Otorhinolaryngology

Otorhinolaryngology Facial Nerve • Be able to describe the course, major branches and function of the facial nerve. Emerges from the pons-medullary junction & crosses posterior cranial fossa à Internal acoustic meatus into the à Facial canal in temporal bone (with geniculate ganglion within canal) Gives off greater petrosal nerve (to stapedius – Temporal prevents excessive movement if loud noise, taste fibres from palate) & Chorda tympani nerve (taste from anterior 2/3 of Facial Nerve tongue + innervates submandibular & sublingual salivary glands) à Exits through Stylomastoid foramen Gives branches to auricular, facial & occipitotemporal muscles à Then enters the Parotid gland (with the parotid plexus) Branches to Posterior auricular – muscles of ear + occipitofrontalis & Temporal, zygomatic, buccal, Cervical mandibular and cervical - motor nerves of facial expression Zygomatic Buccal Marginal Mandibular Nervus intermedius (a branch of VII which runs with CN VIII) takes sensory from external auditory meatus • Recognise the main causes of facial nerve palsy and be able to make a differential diagnosis based on the presenting symptoms. History Onset Severity Symptoms related to VII palsy Otological symptoms? Other neurological symptoms? Parotid disease? Systemic illnesses? Head / facial trauma? - Congenital, rapid or slowly progressive - Complete or incomplete - Eye closure, drooling, hyperacusis - Deafness, otorrohea, otalgia, vertigo, tinnitus - CVA, multiple sclerosis, Guillain-Barré etc - Masses, pain - Symptoms of infection, sarcoid - # Skull base, stab injuries O/E Test facial movements (raise eyebrow, close eyes, smile, puff out cheeks) Graded using House-Brackman scale (see below) If LMN – forehead affected (unable to raise eyebrow) If UMN – forehead spared as bilateral innervation Always check CNV & VIII + lower nerves & cerebellar function Check ear for signs of infection or tumour Check parotid for mass – if mass found = malignant until proven otherwise A deep lobe of parotid tumour can present as an oropharyngeal mass à medial displacement of tonsil, different to peritonsillar abscess as lacks infection signs Check in mouth for vesicles, palate weakness or displaced tonsil Causes to exclude - Children Congenital Moebius Syndrome (bilat VI, bilat VII with uni or bilat XII N palsies) Hemifacial microsomia (unilat VII + microtia, hemifacial hypoplasia) Acquired Forceps delivery Chicken pox (Herpes zoster) Acute OM Causes to exclude in Adults (and children) Peripheral Trauma More likely in early life – esp. forceps delivery Any penetrating injury Iatrogenic Damage from surgery - parotid or submandibular Tumours Malignant parotid tumours including lymphoma Inflammatory conditions of the parotid E.g. sarcoidosis Middle Ear Iatrogenic Surgery (mastoid & ear) - must be warned of the risk to the nerve! Infection Discharging ear + facial palsy = cholesteatoma = medical emergency Rx - Abx + exploration of the mastoid to remove the cholesteatoma Acute otitis media. Rx with Abx & often myringotomy to drain pus Mastoiditis Herpes zoster Tumours Squamous cell, rhabdomyosarcoma (children) Glomus jugulare or glomud tympanicum Petrous temporal bone Trauma Transverse fractures of the skull (see ENT emergencies chapter) Tumour Squamous cell, metastases, petrous apex cysts/cholesteatoma Intracranial Tumour Acoustic / Facial nerve neuromas, Meningioma, Carcinomatous meningitis Iatrogenic - Skull base surgery Vascular - Stroke Neurological - e.g. multiple sclerosis Site variable Bell's palsy (Idiopathic lower motor palsy of VII Nerve (Diagnosis of exclusion)) 20 / 100,000 Criteria - acute onset, hemi-facial, no CNS / ear pathology Cause largely unknown: viral ? ( immunological ??) Rx - Oral steroids may help speed recovery if given early Prognosis - Signs of recovery begin within 2 months, 90% of patients have a satisfactory return of facial function, Poorer if é age, pain, complete palsy, longer before recovery Infection Ramsay-Hunt syndrome - Caused by Herpes zoster virus Features: Facial palsy (often severe and irreversible), Facial pain, Vesicles ear canal, pinna (and soft palate), +/- sensorineural deafness, +/- vertigo Guillain-Barré syndrome • Grading the severity of a facial nerve palsy - House Brackman Scale I Normal II Slight weakness noticeable only on close inspection III Obvious weakness but not disfiguring IV Severe reduction in movement - incomplete eye closure V Asymmetry at rest – motion barely perceptible VI Asymmetry at rest - no facial movement • Be able to describe the key investigations and management of patients presenting with facial nerve palsy. Investigations Pure tone audiogram Stapedial reflexes Electroneuronography – guide to progress and prognosis MRI/ CT in selected cases • Know the key principles of the management of a patient with a facial nerve palsy. Eye care: Reduced eye closure à eye prone to drying & corneal abrasions à blindness Rx – hypromellose drops & lacrilube ointment, eye patch at night Ophthalmology help may help - temporary lateral tarsorrhaphy (lateral eyelid sutures) or gold weight in the eye helps eye closure. General: Bell’s palsy & Ramsay Hunt Syndrome Oral steroids if no contraindications – 80mg daily, reduced to 0 over 2 weeks Acyclovir if Ramsay Hunt diagnosed within few days of onset & severe weakness If permanent weakness Facial slings can restore symmetry – strips of fascia lata from the thigh to suspend the corner of the mouth from the zygomatic arch. Ear Anatomy SOUND Pressure variations above and below atmospheric levels in AIR Amplitudes are on a log scale (dB) 0dB = lowest hearing threshold 140dB = loudest audible à damage THE EAR Outer – pinna, external canal and concha Middle – tympanic membrane + 3 ossicles (maleus, incus & stapes) opening to round & oval windows + eustachian tube. Cavity is air filled and amplifies the pressure Inner ear – cochlear, bony labyrinth, utricle & sacule – all fluid filled HEARING Vibration transmitted through oval window and through fluid Travels on basilar membrane Maximum amplitude of wave = frequency. Near oval window = increased frequency because stiffness is increased Transduction of sound converts vibrations to voltage using hair cells (tectorial membrane moves in shearing pattern à bending of stereocillia à ion movements à voltage change The 3 layers of outer hair cells change space in response to sound à Act as motors to overcome the friction of the basement membrane NB: frequency of ON/OFF = freq of sound OTOCOUSTIC EMISSIONS Sounds coming out generated by outer hair cells. Can be used as hearing test for neonates Impulses à acoustic nerve à inferior colliculus à MGB of thalamus à auditory cortex Hearing • Distinguish between conductive and sensorineural hearing loss with tuning fork. Rinne tuning fork test Compare air (adjacent to external meatus) with bone (mastoid) conduction Rinne negative – BC > AC = Conductive deafness Rinne positive – AC > BC = Sensorineural deafness AND normal ears Weber tuning fork test Tuning fork on the forehead Conductive deafness = sound better on affected side Sensorineural deafness = sound better on contralateral side • Interpret pure tone audiograms and tympanograms Conductive loss – e.g. impacted wax, otitis media with effusions Ossicular loss à Carhart’s notch (a drop in bone conduction at 2KHz) & poor air conduction. E.g. otosclerosis & ossicular disarticulation Presbycusis – a drop at the upper end of the frequency range in both air and bone conduction Noise induced hearing loss – drop at approx 4KHz with increase again at 8KHz Tympanometry Measures the compliance of the tympanic membrane 1. Static compliance = ear canal volume 2. Middle ear compliance (peaks at pressure in middle ear) A. Serous otitis media – no middle ear compliance – middle ear so gunked that it wont move for any pressure B. Tympanic perforation – a hole means no pressure difference, large static compliance C. Ossicular disarticulation – eardrum is floppy so only the compliance of the membrane is measured = large volume A 1. 2. C B • Otoscopy ACUTE OTITIS MEDIA NORMAL GROMMET GLUE EAR CHOLESTEATOMA INF PERF + Typanosclerosis • Causes of conductive deafness Otitis media with effusion - (OME, glue ear, secretory otitis media) Sterile collection of fluid in the middle ear cleft à Conductive deafness of 10-40 dB & flat tympanogram Most common on children (some assoc with large adenoids, previous infective otitis media & cleft palate), often follow URTI If unilateral / in adults need to exclude carcinoma of post-nasal space (obstructs eustachian tube) Persistent OME may à thinning of membrane à retraction pockets & collapse Prognosis High spontaneous resolution rate (often within a few weeks) Usually follow-up for 3 months – 50% will improve, others needs grommets Treatment Based on adverse effects of hearing loss (social, educational, speech deficits) Grommets (typanotomy tube) aerate the middle ear (not drain it) Most expelled spontaneously (average 9 months - may be up to 2 yrs) 20% will need 2nd grommets for recurrent OME Decongestants, antihistamines & Abx have no effect Adenoidectomy can reduce recurrence, tonsillectomy is no benefit Acute suppurative otitis media Bacterial infection in middle Pus à eardrum bulges out à pain à ruptures drum à pus & blood drains Eardrum heals within 4-5 days Treatment 1st line = amoxycillin + clavulanic acid = Augmentin Myringotomy if fails to resolve, facial nerve palsy or other complications Cholesteatoma A deep bag of meatal skin protruding into the middle ear, continually producing keratin causing the bag to further enlarge. Anaerobic bacteria à purulent foul smelling discharge Complications – linked to erosion & invasion Into the ossicles causing a conductive deafness of 50 dB or more Into the lateral semicircular canal causing vertigo Into the 7th (facial) nerve canal causing a facial palsy Into the cochlea causing a sensorineural deafness which may be total, or partial, Through the roof (tegmen) into the brain causing an intracranial abscess or sepsis, Into the sigmoid sinus causing it to thrombose. Treatment – by surgical removal of sac via mastoid surgery Retraction pockets In-drawing of tympanic membrane Self cleansing – if debris accumulates = cholesteatoma Prognosis – many stay stable, some progress to cholesteatoma so follow-up required Tympanosclerosis Calcification of collagenous scar tissue from previous infection / trauma May be a chalky patch on drum or totally obliterate the middle ear à 50dB hearing loss Otosclerosis Familial condition – autosomal dominant with incomplete penetration Spongy bone around the oval window à grows & fuses with stapes à conductive deafness Treatment – replace stapes with prosthesis (stapedectomy) / hearing aid – surgery has slight risk of sensorineural deafness Chronic suppurative otitis media (CSOM) Middle ear mucosa repeatedly infected, hypersecretory & hypertrophic à micro abscess & inflammatory cell infiltrates. Drum may perforate à Odourless, chronic discharge – can be clear mucus to pus Conductive deafness usually present Treatment