ENT Flashcards
Label the parts of the tympanic membrane
Describe the blood supply of the external ear
Arterial - branches of external carotid
* Posterior auricular
* Superficial temporal
* Occipital
* Maxillary
Veins follow arteries and drain to external jugular
What are the auditory ossicles? Describe their anatomy and function.
Malleus, incus and stapes
Connect tympanic membrane to oval window, transmit vibrations to detect sound
Muscles attached which contract to prevent vibrations when there is a loud noise to prevent damage to inner ear (acoustic reflex)
Tensor tympani attached to handle of malleus, innervated by tensor tympani nerve from mandibular nerve
Stapedius attached to stapes, innervated by facial nerve
Why is otitis media more common in children?
Eustachian tubes shorter, straighter, ‘floppier’ than in adults, transmit URTIs to ear
Describe the anatomy of the inner ear
Bony labyrinth - contains cochlea, semicircular canals, vestibule
Membraneous labyrinth - within bony labyrinth, contains cochlear duct, semi-circular ducts, utricle and saccule, filled with endolymph
Oval window and round window connect middle ear to inner ear
Vestibular apparatus (balance) = semi-circular ducts, saccule and utricle
Hearing - cochlear duct, containing organ of Corti
Vestibulocochlear nerve innervates
Describe the anatomy of the oral cavity
Vestibule anteriorly - between lips/cheeks and teeth/gums
Roof - hard (bony) palate anteriorly, soft palate posteriorly
Cheeks formed by buccinator muscle
Floor - muscular diaphragm (mylohyoid muscles), geniohyoid muscles, tongue connected by frenulum, salivary glands/ducts
Innervation
Taste - anterior 2/3 is facial nerve, posterior 1/3 is glossopharyngeal nerve
Motor - hypoglossal nerve
Sensation - lingual and glossopharyngeal nerve
Describe the borders of the anterior triangle of the neck
Superior - inferior angle of mandible
Lateral - anterior border of sternocleidomastoid muscle
Medial - sagittal line down midline of neck
Describe the important contents of the anterior triangle of the neck
Muscles - divided into above and below hyoid bone
* Suprahyoid - stylohyoid, digastric, mylohyoid, geniohyoid
* Infrahyoid - omohyoid, sternohyoid, thyrohyoid, sternothyroid
Vascular
* Common carotid artery - bifurcates into internal and external
* Internal jugular vein
Nerves
* Facial
* Glossopharyngeal
* Vagus
* Accessory
* Hypoglossal
Describe the borders of the posterior triangle of the neck
Anterior - posterior border of sternocleidomastoid muscle
Posterior - anterior border of trapezius muscle
Inferior - middle 1/3 of clavicle
Describe the important contents of the posterior triangle of the neck
Muscles
* Omohyoid
* Levator scapulae
* Anterior, medial and posterior scalenes
Vascular
* External jugular vein
* Subclavian vein
* Distal part of subclavian artery which becomes axillary artery as it crosses first rib
Nerves
* Accessory nerve
* Cervical plexus including phrenic nerve
* Brachial plexus
Describe the anatomical location and blood supply of the thyroid gland
Anterior neck, C5-T1 level
Two lobes with central isthmus
In visceral compartment of neck with trachea, oesophagus and pharynx, bound by pre-tracheal fascia
Lies in close proximity to recurrent laryngeal nerve - can be damaged during thyroid surgery
Arterial supply
* Superior thyroid - first branch of external carotid
* Inferior thyroid - thyrocervical trunk from subclavian
Venous drainage - superior, middle and inferior thyroid veins, superior and middle drain to internal jugular and inferior into brachiocephalic
Describe the anatomy of the pharynx
Connect oral cavity and nose to larynx and oesophagus
Begins at base of skull and ends at cricoid cartilage (C6 level)
Nasopharynx (base of skull to soft palate) -> oropharynx (soft palate to epiglottis) -> laryngopharynx (epiglottis to cricoid cartilage)
Adenoid tonsils in posterior nasopharynx
Lingual and palatine tonsils in oropharynx
Circular muscles which constrict to propel food bolus - superior, middle and inferior pharyngeal constrictors
Mainly innervated by vagus and glossopharyngeal nerves
Arterial supply - branches of external carotid
Venous drainage - pharyngeal venous plexus –> internal jugular
Describe the anatomy of the larynx
Anterior compartment of neck, spans C3-C6, from laryngopharynx to trachea
Formed by cartilaginous skeleton held together by ligaments and membranes
Supraglottis (inferior epiglottis to vestibular folds) –> glottis (vocal cords and 1cm below) –> subglottis (inferior glottis to inferior cricoid cartilage)
Vascular
* Arterial - superior and inferior laryngeal arteries
* Venous - superior and inferior laryngeal veins
Innervation
* Recurrent laryngeal nerve and superior laryngeal nerve
Describe the cartilages of the larynx
Unpaired
* Epiglottis - flattens during swallowing to block off larynx and prevent aspiration
* Thyroid - anteriorly forms laryngeal prominence (Adam’s apple)
* Cricoid - signet ring shaped
Paired
* Arytenoid
* Corniculate
* Cuneiform
Describe the clinically important anatomy of the laryngeal soft tissue structures
Cricothyroid ligament - incision made during cricothyroidotomy for upper airway obstruction to insert ET tube and secure airway
Vocal folds (true) - soft tissue folds which move under control of muscles of phonation to control the pitch of sound
Vestibular folds (false vocal cords) - superior to true, protect larynx
List the important anatomical structures which pass through the parotid gland
Facial nerve - splits into terminal branches within parotid (temporal, zygomatic, buccal, marginal mandibular, cervical)
External carotid artery - gives off posterior auricular then splits into terminal branches (maxillary artery and superficial temporal artery)
Retromandibular vein - formed in parotid by convergence of superficial temporal and maxillary veins
List the salivary glands and describe their drainage
Sublingual - smallest, drain via minor sublingual ducts of Rivinus under tongue
Parotid - drain via Stensen duct, opens near second upper molar
Submandibular - drain via Wharton’s duct, opens at base of lingual frenulum
Describe the physiology of swallowing
Voluntary phase - food bolus formed by mastication, moved to pharynx by tongue, stimulated swallowing reflex
Pharyngeal phase - pressure receptors in pharynx stimulated which activate swallowing centre in brainstem to inhibit respiration, raised larynx, close glottis, open upper oesophageal sphincter
Soft palate elevated to block nasopharynx
Bolus moved down via peristalsis of pharyngeal constrictors
Oesophageal phase - larynx lowers to normal position, cricopharyngeus muscle contracts to prevent reflux, respiration begins again
Bolus moved down by peristalsis
Describe the anatomy of the nasal cavity
Superior, middle and inferior turbinates (or conchae) with corresponding meatuses between - slows air flow to allow for humidification
Paranasal sinuses, nasolacrimal duct and Eustachian tube empty into nasal cavity
Cribiform plate forms portion of roof of nasal cavity - where olfactory nerve fibres enter
Vascular supply
Internal carotid branches - anterior and posterior ethmoidal
External carotid branches - sphenopalatine, greater palatine, superior labial, lateral nasal
Lots of anastomoses, anteriorly form Kiesselbach’s plexus, posteriorly form Woodruff plexus
Veins drain to pterygoid plexus, facial vein or cavernous sinus (intracranial spread of infections)
Define stridor
Externally audible, high-pitched sound caused by turbulent airflow due to obstruction of the upper respiratory tract (pharynx, larynx or trachea)
Describe the clinical presentation of acute airway obstruction
Mild
* Hoarse voice
* Intermittent stridor
* Minimal impact on work of breathing
* Good air entry
Moderate
* Tachypnoea
* Stridor
* Prolonged inspiratory time
* Increased work of breathing
* Decreased air entry
Severe to complete obstruction
* Hypoxia
* Slow respiratory rate or marked tachypnoea
* Tripod position
* Agitated or drowsy
* Severe work of breathing
* Markedly reduced or no air movement
* Silent gagging/coughing
* Progresses rapidly to unconsciousness and cardiorespiratory arrest
Describe the immediate management of acute airway obstruction
Suction secretions or remove foreign body from airway if visible
Oxygen - heliox if available
Alert seniors including ENT/anaesthetics
Consider nebulised adrenaline
Consider nebulised salbutamol
Consider dexamethasone oral/IM/IV
Definitive airway management
Endotracheal intubation if able
Emergency cricothyroidotomy if upper airway obstruction
If due to tumour - radiotherapy, laser, stenting
Describe the immediate management of ear foreign bodies
Ask about pain/discharge from ear, hearing loss
Examination - otoscopy to visualise foreign body
Live insects - drown in oil
Remove using Zoelner sucker, crocodile forceps, Jobson-Horne probes, wax hooks etc.
