or wheezing while others may
have a normal examination.
Vegetative foreign bodies tend to swell with secretions and cause bronchial
obstruction and/or respiratory distress.

Diagnosis.
Radiographic evaluation of the neck and chest is essential although not always
diagnostic and should be taken during inspiration and expiration.
If the foreign body allows airflow into the lungs during inspiration with occlusion
during expiration it will act as a ball-valve. Hyperinflation distal to the foreign
body and shift of the mediastinal structures to the opposite side will occur. If the
foreign body completely obstructs the bronchus, distal atelectasis and collapse
will shift the mediastinum to the side of the foreign body.

Treatment.
Close co-operation between the Anaesthesiologist and the Otolaryngologist is
essential.
Rigid bronchoscopy with a ventilating endoscope is the preferred method for
extraction of tracheobronchial foreign bodies. Atraumatic removal under direct
vision while the patient is ventilated through the side port of the instrument is the
primary goal of therapy.
Specialised forceps have been designed to deal with the potential range of objects
which may be inhaled eg. a peanut, the forceps has a curved tip with an open cup
to allow complete removal without crushing the peanut.
Patients should be observed for at least 24 hours following foreign body removal.

Complications.
Minor complications include atelectasis and wheezing.
Airway obstruction, laryngeal oedema, bleeding and post-operative laryngospasm
are potential problems that may be encountered following bronchoscopy.
Persistent pneumonia is common after removal of long-standing objects.
Bronchial stenosis, pneumothorax, fistula formation and lung abscess are other
rare potential sequelae.

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EMERGENCIES.

Epiglottitis.

Epiglottitis or more appropriately supraglottitis is caused by a group B Haemophilus Influenza

infection. It is characterised by acute severe swelling of the supraglottic mucosa. It is seen
mainly in the age group 3 to 7 though adults may also be affected. It is characterised by:

Sudden onset of severe pyrexia.

Severe sore throat and dysphagia.

Drooling.

The child tends to sit in the trip position ie. sitting erect with hands behind for
support.

In summary the diagnosis is based on the sudden onset, the toxicity, the presence of drooling and
the patient in the characteristic position.

On examination the oral cavity may be inflamed but not severe enough to account for the
severity of symptoms and signs. At the slightest hint of the diagnosis the patient should be
immediately transferred to hospital, taken to the operating theatre, it is imperative that the child
is not put into an X-ray department or made lie flat for bloods to be taken. In these
circumstances total airway obstruction can occur. The patient should be taken to theatre, put
under anaesthesia by the administration of inhalation anaesthetic. It is imperative that a muscle
relaxant is not given. Once the patient is asleep airway control can be achieved by the insertion
of a rigid bronchoscope or endotracheal tube or in certain circumstances a tracheostomy may be
performed. Once the airway is secured blood should be taken for culture and intravenous third
generation cephalosporin antibiotics commenced.
Siblings should be given prophylactic antibiotics, the patients usually can be extubated after 48
hours.

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EMERGENCIES.

Laryngotracheal Injury.

Trauma to the larynx may be missed in a clinical setting where the symptoms and signs are
masked by more severe accompanying trauma to the skull or spine. The incidence of
laryngotracheal trauma has decreased with the compulsory wearing of seat belts. Most injuries
occur due to sporting activities but penetrating injuries may occur from knives and bullets and
the larynx is in danger of damage from inhalation injuries or ingestion of corrosives.

Clinical Features.

The clinical features of trauma to the larynx are dependant upon the severity of the injury.
The main features include:

Bleeding which may be frothy, if there is penetration to the artery due to the mixing of air
and blood. The possibility of aspiration may lead to fatal consequences.

Stridor if the airway has been narrowed by the trauma, stridor will be inevitable. If the
patient is moving very little the stridor may not be clinically manifest.

Dysphonia, alteration of the quality of voice may be due to damage to the vocal cords due
to haemorrhage or paralysis of the recurrent laryngeal nerves.

Painful speech or swallowing. Both speech and swallowing may be painful but not overt
because of the severity of the accompanying injuries.

Emphysema, the presence of crepitus on palpation of the neck is an indication of

penetration of the laryngeal lumen.

Anatomical Changes.

Loss of the normal neck contour due to flattening of the thyroid cartilage is often overlooked
when assessing the patient for neck injury.

In all cases of blunt or sharp trauma to the neck consider the possibility of damage to the
larynx. Examine the external neck for loss of contour, palpate the neck for the presence of
crepitus, if there is any evidence of stridor or airway compromise the patient requires
protection of the airway by intubation of the performance of tracheostomy.

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TUMOURS.

ORAL SQUAMOUS CELL CARCINOMA.

Squamous cell carcinoma of the oral cavity comprises 4% of cancers in males and 2% in
females. It accounts for approximately 46% of head and neck cancers. The majority occur in the
sixth decade of life and the incidence is rising in women. Many survivors of oral cancer have to
cope with severe functional alterations. Speech, swallowing and taste may be affected by the
disease and the physical appearance of many patients may be significantly altered by the disease
process itself and/or its treatment.