Grafting of drum (myringoplasty) may be curative if confined to middle ear If mastoid is involved – cortical mastoidectomy Prognosis Can cause intracranial sepsis if untreated Perforations - dry Dry perforations can be due to viral infections in childhood or scarlet fever Leave alone unless causing significant deafness to patient / preventing sports If troublesome – grafting (myringoplasty) is successful in 80% cases Tumours Benign tumours are very rare Malignant (usually squamous) are rare Usually in previous mastoid surgery – suspect if previously stable mastoid cavity starts discharging (inc blood) & assoc with pain Trauma – head injuries / skull base fractures Haemotympanum Blood in middle ear à drum looks dark red/blue, may be lacerated Conductive loss of 30dB or less DO NOT intervene – blood will be spontaneously reabsorbed & membrane will heal CSF (watery rhinitis) leak may also be present – will usually seal spontaneously NB: Unilateral rhinitis is CSF until proven otherwise Rx with aim to prevent secondary infection Ossicular fracture or disruption As haemotypanum but hearing loss approx 50 dB & doesn’t resolves Explore once blood has reabsorbed & put things right If delayed the ossicle may be reabsorbed Congenital There are some genetic causes of conductive deafness but these are rare. • Causes of sensorineural deafness Presbycusis Most common sensorineural deafness - hearing loss due to ageing High frequencies lost first (d, n, t, s) à unable to understand speech = muffled Treatment - Hearing aid NB: if unilateral suspect acoustic neuroma Acoustic neuroma Benign tumours of auditory nerve 1st symptoms = unilateral hearing loss / tinnitus Early diagnosis essential as mortality/morbidity linked to tumour size (less damage to facial nerve & hearing, able to preserve blood flow to brain Investigations: Pure tone audiometry Magnetic resonance imaging or CT scanning Electric response audiometry Treatment: Surgical removal. Best results are achieved by a joint neuro & otological approach. Sudden sensorineural hearing loss Medical emergency – urgent ENT assessment needed Management Early - Bed rest, v/d, Carbogen gas (a mixture of 5% CO2 and 95% 02), Steroids. Late - Exclude acoustic neuroma/other disease (e.g. syphilis in auditory system) Prognosis: Guarded; low frequency losses recover better than high frequency deficits and severe vertigo is an unfavourable factor. Noise-induced hearing loss Inner ear damage due to sudden acoustic trauma (gunfire etc) Or prolonged exposure to excessive noise (may initially be reversible) – due to cochlear fatigue (temporary threshold shift), occurs within 2 hrs Notch at 4KHz with gradual loss of lower frequencies Non-organic hearing loss Most likely if wanting compensation / psychological need Electric response audiometry will confirm the response Meniere's disease See chapter on dizziness Barotrauma and perilymph fistula Sudden pressure changes à ruptured membranes à leakage of perilymph into middle ear / mixing in inner ear à sensorineural hearing loss, tinnitus & vertigo Can be surgically repaired Trauma to the ear and skull base 20% of temporal bone fractures are transverse à risk to inner ear & facial nerve AIDS and the ear External Ear Kaposi's sarcoma, Fungal otitis externa, Necrotizing ('malignant') otitis Middle Ear Acute and Serous otitis media. Mastoiditis, Most common in Paediatric AIDS. Inner Ear Sensorineural hearing loss (neuropathy of auditory nerve), iatrogenic (vincristine, anti-fungal agents). Hearing loss progresses with disease. Exclude neurosyphilis. Ototoxicity Mainly aminoglycosides, diuretics (frusemide), salicylates and chemotherapeutic agents Take care with RF patients Monitor serum levels Serial audiometry is helpful Glomus tumours Rare benign tumours from non-chromaffin paraganglionic tissue (widely distributed in the head and neck). In the neck, these cells give rise to carotid body tumours. Symptoms: Tinnitus synchronous with the pulse, hearing loss (conductive or sensorineural), facial paralysis, paralysis of cranial nerves IX to XII. Examination: Pulsatile red mass behind the eardrum ('setting sun') audible bruit over the temporal bone, facial paralysis, paralysis of cranial nerves IX to XII. Treatment: Surgery, radiation therapy or by a combination of both Herpes zoster oticus (ramsay hunt syndrome) Virus may attack spiral / vestibular ganglion in inner ear Intense pain in ear à vesicular eruption on pinna & external ear à Sensorineural deafness, vertigo and facial paralysis may ensue Treatment: Acyclovir (improve prognosis and reduce the likelihood of post herpetic neuralgia) • Intracranial complications of temporal bone infections Brain Abscess Pus surrounded by a region of encephalitis in cerebrum / cerebellum Otogenic brain abscess Occurs at any age, 1/3 in children has ENT cause Starts from venous thrombophlebitis à solitary lesion in temporal lobe / cerebellum Most commonly Gr-ve bacilli (can be aerobes / anaerobes / mixed) Mortality 10% Diagnosis Cause often missed – suspect in anyone with ear sepsis Develops over weeks-months Stage Pathology 1 Invasion Initial Encephalitis 2 Localisation Latent Abscess Clinical Low-grade fever, loss of concentration, drowsiness, headache, general malaise. Duration - days. Usually no symptoms. Duration - several weeks. 3 Enlargement Manifest Abscess 4 Termination Rupture of Abscess into ventricle or subarachnoid space. Aphasia, visual field defects, ataxia, motor or sensory paralysis, generalised or focal seizures, fever, lethargy, impaired consciousness, headache and vomiting. 2/3 will have papilloedema Death. Management Refer to neurosurgeon Abscess should be visible on CT/MRI Give intravenous antibiotics penicillin, metronidazole & a 3rd Abx Aspirate pus through a burr hole Operate 2 days later (once Abx working & patient stable) Cholesteatoma usually found, modified radical mastoidectomy performed If untreated will recur within days-weeks Extradural abscess Infection of extradural space (between dura & bone) Manifests as pus, granulation tissue or effusion Usually asymptomatic, often found at mastoidectomy) Can à sigmoid sinus thrombophlebitis, thrombosis & otitic hydrocephalus Sigmoid sinus thrombophlebitis Localised phlebitis à mural thrombus formation à occlude lumen à thrombus propagates proximally/distally to IJV à painful swelling in neck If infected à septicaemia Often à general malaise, headache, spiking fever, rigors & increased ICP Can à oedema over mastoid process if vein blocks Subdural abscess Collection of pus walled off from the remaining subdural space Meningitis Bacterial (usually) infection of meninges & CSF 90% of cases occur in 1 month-5yrs (86% have acute otitis media) Can be caused by direct invasion of cholesteatoma • Be able to recognise the main causes of tinnitus Subjective (intrinsic) tinnitus A hallucination of noises in the head or ears (A symptom and not a diagnosis) It may occur on its own or be associated with hearing loss and vertigo. Objective (extrinsic) tinnitus A noise in the head/ears that can be heard by another individual. E.g. the regular clicking of the soft palate in palatal myoclonus and vascular bruits. Management Counselling Hearing aid if hearing impairment (by hearing better, the patient 'ignores' the tinnitus) Night time sedation / Masker Self help and support groups are useful and help to maintain morale. Balance • Be able to recognise the main causes of dizziness. Central From vestibular nuclei, brainstem and upwards Can be of a central nervous system or cardiovascular origin (probably small vessel disease). E.g. presbystasis - A feeling of momentary dysequilibrium or tending to veer when walking. Common in the over 60s. Thought to be ischaemic in origin and due to small vessel disease in the brain. Cardiovascular Feelings of faintness; ‘weak at the knees’. General syncopal symptoms and are not uncommon in the over 60s. Associated with, hypertension (or its therapy), cardiac arrhythmia's, vasovagal attacks. Peripheral Labyrinth (semicircular canals, the sacule and utricle) and the vestibular nerve. • Be able to define vertigo and understand the significance of spontaneous and induced nystagmus. Vertigo A hallucination of movement, a feeling that either the world is spinning around you or that you are moving with respect to your surroundings usually in a horizontal plane, but can be in the vertical plane like a see-saw. Often accompanied by vegetative symptoms such as nausea, vomiting, pallor and diarrhoea, the first two being the most common. Nystagmus An involuntary conjugated rhythmic to and fro movement of the eyes Clinical sign of a vestibular abnormality Peripheral vestibular nystagmus can be either horizontal or rotatory Vertical nystagmus or nystagmus that changes direction is always signs of a central lesion. Spontaneous nystagmus - follow a finger held 60cm away to the left and then the right, and then up and down. A normal physiological nystagmus is present in the majority of individuals if the irises of the eyes are deviated horizontally further than the punctum of the lacrimal sac, so when looking for a pathological nystagmus don’t deviate the eyes more than this. Destruction of labyrinth function = away from the damaged ear Irritative lesion = towards affected ear Cerebellar lesion = to the ipsilateral side Degree of nystagmus 3rd degree – sudden total vestibular failure (e.g. on right)à nystagmus with a left direction when looking to the right, straight ahead and to the left 2nd degree – several days later – on looking left and straight-ahead 1st degree – a few weeks later - only when looking to the left Will go completely over several months due to CNS compensation • Know the basic patterns of vestibular neuronitis, labyrinthitis, Meniere’s, benign vestibulopathy, benign paroxysmal positional vertigo, presbystasis. Central Nervous System Origin Space-occupying lesion: Degenerative diseases: Post-trauma Intoxication: Vascular processes: Infratentorial tumours, cerebellopontine angle tumours. Multiple sclerosis, Cerebellar degeneration (often ageing) Head injury Alcohol, Barbiturates Vertebro-basilar ischaemia Basilar migraine Transient Ischaemic Attacks (TIA's) Presentation: Ataxia, unsteadiness on one's feet, usually gradual in onset Central vertigo - mild not associated with n/v, hearing loss or tinnitus. Other symptoms and signs of cerebellar / brainstem / central lesion Presbystasis In the elderly An episode of unsteadiness lasting a few seconds, worse on movement. No loss of consciousness, nausea or vomiting. Improves spontaneously. No Rx needed Cardiovascular Causes Postural hypotension, HT, cardiac arrhythmias, vasovagal, drugs, hyperventilation Presentation: Syncope, light-headedness, vague, unsteadiness, faints, global ischaemia - Blackouts (with loss of consciousness) never associated with peripheral cause of dizziness - Fainting / feeling of light headedness on long standing e.g. 20 minutes or more - Carotid sinus syndrome Peripheral vestibular causes Peripheral vestibular problems are characterised by sudden episodes of vertigo Vertigo is