If unable to be removed can be discharged and scheduled for foreign body to be removed under GA (unless button battery which needs to be immediately removed)
Describe the immediate management of a nose foreign body
Ask about issues with breathing and nasal discharge
Examine with Thucidum speculum and a light
Attempt to remove
If distressed or has breathing difficulty - emergency removal under GA
Describe the immediate management of throat foreign bodies
Clarify nature of object (sharp or soft), ask about dysphagia
Visual examination of oropharynx using tongue depressor and torch, fexible nasal endoscopy if not visible on initial assessment
If moderate clinical suspicion of ingested foreign body (which is radio-opaque) can use plain film radiographs, or CT neck for further assessment
If visualised can attempt removal with Magill forceps
Otherwise should be under GA with endoscopy
List causes of tympanic membrane perforation
Secondary to acute otitis media - most common
Barotrauma
Noise trauma
Blunt/penetrating trauma
Iatrogenic - Grommet insertion
Describe the clinical presentation of tympanic membrane perforation
History of trauma/infection
Acute ear pain
Discharge
Conductive hearing loss
How is tympanic membrane perforation managed?
Examination - otoscopy
If uncomplicated usually heal spontaneously after 6-8 weeks
Supportive measures - NSAIDs, hot compresses
Avoid getting waer in ear while healing to prevent secondary infections
If due to acute otitis media usually give antibiotics
If not healing - myringoplasty
Describe the immediate management of nasal fracture
Assessment - mechanism of injury, ?immediate deformity, ?new nasal obstruction, previous nasal fracture/injury
Inspect for ecchymosis, swelling over nasal bridge, visible deformity of bones, epistaxis
Anterior rhinoscopy with nasal speculum - look for epistaxis, septal deviation, septal haematoma (requires immediate ENT referral)
Imaging not required unless other injuries are suspected e.g. skull fracture
Allow swelling to go down and re-examine in 5-7 days, if still deformity causing cosmetic concern can undergo manipultation under anaesthesia (must be <14 days after injury)
If manipulation unsuccessful, severe deformity and septal deviation with nasal obstruction >14 days after injury - septorhinoplasty
How should nasal septal haematomas be managed? Why?
Formation of haematoma deprives cartilage of blood supply, becomes ischaemic leading to necrosis and septal perforation - saddle nose deformity
Can also become infected - septal abscess
Management
Incision and drainage - usually under GA
Antibiotics
What are the potential complications of nasal trauma?
Epistaxis
Septal haematoma - risk of saddle deformity
Septal abscess
Associated serious head injury/facial fracture
List the blood vessels which make up Kiesselbach’s plexus
Greater palatine
Anterior ethmoidal
Superior labial
Sphenopalatine
Describe the classification of epistaxis based on location
Anterior - majority, from Little’s area (Kiesselbach’s plexus), tends to be younger patients
Posterior - 10%, usually from sphenopalatine artery, more likely in older patients
Describe the aetiology of and risk factors for epistaxis
Primary - spontaneous
Secondary
Trauma
Intranasal drugs - decongestants, steroids, illicit drugs
Weather
Anatomical variants e.g. deviated septum
Systemic causes
Tumours
Risk factors:
Rhinitis
Viral/bacterial sinusitis
Septal deviation
Bleeding disorders
Decompensated heart failure
Trauma with facial injury
Hepatic or renal impairment
Anticoagulant or antiplatelet drugs
Uncontrolled hypertension
What are the important differentials for secondary causes of epistaxis in adults and children?
VINDICATE
Vascular - juvenile nasopharyngeal angiofibroma
Infective/inflammatory - sarcoidosis, tuberculosis, acute sinusitis
Neoplastic - juvenile angiofibroma, squamous cell carcinoma, adenoid cystic carcinoma, inverted papilloma
Degenerative
Iatrogenic/intoxication - topical antihistamines/decongestants/steroids, alcohol, snorting cocaine, NG tube, ET intubation
Congenital - hereditary haemorrhagic telangiectasia, Von Willebrand disease, haemophilia
Autoimmune - granulomatosis with polyangiitis, sarcoidosis
Trauma - facial fracture, nose picking, foreign body
Endocrine
Describe the immediate management of epistaxis
First aid initially:
Sit up and lean forwards, allow blood to pass out of nose/mouth
Compression of the anterior nose (the soft part) for 20 minutes continuously
Ice over bridge/back of neck/in mouth - encourages vasoconstriction
A-E assessment
FBC, U&Es, coagulation screen
Do they need fluid resuscitation? Is there evidence of shock?
Anterior rhinoscopy - can a bleeding point be identified?
Can use silver nitrate cautery if bleeding point visible
Check posterior pharynx for dripping blood
Nasal packing:
Anterior nasal packing is second-line after first aid, insert nasal tampon or rapid rhino aiming medially and inferiorly
Can use adrenaline soaked packing materials to cause local vasoconstriction
If no improvement may need to pack contralateral nostril
Posterior nasal packing - foley catheter
Uncontrolled bleeding - contact senior, A-E assessment, IV access, bloods including FBC, group + save
After bleeding controlled - prescribe naseptin cream, advise to avoid blowing nose, strenuous exercise, drinking alcohol/hot drinks for a few hours
Describe definitive management for uncontrolled epistaxis which fails to respond to initial measures
Surgical management:
Ligation or embolisation of bleeding artery
Usually sphenopalatine, anterior ethmoidal (never embolised due to ICA origin) or external carotid artery as last resort
What is the difference between a tracheostomy and laryngectomy, how can they be distinguished clinically and what are the implications of this?
Tracheostomy - opening from skin to trachea but normal anatomy of upper airway, connection between mouth/nose and airway still present, can be temporary or long-term, may or may not be able to speak
Laryngectomy - part/all of larynx removed, proximal part of airway communicates with skin, no connection between mouth/nose and airway, are permanent, not able to speak naturally
Can be difficult to distinguish clinically, sign above bed to indicate
If have a laryngectomy and require ventilation can only ventilate via stoma (no connection between mouth/nose and lungs)
If have a tracheostomy can ventilate via both mouth/nose and stoma, put oxygen masks over both
In both need to consider obstruction as cause of airway problem - suction, remove tube if blocked
What are the common reasons for creation of a tracheostomy?
Long-term mechanical ventilation - often weaning off ventilation in ICU patients
Upper airway obstruction
Secure and maintain a safe airway in cases where upper airway may be unsafe e.g. injuries to face/head/neck
Bronchial toilet and secretion removal
Airway protection e.g. neuromuscular disorders
Describe the resuscitation of a patient with a tracheostomy
- Check bedside sign
- Call for airway expert help - anaesthetist, ENT
- Look, listen and feel at mouth and tracheostomy
- If not breathing call resuscitation team, CPR if no pulse or signs of life
- If breathing apply high-flow oxygen to tracheostomy and face
- Assess tracheostomy patency, remove speaking valve or cap if present, remove inner tube
- If can pass a suction catheter tracheostomy tube is patent, perform suction, ventilate via tracheostomy if not breathing, continue A-E assessment
- If can’t pass suction catheter deflate cuff, look, listen and feel at mouth and trachestomy
- If patient still unstable/not improving - remove tracheostomy tube
- If still not breathing - perform standard oral airway manoeuvres while covering stoma (bag-valve-mask, airway adjuncts)
- If still unsuccessful may need to orally intubate (likely to be difficult) or attempt to intubate stoma
Describe the resuscitation of a patient with a laryngectomy
- Check bedside sign
- Call for airway help - anaesthetist, ENT
- Look, listen, feel at mouth and laryngectomy stoma
- If patient is breathing apply high flow oxygen to laryngectomy stoma
- If patient not breathing call resuscitation team, begin CPR if no pulse/signs of life
- Assess laryngectomy stoma patency, remove stoma cover and inner tube if present
- If you can pass a suction catheter the laryngectomy stoma is patent, suction and ventilate via stoma if not breathing, continue A-E assessment
- If cannot pass suction catheter deflate cuff, look, listen and feel at laryngectomy stoma
- If patient not improving remove tube from stoma, re-apply oxygen to stoma
- If still not breathing give laryngectomy stoma ventilation via paediatric face mask applied to stoma or LMA applied to stoma, may need to attempt intubation of stoma
List findings on observation of oral cavity
Face - parotid or submandibular gland swelling
Lips - angular stomatitis, hyperpigmented macules (Peutz-Jeghers syndrome), ulceration
Teeth - missing teeth, tar staining, tooth decay
Gums - gingivitis, periodontitis, ulceration
Tongue - oral candidiasis, glossitis, ulceration, hairy leukoplakia
Buccal mucosa - aphthous ulcers, other ulcers
Parotid duct - swelling, erythema, discharge
Palate - oral candidiasis, ulceration, papillomas
Tonsils - enlargement, asymmetry, ulceration, stones
Peritonsillar swelling
Pharyngitis
Uvular deviation
Floor of mouth - submandibular gland sialolithiasis/sialodenitis, ulceration
Findings on nasal cavity examination
External nose - basal cell carcinomas, squamous cell carcinomas, keratoacanthoma, deformity
Nasal cavity
Septum - deviation, perforation, haematoma, previous cautery
Mucosa - inflammation, ulceration, oedema
Inferior turbinates - asymmetry, inflammation, polyps
How is a Thudiculum’s speculum used?