Unfortunately cancers of the oral cavity are often diagnosed at an advanced stage thereby
reducing the likelihood of cure and the length of survival. The symptoms of oral cancer are
sometimes confused with trauma, inflammatory and infectious conditions leading to a delay in
diagnosis.

Oral cavity SCC progresses through a series of histological alterations and considerable
individual variation exists in the temporal rate of these changes. The earliest mucosal
abnormality is benign hyperplasia. In the presence of continuous mucosal irritation and/or
carcinogen exposure the epithelium may undergo dysplasia

Predisposing Factors.

Excessive use of alcohol.

Tobacco consumption.
Poor oral hygiene.

Symptoms.

Early Symptoms.

Pain.
Ulcers that fail to heal.
Dentures that become ill-fitting.

Late Symptoms.

Decreased tongue mobility.

Otalgia.
Odynophagia.
Cervical lymphadenopathy.
Wart-like, bulky lesion.
White, lace type patterned lesion.

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Examination.

Oral cancer has a tendency to spread to cervical nodes, with an estimated 30% to 40% having
involvement at presentation. The neck must be included in the initial treatment plan. Metastatic
nodal disease is generally treated with a neck dissection, although some studies have shown that
small nodes can be controlled with irradiation.

The type and extent of neck dissection is dictated by the extent of the primary tumour and
location of nodal disease.

Staging.

The staging system is based on the extent of the disease and the appropriate imaging prior to
initial treatment. The purpose of the present staging system is to help to give an indication of
prognosis and to assist in the evaluation of treatment results. Together the T and N classification
determine the overall stage (I, II, III or IV). The currently accepted staging system is as
follows:-

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TREATMENT OPTIONS FOR ORAL CAVITY CANCERS.

It is now recognised that patients with oral cancer are best managed by a multidisciplinary team
approach. This is usually comprised of Otolaryngologists / Head & Neck Surgeons, Plastic and
Reconstructive Surgeons, Radiation Oncologists, Pathologists, Dental Surgeons, Nurses, Social
Workers, Speech Pathologists as well as allied health care personnel.

The majority of patients are treated with

surgery,
radiation or
a combination of both modalities.

N.B. Chemotherapy has not been proven to be an effective form of primary therapy
when administered alone. Its role as an adjunctive treatment modality is uncertain.
There is some evidence that a response to chemotherapy predicts a subsequenct response
to radiation therapy.

Recent advances in reconstruction with myocutaneous and free vascularised tissue flaps has
facilitated an improvement in cosmesis and function following major ablative surgery.

Treatment is considered on an individual basis and is dependent on the:

site of the tumour,

stage of the tumour,
impact on functional status of any type of intervention,
individual patient circumstances.

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Early oral cavity cancers.

(T1, T2) can be treated effectively with either radiation or surgery. Generally, most
patients are offered primary surgery and usually one treatment modality suffices for early
stage disease.

Advanced oral cavity cancers.

When tumours are more advanced (T3, T4), combined treatment with pre-operative or
post-operative radiation and surgery is the treatment of choice.

Deeply infiltrative lateral tongue oral cavity

squamous cell carcinoma.

Surgery.

Surgery has the advantage of being a once-off procedure and for small tumours has minimal
impact on speech, swallowing or appearance. One of the most important prognostic factors in
patients with oral cavity SCC is complete surgical removal of the neoplasm. A failure to
eradicate the primary tumour will lead to local recurrence and death in most cases. In addition,
when microscopic cancer is present at the resection margin the rate of local recurrence increases
and the survival rate decreases. The aim is to:

Resect the primary tumour with a margin of normal mucosa and any involved
lymph nodes.
Frozen section analysis is usually undertaken to ensure a clear margin of
resection.

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Tumours that abut the mandible may require a marginal mandibulectomy (where
part of the mandible in proximity to or involved with the tumour is resected).

It can be difficult to determine whether the mandible is invaded by disease. Good clinical
judgment combined with modern imaging helps in the decision making process. More advanced
cancers require a mandibulectomy, which is usually segmental in nature. Much of our
understanding of the mechanism of mandible invasion by carcinoma has come from research.

The role of neck dissection or irradiation of the neck in the clinical setting of T1N0 and T2N0
stage disease is controversial. The metastatic potential for T1 and T2 disease is 20% to 30% and
therefore a prophylactic neck dissection is offered by many surgeons in the belief that
microscopic disease can be removed with this approach. Performing a neck dissection has the
distinct advantage that the nodal status of the neck can be analysed histologically and therefore
the information obtained can be used to aid prognosis. The disadvantage of performing a neck
dissection in the N0 patient is the attendant deformity and resulting shoulder dysfunction
associated with the surgery

Radiation Therapy.