almost always associated with nausea and/or vomiting Hearing loss and tinnitus, if present, point to cochlea involvement The duration of the vertigo, the presence or absence of hearing loss / tinnitus are clues to the specific diagnosis. Benign Paroxysmal Positional Vertigo (Cupulolithiasis, Candolithiasis) Spontaneous, occasionally after head injury Typical history: Middle aged or older patient Hx recurrent episodes vertigo, sudden in onset, assoc with n&v Starts on head movement to a particular side in bed / while driving / bending down. It usually lasts at most 1 to 2 minutes. There are no otological symptoms at all. On examination: Hallpike's Positional Head Test will be positive in the initial stage with vertigo and rotatory nystagmus stimulated by turning the head to the affected side. The vertigo and nystagmus disappear in about 30-40 seconds (fatigability) if the head is kept in that position. If it does not fatigue look for a central cause. ENT and neurological examination should otherwise be normal. Treatment: Reassurance, Positioning = Epley, Semont, Cawthorne-Cooksey exercises. Prognosis: Usually gets better spontaneously over 12-18 months. Meniere's Disease Tends to be over diagnosed. Typical history: Middle aged person (35 - 55) - classical triad of symptoms: - Recurrent attacks of vertigo lasting from about 10 minutes to 24 hours - Tinnitus (usually low frequency) - Fluctuating but progressive sensorineural hearing loss Often preceded by feeling of fullness in affected ear à sudden onset symptoms Usually have horizontal nystagmus After – hearing recovers but not to pre attack level à sensorineural loss Can occur in clusters or widely spaced Cause: Unknown (? due to an excessive fluid in the endolymphatic fluid compartment) Investigations: Pure tone audiometry Electric response audiometry is useful in excluding a retro-cochlear cause (i.e. an acoustic neuroma) and electrocochleography may sometimes be diagnostic Blood for serological testing to exclude syphilitic ear disease CT scanning and MRI may be necessary to exclude acoustic neuroma. Treatment: 70% spontaneous resolution - Reassurance is extremely important. Medical- Acute phase: bed rest, vestibular sedatives (diazepam is best), anti-emetics (phenothiazines) e.g. for nausea and vomiting Prochlorperazine (Stemetil or Bucastem) For vertigo Cinnarizine 30mg tds (Stugeron) if fails Betahistine (Serc) 16mg tds Prophylaxis: ? Cinnarizine and beta histine hydrochloride (Serc). ? salt restriction. Surgery: For resistant cases uncontrolled by medical therapy: Intratympanic gentamicin (Chemical neurectomy) Surgery: Endolymphatic Sac Decompression, Vestibular nerve section, Labyrinthectomy Benign Vestibulopathy Cause: Unknown Typical history: Middle-aged Clusters of attacks of vertigo, similar to Meniere's but without the otological symptoms of hearing loss or tinnitus. Also unlike Meniere's, this condition usually resolves in about 2 years Treatment: Reassurance, Cawthorne-Cooksey exercises, Usually gets better spontaneously over 12-24 months. Acute Labyrinthine Failure Causes: Usually idiopathic? viral? local vascular occlusion? autoimmune Fracture of the temporal bone, post surgery, bacterial labyrinthitis secondary Typical history: Any age Sudden attack of deafness and severe vertigo, nausea and vomiting The vertigo is generally prostrating and the patient is confined to bed. O/E a distressed patient who is afraid to move and has nystagmus. Tuning fork tests show a SNHL on the affected side. The audiogram usually shows a moderate to profound sensorineural hearing loss. The attack usually lasts 10 days to 3 weeks, with gradual improvement in symptoms of vertigo. The SNHL often does not recover, even partially. Treatment: Admit for symptomatic treatment of vertigo including intravenous (iv) fluids, antiemetics and vestibular sedatives. Plasma expanders (e.g. Dextran 70) given i.v. and inhaled Carbogen (5% Carbon dioxide, 95% Oxygen) given to try to improve blood supply to labyrinth. Steroids, Cyclophosphamide in lieu of possible autoimmune aetiology. Vestibular Neuronitis Causes: Probably viral in aetiology Typical history: Sudden onset of vertigo with nausea, vomiting and nystagmus but, without hearing loss or tinnitus. Lasts several hours to a few days. Rarely require admission and usually managed by GP. Often occurs in small epidemics Treatment: Symptomatic, vestibular sedatives/anti-emetics. Drug induced Aminoglycosides, chemotherapy, antidepressants and sedatives in the elderly. Often not recognised until patient recovers from the illness that required the antibiotics or chemotherapeutic agents. Otological Emergencies and Infections • Understand the aetiology, presentation, differential diagnosis, principles of management and complications of: o Trauma to pinna (cauliflower ear) Bleeding strips the vascularizing perichondrium from the underlying cartilage of the external ear. If not drained can become infected or the cartilage can become ischaemic à perichondritis, necrosis and later atrophy, distortion of the pinna & cosmetic deformity. A perichondrial haematoma can be drained under LA. A pressure dressing is needed to prevent the haematoma reforming Give prophylactic antibiotics o Trauma to the middle ear Usually caused by poking things into the ear to remove wax/relieve itch! Can be sudden change in pressure (barotraumas) e.g. explosion Usually rupture of the tympanic membrane and the ossicular chain may also become disrupted e.g. fracture of the stapes crura + conductive hearing loss in the region of 50-60dB. If the shock wave is great enough it can rupture Reissner's membrane and result in a severe sensorineural hearing loss. Uncomplicated traumatic perforations often have an irregular edge (c.f. CSOM) and are associated with a 10-20dB conductive hearing loss. They usually heal spontaneously. o Acoustic trauma Results from single loud noises or long-term noise exposure of over 85dB. à progressive hearing loss, o Trauma to the skull base # to petrous temporal bone often passes through the middle ear à conductive loss and a haemotympanum. The external auditory canal can be stenosed due to a fracture of the tympanic ring. Longitudinal # (80%) - CSF leakage is usually short-lived and damage to the facial nerve is rare. Antibiotic cover is indicated. Transverse fractures (20%) (i.e. perpendicular to the long axis of the petrous temporal bone) Usually from frontal or occipital blows Often pass through the labyrinth or internal auditory meatus producing a sensorineural hearing loss, vestibular damage with vertigo and facial nerve palsy (can be decompressed with urgent surgery). Cochlear damage is shown by nystagmus and hearing loss Urgent CT scan is required A delayed palsy is more common and is due to oedema and bruising around the nerve. Rx - high dose systemic steroids. Vertigo may persist for several weeks while the brain learns to compensate 'labyrinthine concussion' if less severe concussion - symptoms include tinnitus, vertigo, permanent hearing loss (at 4 KHz) and benign positional paroxysmal vertigo. Most resolve in 2 yrs, ¼ have some residual loss o Otitis externa 3 main types = diffuse , furuncle, malignant • Diffuse otitis externa o Generalized inflammation of ear canal (external auditory meatus (EAM)) o May be part of generalized skin condition e.g. eczema, psoriasis, seborrhoeic dermatitis or o Localized due to trauma from cotton buds, instrumentation, scratching with dirty finger nails, putting head under water when taking a bath o Infective causes due to § Bacterial: Pseudomonas (secondary colonisation), Staphylococcus aureus § Fungal: Candida, Aspergillus § Viral: Herpes zoster o Other non-infective causes Allergic/irritant e.g. shampoos, medicated ear drops Neurodermatitis as part of an anxiety disorders – results in itching/scratching/eczema cycle o Symptoms include § Itchiness § Irritation § Pain and swelling § Otorrhoea § Deafness due to occlusion of EAM o Signs § Pain of moving pinna or inserting aural speculum to examine ear § Otorrhoea • Bacterial: Pus and debris in EAM • Fungal: Dry or wet debris (looking like blotting paper) or yellow or black spores (Aspergillus flavum or niger respectively) • Viral: vesicles around introitus of EAM (Herpes zoster), soft palate or haemorrhagic vesicles on tympanic membrane (‘bullous myringitis’) associated with thin, watery bloodstained discharge • NB if mucus is present then this must be coming from the middle ear and a perforation must be present as the eam does not contain any mucus secreting glands § Enlarged pre- and postauricular and upper deep cervical lymph nodes may be present o Treatment § Analgesia § Aural toilet – removal of as much debris as possible by dry mopping the EAM or suction clearance § Topical medication: • with antibiotic/steroid ear drops (e.g. Gentamicin + hydrocortisone), astringents (e.g. Aluminium acetate) or anti-infective drops (e.g.Locorten-Vioform) • a ribbon gauze wick or Pope otowick can help the drops reach the deeper aspects of the EAM • antibiotic/steroid ointment injected or applied on a dressing in the EAM § Systemic antibiotics for gross cellulitis o Outcome § Most cases respond to the above § The infection can spread to involve the whole of the pinna (cellulitis) requiring systemic antibiotics § Some patients are ‘prone’ to recurrent infections due to an underlying skin condition, their personal habits/hygiene § NB systemic antibiotics given without aural toilet and/or topical medication can lead to recurrence as infected debris may remain in the eam when skin inflammation has settled Furuncle o A furuncle is a painful infection of one of the hair follicles of the outer 1/3 of the EAM usually due to Staphylococcus o It usually arises after one of the hairs has been plucked or the EAM scratched as above o The main sign is of a red swelling arise from one aspect of the outer wall of the EAM bulging into the meatus o Treatment is with analgesia, astringents (such as glycerin and ichthammol) o Antibiotics may help in more severe infections when there is a lymphadenitis Malignant otitis externa o This is an aggressive form of otitis externa (not a cancerous condition but can be lethal) o Due to Pseudomonas aeruginosa o More common in diabetics or immunocompromised patients § § • • It spreads from the EAM to bone causing an osteitis, severe pain and the VII, IX,X and XI cranial nerve palsies as it spreads across the skull base Treatment is with high dose intravenous antibiotics o • o Otitis media Infection of the middle ear 50% viral in origin Bacterial (Strep pneumoniae, H influenzae, Moraxella catarrhalis) Common in children and usually associated with upper respiratory tract infection Symptoms include - Hearing loss, Pain, Otorrhoea (when the TM bursts), Pyrexia, Systemic upset, In infants a red bulging TM may only be found on careful and thorough examination in a child who is febrile and unwell and there may be few other localising symptoms or signs Pathology The inflamed eardrum bulges outwards due to the formation of pus under pressure - this is painful The drum frequently