Widens the nasal cavity to allow for inspection
Insert index finger into bend, support above with thumb, middle and ring fingers manipulate prongs
Press prongs together to allow insertion then allow them to widen to get optimal view
Findings on inspection neck examination
- General - scars, hoarse voice, dyspnoea/stridor, hyperthyroidism symptoms (anxiety, hyperactivity, heat intolerance, exophthalmos)
- Swallowing
- Tongue protrusion - thyroglossal cysts move upwards
- Lumps - site, size, shape, consistency, mobility, fluctuance, temperature, skin changes, pulsatility, tenderness
- Thyroid - size, symmetry, consistency, masses, thrill
Findings on inspection ear examination
External ear
* Pinna - asymmetry, deformity, erythema, oedema, scars, skin lesions
* Mastoid - erythema, swelling, scars
* Pre-auricular - sinus/pit, lymphadenopathy
* Conchal bowl - erythema, purulent discharge
External auditory canal
* Ear wax
* Erythema/oedema
* Discharge
* Foreign bodies
Tympanic membrane
* Erythema
* Bulging
* Retraction
* Absence or distortion of the light reflex
* Perforation
* Scarring
Which clinical tests can be used to assess balance?
Romberg test - assess proprioception with visual stimulus removed, abnormal if unable to stay upright
Dix-Hallpike test - used to diagnose BPPV and confirm affected side, nystagmus and dizziness when moving head 45 degrees to side and going from sitting to lying
HINTS - head-impulse, nystagmus, test of skew
Unterberger - march in place with eyes closed, rotate to side of labyrinthine lesion
Tandem gait
List the potential complications of flexible nasal endoscopy
Pain in nose and pharynx
Sneezing
Epistaxis - usually mild
Laryngospasm - rare and serious
Rare to cause damage to structures - more common with rigid scopes
What are the indications for nasal endoscopy?
Evaluating nasal symptoms e.g. discharge, congestion, obstruction
Taking biopsies of nasal lesions/masses
Removing foreign bodies
Investigation of symptoms of malignancy - dysphagia, hoarseness, pain
Describe the principles of fine needle aspiration for cytology
Use narrow gauge needle into mass to sample cells which are examined under microscopy
Does not show architecture of lesion
Safe, few complications compared with major open biopsy
Define otitis externa
Infection of the external auditory canal
Describe the aetiology of and risk factors for otitis externa
Infectious:
Bacterial - pseudomonas aeruginosa, staph aureus
Fungal - candida albicans, aspergillus
Non-infectious:
Eczema
Seborrhoeic dermatitis
Contact dermatitis
Risk factors:
Swimming
Immunosuppression e.g. diabetes
Anatomical abnormalities of ear canals e.g. Down’s
Describe the clinical presentation of otitis externa
Ear pain
Itch
Discharge
Conductive hearing loss
Fever
On otoscopy - erythema, oedema, eczematous canal, serous or purulent discharge
Regional lymphadenopathy
How is otitis externa managed?
Usually clinical diagnosis, can take swabs if recurrent/not responding to treatment
Self-care measures - keep ears clean and dry
Acetic acid drops
Analgesia
Aural toilet - clean external auditory canal to allow effective application of topical treatments
Topical antibiotic (gentamicin not if perforation, ciprofloxacin) +/- topical steroid
If fungal - clotrimazole
Can use otowick to allow topical treatments to permeate deeper
List the potential complications of otitis externa
Malignant otitis externa
Pinna/peri-auricular cellulitis
Cranial nerve palsy - facial nerve
Meningitis
Intracranial thrombosis
Myringitis and tympanic membrane perforation
Define malignant otitis externa, describe its epidemiology
Spread of infection beyond soft tissue of ear to temporal bone and skull base
More common in elderly and diabetics (or otherwise immunocompromised)
Describe the presentation and complications of malignant otitis externa
Non-resolving otitis externa despite adequate topical treatment
Pseudomonas most common cause
Severe ear pain
Headaches
Fever
Granulation tissue in the ear canal (at junction between bone and cartilage)
Can cause osteonecrosis, cranial nerve palsies, meningitis, intracranial thrombosis
How is malignant otitis externa managed?
Admission under ENT
Imaging - CT/MRI to assess extent of infection
IV antibiotics
Debridement
Define skull base osteomyelitis and describe its aetiology
Infection of temporal, sphenoid or occipital bones
Usually spread from ear or sinonasal infections in elderly patients with diabetes or otherwise immunocompromised
Pathogens - pseudomonas, staph aureus
Describe the clinical presentation of skull base osteomyelitis
Often non-specific
Headache
Facial pain
Symptoms of original infection - otitis externa, sinusitis
Cranial nerve palsy - VII, VIII, VI
How should skull base osteomyelitis be investigated and managed?
CT head with contrast/MRI
IV antibiotics
May need surgical debridement
Define acute otitis media, chronic otitis media, otitis media with effusion and recurrent acute otitis media
Acute otitis media - acute inflammation of middle ear, <3 weeks, causing pain, fever, hearing loss
Recurrent acute otitis media - 3 or more episodes in 6 months or 4 or more in 12 months
Otitis media with effusion - collection of fluid in middle ear without acute signs of infection, causing pain/hearing loss
Chronic otitis media - chronic inflammation of the middle ear with recurrent ear discharge, tympanic perforation, >6 weeks
Describe the risk factors for and aetiology of acute otitis media
Risk factors:
Children - peak incidence 9-15 months
More common in winter
Smoking/passive smoking exposure
Nursery
Formula feeding
Craniofacial abnormalities
FHx
Prematurity
Immunodeficiency
Pathogens
Bacterial - haemophilus influenzae, strep pneumoniae, moraxella catarrhalis, strep pyogenes
Viral - RSV, rhinovirus, influenza, parainfluenza
Describe the presentation of acute otitis media
Acute onset
Symptoms
* Ear pain - tugging/rubbing ear, irritable, poor feeding
* Fever
* URTI - cough, rhinorrhoea, sore throat
* Tympanic membrane perforation - discharge
* Vestibular involvement - vertigo, balance problems
Signs
* Red/yellow/cloudy tympanic membrane
* Bulging tympanic membrane, loss of normal landmarks
* Effusion - dull, retracted, bubbles, air-fluid level
* Perforation, discharge in auditory canal
* Conductive hearing loss
Describe the differential diagnoses for acute otitis media and their features
- Otitis media with effusion – no signs of acute infection, air fluid level/bubbles on otoscopy, conductive hearing loss
- Chronic suppurative otitis media – persistent inflammation and perforation of tympanic membrane with draining discharge >2 weeks
- Myringitis – erythema and injection of tympanic membrane, no other features of otitis media
- Other causes of earache – otitis externa, eustachian tube dysfunction, mastoiditis, malignancy, referred pain
How is acute otitis media managed?
Usually resolves without treatment within 3 days (up to 1 week)
Supportive management - paracetamol/ibuprofen for pain
Antibiotics
Immediate prescription - systemically very unwell, symptoms/signs of more serious condition, high risk complications
Otorrhoea/perforation, <2 with bilateral infection - consider Abx, ?delayed prescription if symptoms don’t start to improve within 3 days or significantly worsen at any time
If antibiotic required - 5-7 days amoxicillin (clarithromycin if allergic, erythromycin if allergic and pregnant)
Important to safety net - seek medical attention if deteriorating
What are the potential complications of acute otitis media?
Persistent otitis media with effusion
Recurrent infection
Hearing loss – usually conductive and temporary
Tympanic membrane perforation
Labyrinthitis
Rare and serious:
Acute mastoiditis
Meningitis
Intracranial abscess
Sinus thrombosis
Facial nerve paralysis
How does acute mastoiditis present? How is it managed?
Mastoid pain and tenderness
Fluctuant erythematous retro-auricular swelling
Auricle proptosis
Management:
CT temporal bone and brain
IV antibiotics
Fluid resuscitation
Analgesia, antipyrexial agents
Failure to improve - incision and drainage +/- cortical mastoidectomy +/- grommets
Describe the aetiology of otitis media with effusion
Often occurs following acute episode otitis media
Children:
Chronic inflammatory changes + Eustachian tube dysfunction
Adenoidal infection or hypertrophy
Risks - bottle feeding, smoking exposure, atopy, mucociliary disorders (CF, PCD), craniofacial disorders
Adults:
Blockage of Eustachian tube e.g. infection, occlusive mass (including malignancy)
Describe the clinical presentation of otitis media with effusion
Hearing loss - conductive
In children may be noticed as poor speech and language development or difficulty in school
Sensation of pressure in ear, popping/crackling noises
Mild intermittent ear pain
Tympanic membrane dull, loss of cone of light, bubbles, fluid level
Retracted tympanic membrane
How should otitis media with effusion be investigated?
Pure tone audiometry
Tympanometry
Adults - flexible nasoendoscopy (exclude post-nasal space mass)
How is otitis media with effusion managed?
