ENT Flashcards
What is stridor?
High pitched noise resulting from turbulent airflow through a partially obstructed upper airway
What is an inspiratory stridor indicative of?
Obstruction is glottic (at level of vocal cords) or supraglottic
What type of obstruction is an expiratory stridor indicative of?
Tracheal obstruction
What type of obstruction is a biphasic stridor suggestive off?
Subglottic obstruction
How might an airway emergency present?
Stridor
Respiratory arrest
Hoarse voice (tumour or the larynx)
Pain and discomfort
Drooling (epiglotisits)
What might cause paediatric stridor?
CONGENITAL:
Laryngomalacia
Vocal cord paralysis
Subglottic stenosis
AQUIRED:
Laryngotracheobronchitis / tracheobronchitis (croup)
Epiglottitis
Retropharyngeal abcess
Foreign bodies
Iatrogenic
What is laryngomalacia
Congenital softening of the tissues in the supraglottic portion of the larynx. The epiglottis is malformed and floppy causing the tissues to fall over the open airway and partially block it.
Cause of stridor (inspiritory)
Slow feeding, failure to gain weight, noisy breathing
Tracheal tug
Subcostal recession
Flexible office laryngoscopy can be offered to diagnose
Management
Watchful waiting: resolution by 18-24 months
Anti reflux meds (H2 blockers, PPIs)
Microlaryngobronchoscopy, supraglottoplasty
What is Subglottic stenosis
May be congenital of acquired from repeated intubation
Cricoid cartilage (only COMPLETE ring in the airway) is damaged, causing stenosis and scarring which can result in a stridor
What is laryngotracheobronchitis known as commonly
Croup
What organism causes epiglotititis
Haemophilus influenzae
Epiglottitis is a life threatening emergency, which group of patients are typically effected?
2 to 6 year olds
What triad of symptoms does epiglotitis typically present with?
Drooling
Dysphasia
Respiratory distress
(Stridor
Pyrexia)
How might a child with epiglotitis hold themselves
Neck extended, sniffing to reduce air hunger
How might you differentiate epiglotitis from croup?
Child cannot breathe unless sitting up
Worsening “croup”
Child cannot swallow saliva and drools
An X ray should never be taken in suspected Epiglotitis as the child should not be upset and, but what would be seen if one was taken?
Significant swelling of the epiglotitis
How might a retropharnageal abcess present?
Typically a young child
Odynophagia (painful swallow)/ dysphagia
Neck held ridgid and upright, pt reluctant to move (toriciollis)
Pyrexia and systemic unwell
Drooling
Widening of the retropharyngeal space of lateral X ray
How is retropharyngeal abcess managed?
Secure airway (intubation)
Drain abcess surgically (I+D)
IV Abx
What level on CT would the hyoid bone be seen?
C3
What is torticollis?
Twisting of the neck that causes the head to rotate and tile at an odd angle (also known as wryneck)
Adult airway emergencies?
Infection: Paraphyrangeal, peritonsillar (quinsy) abcess, Ludwig’s angina (submental abcess, dental aetiology) epiglotitits/supraglottic
Tumours
Foreign bodies
Allergic reactions, angioodema
Trauma (iatrogenic)
Vocal cord paralysis
How might a peritonsillar abscess appear?
Complete or partial oropharynx obstruction
Uvula may not be visible
Buldging around soft pallet
What is Ludwig’s Angina
Submandibular space infection
Usually odontogenic (dental problems)
How might you manage laryngeal cancers presenting with an acute airway problem
Tracheostomy, possibly under local anesthesia (intubation not possible)
What is an important risk of a tracheostomy in a patient with laryngeal cancer, and how can it be avoided?
Potential seeding
Ideally intubate patient and debulk tumour
What is the most common type of larngeal tumour?
SCC
What might be seen on x ray of a pt with a forgiven body airway obstruction?
The forgiven body
Surgical emphysema (air seen in soft tissue)
A ruptured AAA cause a posterior pharyngeal wall haematoma leading to airway obstruction, what will be seen on X ray?
Prevertabral space increased in size
How large is the prevertabral space usually?
5-8mm
Diagnosis and initial management of airway obstruction?
ABC
Secure airway first
Rapid history and careful examination
Give O2/Heliox
Pharmacological management: adrenaline steroid antihistamine abx
Nasopharyngeal/orophrangeal airway
Intubation
Cricothyroidotomy (needle/surgical)
Surgical tracheostomy
What is heliox and why is it used?
Helium and oxygen mixture
Helium decreases viscosity of oxygen so it can get to the lungs easier
What pharmacological management might be implemented in an airway emergency?
Oxygen or heliox
Adrenaline
Steroids
Antihistamines
Antibiotic is
What is a crycothyroidotomy
Space between crycoid cartilage and thyroid cartilage incised or needle inserted during airway emergency
What are the potential indications for a tracheostomy?
Airway obstruction
To protect tracheobronchial tree (e.g. patients who can’t protect their own airway following a stroke)
Ventilatory insufficiency (e.g. advanced lung disease)
Airway risk during oropharyngeal and laryngeal surgery
Where are the thyroid gland and cartilage in relation to the trachea?
Thyroid gland anterior to trachea
Thyroid cartilage superior to the cricoid cartilage
Where is a tracheostomy inserted?
Window created between the 2nd and 4th tracheal rings, which is where the tracheostomy is inserted
How is the airway protected when swallowing?
Larynx moves up
Epiglottis comes down and closes off airway
Vocal cords close to protect the airway
Where does the larynx start and end?
Epiglottis to the cricoid cartilage
What is the nervous inner action of the larynx?
Vagus nerve
Recurrent, internal and external laryngeal nerves
RLN: Motor with exception of the cricothyroid muscle
ILN: Sensory
ELN: Motor to cricothyroid muscle
What is the difference between acute otitis media and glue ear?
Acute otitis media: Bacterial infection of the MIDDLE EAR
Glue ear is otitis media with effusion - not infective but can become infected leading to acute otitis media - commmon cause of childhood deafness
What is a bacterial infection of the middle ear called?
Acute otitis media
How might acute otitis media present?
preceding URTI, unwell
Fever
Otalgia (or signs of - tugging at ear)
Hearing loss
Later otorrhoea (if TM ruptures) - pain will settled once this happens due to resolution of increased pressure in the tympanic cavity
What causes otalgia in acute otitis media?
Increased pressure in the tympanic cavity
Accumulation of pus within the middle ear cavity (cleft) but eardrum remains intact (pain improves if perforated)
What might be seen on otoscopy in acute otitis media?
Erythamatous and buldging tympanic membrane
If the fluid pressure has perforated the TM a small tear with purulent discharge in the auditory canal may be visible
What type of hearing loss does otitis media with effusion cause?
Conductive
Complications of acute otitis media?
Acute mastoiditis (osteomyelitis)
Intracranial infections: cerebellar abcess, extradural abcess, meningitis, temporal lobe abcess
Thrombosis of the sigmoid sinuses (vein travels in close proximity to the mastoid air cells)
Bacterial Labyrinthitis
Facial nerve palsy - facial paralysis
Petroys apicitis
Gradanigo’s sybdrome
Citelli abscess
Temp. hearing loss
OME
How does acute mastoiditis present and how is it managed
Children present unwell
Protrusion of the pinna
Loss of posterior sulcus
Mastoiditis may cause posturicular swelling (abcess formation)
Surgical management and IV abx
How is acute otitis media managed?
Paracetomol to control fever - this is the only treatment required usually
Sometimes abx required to prevent complications or if complications have occured - (Amoxicillin for 5-7 days first-line, Clarithromycin (in pencillin allergy), Erythromycin (in pregnant women allergic to penicillin))
In severe or recurrent cases myringotomy to insert grommet to release pus
How to examine a child with forgiven body’s inserted in the nose?
EXAMINE BOTH SIDES
Use auriscope
What is the most common inhaled foreign body and why can it cause inflammation?
Peanuts, peanut oil invokes inflammation
Where are inhaled forigen bodies typically found and why?
Right main bronchus
Wider and has more direct extension of trachea
When might nasal trauma be an emergency?
Septal haematoma
Haematoma becoming in an abcess is not drained/vascular necrosis of cartilage to leading to saddle nose deformity/ infection pain and fever
How do you treat a septal haematoma?
Surgical drainage +/- abx
What is periobital cellulitis?
URTI leads to infection from anterior ethmoidal space, spreading into the orbit.
Lateral deviation of medial recuts
Can cause proptosis, loss of colour vision
How is periorbital cellulitis managed?
Just cellulitis then IV abx sufficient
Involve ophthalmology, assess colour vision (pressure on optic nerve), if compromised incision and drainage in theatre
Symptoms of tonsillitis?
Sore throat
Pyrexia
Neck lymphadenopathy
Why must tonsillitis be differentiated from glandular fever?
Glandular fever - hepato/splenomegaly, no contact sports for six weeks, and do not give amampacillin can cause rash
Common complication of tonsillitis?
Quinsy - peritonsillar abcess:
Buldging of the soft pallette
Uvula deviation
How is a peritonsillar abcess managed?
Drainage under local anaesthetic
Management of epiglottitis
Keep child calm as the airway may close if they cry (laryngospasam)
Give wafting oxygen
Intubation in theatre to protect airway
Emergency tracheotomy in rare cases
IVabx broad spectrum
Neck abscess is very common in children, how might it present?
Typically follows URTI,
Cervical lymphadenitis
Usually bacterial - painful, spinning temp, neutrophils raised
Atypical mycobacteria - purple discolouration - painless, bloods may be normal or lymphocytic picture
Rarely, TB is cause
How is neck abscess managed?
Incision and drainage
Pus to microbiology
How does an abscess appear on CT
Ring enhancement
Which types of neck abscess are considered surgical emergencies?
Paraphyrangeal abscess
Retropharyngeal abscess
Causes of neck swelling?
Abscess: Retropharyngeal, parapharyngeal
Cystic hygroma (lymphangioma)
problems
Cervical teratoma
What is a cystic hygroma and how is it managed
Also known as lymphangioma
Benign congenital neck swelling
Respiratory and feeding problems
Soft, compressible
Managed by excision once airway secured
What is a cervical teratoma and how is it managed?
Benign congenital neck swelling
Firm consistency
Extreme cases require tracheostomy
Blood supply to lateral nasal wall
Branches of the internal carotid artery :
Anterior and posterior ethmoidal arteries (branches of the opthalmic artery
Branches of the external carotid artery:
Sphenopalatine
Descending palatine
Greater and lesser palatine
Blood supply to nasal septum
Branches of the internal carotid artery:
Anterior and posterior ethmoidal
Branches of the external carotid artery:
Septal branches of Sphenopalatine artery
Septal branch of the superior labial artery
Branch of greater palatine
From which area of the nose do most bleeds arise from?
Little’s area / Kiesselbach’s plexus - in the septum
Area of nasal mucosa at the front of nasal cavity
This is where all the branches of ICA and ECA supplying the septum meet
When mucosa is disrupted and blood vessels are exposed they become prone to bleeding
Local aetiology of nose bleeds.
Idiopathic
Traumatic (fracture foreign body picking)
Inflammatory (rhinitis)
Neoplastic
Environmental
Iatrogenic (surgery, steroid nasal spray)
General causes of nosebleeds?
Anticoagulants
Coagulapathies
Hereditary haemorrhaged telangiectasia (abnormality of the blood vessel wall)
HTN
Management of nose bleeds?
Pinch cartilaginous part of nose (soft lower portion)
Topical adrenaline +/- cautery with silver nitrate sticks
Anterior nasal lacking (merocel tampon, BIPP)
Posterior nasal pack (Foley catheter, Brighton balloon)
Surgical intervention
What can be used for anterior nasal packing
Merocel tampon
BIPP
What is used for posterior nasal packing?
Brighton balloon
How is nasal cautery undertaken?
Anterior bleed visualised with a thudiculum speculum
Visualise bleeding point
Local anaesthetic spray
Control with adrenaline And or
Cauterise bleeding point and 5mm radius circle around the bleed
How should a nasal pack be inserted?
Horizontally, along floor of nose, to avoid damage to skull base
What kind of surgical intervention might be involved in epistaxis management when other methods have failed?
Rigid nasendoscope with electrocautery
Sphenopalatine artery ligation
Anterior ethmoid artery ligation
External carotid artery ligation
Embolization of vessels under radiographic control
Basic pathophysiology of otitis media?
The Eustation tube (connecting the middle ear to the back of the throat) becomes blocked and causes middle ear secretions to build up in the middle ear space.
.Build up of fluid causes loss of hearing in that ear
May result in infection (acute otitis media)
Otitis media with effusion (glue ear): ET tube dysfunction leading to presence of fluid in the middle ear with intact TM - non infective but can lead to infection
Unlike the external ear the epithelium lining the middle ear is respiratory epithelium or pseudostratified collumnar epithelium - regarded as a continutation of the upper respiratory tract and hence susceptible to similar pathogens - streptococcus pneumoniae, haemophillus influenzae, moraxella species (AOM)
Investigations and management of glue ear/otitis media with effusion?
Referral to audiometry to establish extent of the hearing loss - pure tone audiogram, tympanogram
Conservative management unless persists past 3 months or child has comorbidities (Down’s syndrome, clef palate)
Surgical: Grommet insertion (ventillation tubes) +/- adenoidectomy
Hearing aids
What is a grommet?
Device inserted by ENT surgeon. This allows fluid from the middle ear to drain through the tympanic membrane to the ear canal. Usually grommets are inserted under general anaesthetic as a day case procedure.
How long do grommets typically last?
Grommets usually fall out within a year, and only 1 in 3 patients require further grommets to be inserted for persistent glue ear.
What would be seen on otoscopy and examination in glue ear?
On examination, the tympanic membrane will appear dull (Fig. 2) and the light reflex will be lost, indicating fluid in the middle ear.
Air fluid level
There may also be a bubble seen behind the TM. The external ear will be normal.