ruptures and the pus, often accompanied by blood, enters the outside world with relief of the pain The eardrum heals within 4-5 days. Treatment - First line treatment is with amoxicillin (ask about drug allergies first!), Myringotomy is required if condition fails to resolve or facial nerve palsy or other dire neuro-otological complications develop Complications - Brain abscesses still occur due to neglect or inadequate treatment and this is a potentially fatal condition. o Acute mastoiditis Uncommon complication of AOM these days. Pathology - Infection spreads from the middle ear cavity and pus forms in the mastoid air cells causing bony erosion, The pus may spread out through the bone either subperiosteally or into the subcuticular region in the postauricular region History - an AOM that fails to settle associated with persistent otalgia, otorrhoea and hearing loss. A unilateral headache should ring alarm bells as it may be a sign of the development of an intracranial complication OE - The patient is frequently systemically unwell, the canal may be full of pus and a polyp may be seen through a perforated tympanic membrane, sagging of the postero-superior canal wall, tenderness over the bone immediately above the ear canal (McEwen’s triangle). If the pus breaks through posteriorly the skin becomes oedematous and erythematosus and the pinna may become pushed forward Treatment - In the early stages the patient may be treated with high does intravenous antibiotics in hospital but if it does not settle within 48hours or complications arise e.g. subperiosteal abscess, facial nerve palsy, labyrinthitis, petrositis (spread medially into the petrous bone causing Vth and VIth cranial nerve palsies) or spread outside the temporal bone, the patient should have a cortical mastoidectomy Understand the presentation, principles of management and complications of foreign bodies in the ear Patients present with deafness, discharge, bleeding or pain. Occasionally insects can crawl in e.g. ants, cockroaches (both of which I have seen!) and they cause intense irritation. Insects are best drowned in oil and then syringed or sucked out. Solid objects can be removed with hooks while softer objects may be grabbed with forceps. Rhinology • Examine the external nose, bony and cartilaginous parts. The internal nose and nasal septum, middle and inferior turbinates. • Recognise septal deviation, perforation (ulceration) of the septum, polyps and adhesions • Septal Deviation Septal deviation can occur from decent down birth canal or trauma later in life. This deviation can be columella (at the free edge) or further back in the septum. Both can à symptomatic obstruction • Septal perforation Can be due to Trauma Surgical or nose picking Avascular necrosis 2o to cocaine use, septal haematoma, abscess, sickle cell Granulomatous inflammation Wegeners’ granulomatosis, syphilis, TB or sarcoidosis Tumours T cell lymphoma à lethal midline granuloma • Septal haematoma Occurs either after septal surgery / complication of blunt trauma. Blood accumulates between the cartilage and mucoperchondrium à septum swells & fills nasal cavity Untreated à avascular necrosis à perforation & nasal collapse Infection of haematoma à abscess Adhesions – due to damage & poor healing Polyps – translucent grey & mobile Turbinates – are not mobile, are painful • Differentiate between rhinitis (allergic, seasonal and perennial) from rhinosinusitis. Rhinosinusitis is an inflammatory process involving the mucosa of the nose and sinuses. Acute (<4 weeks), Sub acute (4-12 weeks), chronic (>12 weeks) Anatomy Maxillary, Frontal & ant Ethmoid sinuses drain to middle meatus (between the inf & middle turbinate) Posterior ethmoids drain to the superior meatus Sphenoid sinus drains to the sphenoethmoidal recess in the posterior nasal cavity. Acute One, some of all of sinuses involved (maxillary > ethmoid > frontal > sphenoid) Pathology Most follow viral URTI involving respiratory epithelium & paranasal sinuses à Hyperaemia & oedema of mucosa à blocks sinus drainage Stasis of secretions à 2o bacterial infection (Strep pneumoniae / H.Influenzae) Clinical features Severe, unilateral pain over the infected sinus + malaise & pyrexia Can have nasal obstruction, mucopurulent rhinirroea & poor smell Acute facial pain without nasal symptoms = unlikely to be ARS Pain in cheek/upper teeth = maxillary sinus Pain above eye & tender around supraorbital margin = frontal sinus Pain retroorbital or at vertex of head (referred to temporal/whole head)= sphenoid Tender on percussion of upper molars = dental origin Periorbital swelling = cellulites / abscess à urgent referral & IV Abx OE Anterior rhinoscopy à inflamed / oedematous nasal mucosa + mucopurulent secretions May also be mucopurulent secretions in posterior oropharynx Ix - Rarely necessary Treatment Simple analgesics & steam inhalations Decongestant à reduce oedema & improve drainage Topical (xylometazoline spray) – but only for 5 days (otherwise rebound) Abx only in severe cases (maxillary = pen/amoxycillin 7-14 days) Referral for surgery If not responsive to treatment If periorbital cellulites, severe headaches, focal neurology or symptoms of meningitis à maxillary washout / trephining of frontal sinus Chronic (>12 weeks) Multi-factorial disease (bacterial infection, allergy, mucocilliary impairment) Significant impact on quality of life Pathology Main pathogens – staph aureus, coag –ve staphs, aerobes & Gr -ves Can be linked with mucosa hypersensitivity Clinical features Nasal obstruction & discoloured discharge (nasal/post nasal) > 12 weeks Usually painless – facial pain alone is unlikely to be CRS Differentials – Mid-facial segment pain, migraine, cluster headache Worsens if URTI / with flying, should improve with treatment May be smell disturbance & intermittent frontal pain Discharge should be all day (if only in morning consider snoring) O/E Should be - Mucosal swelling, inflammation, discharge May be – mucopus, nasal polyps Differentials Allergic rhinitis – nasal obstruction, hyposmia, nasal irritation, sneezing, yellow discharge (eosinophils), pale swollen turbinates Idiopathic rhinitis (non infective, non allergic) – nasal obstruction, clear rhinorrhoea, post nasal discharge, less itching & sneezing that allergic NB – these can occur concurrently with CRS Treatment Aim to ventilate the sinuses & restore mucocilliary clearance Trial of medical therapy – augmentin/clindamycin/metronidazole + penicillin (min 3 weeks) Topical nasal steroids - betamethasone (2 drops tds) for 2 months f.b. spray Advise douching - ½ teaspoon of salt, ½ teaspoon of sugar and ½ teaspoon of bicarbonate of soda in 2 pints of boiled water, sniff/squirt up nostrils Treat any co-existing pathologies Referral for surgery If no improvement after 8 weeks Nasendoscopy to confirm diagnosis (+/- CT) Functional endoscopic sinus surgery (FESS) to clear drainage passages • Understand the principles of septal and turbinate surgery and the medical treatment of rhinitis and rhinosinusitis Turbinate surgery is used in cases of permanent turbinate hypertrophy May be excised totally or partially or scarring can be induced à shrinkage (by cryotherapy, hot wire, laser, submucus diathermy or filleting of turbinates) Complications – bleeding, atrophic rhinitis, nasal adhesions (à obstruction) • Be able to recognise the complications of rhinosinusitis Peri-orbital cellulitis and orbital abscess Commonest serious complication Direct or blood-borne spread Ethmoid sinuses separated from orbit by thin plate of bone (lamina papyracea) Ethmoiditis can be associated with: § Cellulitis i.e. inflammation of skin anterior to orbital septum ‘pre-septal cellulitis’ § Orbital abscess – subperiosteal pus (confined by periosteum of lamina papyracea) but posterior to orbital septum Management Peri-orbital cellulitis - high dose antibiotics and careful observation Orbital abscess - requires urgent drainage (vision at risk due to pressure) – monitor colour vision, visual acuity & eye movements Facial Cellulitis May be an extension of orbital cellulitis, frontal sinusitis (pus in soft tissues of forehead = Potts tumour) or maxillary sinusitis or osteomyelitis Treat with high dose Abx & sinus drainage Mucoceles Usually form as a late complication of acute sinusitis Collections of sterile mucus occupying an obstructed sinus (especially frontal and ethmoidal) Present with facial swelling, visual disturbances due to displacement of eye or secondary infections Treatment is by surgical drainage (usually endoscopic) Intracranial complications Can occur by direct spread, by venous thrombophlebitis or along the perineural tissue of the olfactory nerve Meningitis is the commonest complication Cavernous sinus thrombosis § Due to spreading thrombophlebitis from the frontal, ethmoidal and sphenoid sinuses § There is decreased venous return from the eye causing the orbit to swell and congestion of the retinal vessels § Symptoms include high fever with rigors, severe headache, reduced level of consciousness and cerebral irritation § Signs include IIIrd, IVth, VIth nerve palsies causing opthalmoplegia in addition to paraesthesia of the upper two divisions of the Vth (due to the close proximity of these nerves to the cavernous sinus) § Frequently the symptoms become bilateral § Treatment is with high dose antibiotics but there is still a high associated mortality Brain abscesses secondary to frontal sinusitis § Occur most commonly in the frontal lobe § May cause subtle changes in personality, headaches, a grand mal convulsion or may be found incidentally on a CT scan § Treatment requires neurosurgical drainage or aspiration Extradural abscess secondary to frontal sinusitis § May be found on CT scan and is usually due to a dehiscence of the posterior wall of the frontal sinus § Are usually drained into the frontal sinus and hence externally Subdural abscess secondary to frontal sinusitis § Is difficult to diagnose in early stages § Patients have general malaise, headache and some neck stiffness and signs of raised intracranial pressure § The diagnosis is generally made on the examination and CT scan § The prognosis of this rare complication is poor Snoring & Obstructive Sleep Apnoea • Know the specific questions in the history that distinguishes simple snoring from Obstructive Sleep Apnoea Simple snoring is disruptive snoring without any impact on the patients sleep pattern or increased daytime sleepiness. As the severity of the obstruction increases, greater respiratory effort is required which leads to increased sleep disruption and resultant daytime sleepiness. Upper airways resistance syndrome (UARS) is categorised by the presence of these symptoms without evidence of obstructive apnoeas or de-saturations. It is characterised by increased respiratory effort identified by oesophageal pressure analysis. Further progression of airway obstruction leads to near total or total obstruction of airflow. Obstructive sleep apnoea hypopnoea syndrome (OSAHS) is categorised by the co-existence of excess daytime sleepiness with interrupted and repeated