50% resolve within 3 months - active surveillance often utilised
Non-surgical - hearing aid
Surgical - myingotomy and grommet insertion
Persistent disease and multiple grommet insertion - consider adenoidectomy
Describe the types of chronic otitis media
Mucosal - aka chronic suppurative otitis media, due to tympanic membrane perforation and subsequent inflammation of middle ear mucosa
Squamous - due to retraction of tympanic membrane, associated with formation of a cholesteatoma
Describe the clinical presentation of chronic mucosal otitis media
Chronically discharging ear (>6 weeks), absence of fever or otalgia
Visible perforation of tympanic membrane
History of reurrent acute otitis media, previous ear surgery, trauma to ear
Hearing loss - usually conductive
How is chronic mucosal otitis media managed?
Aural toileting - keep ear clean and ry
Topical antibiotic or steroid
If symptoms >6 weeks and large amount of debris - ENT referal
Most perforations heal spontaneously, if not can be surgically managed (myringoplasty or tympanoplasty)
Describe the pathophysiology of chronic squamous otitis media
Congenital or acquired
Congenital - epidermoid cysts in middle ear
Acquired - chronic negative middle ear pressure from Eustachian tube dysfunction, leaves a retraction pocket which can trap keratinised squamous cell debris, leading to formation of a cyst-like structure which may evolve into a cholesteatoma
Cholesteatomas can induce inflammatory process in temporal bone, leading to local destruction of ossicles (conductive hearing loss), semicircular canals (vertigo), cochlea (sensorineural hearing loss) and facial nerve (facial nerve palsy)
Describe the clinical presentation of cholesteatomas
Initially asymptomatic
Conductive hearing loss (can progress to sensorineural if cochlear destruction)
Purulent, foul-smelling discharge
Tinnitus
Vertigo
Facial nerve palsy
Usually no pain
On examination - pearly, keratinised, waxy mass in attic region on otoscopy
How is a cholesteatoma investigated?
Pure-tone audiogram
CT scan of petrous temporal bone
How is a cholesteatoma managed? What are the potential complications of management?
Surgery - usually via pre- or post-auricular incision into mastoid, remove cholesteasoma
Reconstruction of ossicles
Complications:
Facial weakness
Altered taste
Recurrence of disease
Hearing loss
Tinnitus
Describe the anatomical course of the facial nerve
Intracranial - arises from pons as motor and sensory root, travels through internal acoustic meatus of temporal bone, enters facial canal and fuse, form geniculate ganglion, gives off greater petrosal nerve, nerve to stapedius and chorda tympani, exits facial canal via stylomastoid foramen
Extracranial - gives of posterior auricular nerve, nerve to posterior belly of digastric muscle and stylohyoid muscle, motor root continues into parotid gland, splits into 5 terminal branches which supply the muscles of facial expression
List the terminal branches of the facial nerve and the muscles they innervate
Two zebras bit my cat
Temporal
Zygomatic
Buccal
Marginal mandibular
Cervical
Describe the functions of the facial nerve
Motor – muscles of facial expression, stapedius, posterior digastric, stylohyoid and platysma muscles
Sensory – taste to anterior 2/3 of tongue
Parasympathetic – submandibular and sublingual salivary glands, lacrimal gland
How can upper and lower motor neurone lesions affecting the face be distinguished? Why?
Upper (e.g. stroke) - forehead spared, bilateral innervation from brain
Lower (e.g. Bell’s palsy) - forehead not spared, unilateral innervation from cranial nerve
List the causes of facial nerve palsy
UMN
* CVA - unilateral
* Tumours - unilateral
* Pseudobulbar palsy - bilateral
* Motor neurone disease - bilateral
LMN
* Bell’s palsy
* Ramsay-Hunt syndrome
* Infection - otitis media, malignant otitis externa, HIV, Lyme’s disease
* Systemic disease - diabetes, sarcoidosis, leukaemia, MS, Guillain-Barre
* Tumours - acoustic neuroma, parotid tumours, cholesteatomas
* Trauma - direct facial nerve trauma, damage during surgery, base of skull fractures
Describe the presentation of facial nerve palsies
Usually painless unilateral weakness of facial muscles – drooping of eyebrow and corner of mouth, loss of nasolabial fold, incomplete eye closure, speech difficulty, drooling
Hyperacusis – nerve to stapedius
Altered taste – chorda tympani
Reduced lacrimation – greater petrosal nerve
How are facial nerve palsies graded?
House-Brackmann classification
Grade I - normal
Grade II - mild dysfunction
Grade III - moderate dysfunction (obvious but not dysfiguring asymmetry with movement, complete eye closure with effort)
Grade IV - moderately severe dysfunction (normal symmetry at rest but unable to completely close eye)
Grade V - severe dysfunction (asymmetry at rest, barely any facial muscle movement)
Grade VI - complete paralysis (no movement)
Define Bell’s palsy
Acute, unilateral, idiopathic facial nerve paralysis
Lower motor nuerone facial nerve palsy
Describe the clinical presentation of Bell’s palsy
Rapid onset <72 hours
Ear and postauricular pain - 50%
Numbness or tingling of cheek/mouth
Peak incidence 20-40 years
More common in pregnant women
How is Bell’s palsy managed?
Most recover fully within 3-4 months
If within 72 hours of symptoms onset give prednisolone e.g. 50mg daily for 10 days
Eye care (risk of keratopathy) - lubricating drops, taping/patch at night
Persistent weakness - >3 weeks ENT referral, plastic surgical referral
Surgical management - botox injections, anterior belly of digastric transfer, fascia lata sling, cross-facial nerve grafting
Opthalmology referral for corneal exposure
Describe the aetiology of Ramsay-Hunt syndrome
Reactivation of varicella zoster virus from geniculate ganglion (nucleus of facial nerve)
Describe the clinical presentation of Ramsay-Hunt syndrome
Moderate - severe otalgia, progresses to facial palsy with vertigo, hyperacusus and tinnitus
Vesicular skin rash - in ear canal, pinna, around ear, anterior 2/3 of tongue and hard palate
Tends to be more severe than Bell’s palsy
How is Ramsay-Hunt syndrome managed? Describe the prognosis
Oral aciclovir and steroids
Lubricating eye drops
Poor prognosis - only 75% resolve
Complications - chronic tinnitus, vestibular dysfunction
List the symptoms of facial nerve palsy which suggest a cause other than Bell’s palsy or Ramsey Hunt syndrome
Forehead sparing - UMN
Insidious, painful onset - infectious or neoplastic
Progressive and prolonged (>3 months) duration of symptoms with frequent relapses - neoplastic
Systemic illness, fever
Vestibular or hearing abnormalities (other than hyperacusis), otorrhoea, diplopia or dysphagia
Parotid gland masses
Lesions suggestive of skin cancer
Define otosclerosis and describe the pathophysiology
Abnormal remodelling of ossicles - normal bone replaced by vascular spongey bone
Causes impaired vibration of ossicles and conductive hearing loss due to reduced transmission of sound
Particularly affects stapes - becomes stiffened and fixed to oval window
Autosomal dominant inheritance
Describe the clinical presentation of otosclerosis and the typical findings on examination/investigation
<40, unilateral or bilateral progressive hearing loss and tinnitus
Family history - autosomal dominant
More common in women
Low pitched sounds affected more - struggle to hear male speech
Rinne’s test negative on affected side, Weber’s test lateralises to affected side
Audiometry - large air-bone gap, Carhart notch (at 2kHz) in bone conduction
Tympanometry - reduced absorption of sound, membrane stiff and non-compliant
High-resolution CT scans - detect boney changes
How is otosclerosis managed?
Conservative - hearing aids
Surgical - stapedectomy or stapedotomy (stapes prosthesis)
Surgery only done if very poor result with trial of hearing aids and no sensorineural hearing loss in contralateral ear - risk of complete sensorineural hearing loss in affected ear
Describe grommet insertion
Small plastic tube that sits in the tympanic membrane to allow air to pass in and out of ear and prevent development of effusion that causes glue ear
Can be done under GA or sedation, usually as day case
Small opening made in tympanic membrane using microscope, fluid suctioned out of ear, grommet placed in opening in tympanic membrane
Usually fall out after 6-18 months - varies person to person
List the potential complications of grommet insertion
Intra-operative
* Bleeding
* Failure to insert grommet
* Grommet falling into middle ear
Early
* Bleeding
* Infection - most common, 5%, presents with painful otorrhoea, antibiotics ear drops and strict water precautions post-op
* Early grommet extrusion (<6 months)
Late
* Tympanosclerosis - scarring
* Residual tympanic membrane perforation - 1-2% risk
* Failure to improve hearing
* Recurrence of glue ear - more likely with early grommet extrusion
Define vertigo
False sensation of movement - body or environment
Describe the causes of vertigo
Sensory inputs responsible for maintaining balance and posture - vision, proprioception, vestibular system
Peripheral (vestibular):
Benign paroxysmal positional vertigo
Meniere’s disease
Vestibular neuronitis
Labyrinthtis
Trauma to vestibular nerve
Vestibular nerve tumours - acoustic neuromas
Otosclerosis
Hyperviscosity syndromes
Varicella zoster infection - Ramsay Hunt syndrome
Central (cerebellum or brainstem)
Posterior circulation stroke
Tumour
Multiple sclerosis
Vestibular migraine
How can central and peripheral causes of vertigo be distinguished?