Main presenting complaint of glue ear?
Hearing loss - conductive
May be sensation of pressure in the ear accompanied by popping or cracking noises
Disequilibrium and vertigo (rare)
Why are children more likely to suffer from otitis media with effusion?
of chronic inflammatory changes and Eustachian tube dysfunction.
The anatomy of the Eustachian tube in younger children is immature, typically short, straight, and wide (only becoming more oblique as the child develops), therefore infection is more likely.
Why should any new case of unilateral OME in an adult should be investigated as a ‘red flag’ for a malignant underlying cause?
Adults should have mature anatomy of the ET tube
The condition is less common in adults, however will occur if there is any blockage of the Eustachian tube, either from infective causes or from occlusive masses
Main risk factors for OME/glue ear?
Bottle fed
Paternal smoking
Atopy (e.g eczema, asthma)
Genetic disorders
Mucociliary disorders, such as Cystic Fibrosis or Primary Ciliary Dyskinesia
Craniofacial disorders, such as Downs Syndrome
How might glue ear be noticed in young children?
In young children this may be noticed as difficulty with attention at school or poor speech and language development
How should otitis media with effusion be investigated?
Clinical diagnosis
Both pure tone audiometry and tympanometry are nearly always performed in such cases, which will reveal a conductive hearing loss and reduced membrane compliance (a type B tracing) respectively.
In adults, a full ENT examination should be performed, including flexible nasoendoscopy (to exclude a post-nasal space mass).
Who are recomeded for grommet insertion to manage OME?
> 3 months of bilateral OME and hearing level in better ear < 25-30dBHL
Any child with persistent disease and multiple grommet insertion should be considered for what?
Potential adenoidectomy
Pathophysiology of acute otitis media?
Bacterial infection of the middle ear results from nasopharyngeal organisms migrating via the eustachian tube.
The anatomy of the eustachian tube in younger children is immature, typically being short, straight, wide (only becoming more oblique as the child grows), meaning infection is more likely.
Common causative bacteria include S. pneumoniae (most common), H. influenza, M. catarrhalis, and S. pyogenes, all common upper respiratory tract microbiota. Common viral pathogens are respiratory syncytial virus (RSV) and rhinovirus.
Why do clefte pallete and Down’s Syndrome increase risk of otitis media?
Children with cleft palate, or with genetic conditions such as Down’s syndrome, may be more likely to get glue ear as they often have smaller eustachian tubes that don’t function well.
RIsk factors of acute otitis media?
Risk factors for AOM include age (peak age 6-15 months), gender (more common in boys), passive (parenteral) smoking, bottle feeding, and craniofacial abnormalities
When might recurrent acute otitis media be more common?
Recurrent AOM is seen more commonly with the use of pacifiers, who are typically fed supine, or their first episode of AOM occurred <6months. AOM is most common in the winter season.
What should be further examined in a patient with suspected acute otitis media, supported by otoscopy?
It is important to test and document the function of the facial nerve (due to its anatomical course through the middle ear).
Examination should also include checking for any intracranial complications, cervical lymphadenopathy, and signs of infection in the throat and oral cavity.
When should oral antibiotics be considered to treat acute otitis media?
- Systemically unwell children not requiring admission
- Known risk factors for complications, such as congenital heart disease or immunosuppression
- Unwell for 4 days or more without improvement, with clinical features consistent with acute otitis media
- Discharge from the ear (ensure swabs are taken prior to commencing antibiotic therapy)
- Children younger than 2 years with bilateral infections
- Systemically unwell adult, provided not septic and with no signs of complications
When should inpatient admission be considered for otitis media?
All children under 3 months with a temperature >38c, or aged 3-6 months with a temperature >39c, for further assessment.
Also, consider admission for those with evidence of an AOM complication or the systemically unwell child. Patients with a cochlear implant will need to be seen by a specialist and may require inpatient treatment.
What make mastoiditis concerning in relation to AOM?
The middle ear and mastoid are one cavity, and as such, there will nearly always be a degree of mastoiditis with AOM. However, if the inflammation within the air cells progresses to necrosis and subperiosteal abscess, this is of significant concern.
How does mastoiditis present?
It presents clinically as a boggy, erythematous swelling behind the ear, which if left untreated progressing to pushing the pinna forward
How is mastoiditis managed?
Any suspected cases should be admitted for IV antibiotics and investigated further via CT head if no improvement is seen after 24 hours of IV antibiotics.
There is a higher risk of intracranial spread and meningitis, hence cases are often considered for mastoidectomy as definitive management if there is no improvement with IV antibiotics
What is considered the middle ear?
The middle ear is the space that sits between the tympanic membrane (eardrum) and the inner ear.
What oral antibioitics does NICE recommend for AOM if required?
Amoxicillin for 5-7 days first-line
Clarithromycin (in pencillin allergy)
Erythromycin (in pregnant women allergic to penicillin
What is conductive hearing loss?
Conductive hearing loss relates to a problem with sound travelling from the ENVIRONMENT TO INNER EAR.
The sensory system may be working correctly, but the sound is not reaching it. Putting earplugs in your ears causes conductive hearing loss.
What is sensioneural hearing loss?
Problem with the sensory system or vestibulocochlear nerve in the inner ear
Basic structures of the ear (outside to in)
Pinna
External auditiory canal
Tympanic membrane
ET
Malleus, incus and stapes (small bones in the middle ear that connect the tympanic membrane)
Semicircular canals (responsible for sensing head movement (vestibular system)
Cochlea (converting vibration into nervous signal)
Vestibulocochlear nerve (transmits nerve signals from the semicircular canals and chochlea to the brain)
What symptoms might be associated with hearing loss?
Tinnitus (ringing in the ears)
Vertigo (the sensation that the room is spinning)
Pain (may indicate infection)
Discharge (may indicate an outer or middle ear infection)
Neurological symptoms
Sudden onset (less than 72hrs) requires a thorough assessment to establish the cause
Cognitive benefit of hearing aids?
Reduces risk of dementia (hearing loss increases)
Improved speech and language development in children
What is the vestibulocular reflex and how can it be demonstarted?
Information about the position of the head is used to coordinate balance and the vestibulo-ocular reflex. The vestibulo-ocular reflex (also called the oculocephalic reflex) allows images on the retina to be stabilised when the head is turning by moving the eyes in the opposite direction. It can be demonstrated by holding one finger still at a comfortable distance in front of you and twisting your head from side to side whilst staying focused on the finger.
Simple three neuron system: vestibular nerve to vestibular nuclei to ocular muscle nuceli to eye muscles
The ability to remain focused upon and object as the head is turned rapidly from or towards the object and maintain balance
Lateral semicircular canals engaged when head moved sideways (horizontal acceleration) action potentials increase in nerve on side the head turns, decreased input on the contra lateral side
Eyes move to contra lateral side
Gain: ratio of the lapse between one command in another
The gain in this reflex is nearly 1
Most common non ENT causes of balance problems in the elderly?
Postural hypotension - drop of more than 20mm in systolic BP, loss of blood pressure control with age and polypharmacy
OA
In which direction does nystagmus beat in a peripheral vestibular lesion?
In the opposite direction to the defect
Eyes move wrong way as no input from the vestibular nerve when head is turned in direction of defect (loss is vestibulocular reflex)
Labyrinthitis vs vestibular neuritis
What is a vestibular migraine?
CT orientations?
Coronal
Axial
Saggital
CT windows?
Soft tissue windows - expansion of the greys pertaining soft tissue
Bone windows - detail of the bone including density
How to differentiate between cause of nasal septum defect on CT?
Trauma - same size inferior terminal on both sides of CT
Developmental - hypoplastic terminal and enlarged terminal on CT
What causes a nasal pseudohump?
Loss of cartilage (secondary to repeated trauma for example)
Repaired with costal cartilage
What type of obstruction causes stertor?
Above the larynx e.g. large adenoids and tonsils, oropharngeal mass, etc
Snoring - obstruction is above the larynx e.g. nose, tongue, younger base, back of nose
Why is a biphasic stridor more concerning than monophasic?
Obstruction is at level of the vocal cords or below
Subglottic stenosis
What is rhinosinusitis?
Inflammation of the nose and paranasal sinuses characterised by two or more symptoms, one of which should be nasal blockage/discharge/congestion or nasal discharge - anterior or posterior
+/-Facial pain or pressure
+/-reduction/loss of smell
Classiification of rhinosinusitus?
Acute: resolution within 12 weeks VS chronic with and without nasal polyposis
Allergic vs non allergic
History in rhinosinusitis
Nasal blockage/congestion and discharge
Loss/reduction of smell
Itchy runny eyes
Permenant/intermittent
Time of day
Jobs/hobbies
Pets- Cats - wash them with grooming glove and damp water!
Aetiology and pathogenesis of allergic rhinitis?
Type 1 hypersensitivity reaction to allergens
Increased permeability of capillaries
Mucosal infiltration of oesinophils and oedema
CRS management
Conservative - allergy avoidance
Medical - nasal sprays, long course of macrolides (calithromycin, up to 12 weeks)
Surgical management of sinus: septoplasty, turbinate surgery (SMD reduction of inferior turbinates)
Nasal polypectomy
Functional endoscopic sinus surgery (FESS)
Nasal cautery dos and don’ts
Use local anesthetic lignocaine with adrenaline on cotton wool
Don’t simply spray
Don’t allow silver nitrate to drop out the nose
Don’t use silver nitrate for more than 20 seconds each side
Inner ear symptoms?
Hearing loss (sensioneural)
Vertigo
Tinnitus
Outer ear symptoms
Pain
Discharge - scant serous
Late hearing loss (conductive hearing loss)
Otology examination
Wash hands, intro
Tenderness
Which ear is better
Inspect pinna, mastoid area,
Otoscopy: external auditory canal, tympanic membrane
Hearing test
Cranial nerve VII, co-ordination and Romberg
Otological investigations?
Pure tone audiogram
Tympanogram
CT
MRI
Rinne Test
Air conduction should be better than bone conduction and persiist) - POSITIVE TEST
Begin by striking a 512 Hz tuning fork against your knee or elbow.
Place the base against the patient’s mastoid process (for those who like to watch it on a video, check one out here)
Allow it to stay there for 2-3 seconds to allow them to appreciate the intensity of the sound then promptly raise the fork off the mastoid process and place the vibrating tips about 1cm from their external auditory meatus
Leave it there for a few seconds before taking the tuning fork away from their ear
Ask the child whether the sound was louder at the beginning (when it was held against their mastoid) or whether it became louder (when it was held in front of their ear).
If bone conduction is better than air conduction (negative test) indicates conductive hearing loss
Webers test
Should not localise
Localises to affected ear in conductive hearing loss
Localises to the unaffected ear in sensioneural hearing loss
As in Rinne’s test, begin by striking the 512 Hz tuning fork against your knee or elbow
Then, place the base of the fork in the midline, high on the patient’s forehead
Ask whether they hear the sound in the midline or if the sound lateralises to either the affected or good ear.
What is Haematoma/Seroma of the Pinna and how is it managed?
Collection of blood between skin and cartillage, can lead to avascular necrosis and change in shape of the ear (cauliflour ear)
Aspirate x2 in sterile conditions and apply compression bandage (review in 24 hours)
What is otitis externa?
Otitis externa is inflammation of the skin in the external ear canal, also known as swimmers ear.
What predisposes to otitis externa?
Water exposure (swimming)
Removal of earwax (as it is protective)
Ear canal trauma (ear plugs, cotton buds)
Immunosupression
What causes inflammation in otitis externa?
Bacterial infection
Fungal infection (e.g., aspergillus or candida)
Eczema
Seborrhoeic dermatitis
Contact dermatitis
Main causative organisms of otitis externa?
Pseudomonas aeruginosa (gram-negative aerobic rod-shaped bacteria. It likes to grow in moist, oxygenated environments, also causes resp problems in CF pts)
Staphylococcus aureus
Typical symptoms of otitis externa?
Ear pain (severe due to stretching of nerve fibres with inflammation)
Discharge (serous)
Itchiness
Conductive hearing loss (if the ear becomes blocked)
*Tympanic membrane is intact - if not points to OM
Signs seen in otitis externa?
Erythema and swelling in the ear canal
Tenderness of the ear canal
Pus or discharge in the ear canal
Narrowing or ear canal
TM may be red but often obstructed by debris (earwax, discharge)
Lymphadenopathy (swollen lymph nodes) in the neck or around the ear
What is seen on otoscopy in otitis externa?
The tympanic membrane may be obstructed by wax or discharge
It may be red if the otitis externa extends to the tympanic membrane.
If it is ruptured, the discharge in the ear canal might be from otitis media rather than otitis externa.
Most common treatment for otitis externa?
Otomize spray (Neomycin/Dexamethasone/Acetic Acid)
How is mild otitis externa managed?
Mild otitis externa may be treated with acetic acid 2% (available over the counter as EarCalm). Acetic acid has an antifungal and antibacterial effect.
This can also be used prophylactically before and after swimming in patients that are prone to otitis externa.
Topical toilet
How to differientate between UMN and LMN facial palsy?
Forehead sparing - upper motor neuron
How is moderate otitis externa managed?
Moderate otitis externa is usually treated with a topical antibiotic and steroid, for example:
Neomycin, dexamethasone and acetic acid (e.g., Otomize spray)
Neomycin and betamethasone
Gentamicin and hydrocortisone
Ciprofloxacin and dexamethasone
When do aminoglycosides need to be used with caution to treat otits externa and what should be ruled out)
Typmanic membrane perforation or when it cannot be visualised
Aminoglycosides (e.g., gentamicin and neomycin) are potentially ototoxic, rarely causing hearing loss if they get past the tympanic membrane.
Therefore, it is essential to exclude a perforated tympanic membrane before using topical aminoglycosides in the ear.
(This can be difficult if the patient has discharge, swelling or wax blocking the ear canal. Patients with a blocked ear canal may need to be seen by ENT to microsuction the debris from the canal and visualise the tympanic membrane. They will also require a referral if the canal is so blocked or swollen that topical treatments cannot reach the site of infection.)