collapse of the upper airway during sleep, usually with associated de-saturations. This collapse can be complete with total cessation of airflow (apnoea) or partial with significant hypoventilation (hypopnoea). Symptoms associated with Obstructive sleep apnoea Excessive daytime sleepiness, Un-refreshed after sleep, Restless sleep, Nocturia Snoring, Choking episodes during sleep, Witnessed apnoeas Impaired concentration, Irritability/personality change, decreased libido Children Adults Age Peak- 2-5 years Increases with age Gender Male = Female Male>>Female Weight Usually undernourished Usually Obese Daytime Uncommon Primary symptom somnolence Neuro-behaviour Hyperactive, Developmental Cognitive impairment Delay Impaired vigilance Children with OSAHS frequently show signs of failure to thrive rather than obesity. They often demonstrate restlessness and hyperactivity. Other potential consequence in children includes secondary enuresis. • Be able to identify the risk factors for and complications of obstructive sleep apnoea The airway between the posterior end of the nose and the larynx is unprotected by cartilaginous or bony structures and reliant on muscle tone for its patency. With the onset of sleep, pharyngeal muscle tone falls progressively as sleep condenses to deeper levels. a) Age. Incidence increases up to 6th & 7th decades of life – independent of BMI b) Sex. Men have 2-5 fold increase risk compared to women, women increase post menopause, Oestrogen + Progesterone HRT decreases the incidence c) Obesity – Most important – direct correlation with BMI. Central obesity indicators such as neck circumference index and waist hip ratio are better predictors of OSAHS than obesity or BMI d) Obstructive Upper airway anatomy. Craniofacial abnormalities (retro or micrognathia, midfacial or mandibular hypoplasia and macroglossia), Adenotonsillar hypertrophy (in children, but less in adults). Decreased nasal airway due to turbinate hypertrophy, septal deviations or nasal polyposis significantly increases upper airway resistance. These can contribute to snoring and UARS, but are unlikely to be the sole cause for OSAHS. e) Social Habits such as smoking and alcohol increase the risk of SRBD. f) Other risk factors First-degree relatives - Two- to fourfold greater Medical conditions such as Hypothyroidism and acromegaly Neuromuscular diseases - predispose to OSAHS though central apnoeas more likely Drugs assoc with central depression (hypnotics and opioids) Chronic lung disease makes OSAHS & its effects (desaturations) more severe Anatomy - choanal stenosis/atresia, macroglossia, micrognathia, mid face hypoplasia (e.g. Down’s, Crouzon’s and Apert’s syndromes, achondroplasia) and Mandibular Hypoplasia (e.g. Pierre-Robin and Cornelle De Lange syndrome). Complications & consequences a) Neuro-cognitive effects. Excessive daytime sleepiness (EDS) most common. Cognitive performance impaired with deterioration in memory, intellectual capacity and motor co-ordination. Increased accident rate. b) Cardiovascular consequences. OSAHS contributes to systemic hypertension. Treatment with continuous positive airway pressure (CPAP) reduces blood pressure. c) Others. Problems with impotence and increased likelihood of gastro-oesophageal reflux. • Understand the principles of investigation and treatment of patients who snore and who suffer with obstructive sleep apnoea Assessment The aims of the history, clinical examination and investigations are 1) Identify if the patient has OSAHS 2) Identify the potential causes and predisposing factors 3) Localise the level(s) of obstruction in the upper airway a) Physical examination although poor correlation with severity. Endoscopy to check anatomy inc tonsils & tongue. Always consider possibility of hyperthyroidism, acromegaly and Marfan’s. b) Epworth sleepiness scale (ESS) - identifies excessive daytime sleepiness. c) Sleep Studies in all patients (urgent if COPD + Snoring) esp if driver/operates machinery. i) Polysomnography (PSG) gold standard. In-patient study involving overnight assessment including- EEG, electromyogram, electro-oculogram, respiratory airflow, thoraco-abdominal movement, ECG, oximetry, body position, snoring sound and video. ii) Ambulatory Pulse Oximetry - useful screening tool to diagnose but not exclude OSAHS iii) Limited Sleep Studies – ambulatory but not as detailed as PSG d) Upper airway pressure assessment. New technology, still expensive Treatment The choice of treatment is dictated by the diagnosis In the simple snorer the aim is a reduction of the duration and intensity of snoring to socially acceptable levels. Here life style changes, oral devices and limited surgery is appropriate. In UARS and mild OSAHS the goal is reduction in snoring but also the upper airway resistance and associated sleep fragmentation To eliminate the episodes of apnoeas/hypopnoea, de-saturations, and associated daytime sleepiness. Gold standard of treatment is Continuous positive airway pressure (CPAP) a) Behavioural Changes. partner sleep first, earplugs, or sleeping on your side not back b) Weight Loss. reduces snoring, apnoeas and hypopnoeas, improves oxygenation c) Lifestyle changes. Stop smoking. Avoid alcohol (esp close to bed time as it exaggerates loss of pharyngeal muscle tone during sleep and episodes of airway collapse). Also avoid sleeping tablets, sedative antihistamines and tranquillizers d) Continuous Positive Airway Pressure. Eliminates apnoeas/hypopnoeas, improve daytime alertness, neurocognitive functions, mood and cardiovascular sequelae. e) Intra-Oral Appliance. Designed to enlarge pharyngeal airway by moving and fixing the mandible in an anterior position. f) Pharmacological Treatments. Respiratory stimulants (protrytyline, acetozolaminde and progesterone) increasing upper airway muscle tone g) Upper Airway Surgery. i) Tracheostomy. rarely performed today. ii) Nasal Surgery. Correcting polyposis & turbinate hypertrophy iii) Uvulopalatopharyngoplasty (UPPP). Longest track record. Tonsillectomy, uvulectomy and excision of a variable segment of the soft palate. iv) Laser-Assisted Uvulopalatoplasty (LAUP). v) Radiofrequency (RF) reduce volume & scarring without vi) Maxillofacial and Multilevel Surgery These procedures are extremely invasive and there use is limited to patients who fail to use CPAP. Rhinological Emergencies and Infections • • Understand the aetiology, presentation, differential diagnosis, principles of management and complications of: o Trauma to the external nose and septum Check head injury, concussion, zygomatic fracture and CFS leak as well as deformity. Unless you can examine the patient shortly after the injury there is often so much swelling that the extent of any nasal or zygomatic deformity may be impossible to assess clinically ALWAYS exclude septal haematoma – bluish bulge on either side of septum. (A haematoma will feel soft while a deformed cartilage will feel hard). Eye movements – check to ensure no blow-out fracture/zygomatic fracture (à diplopia). Compression of the orbital contents can result in herniation of the orbital fat through the damaged orbital floor – confirm by CT. The inferior rectus muscle can become trapped in the defect causing the diplopia. Periorbital swelling - 'crackles' when palpated / increases in size when the patient blows their nose is due to surgical emphysema, and results from a frontoethmoidal fracture. An immediate repair is indicated. CSF leaks – often heal spontaneously. Test for CSF by looking for β-transferrin. Nurse head up, don’t blow nose, give Abx cover. The need for nasal reduction can only be thoroughly assessed immediately after an accident or at 5-10 days afterwards when any soft tissue swelling has settled. Fractured noses should be reduced within 14 days of the injury. o Epistaxis Mostly self-limiting. Children - usually arise from the retrocolumellar vein at the anterior end of Little’s area. Adults - the anterior septum is the commonest site of bleeding in adults and prominent vessels, an area of excoriation or a tiny prominence (the end of a vessel usually capped with a scab) can be seen. Causes - following URTI, allergic rhinitis, nose picking, facial / nasal trauma, rarely tumours. Very rarely an angiofibroma à severe unilateral epistaxes in adolescent boys. Risk factors – hypertension, anticoagulant medication, hereditary haemorrhagic telangiectasia (multiple abnormal capillaries throughout the respiratory, gastrointestinal and urogenital tract), coagulopathies (Von Willebrand’s disease, leukaemia and disseminated intravascular coagulation (DIC)) Management First aid Resuscitation – estimate loss, monitor pulse & BP, IV access + fluids, FBC, Coag, Group & Save. Remove clot fb anaesthetic & vasoconstrictor spray. If bleeding point is seen use silver nitrate or bipolar diathermy. If not insert pack / posterior balloon (leave in 36-48hrs). Abx to prevent 2o infection Understand the presentation, principles of management and complications of ENT and airway foreign bodies Nose Foul smelling unilateral nasal discharge, unilateral nasal obstruction, vestibulitis or epistaxis Children may be able to blow the foreign body out. Others require removing with forceps or rounded probes. If there is a good history and signs but nothing seen anteriorly an examination under anaesthetic should be performed to check further back in the nose. Laryngology and Upper Airway • Examine the neck, palpate, hyoid bone, laryngeal cartilages, elicit laryngeal crepitus, palpate tracheal rings, thyroid, carotid artery and deep cervical lymph nodes. • Know the significance of stertor and stridor and the common causes and their management. Stridor • Definition: ‘noisy breathing’ • Listen to the phase of respiration as guide to level of narrowing of air passages o Inspiratory stridor: laryngeal level o Expiratory stridor: the wheeze of asthma (bronchi/bronchioles) o Mixed inspiratory & expiratory stridor: tracheal or laryngeal and lower airways Stertor • Noises produced at the level of the oro/nasopharynx i.e.snoring • To be able to list the common causes of upper airway obstruction Congenital • Laryngomalacia – floppy larynx (causes stridor in infants). Usually self limiting • Vocal cord palsy – due to damage to recurrent laryngeal nerve • Vocal cord web • Subglottic stenosis Acquired • Trauma e.g. fracture of larynx Obstruction can be delayed as bruising & oedema take time to develop Smoke inhalation & ingestion of caustic agents also à oedema • Epiglottitis Affects both children and adults and is potentially LIFE THREATENING Most commonly HIB (erythema, oedema of epiglottis with extension to larynx Often starts as URTI à unwell, toxic, febrile à drooling & stridor Rx – expert intubation, blood cultures, IV ceftriaxone & steroids • Croup (laryngotracheobronchitis) Oedema and vascular engorgement of airways particularly of subglottis Low grade RTI (para-influenza) à stridor with seal bark cough NB: Inspiratory stridor + recession = significant subglottic oedema = life-threatening Mild Mod Place of management Home Hospital, ward Severe Hospital, Intensive