Peripheral
* Sudden onset
* Short duration - seconds-minutes
* Hearing loss or tinnitus often present
* Coordination intact
* Severe nausea
Central
* Gradual onset, except stroke
* Persistent
* Usually no hearing loss/tinnitus
* Coordination impaired
* Milder nausea
How should vertigo be assesed?
Examination:
Ear examination
Neurological examination - cranial nerve, cerebellar etc.
Cardiovascular examination - dizziness causes
Special tests - Romberg’s, Dix-Hallpike manoeuvre (diagnose BPPV), HINTS
Describe the aetiology of benign positional paroxysmal vertigo
Presence of otoconia (calcium carbonate crystals), become displaced into semicircular canals
Once in canal, movement of head causes movement of crystals which disrupt the flow of endolymph through the canals
Most commonly in posterior semicircular canal
Can be displaced by viral infection (e.g. labyrinthitis), head trauma, aging
Describe the clinical presentation of benign positional paroxysmal vertigo
Attacks of vertigo lasting seconds (20-60 seconds)
Triggered by typical movements e.g. turning over in bed
Can cause nausea/vomiting
Asymptomatic between episodes
How is benign positional paroxysmal vertigo diagnosed?
Dix-Hallpike manoeuvre - positive if symptoms triggered and nystagmus observed
Usually rotatory nystagmus with crystals in posterior canal
Clockwise rotation - left ear affected
Anti-clockwise rotation - right ear affected
List the risk factors for benign positional paroxysmal vertigo
Age
Female
Migraines
Recent viral infection
Ear surgey
Prolonged recumbent positions
Inner ear pathology
How is benign positional paroxysmal vertigo managed?
Epley manoeuvre (if crystals in posterior canal)
Post-epley - don’t drive, sleep upright, don’t bend down or look up for 48 hours
Brandt-Daroff exercises - performed by patient at home to improve symptoms (vestibular rehabilitation)
Sometimes betahistine prescribed - doesn’t do much
Surgery - intractable symptoms
Denervate/obliterate posterior semi-circular canal
Define vestibular neuronitis and describe its aetiology
Disorder characterised by acute, isolated, spontaneous and prolonged (days) vertigo of peripheral origin
Due to inflammation of vestibular nerve - ?viral cause
Describe the clinical presentation of vestibular neuronitis
Rotational vertigo which occurs spontaneously, usually sudden onset
Exacerbated by changes of head position but initially constant even when head still
Autonomic symptoms - nausea/vomiting, malaise, pallor, sweating
Balance affected - increased risk of falls
Veer to affected side
Nystagmus - usually fine horizontal, unidirectional
Head impulse may be positive
Otoscopy normal
No hearing loss or tinnitus
No focal neurological symptoms
How is vestibular neuronitis managed? Describe prognosis.
Usually acute symptoms resolve within a week but can have long-term vestibular deficit after acute episode with unsteadiness while brain compensates
During acute episodes:
Vestibular sedative - betahistine, antihistamines, dopamine receptor antagonists, use for up to 3 days
IV fluids if dehudrated due to vomiting
If persistent problems with vestibular function - vestibular rehabilisation (Cawthorne-Cooksey exercises)
Complications:
10-15% develop BPPV
Risk of falls
How is the head impulse test performed and interpreted?
Used to diagnose peripheral cause of vertigo
Patient sits uprights, fixes gaze on examiners nose
Examiner holds patient’s head and rapidly jerks it 10-20 degrees in one direction while patient continues to look at examiners nose
Repeat movements
Normal – keep eyes fixed
Abnormal – corrective saccades back to point of fixation (indicates peripheral cause, reassuring as unlikely to be a central cause of vertigo)
Describe the aetiology of and risk factors for Meniere’s disease
Not fully understood
Many have endolymphatic hydrops - excess of endolymph in membraneous labyrinth, increased pressure
Risk factors:
Family history
Usually 40-50 years old
Describe the presentation of Meniere’s disease
Recurrent spontaneous vertigo - 20 minutes - several hours
Progressive or fluctuating hearing loss - sensorineural hearing loss, initially affecting low frequencies
Tinnitus
Aural fullness
Horizontal nystagmus
How is Meniere’s disease investigated?
Audiology assessment - low-frequency sensorineural hearing loss usually
Criteria for definite diagnosis:
Two or more spontaneous episodes of vertigo, lasting 20 minutes to 12 hours
Audiological assessment demonstrating low-moderate sensorineural hearing loss on affected side
Aural fullness
How is Meniere’s disease managed?
Lifestyle - minimise salt and caffeine intake
Vestibular rehabilitation
Medical -
Betahistine - histamine H1-receptor agonist (prophylaxis)
Vestibular sedatives - prochlorperazine (acute episodes)
Surgical -
Steroid/gentamicin injection intratympanically (gentamicin ototoxic)
Labyrinthectomy
Vestibular neurotomy
Inform DVLA
Majority resolve after 5-10 years
List risk factors for acoustic neuroma
High-dose ionising radiation to head/neck
Neurofibromatosis type 2
Describe the clinical presentation of Meniere’s diease
Symptoms:
Unilateral sensorineural hearing loss and/or tinnitus
Dizziness and disequilibrium
Facial pain and numbness - trigeminal nerve compression
Facial weakness - facial nerve compression
Headache, nausea, vomiting - raised ICP
Signs:
Rinne’s - air > bone
Weber’s - sound lateralises to unaffected ear
How is acoustic neuroma diagnosed?
Pure-tone audiometry - confirm presence of sensorineural hearing loss
Imaging - MRI
How are acoustic neuromas managed?
Active observation with annual neuroimaging - small tumours, no impairment of facial nerve function, elderly with co-morbidities
Microsurgery - treatment of choice
Stereotactic radiosurgery - small tumours, uses high energy gamma rays to deliver single dose of radiation to tumour
Less invasive, better hearing preservation
List potential complications of acoustic neuroma
Hearing loss
Facial paralysis
Hydrocephalus
Compression of cerebellar peduncles, cerebellum, brainstem and cranial nerves
How are prominent ears managed?
Otoplasty
Young children under GA, older/adults with local anaesthetic
Post-auricular incision to expose cartilage, remove small amount of cartilage if necessary, suture ear to reshape/reposition
Incisionless otoplasty
Insert needle into ear cartilage to loosen, suture ear into shape
What are the potential complications of otoplasty for prominent ears?
- Scarring
- Pain
- Nerve damage - numbness/tingling, usually resolves in weeks
- Haematoma
- Asymmetry
- Bleeding
- Infection
List risk factors for head and neck cancers
Smoking
Chewing tobacco
Chewing betel nuts (South-East Asia) - oral
Alcohol
HPV (strain 16) - oropharyngeal
EBV – nasopharyngeal
Occupational exposure e.g. wood dust – nasopharyngeal
What are the red flag symptoms for head and neck cancers?
Lump in the mouth or on the lip
Neck lump (persistent and unexplained, >45)
Hoarseness (persistent and unexplained, >45)
Oral cavity red or red and white patch consistent with erythroplakia or erythroleukoplakia
Ulceration in oral cavity (unexplained, >3 weeks)
Thyroid lump (unexplained)
Describe the presentation of head and neck cancers
Oral cavity
* Painless mass on inner lip, tongue, floor of mouth or hard palate
* Oral cavity bleeding
* Ulceration
* Localised pain
* Jaw swelling
* Pre-malignant conditions e.g. erythroplakia
* Regional lymphadenopathy
Pharyngeal
* Odynophagia
* Dysphagia
* Stertor
* Referred otalgia
* Neck lump
Laryngeal
* Hoarse voice
* Stridor
* Dysphagia
* Persistent cough
* Referred otalgia
How is suspected head and neck cancer investigated?
Biopsy of lesion - method dependent on location
Flexible nasal endoscopy for direct visualisation of lesion
Examination under anaesthesia and biopsy
Lymphadenopathy only - US-guided fine needle aspiration
Staging - usually TNM
CT of neck and chest
PET CT for tumours of unknown origin
MRI for oral cavity and oropharyngeal lesions
How are head and neck cancers managed?
Depends on location, size, stage, grade of tumour and patient factors
Common options:
Surgical resection +/- adjuvant radiotherapy or chemotherapy
Primary radiotherapy +/- adjuvant chemotherapy
Other options – monoclonal antibodies (e.g. cetuximab), palliative
What is the most common type of head and neck cancer?
Squamous cell carcinoma
What are the most common types of oesophageal cancer? What are the risk factors for each type?