Post-operative radiation is usually preferred as pre-operative radiotherapy tends to make surgical

dissection difficult and analysis of tumour margins unclear. However, when tumours are more
advanced (T3, T4) a combination of pre-operative and post-operative radiation and surgery is the
treatment of choice.

Radiation therapy when administered tends to leave the patient permanently xerostomic (dry
mouth), with loss of taste and usually requires 4-6 weeks of treatment. An estimated 30%-40%
of tumours are resistant to radiotherapy. When nodal disease is absent, or in the setting of a
single node without extracapsular spread the patient can be spared a course of radiation therapy.

More often radiation is used as an adjunctive treatment modality to improve local control and
survival in advanced disease (T3, T4). Post-operative radiotherapy also has a role to play in
patients with early stage disease who are deemed to have microscopically involved margins,
perineural or intravascular spread. Patients with multiple positive nodes and/or extracapsular
spread are candidates for radiotherapy.

The usual doses are 50 70 Gy in daily fractions of 1.8 to 2.0 Gy. All T4N0 cancers and T3
cancers with the criteria already mentioned for early stage disease should be offered post-
operative radiation. Brachytherapy, defined as the placement of radioactive sources close to or
into tumour, has a role in the management of selected patients.

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Chemoprevention.

The failure to improve survival statistics despite improvements in conventional modalities of

treatment has led to the development of novel methods of managing this disease.
Chemopreventive agents have recently been employed in an attempt to suppress carcinogenesis
and prevent invasive oral cancer. Whilst some treatment centres use the agents outlined below
they are not in widespread use.

Retinoids - have been shown to have a stabilizing effect on the oral mucosa
and shown some potential in treating leukoplakia and decreasing
the incidence of oral cancer.
Single agent oral etretinate (retinoid with Vitamin A activity)
or
Oral plus etretinate paste therapy - has a reported response rate between 71% to
83% which is maintained by 50% of patients
for 2 years.
13 Cis-retinoic acid - has a significant effect on controlling oral leukoplakia.
Lesions progress after therapy is discontinued and cheilitis,
dermatitis and hypertriglyceridaemia are potential side
effects.
Isoretinoin and -carotene - low dosage maintenance therapy tends to have
improved tolerance.
Isoretinoin - high dosage has been shown to reduce overall incidence of second
primary cancers after initial treatment.

Prognostic Factors.

Residual and recurrent disease following conventional treatment for squamous cell carincoma of
the oral cavity is a continuing problem despite improvements in surgical technique and
radiotherapy over the past two decades. Patients with small superficial lesions:-

T1, T2 in the oral cavity - 75% local control rate.

Patients with more advanced lesions have a much poorer prognosis:-

T3, T4 in the oral cavity - 35-40% with a 5 year disease free survival.

The TNM system helps predict survival although a subset of early cancers recur locally and/or
regionally. Recurrence usually develops within two years of the initial resection or treatment
and is seldom amenable to further curative resection. This may be due to a failure to remove the
primary tumour or nodal disease at the time of initial surgery.

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One of the most important factors in patients with oral cavity SCC is complete surgical removal
of the neoplasm. It is known that

(1) failure to eradicate the primary tumour will lead to local recurrence and death
in most cases.
(2) when microscopic cancer is present at the resection margin the rate of local
recurrence increases and the survival rate decreases.

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LARYNGEAL SQUAMOUS CELL CARCINOMA.

The highest incidence of Laryngeal Squamous Cell Carcinoma (LSCC) occurs most commonly
in the 6th decade of life. It is predominantly a disease of men with a male to female ratio of 5:1,
there has been an increasing incidence in female patients thought to be related to the increased
use of tobacco and alcohol by women during this time. Although highly curable in its early
stages, a diagnosis of laryngeal cancer may result in partial or total loss of voice. Changes in
appearance and functional difficulty which pose a threat to an individuals identity and self
image.

The larynx is divided into supraglottic, glottic and subglottic sites and each site is divided into a
number of subsites as stipulated by the International Union Against Cancer. LSCCs arise most
frequently in the glottis (55%) and supraglottis (40%) with subglottic representing less than 5%
of all laryngeal cancers. Supraglottic cancers have a propensity to spread bilaterally to cervical
nodes due to the rich lymphatic supply draining through the thyrohyoid membrane along the
superior thyroid vessels.

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Generally the risk of occult or actual metastases from supraglottic carcinoma is:-

T1 - 20%.
T2 - 40%.
T3 - 60%.
T4 - 80%.

In contrast, the glottic larynx is virtually devoid of lymphatics and consequently less than 8% of
patients with T1 and T2 carcinomas will have nodal involvement compared to 20% to 40% with
more advanced glottic tumours. Subglottic cancers have a tendency to spread to paratracheal
lymphatics and then to superior mediastinal nodes.

Anatomical Classification of the Larynx (UICC).

Regions. Sites.

Supraglottis Suprahyoid epiglottis including tip, lingual (anterior) and

laryngeal surfaces.
Aryepiglottic golds.
Arytenoids.
Infrahyoid epiglottis.
Ventricular bands (false cords).
Ventricular cavities.