How should patients with severe otitis externa be managed (or if they are systemically unwell)?
Patients with severe or systemic symptoms may need oral antibiotics (e.g., flucloxacillin or clarithromycin) or discussion with ENT for admission and IV antibiotics.
Why are peadatric airways difficult to manage?
Children have narrow airways and respond poorly to small changes in radius
How do paediatric airways differ to adults?
Children have narrow airways and respond poorly to small changes in radius
Obligate nasal breaters
Larger toungues
Laryncy is more cranial and anterior
Subglottiss (cricoid) is the narrowest part of the airway (as opposed to the vocal cords in adults)
How is fungal otitis externa managed?
clotrimazole ear drops
Risk factors for mallignant otits externa?
Diabetes
Immunosuppressant medications (e.g., chemotherapy)
HIV
What is malignant otitis externa?
Malignant otitis externa is a severe and potentially life-threatening form of otitis externa. The infection spreads to the bones surrounding the ear canal and skull. It progresses to osteomyelitis of the temporal bone of the skull.
Malignant otitis externa is usually related to underlying risk factors for severe infection
Presenation of mallignant otitis externa?
persistent headache, severe pain and fever
History of chronic ear discharge despite topical treatment
Deep seated ear pain
Sometimes cranial nerve palsies (CNVII) - facial nerve
Key finding that indicated mallignant otitis externa?
Granulation tissue at the junction between the bone and cartilage in the ear canal (about halfway along) is a key finding that indicates malignant otitis externa.
Management of mallignant otitis externa?
Admission to hospital under the ENT team
IV antibiotics
Imaging (e.g., CT or MRI head) to assess the extent of the infection
Potential complications of mallignant otitis externa?
Facial nerve damage and palsy
Other cranial nerve involvement (e.g., glossopharyngeal, vagus or accessory nerves)
Meningitis
Intracranial thrombosis
Death
Management of otitis sleep apnoea in children?
Adenotonsillectomy
Sleep study
Classic presentation of Meneires Disease
recurrent attacks of vertigo, hearing loss, tinnitus, and the sensation of aural fullness.
Management of chronic otitis externa?
Topical toilet and steroids
Eczema
Which hobby might predispose a patient to exostoses?
Cold water swimmers
What is an osteoma?
Benign neoplasia of the bone, may be visable on otoscopy of external ear if involved
What does a retracted typmanic membrane ocassionally progress to?
Cholesteatoma
Although often no treatment required
When might a TM perforation require repair and when might it not?
Dry: may need no treatment
Recurrent infection: can be repaired
What should be considered in the clinic presentation of a child with an airway complaint?
Onset
Duration
Exaccerbating/relieving factors
Fever
H/O coughing/choking (FB)
Change in voice
Swallowing/feeding
Weight gain/loss
History of prolonged intubation
Management of severe croup?
Humidified O2
Nebulised adrenaline
Systemic steroids
Theatres to secure airway - intubation/tracheostomy if not responding
What is recurrent respiratory papilomatosis and how is it managed?
Recurrent respiratory papillomatosis (RRP) is a disease in which benign (noncancerous) tumors called papillomas grow in the air passages leading from the nose and mouth into the lungs (respiratory tract). Tracheal tug, inspiratory stridor and subcostal recession may be present.
Microlaryngobronchoscopy, surgical debridement
What is vertigo?
A hallucination of movement of oneself or one’s surroundings.
The movement is often rotatory (e.g. pt may feel floor is tilting)
Causes of vertigo?
On held tilt: Benign positional paroxysmal vertigo (BPPV)
Hearing loss and tinnitus: Acute labyrinthitis
No hearing loss nor tinnitus: Vestibular neuritis
Unilateral hearing loss progressing to involve CN 5,6,9,10 and the ipsilateral cerebellum: Acoustic neuroma
Sensioneural hearing loss, tinnitus, feeling of aural fullness: Meniere’s disease
Facial nerve palsy (+/- tinnitus, hearing loss): Ramsay Hunt syndrome
Ototoxicity features: aminoglycoside abx, loop diuretics
What AD disorder can predispose patients to recurrent epistaxis but not other kinds of bleeds?
Heriditary haemorrhagic telangiectasia (Osler Weber Rendu disease - telangiectasia on skin and mucous membranes, malformations within the nasal mucosa prone to bleeding)
After how long can abx be considered for sinusitis?
After 5 days
What can be used it otitis externa if the patient’s ear canal is very swolen?
An ear wick may be used if the canal is very swollen, and treatment with ear drops or sprays will be difficult. An ear wick is made of sponge or gauze. They contain topical treatment for otitis externa (e.g., antibiotics and steroids). Wicks are inserted into the ear canal and left there for a period of time (e.g., 48 hours). As the swelling and inflammation settle, the ear wick can be removed, and treatment can continue with drops or sprays.
What common condition is seen here?
Otitis externa - ‘swimmers ear’
Why are patients advised against cleaning their ears with cotton buds?
Possible trauma/perforation of TM
Likely to further impact earwax
Risk of ear canal trauma - OE
Management of a TM perforation?
Watch + wait
Perform otoscopy and audiogram
Water precautions, keep dry, no more cleaning, avoid FB in ear
Review pt after 4 weeks
If no resolution after 6 months consider surgical intervention - myringoplasty
What is the surgical management (if indicated) of TM perforation?
Myringoplasty
TM perforation
General management of otitis externa?
Topical eardrops empirically (e.g. Gentamycin)
Swab any discharge in resistant cases
Microsuction of pus/debris - allows eardrops to reach source of infection
Wick (severe)
Topical antifungals if fungal
MOE- aggressive IVAbx therapy
What is the sensory supply to the pinna?
Upper lateral surface - CNV3 - auriculotemporal nerve
Lower lateral surface - C3 - greater auricular nerve
Superior medial surface - C/2 C3 - less occiputal nerve
Auricular branch of vagus - external auditory meatus
Potential causes of ear trauma?
Laceration: simple primary closure of the skin with sututres after adequete cleaning is all that is required usually, it is important to ensure that any exposed cartillage is covered with skin - otherwise seek plastics
Bites: significant risk of infection from skin commensals or oral commensals - require hx to ascertain likely organisms involved in potential infection - MUST LEAVE WOUND OPEN - treatment includes wound irrigation and topical abx
Hematoma: Pinna haeamtoma causes disruption in blood supply to the cartillage which would normally obtain nutrients via diffusion from vessels in the overlying perichondrium (hence disruption can lead to avasucluar necrosis - risk of cauliflower ear) REQUIRES URGENT DRAINAGE AND DRESING TO PREVENT RE-ACCUMULATION
Perforation of Tympanic membrane - direct or indirect trauma or otitis media - pain, possible conductive deafness
Haemotympanum (blood in middle ear): May be associated with temporal bone fracture. Can be seen through tympanic membrane and is associated with conductive hearing loss. Conservative treament with follow up to ensure no residual hearing loss from damage to ossicles
When might ear trauma lead to hearing loss - and what kind?
Tympanic membrane perforation and haemotypanum (blood in middle ear) - conductive hearing loss
Haemotympanum
Subtypes of otitis media?
Chronic: squamous (inactive/active) or mucosal
Acute
Oral antibiotics used (if indicated) in acute otits media?
Amoxicillin for 5-7 days first-line
Clarithromycin (in pencillin allergy)
Erythromycin (in pregnant women allergic to penicillin)
What is meant by active chronic otitis media?
Squamous: Cholesteatoma
Mucosal: Chronic discharge from the middle ear through a TM prtforation
Associated with chronic ear discharge and often a conductive hearing loss , can also be associated with complications associated with spread of the disease within the temporal bone and intracranially?
What is meant by inactive chronic otitis media?
Squamous: Retraction pocket which may develop into cholesteatoma
Mucosal: TM perforation without active infection or discharge
SQUAMOUS COM
Active: Cholesteatoma
Inactive: Retraction pocket which may develop into active disease (cholesteatoma)
Active develops when keratinized squamous cells are introduced to the middle ear from a retraction pocket or perforation
MUCOSAL COM
Active: Perforated TM with discharge
Inactive: Perforated TM without discharge or infection
Thought to develop from an episode of AOM where after TM rupture there is failure to heal
Management of COM (chronic otitis media)
Depends on type - active squamous disease (cholesteatoma) requires surgery to clear
No cholesteatoma (often not known if this is the case when there is active ear discharge, initially assume there is not and opt for medical treatment and then surgicl if fails ) medical treatment: topical abx drops and an aural toilet
Surgical management of COM?
When there is known cholesteatoma or ?cholesteatoma (chronically discharging ear that is not responding to medical therapy):
COMPLPETE clearence of cholesteatoma
Often requires surgery to the mastoid bone (mastoidectomy) as the cholesteatoma will often grow from the middle ear into the mastoid bone.
If no cholesteatoma is found during surgery (mucosal COM) repair of perforation and ensure good ventillation of the middle ear and mastoid bone (no need to remove every last trace of disease as in cholesteatoma)
What are the potential complications of mastoid surgery?
Facial nerve palsy
Altered taste from damage to chorda typani
CSF leak
Tinnitus
Vertigo
Compete loss of hearing in the operated ear
Why might a patient complain of altered taste following mastoid surgery?
Accidental damage to the chorda typani
Acute otitis medial - buldging red tympanic membrane
What is this called and what is it?
A cholesteatoma
(an abnormal collection of skin cells in the middle ear)
They’re rare but, if left untreated, they can damage the delicate structures inside the ear ear that are essential for hearing and balance.
What is seen on normal otoscopy
“Pearly-grey”, translucent and slightly shiny. Can visualise the pars tensa, pars flacida, cone of light and lateral process of maleoulus
Name the four key structures
Cone of light/light reflex
Pars flacida
Pars tensa
Lateral process of malleolus
Normal TM
Pearly grey, translucent, slightly shiny
Not budlging
Light reflex present
Able visualise the malleus through the membrane
Cholesteatoma pathophysiology?
Squamous epithelial cells originate from the outer surface of the tympanic membrane
Negative pressure in the middle ear, caused by Eustachian tube dysfunction, causes a pocket of the tympanic membrane to retract into the middle ear.
Essentially, a small area of the tympanic membrane gets sucked inwards.
The squamous epithelial cells of this pocket continue to proliferate and grow into the surrounding space, bones and tissues.
It can damage the ossicles (the tiny bones of the middle ear involved in hearing), resulting in permanent hearing loss.
Cholesteatoma complications?
Permenant conductive hearing loss secondary to damage of the ossicles
Infection
Pain
Vertigo
Facial nerve palsy
Tinnitus
How might neuroimaging be utitilsed in cholestetoma?
A CT head can be used to confirm the diagnosis and plan for surgery. MRI may help assess invasion and damage to local soft tissues.
Is otitis media with effusion painful?
No but may lead to acute otitis media which is (up until TM perforates)
Investigations and examinations in suspected OME + findings
Otoscopy: Tympanic membrane is retracted and usually has a yellowish hue. There may also be air bubbles or increased opacity of TM
Posterior rhinoscopy (to visualize the post nasal space) - tumours in this area can cause ET dysfunction leading to OME - especially important in adults with unilateral OME
Tympanogram: Flat (Type B) Tracing
Pure tone audiogram: conductive hearing loss
Rinne’s: abnormal in affected ear
Weber’s: localizes to effected ear (if unilateral)
What problems might occur in children with OME?
Associated speech delay
Reports of problems at school
Diagnosis and indicative findings?
Otitis media with effusion (GLUE EAR)
Tympanic membrane is retracted and usually has a yellowish hue.
Air bubbles
Increased opacity of the tympanic membrane.
When might you worry about an underlying tumor in a patient with OME, and how do you address this concern?
In adults, especially when otitis media with effusion is unilateral - tumours in the postnasal space, as unilateral adult serous effusion is considered a nasopharyngeal tumour until proven otherwise
Posterior rhinoscopy
How can OME lead to hearing loss?
OME is caused by the build-up of a viscous inflammatory fluid within the middle ear, resulting in a conductive hearing impairment.
Typical presenting features of cholesteotoma?
Foul discharge from the ear
Unilateral conductive hearing loss
What does Rinnes negative mean?
Meaning abnormal test - bone conduction is better than air conduction (normal hearing should mean that air conduction is best)
Suggests conductive hearing loss
If the patient has negative or abnormal Rinne negative, air vibrations are not being transmitted across the external auditory canal, the tympanic membrane, the ossicular chain, or the oval window.
Why might cholesteatoma cause vertigo?
Breach of the otic capsule bone causing dizziness on pressure change transmitted from the middle ear to the vestibular system
What type of hearing loss does cholesteatoma cause and why?
Conductive
Debris or erosion by cholestotoma of the ossicles
What is the most likely diagnosis in patients presentencing with episodic room dizziness with nausea especially with certain head movements and lying down?
BPPV - benign paroxysmal positional vertigo
Gold standard test to diagnose BPPV?
Dix Hallpike maneuver
What is considered an abnormal Dix Hallpike maneuver test?
When affected ear is undermost, the following will be observed:
Latency
Torsional geotropic nystagmus
Fatigue
Habituation on repeating the test
What manouevere is used to manage BPPV?
Epley manouvere
How to perform Dix-Hallpike manouevere?
When performing the Dix-Hallpike test, make sure to warn the patient in advance of each step, so that they know what to expect:
- Ask the patient to sit upright on the examination couch.
- Adjust the patient’s position so that when supine, their head will hang over the edge of the bed, allowing for head extension below the horizontal plane.
- Position yourself standing behind the patient.
- Turn the patient’s head 45º to one side.
- Whilst supporting the neck, move the patient from their sitting position to a supine position in one brisk smooth motion, ensuring their head hangs over the bed 30º below the horizontal plane. Ask the patient to keep their eyes open throughout this process.