Care Treatment Supportive Admitted for observation ? Croup tents ‘cool mist’ nebulized racemic adrenaline systemic steroids +/- antibiotics Heliox (acute presentation) nebulized racemic adrenaline systemic steroids intubation +/- antibiotics • • Age Onset Aetiology Temp 0C Voice Posture Treatment Acute laryngitis any gradual mostly viral <39 hoarse or aphonic indifferent supportive Monitoring No Croup 1-8 years Gradual (post URTI) mostly viral <38 harsh lying nebulised adrenaline systemic steroids ‘croup tents’ Yes Epiglottitis 3-6 years rapid H.influenzae >39 hoarse / muffled sitting & drooling antibiotics intubation Yes Other aquired causes include - Foreign body, Angioedema , Vocal cord palsy, Laryngeal (and large hypopharyngeal) carcinomas, Subglottic stenosis, Laryngeal papillomata, Large laryngeal polyps/cysts, External compression from e.g. thyroid mass Know how to manage acute airways obstruction and an inhaled foreign body. Symptoms - acute dyspnoeic attack fb coughing bouts. Also wheezing, dyspnoea & bloody sputum Ix - CXR (collapse or hyperinflation). Bronchoscopy should not be delayed (Organic matter it quickly breaks down, & some vegetable oils cause a chemical pneumonitis) ‘First Aid measures’ • Remove any visible obstruction • Heimlich manoeuvre (adults) should be performed if there is total laryngeal obstruction • If cyanosed but breathing give Heliox to buy time • Neddle cricothyroidotomy - ‘Brown’ Intravenous cannula(e) through cricothyroid membrane • OR Percutaneous cricothyroidotomy • Know the indications for, complications and management of a patient with a tracheostomy. Indications To bypass an obstruction in the throat or voice box To prevent breathing problems due to swelling of the tissues after major operations on the tongue, throat, jaw or facial skeleton (temporary) To allow easier removal of secretions from the air passages and prevent scarring of the larynx from long-term artificial ventilation To prevent overspill of secretions into the lungs. To provide an alternative means of air entry into the lungs after a laryngectomy (‘removal of the larynx’) Technique End tracheostomy - (Performed as part of a laryngectomy (removal of voice box)) • Inspired air can no longer be warmed and humidified by the nose • Speech needs to be relearned by getting other parts of the pharynx to vibrate in lieu of the vocal cords Side tracheostomy • Here the larynx is still in place and a small hole is created between the skin over the lower neck and the trachea Risks and Complications Early • Tube displacement • Blocked tube from dried secretions or blood clot • Pneumothorax (especially in babies) • Surgical emphysema Rare (late) • tracheocutaneous fistula on removing the tube o normally fistula closes spontaneously, occasionally it requires suturing • tracheo-oesophageal fistula o Tube erodes through posterior wall of trachea into oesophagus behind • tracheal stenosis o usually if too much cartilage has been removed in creating the window Voice disorders • Understand the basic anatomy and function of the larynx and in particular how voice and speech are produced The Pharynx: The pharynx is a chamber with a bony and fibromuscular walls Its openings are guarded by functional muscular mechanisms including: 1) Palatal & salpingopharyngeal muscles at the pharyngeal ostium of eustachian tube 2) The soft palate and sphincter muscle of the nasopharyngeal isthmus 3) The base of the tongue and palatoglossal folds 4) The aryepiglottic folds and muscles 5) The cricopharyngeal sphincter Functions Pharyngeal muscles are concerned with the pharyngeal phase of swallowing. Also involved in sneezing, coughing and vomiting and in the production of speech sounds. The pharynx is also related to the opening of the eustachian tube Anatomically 1. The nasopharynx is posterior to the nasal cavity and sinuses. Contains the adenoid, and the orifices of the Eustachian tube. 2. The oropharynx. This area contains the soft palate and uvula, the anterior and posterior faucal pillar and the palatine tonsil, as well as the posterior 1/3 of tongue. 3. The hypopharynx. This space is clinically divided into two lateral recesses called the piriform fossae The larynx It is divided into three clinical regions 1) the supraglottis: the region of the larynx from the vocal cords to the level of the hyoid bone. It includes the false cords, the aryepiglottic folds, and the epiglottis 2) the glottis: the region of the larynx between the upper and lower limits of the vocal cords including the anterior and posterior commissures 3) the subglottis: the region of the larynx below the vocal cords to the level of the cricoid cartilage. Functions § Protection of the lower airway § Helps generate cough and expel matter from the airways § Produces sound vibration for voice Voice production: o Voice is the acoustic output of the vocal tract as a result of vocal fold vibration o Energy from the movement of air causes the mucosa to be set in oscillation o This oscillation results on the generation of a sound wave o This oscillation of the mucosa is possible due to the layered structure of the vocal cord (more correctly known as a vocal fold) o It is Reinke's space (or superficial lamina propria) that allows the epithelial layer to oscillate backwards and forwards in a superior-inferior direction o o o The sound produced by the vocal folds is periodic and has a fundamental frequency (F0) of vibration (measured in Hertz) and intensity or pressure (measured in dB) Frequency (perceived by a listener as the pitch of the voice) is determined by the mass per unit length of the vocal folds which in turn is changed by tensioning of the vocal fold and muscle contraction § adult males speak at a lower F0 than women as their vocal folds are bigger (i.e. have a greater mass per unit length) § any pathological condition which increase the mass per unit length e.g. Reinke's oedema (q.v.) will lower the F0 Intensity or sound pressure level (perceived by a listener as the loudness of the voice) § is determined by subglottic pressure i.e. the pressure beneath the vocal folds which in turn is determined by the degree and length of time of vocal fold closure during a vibratory cycle § any pathological condition that reduces the contact between the vocal folds i.e. a recurrent laryngeal nerve palsy will result in a reduced subglottic pressure as air escape resulting in a weak voice which is difficult to hear Definitions: Dysphonia: Any impairment of the voice or difficulty speaking Dysarthria: Imperfect articulation of speech due to disturbances of muscular control or incoordination Dysphasia: Impairment of speech and verbal comprehension (sensory dysphasia) or speech and verbal production (expressive dysphasia) usually assoc with brain injury Hoarseness: a perceived rough, harsh or breathy quality to the voice • Know the features of the common causes of hoarseness, including infective laryngitis, muscular tension dysphonia, benign and malignant, vocal cord lesions and vocal cord immobility. • Structural/Neoplastic o Malignant § Laryngeal carcinoma Always consider in patients with persistent hoarseness lasting >6 weeks Causes - smoking, genetic Symptoms - progressive hoarseness or change in voice. stridor, referred otalgia, dysphagia & cervical lymphadenopathy in late cases Signs - raised, thickened, irregular mass with leukoplakia (white patch) and redness, narrowing of airway +/- vocal cord fixation on laryngeal visual examination, cervical lymphadenopathy Treatment - Radiotherapy, partial or total surgical excision (laryngectomy) o Benign § Nodules Causes - Voice abuse, shouting, talking above background noise, ?reflux. Boys = girls, in young adults (<40): women>>>men Symptoms - Husky voice worsens with use, loss of higher range of voice. Peri-laryngeal discomfort Signs - Bilateral swellings in mid-membranous portion of vocal fold giving hourglass appearance Treatment - Voice therapy or surgical excision if unresponsive § § § • Polyps Causes - Shouting when suffering with a cold or extra-oesophageal reflux, men>women 30s-50s Symptoms - Husky voice worsens with use, may be deeper, Voice cuts out during speaking, choking episodes if very large Signs - Usually unilateral grey or haemorrhagic swelling arising from midmembranous portion of the vocal fold, smooth edge Treatment - Surgical excision +/- medical treatment +/-voice therapy Reinke’s oedema Causes - Smoking +/- a lot of talking! +/- extra-oesophageal reflux, Men=women (more noticeable in women) Symptoms - Deep pitched gravelly voice (women often mistaken for men on 'phone), If severe may cause choking episodes Signs - Usually bilateral grey or erythematous swellings along whole length of membranous portion of the vocal fold Treatment - reassure, Stop smoking! Surgical reduction of polypoid swelling +/- medical treatment of reflux +/-voice therapy Cysts Causes - Not known, some may develop after laryngeal inflammation, some may be congenital, 2 types: mucus retention cysts and epidermoid cysts, Men=women Symptoms - Husky voice, pitch breaks, loss of range of voice, increased effort to produce voice Signs - Unilateral nodular swelling / localised bulge / stiffness of vocal fold Treatment - Voice therapy can help reduce secondary muscle tension, Surgical excision Inflammatory (laryngitis) o Infectious § Viral - Part of an upper respiratory tract infection (URTI), Recurrent respiratory papillomatosis (RRP) due to Human Papilloma Virus § Bacterial - Rare § Fungi - Candida secondary to steroid inhalers or immunosuppression Symptoms Acute viral or bacterial laryngitis Hoarse or croaky voice, Complete loss of voice (aphonia) in severe cases Pain on voice use, coughing or swallowing Irritant paroxysmal coughing Generally other symptoms of an URTI Fungal laryngitis Above without symptoms of URTI RRP Can affect infants and children when can be quite aggressive and cause severe dysphonia and airway problems In adults usually less aggressive but can cause severe dysphonia Signs Acute viral or bacterial cases: erythematous or sloughy vocal folds Papillomas are usually multiple, raised erythematous lesions on the vocal folds and anywhere in the larynx Candida appears as white dots of leukoplakia Treatment Acute viral or bacterial laryngitis Condition usually self-limiting and settles with Voice rest, Analgesia, Fluid hydration, Steam inhalations, Cough suppressants as necessary. Occasionally antibiotics required RRP Usually needs surgical excision with a laser or microdebrider o Non-infectious § Extra-oesophageal (or "silent") reflux: damage from acid and pepsin § Allergies (rare) Symptoms Variable huskiness, voice may worsen with use, loss of higher range of voice Associated throat symptoms Chronic throat clearing, cough, excessive mucus in throat, choking episodes, globus sensation, pain/discomfort but not true dysphagia Only 40% will have heartburn hence term "silent reflux" Signs General erythema and oedema of vocal folds and larynx Treatment Vocal hygiene and dietary advice Proton pump inhibitor twice daily before breakfast and evening meal for a minimum