Glottis Vocal cords.

Anterior commissure.
Posterior commissure.

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Subglottis

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PATHOPHYSIOLOGY of LARYNGEAL CARCINOMA.

The clinical presentation and patterns of spread of carcinoma are dictated by the anatomical
location of the lesion.

Glottic carcinomas

constitutes 55% of LSCC.

are frequently associated with an alteration in voice quality (hoarseness) in the early
stages of disease due to an alteration in the mass, shape and mobility of the involved
cord.
present earlier than supraglottic lesions.
airway obstruction and dyspnea represent late features of glottic carcinoma.

Squamous cell carcinoma

has a predilection for the anterior half of the true vocal cord and can spread to Reinkes
space where it extends anteriorly and posteriorly along the vocal fold.
Deep invasion results in involvement of the vocalis muscle and the paraglottic space,
lateral to the laryngeal inlet, resulting in decreased glottic mobility.
Posterior extension to the arytenoids and cricarytenoid joint will further limit cord
mobility.

A significant number of laryngeal carcinomas arise in the supraglottis and most frequently in the
central infrahyoid epiglottis. Patients will often ignore symptoms or do not undergo full
evaluation until the tumour has reached an advanced stage.

Typically the tumour spreads anteriorly through the fenestrae of the epiglottis to reach the pre-
epiglottic space, valleculae and tongue base. Lateral extension will involve the pyriform fossa
and later the post-cricoid region with resulting dysphagia. Deep invasion involves the paraglottic
space allowing spread superiorly and inferiorly.

The term transglottic is given to a tumour from one laryngeal region that crosses the glottis in
continuity with another region. The lesion by definition must have invaded the paraglottic space
and is associated with a high incidence of cartilage invasion and cervical metastasis.

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Since non-specific symptoms are associated with supraglottic carcinoma in the early stages of
the disease, two-thirds are not diagnosed until an advanced stage.

Initially, pharyngeal discomfort or pain and varying degrees of dysphagia are the
presenting features.
Later bulky, exophytic tumour growth or transglottic spread may cause hoarseness,
dyspnoea and/or stridor.
A neck mass may be the presenting complaint due to metastasis or direct tumour
extension.
Odynophagia and unilateral otalgia are acknowledged as more advanced symptoms.
Aspiration is not uncommon at this stage due to an incompetent supraglottic valve
mechanism.

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MANAGEMENT of LARYNGEAL SQUAMOUS CELL CARCINOMA.

In approaching the management of a patient with laryngeal cancer consideration must be given to
the patients

age
general health
personal preferences
location and stage of the tumour
treatment facilities available.

Glottic.

Lesions diagnosed as carcinoma in situ may be managed by microscopic suspension

laryngoscopy with vocal cord stripping of the involved epithelium. Close follow up of these
patients is necessary with repeat laryngoscopy to exclude invasive disease.

Treatment options when recurrent disease is noted are repeat stripping, partial laryngeal surgery
or course of radiation therapy.

Primary radiotherapy or
partial laryngeal surgery are viewed as the treatments of choice for early carcinoma of the
glottic larynx (T1 or T2). Both T1 and T2 are typically treated with 50-70 Gray over a
5 8 week period using a C0-60 unit or 4-MV linear accelerator or
laser microscopic excision is now considered an acceptable method of management for
easily accessible T1 glottic cancer.

All three modalities can achieve primary cure rates of 80-85% with the addition of secondary
surgical salvage yielding over 90% cure rates. The cited advantages of irradiation for early
glottic carcinoma are

superior voice quality,

absence of hospitalisation or
surgical complications.

With laser microscopic excision (LME) these advantages may no longer be valid. The rapid
return to work combined with cost savings with LME indicates its importance in the
management of early glottic tumours.

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The disadvantages of radiotherapy include missing work for a period of time and the possible
complications associated with this treatment modality which restricts recreational and vocational
activity such as:-

radionecrosis
oedema
laryngeal stenosis.
Acute mucositis
pharyngitis

The advantages of external conservation surgery include

precise tumour margin control by histology,

an ability to assess nodal metastasis
earlier return to work
improved chances of salvage without total laryngectomy.

The disadvantages are mainly related to surgical complications such as

haemorrhage
fistula formation
tracheostomy problems
web formation and mortality - < 1%.

Various limited surgical procedures can resect early glottic cancers adequately and preserve
voice, deglutition and maintain the airway. Advances in surgical technique and reconstruction
combined with an improved understanding of the routes of laryngeal cancer spread has
facilitated progress in this area. The patient must be made aware that preservation of the larynx
may not be possible and consented for a complete laryngectomy if deemed necessary.

There is no indication for neck dissection in patients with T1N0 or T2N0 glottic carcinoma.

N1 disease - fields of therapy may be extended to these regions when radiation is the
primary modality of treatment.