- Inspect the patient’s eyes carefully for evidence of nystagmus for at least 30 seconds.
- If no nystagmus is observed, the test is then complete for that side and you should carefully help the patient sit back up.
- After a short break, the test should be repeated on the other side, turning the patient’s head in the opposite direction during step 4.
How to perform Epley manouevere?
- The Epley manoeuvre typically follows on from a positive Dix-Hallpike test, so we will assume the patient is still positioned lying flat, with the head hanging over the end of the bed, turned 45º away from the midline.
- Turn the patient’s head 90º to the contralateral side, approximately 45º past the midline, still maintaining neck extension over the bed. Keep the patient in this position for 30 seconds.
- Whilst maintaining the position of the patient’s head, ask the patient to roll onto their shoulder (on the side their head is currently turned towards).
- Once the patient is on their side, rotate the patient’s head so that they are looking directly towards the floor. Maintain this position for 30 seconds to a minute.
- Sit the patient up sideways, whilst maintaining head rotation.
- Once the patient is sitting upright, the head can be re-aligned to the midline and the neck can be flexed so that the patient is facing downwards (chin to chest). Maintain this position for 30 seconds.
The entire procedure can be repeated 2-3 times if needed, however, this will depend on whether the patient is able to tolerate further manoeuvres (as they often precipitate vertigo).
What should you ask a patient presenting with ‘vertigo’?
Is the room spinning around the patient?
When did it start?
Eposodic?
How long does it last
How often does it happen
Positional? - lying down, head turning
Other specific triggers
Associated hearing loss
Associated tinnitus
Loss of conciousness with episodes
If it has happened before - resolution: spontaneous? treatment?
Indications for the Dix-Hallpike test
The Dix-Hallpike manoeuvre is indicated for patients with paroxysmal vertigo in whom BPPV is considered in the differential diagnosis. These patients experience vertigo in brief episodes lasting less than one minute with changes of head position and return to normal between episodes. Light-headedness or a sensation of nausea might last longer than one minute, however, if the sensation of movement persists for more than one-minute alternative diagnoses should be considered. ¹
Absolute contraindications - Dix-Hallpike and Epley manouveres
Fractured odontoid peg
Recent cervical spine fracture
Atlanto-axial subluxation
Cervical disc prolapse
Vertebrobasilar insufficiency
Recent neck trauma
Relative contraindications - Dix-Hallpike and Epley maneuvers
Carotid sinus syncope
Severe neck or back pain
Recent stroke
Cardiac bypass surgery within the last 3 months
Rheumatoid arthritis affecting the neck
Recent neck surgery
Cervical myelopathy
Severe orthopnea
What is otosclerosis?
Disease affecting the ossicles in the middle ear with both genetic and environmental components.
Remoddling of small bones in ear
Mature bone is gradually replaced with woven bone and symptoms begin as the stapes footplate becomes fixed to the oval window.
Most patients develop bilateral disease and most are female (2:1)
When otosclerosis is prevalent in families what is the inheritance thought to be?
Autosomal dominant tranmission
Before what age does otosclerosis tend to present?
Before 40 years
Pathophysiology of otosclerosis?
The auditory ossicles are the tiny bones in the middle ear that transmit sound vibrations from the tympanic membrane to the cochlea. They are the malleus, incus and stapes. The stapes is connected to the oval window (fenestra ovalis) of the cochlea, where it transmits vibrations into the cochlea, which converts them into sensory signals.
In patients with otosclerosis, these tiny bones in the middle are affected by abnormal bone remodelling and formation. Mature bone is gradually replaced with woven bone. This mainly affects the base of the stapes, where it attaches to the oval window, causing stiffening and fixation and preventing it from transmitting sound effectively. It causes conductive hearing loss and symptoms begin as the stapes footplate becomes fixed to the oval window.
Typical presentation of otosclerosis?
Progressive hearing loss (more so with lower pitched sounds - women are easier to hear, conductive type hearing loss)
Tinnitus
Patient may speak quietly (bone conduction of their voice makes the patient think they are speaking loudly)
Patients in early disease may report improved hearing in noisy surroundings
Family history of hearing loss
Pts presenting before age of 40
Hearing loss in otosclerosis?
Worse with lower pitch/frequency (male voices harder to hear)
Better in noise enviornments (early disease)
Conductive hearing loss with intact sensory hearing so patient experiences their voice being loud compared to the environment (due to bone conduction of their voice) - patients will talk quietly
Examinations and investigations in otosclerosis?
Otoscopy: normal usually, ocassionally Schwatze’s sign (pink hue to tympanic membrane)
Tympanogram: Normal type A trace - reduced admittance of sound as TM is stiff and non compliant and doesn’t absorb sound, reflecting most of it back
Pure tone audiogram: conductive hearing loss, characteristic ‘‘Carhart notch’’ at 2kHz
Weber’s: Localises to worst affected ear but may be normal if even bilateral disease
Rinne’s: Negative - conductive hearing loss - sound easily heard when fork applied to mastoid process (bone conduction > air conduction)
High resolution CT: Can detect bondy changes associated with otosclerosis although not always required
At what frequency is the characteristic ‘‘Carhart notch’’ seen during pure tone audiogram in otosclerosis?
2kHz
What is Schwartze’s sign and when is it seen?
Rare sign in otosclerosis - pink hue to tympanic membrane
Otosclerosis management?
Conservative - hearing aids
Surgical (stapedectomy or stapedotomy) generally scuessful with potential to restore hearing to normal - involves lifting the tympanic membrane and some of the surrounding skin out of the way to access the middle ear through the canal
What are the two types of surgery used to manage otosclerosis and what do they invovle?
STAPEDECTOMY - removal of the entire stapes bone, replacing it with a prosthesis which attacthed to the oval window and hooks around the incus (transmitting sound from incus to choclea the same way the stapes normally would)
STAPEDOTOMY - removal of part of stapes bone and leaving the base (footplate) attatched to the oval window.
A small hole is made in the base of the stapes for the prosthesis to enter, which is added to transmit sound from the incus to cochlea
The inner ear resides in which part of which bone?
Petrous part of the temporal bone
The inner ear consists of a labrynith and canals and can be divided functionally into which two parts?
- The vestibule and semicircular canals.
- The cochlea
Inner ear anatomy: membranous labrynth - what does it contain, what is it surrounded by, what is it suspended in, and what is contained in?
Filled with endolymph
Surrounded by bony labyrinth
Suspended in perilymph
Contained within the bony labyrinth
How does the perilymphatic system (membranous labryinth, endolymph, bony labryinth) communicated with the subarachnoid space and CSF?
The perilymphatic system communicates with the subarachnoid space and CSF via the
cochlear aqueduct
Perilymph fluid resembles CSF, and endolymph fluid resembles
intracellular fluid
What does perilymph fluid in the perilymphatic system resemble?
CSF
What does endolymph in the perilymphatic system resemble?
INtracellular fluid
Features and functions of the cochlea?
Responsible for perception of hearing
- Articulated with oval window causing movement of perilymph and pressure change compensated by the round window
- Vibrations are transmitted through the tectorial membrane
-Low frequency sounds detected at apex (of the cochlea) - High frequency sounds detected at base (of the cochlea)
-Movement of the tectorial membrane causes movement of the hair cells and subsequent depolarization of neuronal fibers - allowing for perception of sound - Transmission of information occurs via the cochlear nerve
- Has 2.5 turns around a bony core- the modiolus
What can the vestibular system be divided into and how does each component detect movement?
Semicircular canals (x3 at 90 degrees to eachother, detect movement in a rotational fashion)
Utricle (detects linear/horizontal movement)
Saccule (detects vertical movement)
(Utricle – Hair cells point Up – Detect linear/horizontal movement
Saccule – Hair cells stick out to the Side – Detect vertical movement)
Central causes of vertigo
Stroke
Migraine
Neoplasms
Demyelination e.g. MS
Drugs
Peripheral causes of vertigo?
BPPV
Menieres disease
Vestibular neuronitis
Pathophysiology of BPPV?
Crystals of calcium carbonate (otoconia) become displaced into the semicircular canals (most often posterior semicircular canal) due to a viral infection, head trauma, ageing or without clear cause
Otoliths (crystals) disrupt the normal flow of endolymph through the canals, causing abnormal stimulation of hair cells giving the hallucination of movement - ie. triggering episodes of vertigo
BPPV presenation?
Attacks of vertigo that settle after around 20-60 seconds
Often episodes occur over several weeks and then resolve but can reoccur weeks or months later
Triggers: lying down, turning head
What exercises can patients perform at home to help BPPV and how do they do them?
BRANDT-DAROFF EXERCISES
Brandt-Daroff exercises can be performed by the patient at home to improve the symptoms of BPPV. These involve sitting on the end of a bed and lying sideways, from one side to the other, while rotating the head slightly to face the ceiling. The exercises are repeated several times a day until symptoms improve.
Peripheral causes of vertigo differentiating symptoms and their management
What is an acoustic neuroma/vestibular schwannoma, how and why might they present?
An acoustic neuroma, also known as a vestibular schwannoma, is a tumour of the vestibulocochlear nerve (cranial nerve VIII).
They are classically benign tumours that are slow-growing but may become symptomatic through local mass effect, and in some cases may be life-threatening if they extend into the cerebellopontine angle, where they behave as a space-occupying lesion and can lead to hydrocephalus.
The most common presentation is unilateral sensorineural hearing loss, with other symptoms including tinnitus, dizziness and balance problems.
With enlarging tumours, compression of local structures may lead to facial paraesthesia/sensory loss, ear pain, ataxia, and in severe cases there may be evidence of raised intracranial pressure (e.g. headache).
How does noise relating hearing loss present
NIHL usually develops after long periods of noise exposure and is usually bilateral in nature.
NIHL typically causes sensorineural hearing loss in both ears.
The ability to perceive higher sound frequencies is lost first, later followed by impairment of lower frequency perception.
Investigations and examinations in noise related hearing loss
Weber’s test does not lateralise if the level of sensorineural loss is equal bilaterally
Rinnes test will confirm that air conduction is greater than bone conduction in both ears (in the absence of conductive hearing loss).
Pure tone audiometry will highlight a bilateral sensorineural hearing loss (i.e. bone and air conduction thresholds in both ears will be above 25dB and within 10 dB of one another).
Normal hearing can be definied as what
Normal hearing can be defined as the ability to detect noises between 0-25dB.
When are abx recommended in AOM?
Antibiotics are generally recommended in patients with AOM If they are:
<6 months of age
6 months to 2 years with bilateral AOM
>2 years or older who
appear toxic
have persistent otalgia for > 48 hours
have temperature > 39 C in the past 48 hours
have bilateral AOM
First line drops for otitis externa
Ofloxacin otic drops are used first-line in both bacterial cases of otitis externa when the tympanic membrane is intact
Clinical features of Ménière’s disease?
Hearing loss (initally fluctuates, associated with vertigo attacks, gradually becomes oermenant, sensorineural, unilateral, low frequencies affected first)
Vertigo
Tinnitus (unilateral)
Aural fullness
Drop attacks (unexplained falls without LOC)
Imbalance which can persist after episodesnresolve
What is MénIères disease and what is the pathophysiology?
Long term inner ear disorder that causes recurrent attacks of vertigo, tinnitus hearing loss and aural fullness.
Excessive build up of ENDOLYMPH in the LABYRINTH of the INNER EAR, causing a higher pressure than normal and disrupting the sensory signal.
This increased pressure of the endolymph is called endolymphatic hydrops.
Ménière’s Disease - disease course
Initially patients are well between attacks
As disease progresses patients may start to develop reduced vestibular function on the side of the disease and a progressive sensioneural hearing loss.
Episodes tend tom come in clusters over several weeks followed by prolonged periods (months) without symtpoms.
Over time the disease often burns itself out so that the patient doesn’t suffer from acute vertigo but will have reduced hearing and maybe generally unbalanced.
If the vestibular system of the other ear is working well this can compensate for the bad ear to improve the overall balance but this can take time especially in the elderly.
How long does vertigo last in Ménière’s disease?
20 minutes to several hours
BPPV vs Ménière’s - history
BPPV: hearing unaffected, vertigo lasts seconds, no associated symptoms except nausea, triggered by movement
Ménèires: hearing loss and tinnitus, lasts up to several hours and no less than 20 mins, aural fullness, drop attacks and persistent imbalance, spontaneous nystagmus NO MOVEMENT OR POSTURAL TRIGGER
Hearing in Ménière’s?
Hearing Initially fluctuates
Hearing loss and tinnitus Associated with vertigo attacks
Hearing loss and tinnitus gradually become permenant
Sensioneural hearing loss
Unilateral
Affecting low frequencies first (male voices worse)
Tinnitus in Ménière’s?
Initial
What neurological sign might you observe during an acute Ménière’s attack?
Spontaneous nystagmus (unidirectional)
Examination and investigations in Ménière’s disease?
Clinical diagnosis made by ENT specialist
Audiology assessment required
Rinnes positive (as sensioneural)
Webers lateralises to unaffected ear
Pure tone audiometry: sensioneural
Electronystagmogram (ENG) to help guide cause of vertigo
MRI/CT head can rule out other causes of vertigo - will not show changes in Ménière’s
How is Ménière’s managed?
Acute attacks (no more than 3 days use):
Prochlorperazine
Antihistamines (cyclizine,cinnarizine and Promethazine)
Prophylaxis of attacks:
Betahistine
Thiazide diuretics e.g. bendrofluazide
Dietary – reduce salt, chocolate, alcohol, caffeine, chinese food
Surgical
o Grommet insertion
o Dexamethasone middle ear injection
o Endolymphatic sac decompression
o Vestibular destruction using middle ear injection of gentamicin
o Surgical labyrinthectomy – very rarely required
Stages of Ménière’s disease and the implications
Stages 1, 2, 3 and 4
1 and 2 are considered early reversible disease susceptible to remission
3 and 4 are considered fixed or not reversible
What age to patients with Ménière’s typically present?