Squamous cell carcinoma - more common in developing world, middle and upper thirds of oesophagus, associated with smoking and excessive alcohol consumption, other risk factors include chronic achalasia, low vitamin A, iron deficiency
Adenocarcinoma - more common in developed world, lower third of oesophagus, occurs due to Barrett’s oesophagus, risk factors e.g. GORD, obesity, high fat intake
Describe the clinical presentation of oesophageal cancer
Dysphagia, progressive - solids then liquids
Significant weight loss
Odynophagia
Hoarseness
Supraclavicular lymphadenopathy
How is oesophageal cancer diagnosed?
Upper GI endoscopy with biopsy
Staging:
CT chest-abdomen-pelvis and PET-CT scan
Endoscopic US - local spread
Cervical LN - FNA
How is oesophageal cancer managed?
Most present with advanced disease - 70% palliative
Curative management
SCC - chemo-radiotherapy
Adenocarcinoma - neoadjuvant chemotherapy or chemo-radiotherapy followed by oesophageal resection
Palliative
Oesophageal stent
Radiotherapy/chemotherapy
Nutritional support - may need gastrostomy
Describe the differences between Hodgkin’s and non-Hodgkin’s lymphoma
Hodgkin’s
* Alcohol-induced lymph node pain
* B symptoms earlier
* Reed-Sternberg cells
* Bimodal age distribution - 3rd and 7th decade
Non-Hodgkin’s
* All others that aren’t Hodgkin’s
* More common
* Extra-nodal disease more common
* Typically >75s, Burkitt in children
List the risk factors for lymphoma
Hodgkin’s
* HIV
* Epstein-Barr virus
* Autoimmune disease - rheumatoid arthritis, sarcoidosis
* Family history
Non-Hodgkin’s
* HIV
* Epstein-Barr virus
* H Pylori - MALT lymphoma
* Hepatitis B/C
* Exposure to pesticides, trichloroethylene
* Family history
Describe the presentation of lymphoma
Lymphadenopathy - non-tender, rubbery, asymmetrical (Hodgkin’s - pain with alcohol)
B symptoms - fever, weight loss, night sweats
Fatigue, itch, cough, SOB, abdominal pain, recurrent infections
Hepatomegaly, splenomegaly
How is lymphoma diagnosed?
- Lactate dehydrogenase - often raised in Hodgkin’s lymphoma, non-specific
- FBC - normocytic anaemia
- Lymph node biopsy - Reed-Sternberg cells in Hodgkin’s (abnormal large B cells with multiple nuclei)
- CT, MRI, PET - staging
How is non-Hodgkin’s lymphoma staged?
Ann Arbor system
I - one lymph node
II - two or more on same side of diaphragm
III - lymph nodes on both sides of diaphragm
IV - involvement of one or more extralymphatic organs or sites
A - no B symptoms
B - symptoms (unexplained weight loss, recurrent unexplained fever, recurrent night sweats)
How is lymphoma managed?
Dependent on sub-type
Watchful waiting, chemotherapy, radiotherapy, monoclonal antibodies (rituximab), stem cell transplantation
Neutropaenia - may need antibiotic prophylaxis
What are the potential complications of lymphoma?
Bone marrow infiltration - anaemia, neutropaenia, thrombocytopaenia
Superior vena cava obstruction
Metastasis
Spinal cord compression
Complications of management - secondary malignancies, infertility etc.
List causes of a goitre
Grave’s disease
Toxic multinodular goitre
Hashimoto’s thyroiditis
Iodine deficiency
List causes of thyroid lumps
Benign hyperplastic nodules
Thyroid cysts
Thyroid adenomas
Thyroid cancer - papillary or follicular
Parathyroid tumour
List the most common subtypes of thyroid cancer and their histological and clinical characteristics
Papillary carcinoma - most common (75%), women 40-50
Mixture of papillary and colloid-filled follicles
Spread via lymphatics
Follicular carcinoma – second most common (15%), usually women 40-60
Usually haematogenous spread to bones and lungs
Medullary carcinoma – 3%, cancer of parafollicular cells, cause raised calcitonin, 20% associated with MEN 2 (A and B)
Spread via lymphatic and medullary routes
Poor prognosis
Anaplastic – rare, 5%, usually in elderly
Aggressive, grow rapidly, early local invasion
Poor prognosis
Lymphoma – 1-2%, >60s, rapid growth, marked compressive and B-cell symptoms
What are the risk factors for thyroid cancer?
Female gender
Family history – including cancer syndromes e.g. medullary type associated with MEN 2A/B
Radiation exposure
Full body radiotherapy for bone marrow transplant
Hashimoto’s – lymphoma type
What are the risk factors for thyroid cancer?
Female gender
Family history – including cancer syndromes e.g. medullary type associated with MEN 2A/B
Radiation exposure
Full body radiotherapy for bone marrow transplant
Hashimoto’s – lymphoma type
Describe the clinical presentation of thyroid cancer
Palpable lump/multiple lumps
Can be incidental finding
Red flags for malignancy – rapid growth, pain, cough, hoarse voice or stridor, enlarged cervical lymph nodes, tethering
How should suspected thyroid cancer be investigated?
TFTs – if evidence of toxic nodule (low TSH or raised T3/4 or radio-nucleotide imaging showing ‘hot’ nodule) no further investigation for malignancy
Serum calcitonin – diagnosis and monitoring of treatment response in medullary carcinoma
US – thyroid, cervical lymph nodes
Features suggestive of malignancy - microcalcification, hypoechogenicity, irregular margin
Score U1-5, U-12 low risk of malignancy, U3-5 need FNAC
FNAC – score Thy1-5 given
Thy1 – inconclusive
Thy2 – non-malignant
Thy3 – follicular, needs diagnostic hemithyroidectomy to differentiate between adenoma or carcinoma
Thy4 – suspicious, need diagnostic hemithyroidectomy
Thy5 – malignant
How is thyroid cancer managed?
Surgery – hemi-thyroidectomy or total thyroidectomy
Will need life-long thyroxine
If locally advanced also need neck dissection to remove lymph nodes
Radioiodine – used for follicular or papillary carcinomas after total thyroidectomy
External beam radiotherapy – curative or palliative
Chemotherapy – lymphomas often response well
What are the potential complications of thyroid surgery?
Bleeding – haematoma formation, can cause airway obstruction
Hypocalcaemia if damage to/removal of parathyroid glands
Vocal cord paralysis if damage to recurrent laryngeal nerves
Bilateral recurrent laryngeal nerve injury can cause life-threatening stridor, may need tracheostomy
How does post-thyroid surgery haematoma formation present? How is it managed?
Difficulty swallowing saliva, swelling in the neck, breathing difficulties, stridor
Management – SCOOP
Contact crash team and surgeon
S – steri-strips (remove)
C – cut sutures
O – open skin
O – open strap muscles to expose trachea
P – pack over wound
Return to theatre to control bleeding and re-close wound
List the main causes of thyroiditis
Autoimmune thyroiditis – Hashimoto’s
Drug-induced thyroiditis
Viral or sub-acute thyroiditis – De Quervain’s
Postpartum thyroiditis
List the drugs which can commonly cause drug-induced thyroiditis and describe the presentation of drug-induced thyroiditis.
Lithium
Amiodarone
Interferons
Monoclonal antibodies – nivolumab, ipilimumab, pembrolizumab
Tyrosine kinase inhibitors – axitinib, sunitinib
Presentation – can cause hyper- or hypothyroidism symptoms
Pain/swelling of thyroid
Describe the cause and presentation of De Quervain’s thyroiditis. How is it managed?
Thyroiditis due to viral infection
Presentation – fever, neck pain, tenderness, dysphagia, features of hyperthyroidism
Hyperthyroid then hypothyroid level, TSH falls due to negative feedback
Usually self-limiting, pain managed with NSAIDs, more severe cases may use steroids especially with hypothyroidism
Can use beta-blockers for hyperthyroidism symptoms
Describe the cause and presentation of a thyroglossal cyst
Remnant of thyroglossal duct which connects tongue to thyroid gland during embryonic development, usually atrophies but can persist in some people and give rise to thyroglossal duct cysts
More common in <20s
Lump, moves superiorly on tongue protrusion, usually midline between isthmus and hyoid bone
May be painful if infected
How are thyroglossal cysts managed? Why?