N2-3 disease - radical neck dissection or modified radical dissection can be performed.

Combined therapy for advanced glottic carcinomas (T3, T4) is widely practiced. This may
involve a combination of radiotherapy and conservative surgery or radical surgery preceded or
followed by radiotherapy. Selected patients may be managed with radiotherapy initially, with
surgery reserved for salvage.

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The management of T3 glottic lesions is somewhat controversial. Some centres advocate

radiotherapy with surgery for salvage (usually a total laryngectomy), or a total laryngectomy
with or without postoperative radiotherapy. A less than total laryngectomy is also practiced by
some surgeons in an attempt to improve quality of life without compromising survival.

Most T4 glottic carcinomas are managed with total laryngectomy with ipsilateral selective neck
dissection. Bilateral neck dissections are recommended if the lesion approaches midline
structures. Currently the trend is towards laryngeal preservation, as studies have indicated that
patients wish to preserve some laryngeal function and therefore improve quality of life, even
though survival may be slightly compromised.

Supra-glottic.

Early supraglottic carcinoma (T1N0, T2N0) can also be successfully managed by a single
treatment modality either radiotherapy or partial laryngectomy. This approach is cost effective
reduces patient morbidity and does not impact negatively on survival. The oncologic principle
behind supragottic laryngectomy stems from the fact that the supraglottis is derived from a
distinct region (buccopharyngeal) to that of the glottis/subglottis (tracheopulmonary)
embryologically. The right and left hemilarynges arise separately. When a supraglottic
laryngectomy is contemplated the patient must have good pulmonary and cardiac status since
aspiration is inevitable in the post-operative period.

Supraglottic squamous cell carcinoma involving the vocal cord.

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Laryngectomy is generally recommended for all T4 supraglottic cancers. Due to the tendency of
supraglottic cancers to present late, the cervical nodes must be considered in the initial treatment
plan.

Radiation may be used as the initial treatment for cure, with surgery reserved for failure. Failed
radiation cases are usually best managed by laryngectomy or near total laryngectomy rather
than partial laryngectomy. Generally T1N0 and T2N0 supraglottic cancers have cure rates of
approximately 75% with either surgery or radiation alone. Combined as opposed to single
modality treatment shows better survival rates in patients with advanced neck disease and
advanced primary cancers.

While subglottic cancers are rare, < 2% of laryngeal cancers, they tend to present late with
cartilage and nodal involvement, necessitating laryngectomy with bilateral neck dissection.
Patients are usually treated with post-operative radiation therapy to the neck and upper
mediastinum. Irradiation can be used alone with a 36% local control rate in patients with T4
tumours. Stomal recurrence is a feature of this disease especially when a tracheostomy is
performed for emergency airway management.

Radiation therapy is clearly used frequently in the management of this disease and occasionally
results in severe tissue reaction. The recent trend towards organ preservation has seen an
increase in severe radiation side-effects. Oedema and mucositis may progress to perichondritis
and frank cartilaginous necrosis. This manifests with:-

severe hoarseness
pain
airway compromise
dysphagia mimicking tumour progression.

Prognosis.

Whilst results for early laryngeal cancer are favourable results for patients with advanced disease
remain poor. A vast array of methods are available for treatment at any stage of the disease.
Decisions with regard to the type of therapy are usually based on a number of factors excluding
biological markers. This due to the lack of reliable tumour markers in LSCC.

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Thyroid cancer, an update on its management

G. Sim1, A. Curran1,2
Professorial Unit of Otolaryngology/ Head & Neck Surgery
1
Royal Victoria Eye & Ear Hospital, Adelaide Road, Dublin 2.
2
S.t Vincents University Hospital, Elm Park, Dublin 4.
School of Medicine & Medical Science, UCD.

It is well recognised that compared with other human cancers differentiated thyroid cancer is a
relatively indolent disease. In 2001 there were 65 cases (51 females, 14 males) of thyroid cancer
in Ireland, accounting for approximately 0.4% of all cancers [1]. Thyroid cancer consists of the
following types:

Well differentiated - Papillary 70-80%

- Follicular 10%
- Hurthle cell rare

Medullary 5-7%
Anaplastic <4%
Lymphoma rare
Sarcoma rare
Metastases rare

Once a thyroid cancer has been diagnosed, surgical resection of the cancer is necessary to ensure
recurrence or metastases do not develop. This is combined with radioactive iodine ablation,
thyroid suppression therapy and occasionally external beam therapy. The incidence of thyroid
cancer is normally twice as common in women than men. Females usually have a better
prognosis in all types of thyroid cancers when compared to males. Typically patients who
present with cancers over the age of 40 tend to have a more aggressive and potentially a more
lethal course of behaviour.

Papillary Thyroid Cancer.

This is the most common form and accounts for 70-80% of thyroid cancer. It usually affects
young females (20-40 years of age) and tends to metastasise to regional nodes. Tumours are
solitary or multifocal and most present as asymptomatic nodules. Patients can present with
hoarseness, dysphagia or neck lumps, if the disease is at an advanced stage. Prognosis is
excellent with current surgical and medical management with a 90% survival rate at 20years [2].