40-50 years old
Presentation of an acoustic neuroma?
The typical patient is aged 40-60 years presenting with a gradual onset of:
Unilateral sensorineural hearing loss (often the first symptom)
Unilateral tinnitus
Dizziness or imbalance
A sensation of fullness in the ear
If tumour grows large enough may be a facial nerve palsy
Acoustic neuromas are usually unilateral, when might they not be?
Bilateral acoustic neuromas almost certainly indicate neurofibromatosis type II.
What are acoustic neuromas and where do they occur?
Acoustic neuromas (vestibular schwannomas) are benign tumours of the Schwann cells (PNS cells providing myelin sheath around neurones) surrounding the auditory nerve (vestibulocochlear nerve) that innervates the inner ear.
They occur at the cerebellopontine angle and are sometimes referred to as cerebellopontine angle tumours.
Investigations in acoustic neuroma?
Audiometry: sensioneural pattern of hearing loss
Brain imagaing (MRI or CT): establish dgx and features of the tumour
Management of acoustic neuroma?
ENT specialist management options include:
Conservative management with monitoring may be used if there are no symptoms or treatment is inappropriate
Surgery to remove the tumour (partial or total removal)
Radiotherapy to reduce the growth
Risks associated with treatment of a vestibular shwannoma/ acoustic neuroma?
Vestibulocochlear nerve injury, with permanent hearing loss or dizziness
Facial nerve injury, with facial weakness
What is vestibular neuronitis?
Vestibular neuronitis describes inflammation of the vestibular nerve. This is usually attributed to a viral infection.
Presentation of vestibular neuronitis?
In this condition inflammation in the inner ear causes
severe incapacitating vertigo lasting
several days
associated with nausea and vomiting.
During an attack patients will have
horizontal nystagmus
but an otherwise normal neurological examination.
Vestibular neuronitis main differentials?
Posterior circulation infarction (neurological signs present)
Labrinythitis (hearing loss present)
In VN no neurological signs (other than horizontal nystagmus) and no hearing loss
Management of vestibular neuronitis?
IV fluids (Patients may need admission if they are becoming dehydrated due to severe nausea and vomiting
For peripheral vertigo, short-term options for managing symptoms include:
Prochlorperazine
Antihistamines (e.g., cyclizine, cinnarizine and promethazine)
(NICE advise that symptomatic treatment can be used for up to 3 days. More extended use may slow down the recovery)
NICE also recommend referral if the symptoms do not improve after 1 week or resolve after 6 weeks, as they may require further investigation or vestibular rehabilitation therapy (VRT) - (Cawthorne-Cooksey exercises)
Prognosis of vestibular neuronitis?
Symptoms are most severe for the first few days, after which they gradually resolve over the following 2-6 weeks. (There is often an associated long term vestibular deficit after the acute episode which can lead to a generalized unsteadiness after the acute episode for a number of weeks while the brain compensates for this)
Benign paroxysmal positional vertigo (BPPV) may develop after vestibular neuronitis.
Pathophysiology of vestibular neuronitits?
Vestibular neuronitis refers to inflammation of the vestibular nerve.
A viral infection may trigger this inflammation.
It distorts the signals travelling from the vestibular system to the brain, confusing the signal required to sense movements of the head.
This results in episodes of vertigo, where the brain thinks the head is moving when it is not.
Cochlea nerve is not affected and hence there is no hearing loss
What are the semicircular canals responsible for detecting?
Rotation of the head
What are the otolith organs (urticle and saccule) responsible for detecting?
Gravity and acceletation
What test can be used to diagnose peripheral causes of vertigo (problems with vestibular system)?
Head impulse test
How is the head impulse test performed?
The head impulse test involves the patient sitting upright and fixing their gaze on the examiner’s nose.
The examiner holds the patient’s head and rapidly jerks it 10-20 degrees in one direction while the patient continues looking at the examiner’s nose.
The head is slowly moved back to the centre before repeating in the opposite direction. Ensure they have no neck pain or pathology before performing the test.
Implications of the results of the head impulse test?
Normal: eyes remain fixed on examiners nose - no problem with vestibular system - either no vertigo or central cause
Abnormal: Eyes will saccade (rapidly move back and forth) and will eventually fix back on examiner - abnormally functioning vestibular system - ie. vestibular neuronititis, labrythitis
What is labyrinthitis and why might it occur?
Labyrinthitis refers to inflammation of the bony labyrinth of the inner ear, including the semicircular canals, vestibule (middle section) and cochlea. The inflammation is usually attributed to a viral upper respiratory tract infection.
Rarely labyrinthitis can be caused by a bacterial infection. This may be an inflammatory response to a nearby infection or the result of bacteria or bacterial toxins entering the labyrinth. It is usually secondary to otitis media or meningitis.
Presentation of labyrinthitis?
(Vestibular neuronititis+hearing loss and tinnitus)
Hearing loss
Tinnitus
Acute onset vertigo
Possible nystagmus
Patients may have symptoms associated with the causative virus, such as a cough, sore throat and blocked nose.
May arise as a compliaction of AOM
How is labyrinthitis diagnosed?
A clinical diagnosis is based on history and examination findings. It is important to exclude a central cause of the vertigo.
The head impulse test can be used to diagnose peripheral causes of vertigo, resulting from problems with the vestibular system (e.g., vestibular neuronitis or labyrinthitis).
Management of labyrinthitis?
Management is the same as with vestibular neuronitis, with supportive care and short-term use (up to 3 days) of medication to suppress the symptoms. Options for managing symptoms are:
Prochlorperazine
Antihistamines (e.g., cyclizine, cinnarizine and promethazine)
Antibiotics are used to treat bacterial labyrinthitis. The underlying infection (e.g., otitis media or meningitis) needs appropriate treatment.
Complications of labyrinthitis?
Patients rarely have lasting symptoms, including permanent hearing impairment. This is more common after bacterial labyrinthitis, particularly associated with meningitis (All patients with meningitis are offered audiology assessment as soon as they are recovered to assess for hearing impairment. )
What is sudden sensorineural hearing loss?
Sudden sensorineural hearing loss (SSNHL) is defined as hearing loss over less than 72 hours, unexplained by other causes. This is considered an otological emergency and requires an immediate referral to the on-call ENT team. The diagnosis is made when someone rapidly loses their hearing, and no conductive cause can be found.
With SSNHL, hearing loss is most often unilateral. It may be permanent or resolve over days to weeks.
Causes of rapid onset CONDUCTIVE hearing loss?
Conductive causes of rapid-onset hearing loss (not classed as SSNHL) include:
Ear wax (or something else blocking the canal)
Infection (e.g., otitis media or otitis externa)
Fluid in the middle ear (effusion)
Eustachian tube dysfunction
Perforated tympanic membrane
Causes of SSNHL?
Most cases (90%) of SSNHL are idiopathic, meaning no specific cause is found.
Other causes of SSNHL include:
Infection (e.g., meningitis, HIV and mumps)
Ménière’s disease
Ototoxic medications
Multiple sclerosis
Migraine
Stroke
Acoustic neuroma
Cogan’s syndrome (a rare autoimmune condition causing inflammation of the eyes and inner ear)
How is SSNHL investigated?
Audiometry is required to establish the diagnosis. A diagnosis of SSNHL requires a loss of at least 30 decibels in three consecutive frequencies on an audiogram.
MRI or CT head may be used if a stroke or acoustic neuroma are being considered.
Criteria for sudden sensorineural hearing loss?
Sensorineural hearing loss over less than 72 hours at least 30 decibels in three consecutive frequeencies on audiogram
Management of SSNHL?
The NICE clinical knowledge summaries (updated September 2019) recommend an immediate referral to ENT for assessment within 24 hours for patients presenting with sudden sensorineural hearing loss presenting within 30 days of onset.
Where an underlying cause is found (e.g., infection), treatment can be directed at this (e.g. antivirals, antibiotics)
Idiopathic SSNHL may be treated with steroids under the guidance of the ENT team. Steroids may be:
Oral
Intra-tympanic (via an injection of steroids through the tympanic membrane)
Other treatments are used e.g. hyperbaric oxygen, carbogen but are not widely
practice
Prognosis of SSNHL?
1/3 recover to normal
1/3 some recovery
1/3 no recovery
What is Presbycusis and it’s pathophysiology?
Age related hearing loss.
Loss of hair cells in the cochlea,
Loss of neurones in the cochlea
Atrophy of the stria vascularis
Endolymphatic potential
Hearing loss in Presbycusis?
Sensorineural
Symmetrical
High pitched sounds lost first (female voices harder to head)
Gradual and insidious
Worse in noisey environments
Presentation of Presbycusis
Sensorineural symmetrical hearing loss, gradual and insidious, loss of high pitched sounds first, harder to hear in noisy environments.
History of ‘not paying attention’ or missing parts of conversations - may be concerns of dementia when the actual issue is hearing loss
May be associated tinnitus
What does use of a hearing aid in Presbycusis reduce the risk of?
Dementia
Risk factors for presbycusis?
Age
Male gender
Family history
Loud noise exposure
Diabetes
Hypertensive
Loud noise exposure
HTN
Ototoxic medications
Smoking
Audiometry in presbycusis?
Sensorineural hearing loss pattern
Normal or near normal hearing at lower frequencies
Worsening hearing loss at higher frequencies
Investigation of choice for presbycusis?
Audiometry
Management of presbycusis?
The effects of presbycusis cannot be reversed.
Management involves supporting the person to maintain normal functioning:
Optimising the environment, for example, reducing the ambient noise during conversations
Hearing aids
Cochlear implants (in patients where hearing aids are not sufficient)
What is cerumen?
Ear wax is also called cerumen.
It is normally produced in small amounts in the external ear canal. It is created from a combination of secretions, dead skin cells and any substances that enter the ear.
Ear wax has a protective effect, helping to prevent infection in the ear canal. In most people, ear wax does not cause any problems.
What problems might impacted ear was cause?
Ear wax can build up and become impacted and stuck to the tympanic membrane. This can result in:
Conductive hearing loss
Discomfort in the ear
A feeling of fullness
Pain
Tinnitus
Impacted ear wax (cerumen)
If earwax is causing problems, how can it be managed?
In most cases, ear wax does not require any interventions. The ears should naturally regulate the amount of wax in the ear canal without any issues.
Inserting cotton buds into the ear should be avoided, as this can press the wax in further and cause impaction.
There are three main methods for removing ear wax:
Ear drops – usually olive oil or sodium bicarbonate 5%
Ear irrigation – squirting water in the ears to clean away the wax
Microsuction – using a tiny suction device to suck out the wax
Ear drops may be enough to clear the ears. If not, ear irrigation can often be performed in primary care. Where there are contraindications to ear irrigation (e.g., perforated tympanic membrane or infection), microsuction can be performed by specialist ear, nose and throat services.
Structures of ear from outside to in
The pinna is the external portion of the ear
The external auditory canal is the tube into the ear
The tympanic membrane is the eardrum
The Eustachian tube connects the middle ear with the throat to equalise pressure
The malleus, incus and stapes are the small bones in the middle ear that connect the tympanic membrane to the structures of the inner ear
The semicircular canals are responsible for sensing head movement (the vestibular system)
The cochlea is responsible for converting the sound vibration into a nervous signal
The vestibulocochlear nerve transmits nerve signals from the semicircular canals and cochlea to the brain
Causes of sensorineural hearing loss
Causes Of Sensorineural Hearing Loss
The causes of adult-onset sensorineural hearing loss are:
Sudden sensorineural hearing loss (over less than 72 hours)
Presbycusis (age-related)
Noise exposure
Ménière’s disease
Labyrinthitis
Acoustic neuroma
Neurological conditions (e.g., stroke, multiple sclerosis or brain tumours)
Infections (e.g., meningitis)
Medications
What medications can cause sensorineural hearing loss?
Loop diuretics (e.g., furosemide)
Aminoglycoside antibiotics (e.g., gentamicin)
Chemotherapy drugs (e.g., cisplatin)
Causes of conductive hearing loss
Ear wax (or something else blocking the canal)
Infection (e.g., otitis media or otitis externa)
Fluid in the middle ear (effusion)
Eustachian tube dysfunction
Perforated tympanic membrane
Otosclerosis
Cholesteatoma
Exostoses
Tumours
What is tinnitus and why does it happen?
Tinnitus refers to a persistent addition sound that is heard but is not present in the surrounding environment. It may be described as a “ringing in the ears”, but it can also be a buzzing, hissing or humming noise.
The additional noise experienced with tinnitus is thought to be the result of a background sensory signal produced by the cochlea that is not effectively filtered out by the central auditory system. In a quiet enough environment, almost everyone will experience some background noise (tinnitus). This becomes more prominent the more attention it is given.
Causes of tinnitus?
Primary tinnitus has no identifiable cause and often occurs with sensorineural hearing loss.
Secondary tinnitus refers to tinnitus with an identifiable cause. Causes include:
Impacted ear wax
Ear infection
Ménière’s disease
Noise exposure
Medications (e.g., loop diuretics, gentamicin and chemotherapy drugs such as cisplatin)
Acoustic neuroma
Multiple sclerosis
Trauma
Depression
Tinnitus may also be associated with systemic conditions:
Anaemia
Diabetes
Hypothyroidism or hyperthyroidism
Hyperlipidaemia
Objective tinnitus refers to when the patient can objectively hear an extra sound within their head. This sound can also be observable on examination by auscultating with a stethoscope around the ear. Actual additional sounds may be caused by:
Carotid artery stenosis (pulsatile carotid bruit)
Aortic stenosis (radiating pulsatile murmur sounds)
Arteriovenous malformations (pulsatile)
Eustachian tube dysfunction (popping or clicking noises)
Tinnitus: history and investigations
Ask about the pattern of symptoms:
Unilateral or bilateral
Frequency and duration
Severity
Pulsatile or non-pulsatile (pulsatile may indicate a cardiovascular cause, such as carotid artery stenosis with a bruit)
A focused history and examination can be used to identify any underlying causes, including:
Contributing factors, such as hearing loss or noise exposure
Associated symptoms (e.g., hearing loss, vertigo, pain or discharge)
Stress and anxiety
Otoscopy to look for causes such as ear wax or infection
Weber’s and Rinne’s tests for hearing loss
How might you investigate tinnitus?