of 2 months +/- alginates and H2 antagonists • Neuromuscular o Underactive § Recurrent laryngeal nerve palsy Causes Surgical trauma (23%), Malignant disease (22%) Symptoms Weak voice, Tires on prolonged talking, Perilaryngeal discomfort, Choking with fluids, Higher pitched voice, Diplophonia ('two tone' voice), Weak (‘bovine’) cough Signs Immobile vocal cord (75% RHS, 15% LHS, 10% bilat) Investigations CXR - Exclude mediastinal mass CT scan skull base to mid-thorax - Check for lesions along nerve ?Ba swallow - If oesophageal lesion or aspiration suspected Treatment None –await spontaneous recovery (up to 1 year) Voice therapy- encourages compensation Vocal cord medialisation = thyroplasty or injection § Myaesthenia (rare) o Overactive § Spasmodic dysphonia (rare) • Muscle Tension Imbalance o Causes § Primary Imbalance of ‘pull’ or excessive tension of the laryngeal muscles • Multifactorial aetiologies Stress, anxiety, depression, conversion disorders, neck/back problems, poor vocal hygiene/loud environments, not drinking enough fluids / too much caffeine, eating late at night/large/fatty meals § Secondary Excessive tension required to overcome a deficiency in the voice producing mechanism e.g. poor respiratory function, structural defect of vocal folds, nasal blockage affecting resonance o Symptoms Variable huskiness of voice, usually worsens with use May be a little deeper or higher than expected for age and sex Voice unstable, perilaryngeal soreness, dryness/uncomfortable sensation in throat o Signs Voice may be croaky/husky, breathy, bizarre or aphonic (no voice) Variable voice quality may occasionally be normal Cough often normal even when voice aphonic Vocal folds usually normal in appearance and movement but either constriction of false cords, antero-posterior constriction or extreme sphincteric closure when the vocal folds disappear from view beneath false cords o Treatment Vocal hygiene and life style advice, Address underlying causative factors Voice therapy Neck Masses • Specific questions, nasal obstruction hoarseness, dysphagia and throat pain/discomfort. Risk Factors SCC are more common in Smokers - Pipe smokers (lip area), chewing tobacco (mouth & gums) Alcohol Sun exposure – increased risk on lips & in ears Chemicals and hardwood dusts increases the risk of cancers of the nose and sinuses Leukoplakia - this condition becomes cancerous in approximately one-third of patients • Know the sites of branchial cysts, thyroglossal cysts, thyroid gland & deep cervical lymph nodes. a. b. c. d. e. f. g. h. i. j. k. l. m. mastoid process Heads of clavicles SCM Trachea Cricoid cartilage Cricothyroid membrane Thyroid prominence Hyoid bone Carotid artery bifurcation Throid gland Parotid gland Submandibular gland Jugulodiastric LN Thyroglossal cyst Congenital but usually present child-early adulthood Midline swelling which should ascend when tongue is protruded (due to attachment) Treatment is to excise whole tract with body of hyoid – otherwise prone to recur Branchial Cyst Tend to present before 30yrs Lump in middle 1/3 of SCM muscle, may be painful if infected Treat by surgical excision • Be able to recognise key patterns of presentation of head and neck malignancy Common presenting features o Pain - in the throat, on swallowing (odynophagia), referred to ear o Difficulty swallowing (dysphagia) o o o o o o o o o o Persistent hoarseness or a change in voice Bleeding in the mouth or throat Enlarging neck node Persistent ulceration, leukoplakia (white patch) or erythroplakia (red patch) Sores or lesions in the mouth can be warning signs Lump or thickening in oral soft tissues Soreness or feeling that something is stuck in the throat Difficulty chewing or opening of mouth or moving the tongue Numbness of the tongue or other parts of the mouth Swelling of the jaw that causes dentures to fit poorly or become uncomfortable • Recognise the significance of leukoplakia and erythroplakia. Leucoplakia – a white patch which can occur on any mucosa surface which cannot be rubbed / scraped off. Occurs in response to chronic irritation (e.g. chewing tobacco) It is associated with dysplasia and malignancy Is a diagnosis of exclusion Erythroplakia – a red patch which occurs on a mucosa surface and from which malignancy can develop • List the main types of head & neck cancer Tumours of the Oropharynx Incidence - 6-8 per million per year Age - main incidence 50 – 70, but increasing incidence of younger patients (30-40y) Sex: - Male : female ratio 5-8/1, but increasing incidence in women Aetiological: Smoking and alcohol abuse, but also betel-nut chewing, radiation, iron deficiency anaemia, HPV infection Histology - Mainly SCC (90%), Non-Hodgkin Lymphomas (8%), minor salivary gland tumours (2%, usually on the palate) Presentation: - Sore throat, odynophagia, dysphagia, otalgia, bleeding, change of voice, trismus, weight loss or a mass in the neck Sub sites - tonsils / lateral pharyngeal wall (60%), tongue base (25%) palate (10%), posterior pharyngeal wall (5%) Hypopharyngeal Tumours Incidence - 10-20 per million per year Age - incidence increasing with age Sex: - postcricoid cancer is the only head & neck cancer that is more common in women Aetiological - smoking and alcohol abuse, but also betel-nut chewing, radiation, iron deficiency anaemia, HPV infection Histology - almost exclusively SCC Presenting symptoms - sore throat, odynophagia, dysphagia, otalgia, haemoptysis, hoarseness, stridor and occasionally weight loss in advanced cases, neck mass (45 % have metastatic neck disease at presentation) Sub sites - piriform sinuses 70%, posterior pharyngeal wall 25% and the postcricoid area 5% Laryngeal Cancer Incidence - 40 per million per year Age - incidence increasing with age (Rare <45yrs) Sex: - male-female ratio: 4 : 1, but increasingly more female (Scotland 2:1) Aetiological - smoking and alcohol abuse, previous neck radiation Histology - 95% of all primary laryngeal cancers are squamous cell carcinomas, with the remainder being minor salivary gland tumours, neuroendocrine tumours and sarcomas Presenting symptoms - change of voice/hoarseness, dyspnoea/stridor, pain/odynophagia, dysphagia, neck mass Sub sites - the glottis or true vocal cords (50%), the supraglottis (40%), the subglottis (5%) Salivary Glands • Examination, know surface marking of parotid gland and identify parotid papilla, displacement of tonsil. Identify submandibular ducts, bimanual palpation of ducts and gland. 1 – branches of facial nerve 2 – transverse facial artery 3 – Parotid duct 4 – sublingual gland 5 – Submandibular duct 6 – Submandibular gland 7 – Parotid gland Minor salivary glands: 600 - 1000 Beneath the mucosa of the upper aerodigestive tract Named according to anatomical position e.g. palatal, buccal, labial, lingual, tongue, tonsillar region, false cords and aryepiglottic folds of larynx Major salivary glands: 3 paired structures Parotid, Submandibular, Sublingual Each situated outside the oral cavity but connected to it by a duct or system of ducts • Be able to describe the key anatomical and physiological features of the salivary glands. Anatomy Parotid Gland (serous) Divided artificially by plane of VII nerve into Superficial lobe (80%) and Deep lobes (20%) Relationships: Posteriorly: zygoma, tympanic bone, cartilaginous external ear canal, stylomastoid fossa, mastoid process, upper ¼ of the sternocleidomastoid m. Anteriorly: overlies posterior ½ masseter m. Superiorly: zygomatic arch Structures within gland: Facial nerve trunk & 5 branches: temporal, zygomatic, buccal, mandibular, cervical Retromandibular vein, External carotid artery à terminal superficial temporal & maxillary arteries, + lymph nodes (<20) mostly in superficial lobe Parotid Duct (Stenson's Duct) leaves gland anteromedially through buccinator m. then medially to ant. border masseter: exits at level of upper 2nd molar Secretemotor fibres: from inferior salivary nucleus and otic ganglion Sympathetic fibres: from sup. cervical ganglion via neural plexuses around arteries Submandibular gland (mixed) Relationships: Larger superficial and smaller lobes in continuity around posterior aspect of mylohyoid m. Fills submandibular triangle below mandible Marginal mandibular branch facial nerve superficial to capsule below mandible Lingual and Hypoglossal nerves close proximity to deep surface Facial artery enters submandibular Δ under post. border of digastric m. crosses the posterosup. aspect of the gland before passing over the mandible Structures within gland: Submandibular (Wharton’s Duct) emerges from middle of deep surface where exits in a papilla to the side of the lingual frenulum. The sublingual glands and lingual nerve are in close proximity to the duct. Secretemotor fibres: from superior salivary nucleus via the nervus intermedius, chorda tympani, lingual nerve and submandibular ganglion Sympathetic: from sup. cervical ganglion via neural plexuses around facial artery Sublingual gland (serous) Floor of mouth, distal to deep lobe of submandibular gland. Same nerve supply as submandibular gland Many small ducts drain into floor of mouth and wharton's duct. • Know the specific questions related to salivary gland disease e.g. swelling after meals, lump, pain, facial palsy, xerostomia, associated arthritis, dry eyes, trismus, displaced tonsil History: age, sex , Unilateral/bilateral swelling, constant/intermittent swelling, constant/intermittent pain, related to food, foul taste in mouth, facial weakness, dry eye/mouth Common causes of Xerostomia (dry mouth) Depression & Anxiety Drugs with antimuscarinic activity Atropine, hyoscine, ipratropium, Tricyclic antidepressants, Monoamine oxidase inhibitors, Phenothiazines, Orphenadrine, benzhexol, and related antiparkinson drugs, Antihistamines with sympathomimetic activity cold cures’ and decongestants e.g. ephedrine, phenylpropylamine, bronchodilators e.g. isoprenaline, appetite suppressants Sjögren’s syndrome Radiotherapy to head and neck region • Be able to make a differential diagnosis of salivary gland swellings including the main types of salivary gland tumour Non-neoplastic Non-salivary swellings Hypertrophy of the Masseter Ageing - absorption of adipose tissue leaving glands more conspicuous In the parotid - neuromas, aneurysms and cysts Infective Lymphadenopathy - skin/scalp, dental, otitis externa, Ludwig's Angina Tumours - Para-pharyngeal space, Mandibular Mastoiditis causing a subperiosteal abscess (drains behind tail of parotid) Parotitis Viral - mumps, echo and coxsackie - do mumps titres Treat with analgesia and hydration HIV - diffuse enlargement, multiple cysts Bacterial - often staphylococcal infection Debilitated, may be on anticholinergics, dehydrated Treat with sialogogues, massage or drain pus if present Tuberculosis - drug treatment, not surgery Fungal - rare, candidiasis in immunosuppressed Other – Sarcoid, Drugs e.g. dextroprophoxyphene Sialectasis Dilation, stenosis and necrosis of acini forming cysts cause unknown Initial event in sialolithiasis (calculus formation) 85% of which affect the submandibular duct Ix - plain X-Ray and sialogram Rx - Remove calculus and marsupialise duct , occ gland needs to be excised Sjögren's Syndrome Classified as follows: 1. Primary Sjögren's Syn (sicca complex) - Xerophthalmia & xerostomia 2. Secondary Sjögren's Syndrome Xerophthalmia, xerostomia and a connective tissue disease (50% of time Rheumatoid arthritis, also systemic lupus erythematosus, scleroderma, and polymyosits) 3. Benign lymphoepithelial lesion ? prelymphomatous condition 4. Aggressive lymphocytic behaviour confined to parotid glands Symptoms: Dry eyes, keratoconjunctivitis, dry mouth, glossitis, secondary candidiasis, stomatitis, dental caries, dry vagina. 