Follicular Thyroid Cancer.

This accounts for approximately 10% of thyroid cancer and affects females in the older age
group (40-60 years) often in areas of iodine deficiency. It spreads by the haematogenous route
and prognosis is influenced by the extent of capsular and vascular invasion.

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Hurthle Cell Carcinoma.

This is a type of follicular tumour in which the follicles consist predominantly of Hurthle cells.
Hurthle cell carcinomas have a higher incidence of metastases compared to follicular cancers.

Medullary Thyroid Cancer.

This is a neuroendocrine tumour and comprises 5-7% of all thyroid cancers. Tumours originate
from the parafollicular C cells and secrete calcitonin. Approximately 60-80% occur as sporadic
thyroid nodules while 20-40% are familial and associated with multiple endocrine syndrome
(MEN) IIa or IIb. Patients are older (40 to 50 years of age) and the 5 year survival rate is 60%.

Anaplastic Thyroid Cancer.

This usually affects elderly females who are over 65 years of age and constitutes less than 5% of
thyroid cancers. Patients present with a rapidly enlarging thyroid mass and are symptomatic
(stridor, dysphagia). Many usually have distant metastases on presentation. Prognosis is dismal
and most succumb to disease about 1 year after presentation.

Investigations.

When a patient presents with a thyroid mass, the aim of workup is to differentiate benign from
malignant disease. A good history, physical examination, blood tests, fine needle aspiration
biopsy (FNA) and imaging studies are the mainstay of evaluation of thyroid masses.

A rapidly increasing mass, neck nodes or associated hoarseness, dysphagia are signs and
symptoms of concern.

Fine Needle Aspirate Biopsy.

This is the most accurate pre-operative diagnostic evaluation and is cheap and easy to perform
with few complications. Four different results may be obtained from FNAB: benign disease,
malignant disease, indeterminate for diagnosis, and non-diagnostic. In their review of several
large series, Gharib and Goellner found 69% of FNAB results to be benign, 4% to be malignant,
10% to be indeterminate and 17% to be non-diagnostic. The false-positive rate was 2.9% and the
false-negative rate was 5.2% [3].

Accuracy of diagnosis can be improved by performing multiple aspirates. The patients

management depends on the FNA results. A diagnosis of malignancy requires surgical
intervention. Whilst it is possible to diagnose papillary and medullary cancers by FNA, it is not
possible to distinguish follicular adenoma from carcinoma. Thyroidectomy is required in such
instances.

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Blood tests.

Thyroid function tests to determine endocrine status should be performed . Serum thyroid-
stimulating hormone (TSH) is a highly sensitive measure for hyperthyroidism or
hypothyroidism. A low serum TSH suggests a functioning nodule, which is typically benign.
However, neither low nor high TSH can exclude malignant disease. A baseline thyroglobulin
level can be useful as a tumour marker in patients with well-differentiated thyroid cancer.
Elevated serum calcitonin is highly suggestive of medullary thyroid carcinoma. With the low
incidence of medullary thyroid carcinoma, serum calcitonin is not a cost-effective screening tool
in the primary workup of thyroid nodules.

Imaging Studies.

Ultrasound is the most sensitive imaging tool for defining thyroid lesions. It can detect nodules
in 25% of asymptomatic patients and can identify thyroid masses that are not palpable.
Ultrasound cannot distinguish benign from malignant nodules.

Radioisotope scanning determines the functional status of a nodule and therefore the probability
of malignancy within a nodule. Malignant nodules are typically non-functional and do not take
up radiolabelled iodine and appear as cold nodules. Benign nodules tend to be hyperfunctioning
and take up higher levels of radioiodine and appear as hot nodules. However, Ashcraft et al, in a
review of 5000 patients who had undergone thyroidectomy, found that 4% of hot nodules
harboured malignancy, irrespective of radioiodine image findings. Therefore carcinoma cannot
be excluded following radioiodine scans [8].

CT and MRI are not used for routine evaluation of thyroid nodules. They can be used to evaluate
soft-tissue extension of large or suspicious thyroid masses into the neck, trachea or oesophagus
and to assess cervical lymphadenopathy (Figure 1, 2.).

Prognostic factors.

Several classifications with different variables have been used to define the risk and prognosis of
patients. In addition to the TNM system, the three other systems most frequently used include
AGES, AMES and MACIS. Almost all of the prognostic systems include extra thyroid invasion,
distant metastases, tumour size and histological grade [4]. Age is the single most important
factor which determines prognosis. Adverse factors included patients over the age of 45 years,
follicular histology, primary tumour >4 cm (T2-3), extrathyroid extension (T4) and distant
metastases [5] [6]. The variables used in the different prognostic systems are outlined in Table 1
[4].

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Treatment.

Well differentiated tumours.