The NICE clinical knowledge summaries (updated March 2020) suggest considering blood tests for possible underlying causes:
Full blood count (anaemia)
Glucose (diabetes)
TSH (thyroid disorders)
Lipids (hyperlipidaemia)
Audiology can be used to assess the hearing in detail and help establish the underlying cause.
Imaging (e.g., CT or MRI) may be rarely required to investigate for underlying causes such as vascular malformations or acoustic neuromas.
Red flags that could indicate a serious underlying cause and the need for specialist assessment in a patient presenting with tinnitus?
Unilateral tinnitus
Pulsatile tinnitus
Hyperacusis (hypersensitivity, pain or distress with environmental sounds)
Associated unilateral hearing loss
Associated sudden onset hearing loss
Associated vertigo or dizziness
Headaches or visual symptoms
Associated neurological symptoms or signs (e.g., facial nerve palsy or signs of stroke)
Suicidal ideation related to the tinnitus
Management of tinnitus?
Tinnitus tends to improve or resolve over time without any interventions.
Underlying causes of tinnitus can be treated, such as impacted ear wax or infection.
Several measures can be used to help improve and manage symptoms:
Hearing aids
Sound therapy (adding background noise to mask the tinnitus)
Cognitive behavioural therapy
Causes of peripheral vertigo?
BPPV
Meniere’s disease
Labyrinthitis
Acute vestibular neuronitis
Trauma to the vestibular nerve
Vestibular nerve tumours (acoustic neuromas)
Otosclerosis
Hyperviscosity syndromes
Varicella zoster infection (often with facial nerve weakness and vesicles around the ear – Ramsay Hunt syndrome)
Causes of central vertigo?
Posterior circulation infarction (stroke)
Tumour
Multiple sclerosis
Vestibular migraine
Clues that vertigo has central etiology as opposed to peripheral?
All the central causes of vertigo will cause sustained, non-positional vertigo.
Posterior circulation infarction will have a sudden onset and may be associated with other symptoms, such as ataxia, diplopia, cranial nerve defects or limb symptoms.
Tumours in the cerebellum or brainstem will have a gradual onset with associated symptoms of cerebellar or brainstem dysfunction.
Multiple sclerosis may cause relapsing and remitting symptoms, with other associated features of multiple sclerosis, such as optic neuritis or transverse myelitis.
Vestibular migraine will cause symptoms lasting minutes to hours, often associated with visual aura and headache. Attacks may be triggered
Potential triggers of vestibular migraine?
Vestibular migraine will cause symptoms lasting minutes to hours, often associated with visual aura and headache. Attacks may be triggered by:
Stress
Bright lights
Strong smells
Certain foods (e.g. chocolate, cheese and caffeine)
Dehydration
Menstruation
Abnormal sleep patterns
Peripheral vs. central vertigo: onset
Peripheral: Sudden onset
Central: Gradual onset (except stroke)
Peripheral vs. central vertigo: duration
Peripheral: Short (seconds or minutes)
Central: Persistent
Peripheral vs. central vertigo: hearing loss or tinnitus?
Peripheral: often present
Central: Usually not
Peripheral vs. central vertigo: coordination
Peripheral: intact
Central: lost
Peripheral vs. central vertigo: nausea?
Peripheral: severe
Central: mild
What should be examined when a patient presents with vertigo?
Ear examination to look for signs of infection or other pathology
Neurological examination to assess for central causes of vertigo (e.g., stroke or multiple sclerosis)
Cerebellar examination
Cardiovascular examination to assess for cardiovascular causes of dizziness (e.g., arrhythmias or valve disease)
Special tests:
Romberg’s test (screens for problems with proprioception or vestibular function)
Dix-Hallpike manoeuvre (to diagnose BPPV)
HINTS examination (to distinguish between central and peripheral vertigo)
What is the HINTs examination?
The HINTS examination can be used to distinguish between central and peripheral vertigo. It stands for:
HI – Head Impulse
N – Nystagmus
TS – Test of Skew
Nystagmus: central vs peripheral vertigo?
Unilateral horizontal nystagmus is more likely to be a peripheral cause. Bilateral or vertical nystagmus suggests a central cause.
What is the role of the ET tube and what happens when it is dysfunctional?
Eustachian tube dysfunction is when the tube between the middle ear and throat is not functioning properly. The Eustachian tube is present mainly to equalise the air pressure in the middle ear and drain fluid from the middle ear.
When the Eustachian tube is not functioning correctly or becomes blocked, the air pressure cannot equalise properly and fluid cannot drain freely from the middle ear.
The air pressure between the middle ear and the environment can become unequal.
The middle ear can fill with fluid.
Eustachian tube dysfunction may be related to a viral upper respiratory tract infection (URTI), allergies (e.g., hayfever) or smoking.
Presentation of ET tube dysfunction?
Reduced or altered hearing
Popping noises/sensation within the ear
A fullness sensation within the ear
Pain or discomfort
Exacerbation of symptoms when the external air pressure changes and the middle ear pressure cannot equalize to the outside pressure - for example when scuba diving, flying in an earoplane
Why is ET tube dysfunction not routinely investigated unless there are persistent, problematic severe symptoms (to establish the diagnosis and cause)?
Often Eustachian tube dysfunction gives a typical set of symptoms and is associated with a clear cause, for example, a recent viral upper respiratory tract infection or hayfever. In this situation, investigations are not required as the symptoms will resolve with time or simple treatments.
In Eustation Tube dysfunction is persistent, problematic or severe symptoms, investigations to help establish the diagnosis and cause include what?
Tympanometry
Audiometry
Nasopharyngoscopy (inspect the ET tube openings)
CT scan (asses for structural pathology)
What does tympanometry involve?
Measurement of compliance of TM, can be done at any age as minimal complience required from patient (small probe in ear only)
A device is inserted into the external auditory canal, creating different ear pressures within the canal
Sound is sent in the direction of the tympanic membrane
The amount of sound reflected back off the tympanic membrane is measured
A tympanogram of the sound absorbed (admittance) is plotted at different air pressures
What is meant by ‘admittance’ in terms of tympanometry?
The amount of sound absorbed by the TM and middle ear (measured at various ear pressures)
Tympanometry - normal
Normally, sound is absorbed best when the air pressure in the ear canal matches the ambient air pressure. The ambient air pressure is equal to the middle ear pressure in healthy ears.
Tympanometry in ET tube dysfunction?
Peak admittance at negative ear canal pressures
This is because the air pressure is lower in the middle ear than the ambient air pressure (new air cannot get through TM to equalise the pressures)
Management of ET tube dysfunction?
None - wait for it to resolve spontaneously - e.g. recovering from URTI
Valsalva maneuverer (holding nose and blowing into it to inflate the ET tube).
Decongestant nasal sprays (short term only)
Antihistamines and a steroid nasal spray (short term only)
Antihistamines - steroid nasal spray for allergies or rhinitis
Sugery may be required in severe or persistent cases
Otovent - OTC device where the patient blows into a balloon which can help inflate the ET tube, clear blockages and equalize pressure
Surgical management of ET tube dysfunction?
Treatment of other pathology that might cause symptoms, for example, adenoidectomy
Grommets (tubes inserted into TM by ENT surgeon allowing air or fluid to drain through the ear canal, fall out typically within about 18 months)
Under local
Balloon dilation ET tuboplasty involves insetring a deflated balloon into the ET tube for a short period of time (a2 mins) to stretch the ET tube, then deflating and removing it, Under GA
What are the potential complications of ET tube dysfunction
Recurrence
Chronic otitis media, a middle ear infection
Otitis media with effusion, or “glue ear,” a fluid buildup in the middle ear that can last for weeks and could damage hearing
Eardrum retraction, when the eardrum is seemingly sucked farther into the ear canal
Risk factors for ET tube dysfunction
Cleft pallette
Nasal polyps
Smoking (damage to cilia)
Obesity (fatty deposits can form around the Eustachian tubes, leading to dysfunction)
Allergies (frequent episodes of mucus production and congestion)
Down syndrome
Young children - 1 - 6 years (narrower ET tube)
What does audiometry involve?
Testing a patients hearing by playing a variety of tones and volumes using headphones (air conduction) and an oscillator (conduction device) .
Audiometry results are recorded on an audiogram. Audiograms can help identify and differentiate conductive and sensorineural hearing loss.
Components of an audiogram
Chart documenting the volume at which patients can hear differnt tones
x axis: frequency/Hz
y axis: volume/decebils (quitest volume that can be heard at given frequency) (gets lower going upwards)
Plotting in an audiogram?
X - left sided air conduction
] - left sided bone conduction
O - right sided air conduction
[ - right sided bone conduction
Sensorineural hearing loss on audogram?
In patients with sensorineural hearing loss, both air and bone conduction readings will be more than 20 dB, plotted below the 20 dB line on the chart. This may affect only one side, one side more than the other or both sides equally.
Conductive hearing loss on audiogram?
In patients with conductive hearing loss, bone conduction readings will be normal (between 0 and 20 dB). However, air conduction readings will be greater than 20 dB, plotted below the 20 dB line on the chart. In conductive hearing loss, sound can travel through bone but is not conducted through air due to pathology along the route into the ear.
Normal hearing on audiogram
When a patient has normal hearing, all readings will be between 0 and 20 dB, at the top of the chart.
Normal audiogram
Conductive hearin loss
Sensorineural hearing loss
Mixed hearing loss - audiogram
Both air and bone conduction readings will be more than 20 dB in patients with mixed hearing loss. However, there will be a difference of more than 15 dB between the two (bone conduction > air conduction).
Both air and bone conduction readings will be more than 20 dB in patients with mixed hearing loss. However, there will be a difference of more than 15 dB between the two (bone conduction > air conduction).
Common causes of congenital hearing loss?
Maternal rubella or cytomegalovirus infection during pregnancy
Genetic deafness can be autosomal recessive or autosomal dominant
Associated syndromes, for example Down’s syndrome
Perinatal causes of hearing loss?
Prematurity
Hypoxia during or after birth
Causes of childhood hearing loss that are neither perinatal nor congenital causes?
Jaundice
Meningitis and encephalitis
Otitis media or glue ear
Chemotherapy
How is hearing tested in neonates?
The UK newborn hearing screening programme (NHSP) tests hearing in all neonates. This involves special equipment that delivers sound to each eardrum individually and checks for a response. This can identify congenital hearing problems early.
How might children with hearing loss present?
Children with hearing difficulties may present with parental concerns about hearing or with behavioural changes associated with not being able to hear:
Ignoring calls or sounds
Frustration or bad behaviour
Poor speech and language development
Poor school performance
How is hearing loss assessed in children?
NHSP - neonates - special equiptment that delivers sound to each eardrum and checks for a response
Looking for basic turning towards a sound - children under 3
Audiometry - headphones at specific tones and volumes
Management of childhood hearing loss?
Establishing the diagnosis is the first step. After the diagnosis is established, input from the multidisciplinary team is required for support with hearing, speech, language and learning:
Speech and language therapy
Educational psychology
ENT specialist
Hearing aids for children who retain some hearing
Sign language
What is a compliance peak in a tympanogram?
The point at which pressure in the canal equals that of the middle ear
Type A tympanogram trace?
Normal result
Peak centred on 0 daPa on x axis
Type A Tympanogram (normal, peak centred at 0daPa on x axis)
Type B tympanogram
Flat tracing
Suggests middle ear effusion or perforation
How can you differentiate between effusion and perforation on tympanogram?
Both type b (flat line)
Effusion: normal canal volume (around 1cm3 in adults)
Perforation: Larger volume measure as both middle and external ear volume
Type B tympanogram
Type C tympanogram
Suggests ET tube dysfunction
The peak of the tracing has negative pressure
Triggers of nosebleeds
Nosebleeds are common in young children and older adults. They can be triggered by:
Nose picking
Colds
Sinusitis
Vigorous nose-blowing
Trauma
Changes in the weather
Coagulation disorders (e.g., thrombocytopenia or Von Willebrand disease)
Anticoagulant medication (e.g., aspirin, DOACs or warfarin)
Snorting cocaine
Tumours (e.g., squamous cell carcinoma)
When a patient swallows blood during a nosebleed, they may present with vomiting blood.
Bleeding is usually unilateral. Bleeding from both nostrils may indicate bleeding posteriorly in the nose. Posterior bleeding presents a higher risk of aspiration of blood.
Management of nosebleed under 10-15 mins
Sit up and tilt the head forwards (tilting the head backwards is not advised as blood will flow towards the airway)
Squeeze the soft part of the nostrils together for 10 – 15 minutes
Spit out any blood in the mouth, rather than swallowing
Management of nosebleed in cases of 10-15 mins, bilateral bleeds, hemodynamic instability?
Nasal packing using nasal tampons or inflatable packs
Nasal cautery using silver nitrate sticks
After treating an acute nosebleed, consider prescribing Naseptin nasal cream (chlorhexidine and neomycin) four times daily for 10 days to reduce any crusting, inflammation and infection. This is contraindicated in peanut or soya allergy.
What should you consider in recurrent or severe nosebleeds?
Recurrent and significant nosebleeds might require further investigation to look for an underlying cause, such as thrombocytopenia or clotting disorders.
What is sinusitis?
Sinusitis refers to inflammation of the paranasal sinuses in the face. This is usually accompanied by inflammation of the nasal cavity and can be referred to as rhinosinusitis. It is very common.
Sinusitis can be:
Acute (less than 12 weeks)
Chronic (more than 12 weeks)
What are the four sets of paranasal sinuses?