Surgical resection – Sistrunk procedure
Can rarely develop thyroglossal duct cyst carcinoma from ectopic thyroid tissue in cyst (most commonly papillary)
Describe the most common types of salivary gland tumours
80% are parotid, 80% of these are pleomorphic adenomas, 80% in the superficial lobe
Pleomorphic – benign, mixed histology, small chance of malignant transformation (5% if not resected or inadequately resected), usually middle-aged males affected, unilateral
Carcinoma ex-pleomorphic adenoma – pleomorphic adenoma which has undergone malignant transformation
Warthin’s tumour (adenolymphoma) – benign, usually middle-aged males affected, mobile, cystic appearance on imaging
Mucoepidermoid carcinoma – most common malignant type, slow-growing but can have phases of accelerated growth, high-grade metastasise to lymph nodes, lung, bone
Describe the presentation and management of salivary gland tumours
Presentation – painless, slow-growing lump around mouth, jaw or neck
Can be mobile or fixed
If large/rapidly growing can cause compression of facial nerve, impairment of muscles of mastication
Features suggestive of malignancy – ulceration of skin overlying lump, pain, local lymphadenopathy
Management – usually pleomorphic adenomas
Extracapsular lumpectomy, partial or total parotidectomy +/- radiotherapy
List the potential complications of parotid surgery
Infection, bleeding, anaesthetic risks
Facial nerve palsy – transient or permanent
Can cause exposure keratopathy
Use electrodes for intraoperative facial nerve monitoring
Greater auricular nerve injury – paraesthesia around ear
Frey syndrome – flushing and sweating of area over parotid when eating, due to mixing of sympathetic and parasympathetic fibres
List causes of salivary gland swelling
Sialolithiasis
Sialadenitis
Neoplasms – benign or malignant
Ranula – mucocele in sublingual gland
Describe the risk factors for and the clinical presentation of sialolithiasis
Risk factors:
Diuretics
Anti-cholinergics
Dehydration
Gout
Smoking
Hyperparathyroidism
Presentation
Most commonly affects submandibular gland due to flow of saliva against gravity and mucoid secretions
Tends to be asymptomatic
Can have intermittent facial swelling, associated with eating
Can be painful or painless
May be able to palpate stone
How is sialolithiasis diagnosed/managed?
Diagnosis – US, X-ray (most stones are radio-opaque)
Usually conservative management – hydration, analgesia, sialologues (e.g. lemon juice), massage gland
If infected – antibiotics
If persistent/recurrent symptoms – removal of stones with interventional radiology or surgical techniques
List causes of sialadenitis
Infective – viral or bacterial
Viral – more common, mumps, coxsackie, parainfluenza, HIV
Bacterial – S. aureus, S. viridans, H. influenzae, S. Pyogenes
Stones
Malignancy
Autoimmune – sarcoidosis (Heerfordt’s syndrome – parotid enlargement, anterior uveitis, facial nerve palsy), Sjogren’s, Wegner’s granulomatosis
Idiopathic
Describe the presentation and potential complications of mumps
Prodromal symptoms – low grade fever, headache, malaise
Bilateral gland swelling
Complications – meningitis/encephalitis, deafness, pancreatitis, orchitis
Describe the clinical presentation of sialadenitis
Painful swelling and tenderness of gland
Pyrexia, lymphadenopathy, erythema
Infectious causes – purulent discharge from duct
How is sialadenitis managed?
Usually conservative management – hydration, analgesia, sialologues e.g. lemon juice, massage gland
Antibiotics if bacterial sialadenitis suspected (purulent discharge, fever)
Abscess – incision and drainage, can cause airway obstruction
If recurrent may warrant surgical removal of gland
Describe the aetiology of acute tonsillitis
Viral – most common (70%)
Rhinovirus – most common
Coronavirus
Parainfluenza
Epstein Barr Virus
Bacterial
Group A beta-haemolytic streptococcus (most common) – strep pyogenes
Haemophilus influenzae
Moraxella catarrhalis
Describe the clinical presentation of acute tonsillitis
Odynophagia
Dysphagia
Cough
Coryzal prodrome
Dysphonia
Pyrexia
Malaise
Red, inflamed, enlarged tonsils, with or without exudate
Anterior cervical lymphadenopathy
Describe the scoring systems used for acute tonsillitis
Centor criteria – used to estimate probability of bacterial cause, if score of 3 or more give antibiotics
Fever >38 – one point
Tonsillar exudate – one point
No cough – one point
Tender cervical lymphadenopathy – one point
Age 3-14 – one point
Age 15-44 – no points
Age >44 – minus one point
FeverPAIN – score of >4 give antibiotics
Fever during previous 24 hours
P – purulence
A – attended within 3 days of onset of symptoms
I – inflamed tonsils (severely inflamed)
N – no cough or coryza
How is acute tonsillitis managed?
Analgesia – Difflam spray, regular paracetamol, NSAIDs
Hydration
May need admission if cannot swallow fluids, immunocompromised, systemically unwell, stridulous, evidence of peritonsillar abscess
If likely to be bacterial (based on CENTOR/feverPAIN score) give antibiotics – penicillin V for 10 days, clarithromycin if allergic
Can give delayed prescription – collect if symptoms worsen or don’t improve over next 2-3 days
Safety net – return if high fever, respiratory distress, can’t swallow fluids
Why is amoxicillin not given for acute tonsillitis?
May be EBV – amoxicillin causes generalised maculopapular rash
List the potential complications of acute tonsillitis
Chronic tonsillitis
Quinsy – peritonsillar abscess
Otitis media
Scarlet fever
Rheumatic fever
Post-strep glomerulonephritis
Post-strep reactive arthritis
List the indications for tonsillectomy
Two episodes of Quinsy
Recurrent tonsillitis:
7 episodes in one year
5 episodes in two years
3 episodes in three years
Other:
Suspected malignancy
Sleep apnoea
Describe the major potential complications of tonsillectomy and how they are managed
Primary (<24 hours) haemorrhage in 2-3% - due to inadequate haemostasis
Secondary (24 hours to 10 days) haemorrhage – due to infection
All need assessed by ENT
Primary – immediate return to theatre
Secondary – admission and antibiotics
Define Quinsy and describe its aetiology
Peritonsillar abscess, collection of pus in the peritonsillar space – potential space lateral to palatine tonsils
Aetiology – complication of acute/recurrent tonsillitis
Most common bacterial pathogen – strep pyogenes (GABHS)
Describe the clinical presentation of Quinsy
Symptoms
Odynophagia, worse on one side, can have referred pain to ear
Dysphonia – hot potato voice
Dysphagia – saliva or small sips only
Signs
Trismus - <3cm opening
Bulging palatine arch on affected side, uvular deviation away from affected side
Signs of sepsis – altered mental state, fever, tachypnoea, tachycardia, hypotension
Describe the scoring system used to diagnose Quinsy
Liverpool peritonsillar abscess score
* Unilateral sore throat – 3 points
* Trismus – 2 points
* Male gender – 1 point
* Hot potato voice – 1 point
3 or less – unlikely
4 or more – likely
6 or more – very likely, PPV of 80%
How is Quinsy managed?
A-E assessment
Airway problems rare but may develop stertor – involve ENT surgeon if concerned about airway
Medical management:
Analgesia – NSAIDs
IV fluids – likely to be dehydrated as reduced oral intake
IV antibiotics – benzylpenicillin and metronidazole
Single dose steroids may reduce inflammation
Surgical management:
Aspiration of abscess – symptomatic management
Incision and drainage
Pus sent for C&S to guide antimicrobial therapy
List the potential complications of Quinsy
Deep neck space infections – retro or parapharyngeal abscess, mediastinitis
Airway compromise
Describe the clinical presentation of deep neck space infections
Severe sore throat
New-onset dysphagia
Voice changes
Neck stiffness!!
Systemically unwell
Stridor
Trismus
Pharyngeal swelling
Cervical lymphadenopathy
How are deep neck space infections diagnosed and managed?
Diagnosis - CT neck with contrast
Management:
Broad-spectrum antibiotics
IV fluids
Oxygen and adrenaline nebulisers if respiratory distress
Low threshold for intubation
Surgical – drainage and washout (may need to repeat if reaccumulates)
Define obstructive sleep apnoea
Intermittent and recurrent collapse of upper airways during sleep –
5 or more respiratory events per hour (detected by polysomnography) plus associated symptoms
List the risk factors for obstructive sleep apnoea
Obesity
Male gender
Smoking
Excess alcohol
Sedating drugs
Children – tonsillar or adenoid enlargement
Describe the clinical presentation of obstructive sleep apnoea
Witnessed apnoeas/noisy breathing/snoring
Excessive daytime sleepiness, reduced concentration
Non-specific symptoms – personality changes, reduced libido, restlessness
How is obstructive sleep apnoea diagnosed/investigated?
Polysomnography is gold standard – measure number of apnoeic or hyponoeic episodes
Can quantify impact during Epworth sleepiness scale – score out of 24
How is obstructive sleep apnoea managed?
Lifestyle – weight loss, increased exercise, smoking cessation, alcohol reduction
Non-pharmacological – continuous positive airway pressure (CPAP) first-line for moderate-severe
Surgical interventions to open airway, tonsillectomy +/- adenoidectomy for children with tonsillar/adenoid enlargement
What are the potential complications of obstructive sleep apnoea?
Daytime sleepiness – impaired working, driving (inform DVLA), reduced quality of life, memory, cognitive function
Significant CV morbidity – hypertension, ischaemic heart disease, stroke
What is a branchial cyst?
Congenital neck lumps – due to incomplete obliteration of the branchial clefts during fetal development
Most commonly 2nd branchial cleft, can also be 1st, 3rd, 4th branchial clefts
Lined by stratified squamous epithelium, fluid filled
Can have sinus to skin or fistula – risk of infections
Describe the presentation of branchial cysts
Soft, non-tender, fluctuant, fluid-filled swellings in anterior triangle of neck
Present in adolescents/young adults
Slowly enlarging, may increase after URTI
Do not transilluminate
May have sinus/fistula with infective symptoms and discharge
How are branchial cysts managed?