Patients presenting with malignancy on needle aspiration, with airway compromise, or a mass
suspicious of malignancy are candidates for surgery. Depending on their prognosis, patients may
be treated by thyroid lobectomy or total thyroidectomy. Patients with good prognosis may be
treated by thyroid lobectomy with TSH suppression. Low-risk papillary carcinoma which is
macroscopically localized in one lobe or patients with occult papillary thyroid cancers, may be
treated with thyroid lobectomy. Indications for lobectomy include unifocal, non-metastatic
papillary carcinomas less than 1.0 cm in diameter, with no previous exposure to radiation and a
clinically normal contralateral lobe.

Most of our patients are treated with total thyroidectomy and radioactive iodine ablation and
thyroid suppression therapy. All thyroid tissue is removed so that post-operative iodine-131 is
more effective in treating occult disease. The regional lymph nodes need to be addressed and the
appropriate neck dissection performed [Figure 3]. This allows serum thyroglobulin levels to be
used to monitor patients following total thyroidectomy.

Follow-up.

A diagnostic radioactive iodine scan is performed at 6 week post-surgery. Radioactive iodine

ablation is used if any residual thyroid tissue is present. Scans need to be repeated annually and
serum thyroglobulin used as a marker with regular neck examination.

Anaplastic cancer

Most patients are usually at an advanced stage of disease at presentation and surgery has a
limited role. External beam radiotherapy and/or chemotherapy are used for palliative purposes.
Nitinol airway stenting is useful with laser to maintain the airway in a palliative setting. A
tracheostomy may be useful to maintain the airway.

Medullary cancer

Patients are best treated by total thyroidectomy and central lymph node clearance. Thyroxine
replacement is given post-operatively and calcitonin is a useful marker for follow up.

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Complications of surgery

The cervical neck scar which may take a considerable time to fade, is the complication that
concerns patients most. There is approximately a 1%-2% risk of damage to the recurrent
laryngeal nerve resulting in hoarseness. The external laryngeal branch of the superior laryngeal
nerve may cause dysphonia if injured. Damage/removal of parathyroids may cause transient or
permanent hypocalcaemia. Haemorrhage results in respiratory compromise, it is potentially life
threatening. This complication occurs in 2% of patients.

Recent surgical advances in thyroid surgery:

Endoscopic thyroidectomy

Current trends in Head and Neck Surgery are moving towards less invasive procedures.
Endoscopic thyroidectomy is being developed due to its superior cosmetic results diminished
pain and the added benefit of requiring a shorter hospital stay.

In 1998, Miccoli et al [7], from the University of Pisa, described the technique of endoscopic
thyroidectomy. Patients with a thyroid nodule less than 35 mm or early papillary carcinoma are
suitable candidates. Other criteria include the absence of previous neck surgery, radiation in the
cervical area, the absence of ultrasound evidence and biochemical signs of thyroiditis, thyroid
volume less than 20 mL, and the absence of suspected lymphadenopathy.

The technique involves a 1.5 - 2.0 cm horizontal incision above the sternal notch. Dissection of
the thyroid lobe is carried out under endoscopic vision through a small skin incision with the use
of laparoscopic and conventional instruments. Two conventional retractors are used to maintain
the operation space [7].

The most obvious and attractive post-operative advantages of endoscopic thyroidectomy are
minimal scarring for patients, diminished pain which alleviates the trauma of surgery for patients
ana significantly shorter hospital stay of approximately 2 days.

At present, endoscopic thyroidectomy has a limited role and most cases are managed in the
traditional fashion. Its role is evolving and further clinical experience is required to fully
determine its place in the treatment of thyroid disorders.

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References

1. National Cancer Registry, Ireland.

2. Hundahl SA, Fleming ID, Fremgen AM, et al. A National Cancer Data Base report on 53,856 cases of
thyroid carcinoma treated in the U.S., 1985-1995.
3. Gharib H, Goellner JR: Fine-needle aspiration biopsy of the thyroid: an appraisal. Ann Intern Med 1993
Feb 15; 118(4): 282-9.
4. Dean D, Hay I: Prognostic factors in differentiated thyroid carcinoma. Cancer Control Journal 2000
May/June; 7(3): 229-239.
5. Shah JP, Loree TR, Dharker D, et al. Prognostic factors in differentiated carcinoma of the thyroid gland.
Am J Surg 1992 164 (6): 658-61.
6. Andersen PE, Kinsella J, Loree TR, et al. Differentiated carcinoma of the thyroid with extrathyroidal
extension. Am J Surg 1995 170 (5): 467-70.
7. Miccoli P, Pinchera A, Cecchini G, et al. Minimally invasive,
video-assisted parathyroid surgery for primary hyperparathyroidism.
J Endocrinol Invest. 1997 20:429430.
8. Ashcraft MW, Van Herle AJ: Management of thyroid nodules II: Scanning
techniques, thyroid suppressive therapy and fine needle aspiration. Head Neck Surg 1981 Mar-Apr; 3(4):
297-322.