Frontal sinuses (above the eyebrows)
Maxillary sinuses (either side of the nose below the eyes)
Ethmoid sinuses (in the ethmoid bone in the middle of the nasal cavity)
Sphenoid sinuses (in the sphenoid bone at the back of the nasal cavity)
What are the paranasal sinuses and how can sinusitis occur?
The paranasal sinuses are hollow spaces within the bones of the face
Arranged symmetrically around the nasal cavity
Produce mucous and drain into the nasal cavities via ostia (holes)
Blockage of the ostia prevents drainage of the sinuses, resulting in sinusitis
Causes of sinusitis?
Inflammation of the sinuses can be caused by:
Infection, particularly following viral upper respiratory tract infections
Allergies, such as hayfever (with allergic rhinitis)
Obstruction of drainage, for example, due to a foreign body, trauma or polyps
Smoking
Patients with asthma are more likely to suffer from sinusitis.
Typical presentation of acute sinusitis?
The typical presentation of acute sinusitis is someone with a recent viral upper respiratory tract infection presenting with:
Nasal congestion
Nasal discharge
Facial pain or headache
Facial pressure
Facial swelling over the affected areas
Loss of smell
What might chronic sinusitis be associated with?
Nasal polyps
What might examination reveal in a patient with acute sinusitis?
Tenderness to palpation of the affected areas
Inflammation and oedema of the nasal mucosa
Discharge
Fever
Other signs of systemic infection (e.g., tachycardia)
In sinusitis investigation is rarely necessary, what might you do if patients have persistent symptoms despite treatment?
Nasal endoscopy
CT scan
When patients with acute sinusitis symptoms persisting past 10 days, what options does nice reccomend?
High dose steroid nasal spray for 14 days (e.g., mometasone 200 mcg twice daily)
A delayed antibiotic prescription, used if worsening or not improving within 7 days (phenoxymethylpenicillin first-line)
Management of chronic sinusitis?
Options for chronic sinusitis are:
Saline nasal irrigation
Steroid nasal sprays or drops (e.g., mometasone or fluticasone)
Functional endoscopic sinus surgery (FESS)
How should patients be instructed to use steroid nasal spray?
Tilting the head slightly forward
Using the left hand to spray into the right nostril, and vice versa (this directs the spray slightly away from the septum)
NOT sniffing hard during the spray
Very gently inhaling through the nose after the spray
If a patient can ‘taste the spray at the back of their throat’ when using steroid nasal spray, what odes this suggest?
Spray has gone past the nasal mucosa
It will be ineffective
What is Functional Endoscopic Sinus Surgery?
Functional endoscopic sinus surgery (FESS) involves using a small endoscope inserted through the nostrils and sinuses.
Instruments are used to remove or correct any obstructions to the sinues.
Obstruction may be cause by swollen mucosa, bone, polyps or a deviated septum.
Balloons may be inflated to dilate the opening of the sinuses.
Patients need a CT scan before the procedure to confirm the diagnosis and assess the structures?
What surgery is used to correct a deviated septum?
Septoplasty
What are nasal polyps?
Nasal polyps are growth of the nasal mucosa that can occur in the nasal cavity or sinuses.
They are often associated with inflammation (chronic rhinitis)
They grow slowly and gradually obstruct the nasal passage
Polyps are usually bilateral
What makes unilateral nasal polyps concerning?
unilateral polyps are concerning for malignancy and require a specialist referral for assessment
What conditions are associated with nasal polyps?
Chronic rhinitis or sinusitis
Asthma
Samter’s triad (nasal polyps, asthma and aspirin intolerance/allergy)
Cystic fibrosis
Eosinophillic granulomatosis with polyangitis (Chrug-Strauss syndrome)
How might nasal polyps present?
Chronic rhinosinusitis
Difficulty breathing through the nose
Snoring
Nasal discharge
Loss of sense of smell (anosmia)
How can you examine nasal polyps?
Nasal speculum - hold the nostrils open
Otoscope with large speculum
Nasal endoscopy to visualize the cavity in detail to assess any polyps
What do nasal polyps look like?
Nasal polyps appear as round pale grey/yellow growths on the mucosal wall.
Nasal polyp
Management of nasal polyps?
Unilateral polyps should be referred for specialist assessment to exclude malignancy.
Medical management involves intranasal topical steroid drops or spray.
Surgical management is used where medical treatment fails. This involves removing the polyps:
Intranasal polypectomy is used where the polyps are visible close to the nostrils
Endoscopic nasal polypectomy is used where the polyps are further in the nose or the sinuses
What is obstructive sleep apnoea?
Obstructive sleep apnoea is caused by collapse of the pharyngeal airway. It is characterised by episodes of apnoea during sleep, where the person stops breathing periodically for up to a few minutes. The partner usually reports this happening, and the patient is unaware of the episodes.
Risk factors for sleep apnoea?
Middle age
Male
Obesity
Alcohol
Smoking
Feature of sleep apnea
Episodes of apnoea during sleep (reported by their partner)
Snoring
Morning headache
Waking up unrefreshed from sleep
Daytime sleepiness
Concentration problems
Reduced oxygen saturation during sleep
Severe cases can cause hypertension, heart failure and can increase the risk of myocardial infarction and stroke.
What can be used to asses the symptoms of sleepiness associated with obstructive sleep apnoea?
Epworth sleepiness scale
Management of sleep apnoea?
Sleep studies under sleep clinic (measuring sats, HR, respiratory rate and breathing to establish any episodes of apnoea and the extent of pts snoring)
Address risk patients (drinking alcohol, stop smoking and lose weight)
CPAP to maintain patency of the airway using continous pressure
Surgery - uvulopalatopharyngoplasty (UPPP) to reconstruct the soft palate and jaw, children –adenotonsillectomy
Mandibular positioning devices in selected cases
Bones and cartillage of the nose and blood supply
Quadrangular cartillage
Ethmoid
Vomer
Anterior ethmoidal, posterior ethmoidal, septal branches of the spheno-palatine, branch of greater palatine, Little’s area , septal branch of superior labial
Local causes of epistaxis?
Local
Idiopathic – 85%
Traumatic
Iatrogenic
Foreign Body
Inflammatory – Rhinitis, Polyps
Neoplastic
Systemic causes of nosebleeds
Hypertension
Coagulopathies
Vasculopathies
Hereditary Haemorrhagic Telangiectasia/Osler-Weber-Rendu disease
Which should be tried first in management of epistaxis- packing or cautery?
Cautery, then anterior packing, then posterior packing (if continues to bleed into the oropharynx
How should cautery be performed as per source of epistaxis?
Anterior bleed: anterior rhinoscopy
Posterior bleed - rigid endoscope
(Topical adrenaline may also help to control the bleed)
Potential complications of nasal bone fracture (often as a result of assult, sports, falls, RTC)
Septal hematoma
CSF leak associated with skull base fracture (rare)
Management of nasal trauma
ABC – epistaxis normally self-limiting
Examine for septal haematoma
No XR required
If deviated nose consider Manipulation under anaesthetic (LA/GA) within 2
weeks of injury
Paranasal sinus anatomy
Structures of importance: lamina papracea forming the medial wall of the orbit, anterior cranial fossa, internal catorid artery
The sites of drainage of the paranasal sinuses?
Sphenoid sinus: spheno-ethmoidal recess
Posterior ethmoid cells: superior meatus
Frontal, maxillary and anterior ethmoid cells: Middle meatus
Nasolacrimal duct: inferior meatus
Potential complications related to the sinuses?
Surgery
Damage to orbit (orbit lies lateral to the ethmoid sinus and superior to the maxillary sinus and its contents are at risk during sinus surgery and in severe cases can cause loss of sight.
Anterior skull base - lies just above the sphenoid and ethmoid sinuses and can be breached during surgery which can cause as CSF leak and even brain damage
Rhinosinusitis:
Orbit - infective rhinosinusitis can spread to the orbit and cause periobrital sinusitis (can be sight threatneing)
Intracranial infection - infective rhinosisitus particularly of the frontal sinuse can spread intracranially to cause menigitis and intracranial abcsess formation
DEFINITION of rhinosinusitis (ie. required criteria)?
Inflammation of the nose and the paranasal sinuses characterised by TWO or more symptoms, one of which should be:
- Nasal blockage/obstruction/congestion or discharge
- Anterior/posterior nasal drip
- Facial pain/pressure
- Reduction or loss of smell
And either of:
- Endoscopic signs of: polyps, mucopurulent discharge or oedema in the middle meatus
- CT changes - mucosal changes within the osteomeatal complex or sinuses
After how long might you consider nasal steroids and oral antibiotics in acute rhinosinusitis?
5 days
Predisposing factors for rhinosinusitis?
Allergy: atopy can predispose and associated
Infections: Bacterial such as Staph aureus and streptococcus pneumonia and fungal infections
Cillary impairment such as CF due to inability of cilia to clear mucus. Nasal polyps are present in about 40% of patients with cystic fibrosis.
An anatomical abnormality such as spetal deviation and abnormal uncinate process leads to narrow infundibulum and occlusion of osteomeatal complex
Immunocompromised host
Aspirin hypersentivity
Atmostpheric irritants: smoking, dusts, fumes
Hormonal: pregnancy and hypothroidism, nasal congestion is high due to oestrogen and progesterone effect on nasal mucosal vascularity
Trauma: surgical (oroantral fistula), nasal sinus fracture
Swimming and diving
How might you investigate CRS?
Skin prick test
Radiology
o CT Sinuses
If surgery planned / Atypical features to history or examination ( Not good for diagnosis as large numbers of asymptomatic patients have changes in the sinuses on CT scanning )
What is ARIA in terms of sinusitis
Allergic rhinosinusitis impact on asthma (classification of allergic rhinosinusitis)
Duration: intermittent (less than 4 days a week less than 4 weeks), persistent (more than 4 days a week for more than 4 weeks)
Severity
Mild: normal daily activities, and sleep. No troublesome symptoms
Moderate to severe: Impairment of daily activities and sleep. Troublesomesymptoms.
Investigating allergic rhinosinusitis?
Skin prick tests (SPT) for specific allergens
RAST blood tests if SPT not possible
How does allergic rhinosinusitis cause symptoms?
Type 1 hypersensitivity reaction
Allergic reaction leads to synthesis and release of arachidonic acid metabolites (prostaglandin D& leukotrienes) and mast cell degranulation to release histamine. The effect is to increase capillary permeability which leads to congestion, oedema, rhinorrhoea, sneezing and irritation
Management of allergic rhinosinusitis?
Conservative
o Allergen avoidance
o Nasal douching
Medical
o Antihistamines
o Topical nasal steroids
Immunotherapy
Peri - orbital cellulitis and odema
This is a site-threatening emergency which is more common in children and often results from direct spread of pus from the ethmoid sinus, or from thrombophlebitis of mucosal vessels in any of the sinuses.
Patients develop pain followed by oedema of the eyelids and with orbital collection, the eye will become proptosed and eye movements will be reduced.
There is a risk of blindness as a result of tension and septic necrosis of the optic nerve.
Colour blindness is an early sign.
A CT scan will confirm the collection and extent of the disease.
Treatment with intravenous antibiotics, nasal decongestants, and urgent surgical drainage of any abscess is indicate
How might a septal haematoma present?
Post traumatic
Palpable buldging septum
Can detect on anterior rhinoscopy
What causes ‘saddle nose deformity’ (obvious step in nose)
Nasal septal haematoma left untreated leading to erosion of the septal cartillage
What recreational drug s commonly implicated in nasal septal defects and what is its method of damage?
Cocaine
Disruption of blood supply to the cartillage
What should be done if a patient with epistaxis controlled by packing starts to spit up blood/.
Use tounge depressor and torch to visualise the oropharynx wall, if fresh blood is running down it remove anterior pack and post nasal pack or inflate nasopharangeal balloon followed by further anterior nasal packign
How is a patient with epistaxis managed if packing and cautery of the bleeding vessels were to fail?
GA to cauterise bleeding point/pack more effectively/ ligate sphenopalaetine and possibly anterior ethmoidal artery
Identify labled structures of the neck
Trachea
Eosophagous
Carotid sheath
Spine
Boundaries of the anterior triangle of the neck
Lateral - Anterior boarder of the SCM (sternocleidomastoid)
Medial - midline of neck
Superior - Lower border of the mandible
Boundaries of the posterior triangle of the neck?
Medial: posterior boarder of sternocleidomastoid
Inferior: middle third of clavicle
Lateral: anterior edge of the trapezius
Sub triangles of the neck?
Submental
Supraclavicular
Occipital
Carotid
Supramandibular (digastric)
Omotracheal (muscular)
How is retropharyngeal abscess investigated?
CT neck
Associated mortality in retropharyngeal abscess
Airway problems
Mediastinitis
What is the retropharyngeal space?
Potential space behind the pharynx and anterior to the prevertable fascia extending from the base of the skull to the mediastinum.
Retropharyngeal abscess
What’s Ludwing’s Angina?
Infection of the space between the FLOOR OF THE MOUTH and MYLOHYOID - associated with dental infection
Presentation of Ludwig’s angina?
Swelling of the floor of the mouth
Painful mouth
Protuding tongue
Airway compromise
Drooling
How might you investigate Ludwig’s angina?
CT neck
OPG
Management of Ludwig’s angina?
Secure airway
IV abx
Surgical drainage of any collections
What is the parapharyngeal space?
Potential space postero-lateral to the oropharynx and nasopharynx which is divided by the styloid process.
Contains carotid sheath
What is a parapharyngeal abscess?
Abcess in parapharyngeal space (potential space postero-lateral to the oropharynx and nasopharynx which is divided by the styloid process)
Presents ins a similar manner to quinsy (peritonsillar abscess)
How might a parapharyngeal abscess present?