Need to exclude malignancy – usually need US, FNAC
Surgical excision is definitive management
Antibiotics for acute infection
What are the key differential diagnoses for strawberry tongue?
Scarlet fever
Kawasaki disease
What are leukoplakia? How do they present?
Oral lesions – white patches on mucous membrane
Premalignant (squamous cell carcinoma)
Asymptomatic, irregular, slightly raised
Fixed in place – can’t be scraped off
How are leukoplakia managed?
Biopsy – to exclude malignancy
Lifestyle – smoking cessation, reduce alcohol consumption
Close monitoring for malignant transformation (occurs in 1%)
Potentially laser removal or surgical excision
What is hairy leukoplakia? How does it present? How is it managed?
Oral cavity lesions
White, hyperkeratotic plaque, usually on lateral border of tongue
Vertical white striations – may appear hairy
Causes – EBV, HIV
Not premalignant, don’t usually need treatment
What is erythroplakia? How does it present?
Similar to leukoplakia but red
High risk for squamous cell carcinoma
Describe the cause, risk factors, presentation and management of oral candidiasis
Most commonly caused by candida albicans
Soft white plaques that can be easily wiped off showing red underlying mucosa
Risks – diabetes, anaemia, immunocompromise
Management – topical miconazole gel or oral fluconazole
Describe the aetiology of and risk factors for lichen planus
Immune-mediated chronic inflammatory condition, T-cell infiltration and destruction
More common in women, age 30-50
Describe the clinical presentation of lichen planus
50% have oral involvement
Reticular – web-like white lines, Wickham’s striae
Erosive lesions – surface layer of mucosa eroded, leaving bright red sore mucosa
Plaques – larger continuous areas of white mucosa
Other symptoms:
Itchy, papular rash on palms, soles of feet, genitalia and flexor surfaces of arms
Koebner phenomenon
Nails – thinning of nail plate, longitudinal ridging
Which drugs can cause lichenoid eruptions?
Gold
Quinine
Thiazides
How is lichen sclerosus managed?
Topical steroids
Benzydamine mouthwash/spray for oral
If extensive may need oral steroids or immunosuppression
Describe the clinical presentation of gingivitis
Inflammation of gums
Bleeding after brushing
Gum pain
Halitosis
List risk factors for gingivitis
Plaque build-up - poor oral hygiene
Smoking
Diabetes
Malnutrition
Stress
How is gingivitis managed?
Good oral hygiene
Stop smoking
Dental hygienist
Chlorhexidine mouthwash
Antibiotics for necrotising - metronidazole
List causes of gingival hyperplasia
Gingivitis
Pregnancy
Vitamin C deficiency (scurvy)
Acute myeloid leukaemia
Medications – calcium channel blockers, phenytoin, ciclosporin
Describe the presentation and causes of aphthous ulcers
Well-circumscribed, punched-out, white appearance
Occur in healthy people, may be triggered by emotional/physical stress, trauma to mucosa or particular foods
Underlying conditions:
Inflammatory bowel disease
Coeliac
Behcet disease
Vitamin deficiency e.g. iron, B12, folate, vitamin D
HIV
How are aphthous ulcers managed?
Usually heal on their own within 2 weeks
Topical treatments for symptoms:
Bonjela (choline salicylate)
Benzydamine e.g. Difflam
Lidocaine
Topical steroids for more severe – reduced duration and severity of symptoms:
Hydrocortisone buccal tablets
Betamethasone soluble tablets
Beclomethasone inhaler
2ww referral in patients with unexplained ulcer lasting >3 weeks
Describe the innervation of the vocal cords
Recurrent laryngeal nerve – branch of vagus
Left nerve loops under aortic arch, right nerve loops under right subclavian artery
Travel alongside trachea
Describe the aetiology of vocal cord paralysis
1/3 idiopathic – post-viral neuropathy
1/3 surgery – thyroid and parathyroid
1/3 neoplastic – lung, lymphoma, neck
Ortner’s syndrome – recurrent laryngeal nerve palsy due to cardiovascular disease (e.g. dilated left atrium due to mitral stenosis, pulmonary hypertension, thoracic aortic aneurysms)
Describe the clinical presentation of vocal cord paralysis
Harsh, hoarse voice
Shortness of breath, noisy breathing
Choking or coughing while eating
Bilateral causes severe airway obstruction
How is vocal cord paralysis managed?
Speech therapy
Surgical interventions
If bilateral paralysis - tracheostomy
Describe the cause, presentation and management of vocal cord polyps
Arise following injury to lamina propria of vocal cords – smoking, chronic cough
Can be pedunculated or sessile
Usually quite large and unilateral
Symptoms – sore throat, hoarse voice
Treatment – surgical excision
Describe the cause, presentation and management of vocal cord granulomas
Damage to arytenoid cartilages (not vocal cords themselves) – affects voice minimally
Caused by continuous damage and subsequent inflammation/healing – chronic cough, intubation trauma, reflux
Symptoms – pain
Management – biopsy to exclude SCC, surgical excision, speech therapy, PPIs
Describe the cause, presentation and management of vocal nodules
Arise due to damage to lamina propria of vocal cords
Excessive use of voice – singers, teachers
Presents with hoarse voice
Management - SALT
Describe the aetiology of a pharyngeal pouch
Herniation of pharynx through area of weakness, Killian’s dehiscence in posterior pharyngeal wall
Cause – reduced elasticity of pharyngeal muscles with aging, increased upper oesophageal tone?
Associated with increased age and male sex
Describe the clinical presentation of a pharyngeal pouch
Dysphagia and repeated aspiration
Feeling of food getting stuck
Regurgitation
Halitosis
Neck lump
Weight loss
Recurrent chest infections
Can cause fistulation into trachea, vocal cord paralysis due to pressure, squamous cell carcinoma of diverticulum
How is a pharyngeal pouch diagnosed?
Gold-standard – fluoroscopy, barium swallow
US if unable to swallow or if barium not tolerated
How are pharyngeal pouches managed?
Conservative – asymptomatic, <1cm
Surgical – symptomatic, endoscopy or open percutaneous
List potential complications of a pharyngeal pouch
Aspiration pneumonia
Ulceration of pouch
Fistulation between pouch and trachea
Vocal cord palsy due to pressure from pouch contents
Squamous cell carcinoma of pouch
Complications of surgical repair:
Recurrent laryngeal nerve damage
Perforation of pouch or oesophagus
Mediastinitis
Pharyngeal fistula
Pharyngeal or oesophageal stricture
Recurrence
Describe the aetiology of acute rhinosinusitis
Acute inflammation of mucosal lining of nasal passage and paranasal sinuses
Inflammation triggered by infection, allergy
Pathogens – usually viral e.g. rhinovirus, influenza, adenovirus
Can be bacterial – strep pneumoniae, haemophilus influenzae, moraxella catarrhalis
Allergens – dust, pollen, cat or dog hair
Inflammation results in blockage of paranasal sinuses which can lead to bacterial infection
List risk factors for rhinosinusitis
Cigarette smoke exposure – active or passive
Air pollution
Anatomical variations – septal deviation, nasal polyps, sinus hypoplasia
Atopy – asthma, hayfever
Describe the clinical presentation of rhinosinusitis
<12 weeks – acute
>12 weeks – chronic
Nasal obstruction
Discoloured nasal discharge
Facial pain or pressure
Altered sense of smell
Acute – sudden onset, <12 weeks
Chronic – two or more of these symptoms, >12 weeks
How is acute rhinosinusitis managed?
Analgesia
Nasal irrigation
Nasal decongestants
Signs of acute bacterial rhinosinusitis (purulent discharge, fever) – antibiotics
No improvement after 7-14 days or red-flag symptoms – referral to ENT
Severe infections/complications – oral steroids, IV antibiotics, surgery
What are the potential complications of acute rhinosinusitis?
Peri-orbital cellulitis
Osteomyelitis
Pott’s puffy tumour – soft boggy swelling on forehead
Intracranial abscess
Venous sinus thrombosis
How is chronic rhinosinusitis managed?
Mild – nasal saline irrigation, topical steroid spray, avoid triggers
Moderate to severe – topical steroids, consideration of surgery
Surgery – functional endoscopic sinus surgery
Describe the cause and presentation of Reinke’s oedema
Smoking, gastroesophageal reflux, chronic overuse of voice
Dysphonia – low-pitched voice with hoarseness
‘Sac-like’ appearance of vocal folds, oedematous, bulging
Describe the cause and presentation of Reinke’s oedema
Smoking, gastroesophageal reflux, chronic overuse of voice
Dysphonia – low-pitched voice with hoarseness
‘Sac-like’ appearance of vocal folds, oedematous, bulging
How is Reinke’s oedema managed?
Control risk factors – smoking cessation, PPIs, vocal rest
Speech therapy
Surgery - microlaryngoscopy