40% feel parotid gland enlargement Other associated conditions: Primary biliary cirrhosis, chronic hepatitis, vasculitis, cryoglobulinaemia, hypergammablobulinaemic purpura, polyarteritis. Thyroiditis pancreatitis. Achlorhydria, disorders of oesophageal motility, nasal and other upper aerodigestive tract crusting Immunological defect: Loss of suppressor T-cell activity and an alteration in the T-suppressorhelper cell relationship Investigations: HLA AI, B8, DR3 (present especially in primary Sjögren’s) Specific antigens: SSA and SSB Schirmer's Test for lacrimation Carlsson-Crittendon for salivary flow Labial biopsy – diagnostic test for Sjögren’s Risks: 1 in 6 with Sjögren’s will develop Non-Hodgkin's B-Cell Lymphoma also Waldenstrom's Macroglobulinaemia and Lymphoblastic sarcoma Treatment: Steroids if parotid swelling. Artificial tears, artificial saliva, lubricants Rapid growth: diagnostic parotidectomy Benign tumours 80% salivary tumours occur in the parotid, 80% of these are benign 60% Submandibular tumours are benign 30% Minor salivary gland tumours are benign Away from the mouth and oropharynx all minor salivary gland tumours are all malignant Incidence: 1 per 100,000 mainly Adults, (rare in children). slight female bias Aetiology: mostly unknown but previous radiation is a factor in some Pathology: most classified according to the resemblance of the tumour cell to normal non-neoplastic cells. Tumours result from abnormal proliferation of reserve (stem) cells that do not go on to terminal differentiation. The reserve cells are present in the intercalated and excretory ducts. Pleomorphic Adenomas (60-70%) Originates: - From intercalated duct reserve cells (progenitor cells for ductal cells and myoepithelial cells) Histology: - More often in superficial lobe, often in tail of gland Macroscopically: Grey/blue cut surface, soft myxomatous, cystic, Lobulated, and bosselated false capsule, Mixed cell tumour (ductal, myoepithelial and mesenchymal cells) Investigations: - Fine needle aspiration cytology, Ultrasound or CT Treatment: - surgical removal Prognosis: - If incomplete removal tendency for multiple tumour recurrence Warthin's Tumour or ‘adenolymphoma’ (2-6%) Originates: - probably from parotid lymph nodes Features: - more often in males (8:1) usually >40yrs. (NOT a type of lymphoma), Present as soft, cystic masses in tail of parotid, May be bilateral Histology: - usually papillary elements lining cystic spaces in lymphoid stroma Treatment: - as above Variable malignancy and clinical behaviour Mucoepidermoid carcinoma Originates: - from epithelial cells of interlobar and intralobular ducts Features: - 90% found in parotid gland, Prevalence highest in 5th decade, Commonest salivary gland carcinoma in children, F>M (2-4:1), Well differentiated (low grade) tumours grow slowly and painlessly while Poorly differentiated (high grade) tumours grow rapidly, painfully, invade local structures and metastasise to local lymph nodes (30%), lungs, bones & brain. Histology: - well circumscribed. Cut surfaces show cystic dilatations with mucous material. 3 cell types: mucin-secreting, epidermoid and intermediate. Treatment: - Low grade tumours - local resection and prolonged follow up. High grade tumours require more radical resection and adjuvant radiotherapy Prognosis: - Up to 30% recurrence rate. Cure rate at 15 years approximately 50% for low grade and 25% for intermediate and high grade tumours Acinic Cell (2-4% of all parotid tumours) Originates: - from reserve epithelial cells of terminal or intercalated ducts Features: - 99% found in parotid gland, Most commin in elderly, Can occur in children, more common in females, Can occur bilaterally (3%), Grow slowly Histology: - Well circumscribed by a large layer of dense fibrous tissue and are much the same consistency and colour as normal parotid tissue. Cellular tumours with basophilic cytoplasm, sparse stroma and a lymphoid infiltrate. Treatment: - Local resection with VII nerve preservation and prolonged follow up. Prognosis: - low grade tumours with a tendency to recur locally (35%), can occasionally metastasise to lymph nodes (10%). Cure rate 55% at 15 yrs Malignant tumours Adenoid Cystic Carcinoma (14% of parotid gland cancers) Originates: - from reserve epithelial cells in the intercalated ducts Features: - commonest malignant tumour , tumours in these sites: 2% parotid, 16% submandibular, 28% sublingual, 13% minor salivary gland Mainly 40-60yrs, submandibular gland mostly women, minor glands M=F Grows slowly and insidiously but can infiltrate CN VII à palsy & pain Histology: - Well circumscribed by a large layer of dense fibrous tissue and are much the same consistency and colour as normal parotid tissue. Small cells in nests fenestrated by round/oval spaces creating a cribriform pattern Treatment:- Wide local resection sometimes with sacrifice of VII nerve, radiotherapy controversial, prolonged follow up. Prognosis: - 15 yr survival 10-26%, Local recurrence 50%, also to bone, liver and lung, distant mets (e.g. lungs) assoc with prolonged survival (up to 5 yrs) Carcinoma ex pleomorphic adenoma (3-12% of all cancers of salivary glands) Can develop within a pleomorphic adenoma (but 10-15yrs later) Pain or a palsy usually heralds onset Adenocarcinoma (2.5-4% of all parotid neoplasms) Highly malignant Several histological types Poor prognosis: 10% 5 year survival Lymphoma (40 of non epithelial salivary tumours) Non-Hodgkin’s lymphoma – commonest, usually 50-70yrs Present as firm rapidly enlarging masses and occasionally lymph node metastases Diagnosis made by open biopsy, Rx depends on clinical stage and histological type Metastases Local skin - Melanoma, Squamous cell carcinoma Distant – lung, breast, kidney or upper gastrointestinal tract • Be able to order the appropriate investigations and form a management plan for a patient presenting with a salivary gland swelling. Investigations: Routine blood tests, Virology, ACE, SSA and SSB , X-Ray Plain, Sialogram, CTSialogram, CXR, USS high definition and Doppler, MRI , Schirmer’s, Carlsson-Crittenden Histological: FNAC, Biopsy gland (if ulcer / minor gland), Management: Partial Superficial Parotidectomy Complications: Facial nerve: - palsy or paresis Frey's syndrome: - skin sweating over parotid gland area on eating, may be helped by antiperspirants or botulinum toxin injections, into the skin Fistula: - saliva leakage from wound especially on eating – usually settles with time Numbness of ear lobe: usually permanent due to division of the greater auricular nerve to gain access to the gland Submandibular Gland Excision Procedure: - remove gland and ligate duct. Avoid damage to marginal mandibular nerve and lingual nerve Complications: Haemorrhage:reactionary Nerve damage: Marginal mandibular (causes asymmetrical smile by causing weakness muscles at corner of lower) Throat Emergencies and Infections • Understand the aetiology, presentation, differential diagnosis, principles of management and complications of: o • Tonsillitis/peritonsillar abscess Pharyngitis Symptoms - Dry sore throat, nocturnal nasal obstruction, often coryza w/o malaise Main viral agents – Adenovirus, Epstein-Barr virus (Glandular fever), Enteroviruses, Cytomegalovirus, Occasionally Herpes simplex Main bacterial agents - b-haemolytic Streptococcus, Pneumococcus Main fungal agent - Candida (assoc with steroids, dentures, immunosupression, Radiotherapy encompassing oral cavity/oropharynx) Follicular tonsillitis Symptoms - Sore throat and pain on swallowing, Enlarged erythematous tonsils with ‘white spots’ (exudates from tonsillar crypts), Systemic illness with fever, malaise, cervical lymphadenopathy and halitosis Main bacterial agents - b-haemolytic Streptococcus Group A (C & G less common), Corynebacterium diphtheriae (if travelled) Treatment - Mainly analgesics and antipyretics, Usually self-limiting with resolution within 5 days, Antibiotics e.g. penicillin shorten course by 1-3 days and are of marginal benefit (see algorithm), Give Erythromycin if allergic to penicillin Surgery - Tonsillectomy is indicated if tonsillitis is recurrent (5 episodes per year for 2 years or more or a significant time is being missed off school or work) Glandular fever Symptoms - Sore throat and pain on swallowing, Enlarged erythematosus tonsils covered with white/grey exudates, Fever, malaise, cervical and generalized lymphadenopathy, hepatosplenomegaly in severe cases Ix - Atypical mononuclear cells on blood film, Diagnosis confirmed with a positive Monospot or Paul Brunnell test Treatment - is with bed rest, hydration, analgesics, antipyretics and oral steroids (in severe cases or when there is a danger of airway obstruction) Quinsy (peritonsillar abscess) A past history of tonsillitis may or may not be present Pathology - Pus develops in the soft tissues superolateral to the tonsil displacing the tonsil and uvula inferomedially Symptoms - severe unilateral tonsillar pain, odynophagia, trismus (the inability to open the mouth because the pterygoid muscles are in spasm because of the local inflammation), referred otalgia, generally malaise and fever, OE - A bulging of the paratonsillar tissues and soft palate is usually seen Ix - Mixed aerobes and anaerobes are usually cultured from the pus Treatment - drainage of the abscess (by lancing or aspiration), antibiotics, analgesia, antipyretics and fluids, A tonsillectomy is indicated if the quinsy recurs Understand the presentation, principles of management and complications of swallowed foreign bodies Swallowed Anatomy - tend to lodge just above the cricopharyngeus, at the level of the arch of the aorta or at the oesophageal cardia. Discomfort tends to be referred upwards Symptoms of sudden discomfort on eating, inability to finish the meal, severe pain at rest and/or on swallowing and referred earache OE - Flinching on swallowing / Pooling of saliva in the hypopharynx is a useful sign. Ix – X-ray of little use. Indirect laryngoscopy to visualise & remove Complications are rare, probably because the majority of those which have the potential to perforate the oesophagus cause sufficient symptoms to result in their early removal. Swallowing corrosives can cause remarkably few symptoms in the short term, but a neutralising agent should be given immediately in large amounts as the consequences of a stricture are not only troublesome requiring repeated dilatation, but in very severe cases an oesophagectomy may be necessary.