Table 1: Prognostic schemes used for thyroid cancer

EORTC AGES AMES MACIS

(1979) (1987) (1988) (1993)
Patient
Age X X X X
Sex X - X -

Tumour
Size - X X X
Histological grade - X - -
Histological type X Y X Y
Extrathyroid
invasion X X X X
Distant
Metastases X X X X

X : variables used
Y: used only for papillary thyroid cancer

EORTC: European Organisation for Research on Treatment of Cancer

AGES: patient age, tumour histological grade, tumour extent and tumour size
AMES: patient age, metastases, extent and size of tumour
MACIS: metastases, age, completeness of resection, local invasion and tumour size

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ANGIOFIBROMA.

Nasopharyngeal angiofibroma is a benign growth found in the back of the nose or upper throat.
Angiofibroma occurs predominantly in adolescent males. Whilst it is histologically benign, it is
aggressive and capable of eroding bone.

Symptoms.

Nasal obstruction difficulty breathing through nose.

Nasal discharge bloody in type.
Epistaxis, prolonged recurrent bleeding.
Hearing Loss.
Tinnitus.
Facial swelling, eye pain or headache.

Signs.

Visible firm greyish-red mass in the nasopharynx.

Bulging palate.
Intra-oral buccal mucosa mass.
Swelling over the zygoma.

Examination.

X-ray or CT Scan of the head will confirm if angiofibroma is present.

Angiography.
MRI.
Nasal mucosal biopsy.

Treatment.

Management of the angiofibroma will be based on staging classification as follows:-

Treatment is required if the angiofibroma is enlarging, obstructing the airway or causing
chronic nosebleeding.
Surgery - removal of the tumour.
Radiotherapy is used only in unresectable lesions as there is a risk of delayed
sarcomatous change.

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ACOUSTIC NEUROMA.

An acoustic neuroma is a benign brain tumour that develops in the middle ear. It is one of the
most common types of benign tumours and causes hearing loss. The auditory nerve connects the
inner ear to the brain. It transmits hearing and balance to the brain. The nerve is covered in
layers of cells called Schwann cells. An acoustic neuroma occurs when the Schwann cells grow
too quickly. This is sometimes referred to as an acoustic or vestibular schwannoma. If an
acoustic neuroma is not treated it can grow through the skull bones that make up the middle ear
and affect important structures in the brain.

Symptoms.

Acoustic neuromas grow slowly and take years before they are large enough to cause signs and
symptoms.

Asymmetrical sensorineural hearing loss usually occurs gradually, but in some

instances can develop suddenly.
Tinnitus buzzing or other repetitive sound in the ear which distorts normal hearing.
Dizziness.
Loss or balance
Facial numbness.
Headache.

Examination.

Full examination of the nose, throat and neck.

Tuning fork to test hearing.
Audiogram.
Check balance.
MRI Scan.

Treatment.

Surgery most acoustic neuromas are treated with surgery. Aim of the surgeon is to
remove the tumour and endeavour to preserve hearing and avoid any damage to the brain.
Radiotherapy is sometimes chosen it may not completely remove the tumour but shrink
it to prevent further growth and avoid surgery.

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RARE CHRONIC INFLAMMATORY DISEASES.

1. HYPOTHYROIDISM.

- hoarseness due to oedema of vocal cords.

2. RHEUMATOID ARTHRITIS.

- hoarseness due to fixation of cricoarytenoid joint and vocal cord

immobility.

3. WEGENERS GRANULOMATOSIS.

- systemic vasculitis.
- nasal obstruction.
- chronic otitis media.
- tracheal granulomas and airway obstruction.
- diagnosis made by presence of granulomata on CXR, abnormal
renal function and a positive cANCA.

4. SARCOIDOSIS.

- lateral neck lump.

- lupus pernio are bluish red nodules of the nasal skin.
- diffuse swelling of the parotid gland.
- raised serum ACE levels and hilar lymphadenopathy on CXR.

Professor Aongus Curran/UCD et al

UCD Student Manual / A Student Guide to Oto-Rhino-Laryngology 95

References.

The ABC of Otolaryngology 3rd Edition by Harold Ludman is recommended.

E.N.T. Diagnosis 2nd Edition - T R Bull.

Lecture Notes on Diseases of the Ear, Nose and Throat 9th Edition - P.D. Bull.

Clinical E.N.T: An Illustrated Textbook - Gerard ODonoghue.

Clinical Methods in E.N.T. - P T Wakode.

Acknowledgements for their valuable contributions go to:-

Alexander Blayney,
Consultant Otolaryngologist,
Mater Misericordiae University Hospital.

Mary Bresnihan,
Special Lecturer in Otolaryngology - 2005,
School of Medicine & Medical Science, UCD.

Eileen Corridan,
Senior Executive Assistant,
School of Medicine & Medical Science, UCD.

Professor Aongus Curran/UCD et al