Hx febrile illness
Odynophagia
Tismus
Reduced neck movement
Swelling in the neck around the upper part of the SCM
Management of parapharyngeal abscess
Secure airway if any concerns
IV abx
Surgical drainage
Management of epiglottitis
Do not examine patient as this may precipitate airway obstruction and keep them in a calm environment with their parents to avoid undue distress (ditto)
If possible, child taken to theatre to be intubated by a pediatric anesthetist with an ENT surgeon on standby to do a surgical airway if intubation not possible, if transfer unsafe intubation in A&E
IV abx, pts usually respond well and can be intubated after a couple of days
How should neck lumps be investigated?
Ultrasound guided fine needle aspiration (except for pulsitile masses)
What might cause a neck lump and where?
Parotid neoplasam - anterior to ear
Jugulodiagastric - angle of mandible
Submandibular gland - inferior border of madnible
Carotid body tumor or aneurysm - at bifurcation of common carotid artery (usually C3-C5 level)
Thryoglossal cysts - in midline between hyoid bone and thyroid gland
Brachial cyst - anterior border of sternocleidomastoid
Thyroid nodule - level of thryoid
Virchow’s node - supravicular fossa node (may represent mets)
Regions of the pharynx and oral cavity?
Oral cavity – Extends from the lips to the posterior soft palate.
Nasopharynx – Superiorly bound by the base of the skull, and inferiorly by an imaginary line at the level of the soft palate
o Contents include the adenoids and eustachian tube opening
Oropharynx – Extends from the level of the soft palate to the superior border of the epiglottis
o Contents include the palatine tonsils, anterior and posterior tonsillar
pillars
Hypopharynx – Extends down from the superior border of the epiglottis to the inferior border of the cricoid cartilage. It is posterior to the larynx.
Muscle of the pharynx vs rest of the GI tract
Unlike the rest of the GI tract where the muscular layers are arranged in circular and longitudinal layers, the pharynx has only a circular layer which is formed in principle by four muscles;
Superior, middle, and inferior constrictors, and cricopharyngeus
What is s Killian’s dehiscence?
Pharyngeal weak point formed between the horizontal fibers of the cricopharyngeus (CP) muscle and the oblique fibers of the inferior pharyngeal constrictors (IPCs)
This is the site of pharyngeal pouch formation
How does a pharyngeal pouch present?
Pharyngeal pouches typically present with dysphagia, delayed regurgitation of food and sometimes recurrent chest infections from aspirated food.
Where do pharyngeal pouches occur?
Killian’s triangle (pharyngeal weak point formed between the horizontal fibers of the cricopharyngeus (CP) muscle and the oblique fibers of the inferior pharyngeal constrictors (IPCs)) - also known as Killian’s dehiscence.
Muscles of the pharynx responsible for its elevation and depression?
stylopharyngeus, salpingopharyngeus, and palatopharyngeus.
What imagaing is this and what does it show?
Barium swallow
Pharangeal pouch
What is the most common cause of sleep apnoea in children (VS obesity in adults)
adenotonsillar hypertrophy
What bloods might you perform when investigating sleep apnoea and why
TFTs - ?hypothyroidism
Why might ECG and CXR be warrented in possible sleep apnoea?
CXR – ?Signs of obstructive lung disease
ECG – ?Signs of right ventricular failure
Bacterial causes of tonsilitis?
Beta-haemolytic Streptococci
Staphylococci
Streptococcus pneumoniae
Haemophilus influenza
Escherischia coli
Viral causes of tonsilitis?
Rhinovirus
Adenovirus
Enterovirus
Epstein-Barr virus (EBV)
Most common cause of bacterial tonisilitis?
group A streptococcus (Streptococcus pyogenes).
Clinical features of tonsilitis?
Pyrexia > 38
Dysphagia
Lymphadenopathy (anterior cervical lymphadenopathy)
Odynophagia
Trismus
Swollen tonsils with or without exudate
Otalgia (Referred pain)
Lymphadenopathy in tonsilitis?
There may be anterior cervical lymphadenopathy, which refers to swollen, tender lymph nodes in the anterior triangle of the neck (anterior to the sternocleidomastoid muscle and below the mandible).
The tonsillar lymph nodes are just behind the angle of the mandible (jawbone).
Why should amoxicillin be avoided in tonsilitis?
Treatment with amoxicillin should be avoided as this will cause a maculopapular rash in
the presence of EBV (glandular fever). Furthermore, patients with EBV should be advised
to avoid contact sports for 2-3 months as the virus commonly causes
hepatosplenomegaly.
Waldeyer’s Tonsillar Ring
In the pharynx, at the back of the throat, there is a ring of lymphoid tissue. There are six areas of lymphoid tissue in Waldeyer’s ring, comprising of the adenoids, tubal tonsils, palatine tonsils and the lingual tonsil. The palatine tonsils are the ones typically infected and enlarged in tonsillitis. These are the tonsils on either side at the back of the throat.
What is the centor criteria?
The Centor criteria can be used to estimate the probability that tonsillitis is due to bacterial infection and will benefit from antibiotics.
A score of 3 or more gives a 40 – 60 % probability of bacterial tonsillitis, and it is appropriate to offer antibiotics. A point is given if each of the following features are present:
Fever over 38ºC
Tonsillar exudates
Absence of cough
Tender anterior cervical lymph nodes (lymphadenopathy)
What is the FeverPAIN score?
The FeverPAIN score is an alternative to the Centor criteria.
A score of 2 – 3 gives a 34 – 40% probability, and 4 – 5 gives a 62 – 65% probability of bacterial tonsillitis:
Fever during previous 24 hours
P – Purulence (pus on tonsils)
A – Attended within 3 days of the onset of symptoms
I – Inflamed tonsils (severely inflamed)
N – No cough or coryza
Management of tonsilitis?
Consider admission if the patient is immunocompromised, systemically unwell, dehydrated, has stridor, respiratory distress or evidence of a peritonsillar abscess or cellulitis.
When tonsillitis is the most likely diagnosis, calculate the Centor criteria or FeverPAIN score.
Educate patients with likely viral tonsillitis and give safety net advice about when to seek medical advice. Advise simple analgesia with paracetamol and ibuprofen to control pain and fever. NICE clinical knowledge summaries suggest advising patients to return if the pain has not settled after 3 days or the fever rises above 38.3ºC. Starting antibiotics or an alternative diagnosis should be considered.
Consider prescribing antibiotics if the Centor score is ≥ 3, or the FeverPAIN score is ≥ 4. Also, consider antibiotics if they are at risk of more severe infections, such as young infants, immunocompromised patients or those with significant co-morbidity, or a history of rheumatic fever.
Delayed prescriptions can be considered. This involves educating patients or parents about the likely viral nature of the sore throat and providing a prescription to be collected only if the symptoms worsen or do not improve in the next 2 – 3 days.
Draining of peritonsilar abcsess
What antibiotic is used to treat tonsilitis
Penicillin V (also called phenoxymethylpenicillin) for a 10-day course is typically first-line. It has a relatively narrow spectrum of activity and is effective against Streptococcus pyogenes.
Clarithromycin is the usual first-line choice in true penicillin allergy.
Complications of tonsilitis?
Peritonsillar abscess, also known as quinsy
Otitis media, if the infection spreads to the inner ear
Scarlet fever
Rheumatic fever
Post-streptococcal glomerulonephritis
Post-streptococcal reactive arthritis
Quinsy (peritonsilar abscess)
What is quinsy?
Peritonsilar abscess
These normally present with a sore throat that is lateralised to one side and a “hot
potato” voice.
They may be amenable to drainage under local anaesthetic
Peritonsillar abscess arises when there is a bacterial infection with trapped pus, forming an abscess in the region of the tonsils.
Peritonsillar abscess is a complication of untreated or partially treated tonsillitis, although it can arise without tonsillitis.
Quinsy can occur just as frequently in teenagers and adults as it does in children, unlike tonsillitis which is much more common in children.
Presentation of quinsy?
Patients present with similar symptoms to tonsillitis:
Sore throat
Painful swallowing
Fever
Neck pain
Referred ear pain
Swollen tender lymph nodes
Additional symptoms that can indicate a peritonsillar abscess include:
Trismus, which refers to when the patient is unable to open their mouth
Change in voice due to the pharyngeal swelling, described in textbooks as a “hot potato voice”
Swelling and erythema in the area beside the tonsils
Quinsy - causative microorganism
Quinsy is usually due to a bacterial infection. The most common organism is streptococcus pyogenes (group A strep), but it is also commonly caused by staphylococcus aureus and haemophilus influenzae.
Management of peritonsillar abscess?
Patients should be referred to the hospital under the ENT team’s care for needle aspiration or surgical incision and drainage to remove the pus from the abscess.
Quinsy typically has an underlying bacterial cause. Therefore, antibiotics are appropriate before and after surgery. A broad-spectrum antibiotic such as co-amoxiclav would be an appropriate choice to cover the common causes, but local guidelines will guide antibiotic selection according to local bacterial resistance.
Some ENT surgeons give steroids (i.e. dexamethasone) to settle inflammation and help recovery, although this is not universal.
Indications for tonsilectomy?
The SIGN guidelines (2010) give the indications for tonsillectomy. The number of episodes of acute sore throat they specify for a tonsillectomy are:
7 or more in 1 year
5 per year for 2 years
3 per year for 3 years
Other indications are:
Recurrent tonsillar abscesses (2 episodes)
Enlarged tonsils causing difficulty breathing, swallowing or snoring
Tonsilectomy - potential complications
Sore throat where the tonsillar tissue has been removed (this can last 2 weeks)
Damage to teeth
Infection
Post-tonsillectomy bleeding (can be significant and an emegrency, can occur as late as 2 weeks after tonsilectomy)
Risks associated with a general anaesthetic
Post-tonsillectomy bleeding - management?
Call the ENT registrar and get them involved early
Get IV access and send bloods including an FBC, clotting screen, group and save and crossmatch
Keep the patient calm and give adequate analgesia
Sit them up and encourage them to spit out the blood rather than swallowing
Make the patient nil by mouth in case an anaesthetic and operation is required
IV fluids for maintenance and resuscitation, if required
If there is severe bleeding or airway compromise, call an anaesthetist. Intubation may be required.
Before going back to theatre there are two options for stopping less severe bleeds:
Hydrogen peroxide gargle
Adrenalin soaked swab applied topically
How do head and neck cancers typically present?
Dysphonia (esp laryngeal malignancy which may cause hoarseness)
Dysphagia/odynaphagia
Dyspnoea –stridor from narrowing of airway, especially laryngeal tumours
Neck Mass
Pain from site of pathology or referred e.g. to ear
Bleeding from nose or mouth depending on site of primary(rare presentation)
Nasal blockage –normally unilateral progressive for nasal/nasopharyngeal pathology
Most common histopathological type of head and neck cancer?
The majority (90%) are squamous cell carcinomas.
TNM staging
T= Tumour size, 1 (small) – 4 (big)
N= Nodal Metastasis, 0 (no nodes) - N3 (big/multiple nodes)
M= Distant metastasis 0 (none) – 1 (present)
Head and neck cancers: risk factors?
Alcohol
Chewing tobacco
Beetle nut chewing for oral cavity malignancies
Chinese ethnic origin for nasopharyngeal malignancy
HPV strain 16
EBV infection
Smoking
Beetle nut chewing increases the risk of which type of cancer?
Oral cavity mallignancies
Investigation of primary tumour - head and neck cancers
Examination under anaesthetic
o Also called Panendoscopy or laryngopharyngo-oesophagoscopy
in H&N
o Purpose – Biopsy for histological diagnosis, assess size of tumour,
look for second primary
CT Neck
o Purpose – assess size of tumour and neck node metastasis
Investigating neck lumps - head and neck cancer
If a patient has a biopsy proven primary squamous cell carcinoma in the head and neck it
can be assumed that any palpable cervical lymphadenopathy is secondary to this primary
and the CT scan of the neck to assess the primary will give all the information required for
staging.
If this is not the case any palpable neck masses should be investigated with an
ultrasound guided fine needle aspiration (FNA). While blind (i.e. no US) FNA can be done
the ultrasound will increase the accuracy of the specimen taken and will give extra
information on the mass being sampled.
Sometimes patients with head and neck squamous cell carcinoma may present with neck
metastases with no obviously primary even after examination under anaesthetic and
imaging - how should these be diagnosed?
These should be diagnosed with a FNA of the neck mass
Role of biopsy in suspicious neck lumps
Biopsy can lead to seeding and poor prognosis, however FNA is not so good for other causes of cervical lymphadenopathy other than SCC, such as tuberculosis and lymphoma which often require an open biopsy so in these cases an FNA should be carried out to exclude SCC before an open biopsy is done
Head and neck cancers - investigation of distant mets
CT chest are routinely done to check for metastasis in the chest, the commonest site of
distant metastasis.
Other investigations are not routinely done unless there is suspicion of other distant
metastesis
Management of head and neck cancers?
Treatment needs to be aimed at the primary site and also any neck metastases. In some
head and neck cancers there is a high rate of metastasis to the neck so even if no neck
metastasis are detected treatment will still be given to the neck (if curative aim)
Radiotherapy – to the primary site +/- to the neck, +/- chemotherapy - curative or palliative
Endoscopic surgery - e.g. laser resection
Open surgery
To primary site – e.g. laryngectomy
To neck – i.e. neck dissection
Descriptions to note the location of a neck lump?
Anterior triangle
Posterior triangle
Midline (vertically along the centre of the neck)
Neck lump differentials - adult
Normal anatomy - ie bony prominence
Skin abcess
Lymphadenopathy
Tumour (SCC, sarcoma)
Lipoma
Goitre
Salivary gland stone or infection
Carotid body tumour/anyerysm
Haematoma
Thyroglossal cyst
Brachial cyst
Neck lump differentials more specific to children?
Cystic hygromas
Dermoid cyst
Haemangioma
Venous malformation
What should be looked for when examining a neck lump to distinguish its features?
Location (anterior/posterior triangle or midline)
Size
Shape (oval, round, irregular)
Consistency (hard, soft, rubbery)
Mobile or tethered to underlying tissue or skin
Warmth
Tenderness (?infection)
Pulsatile (think carotid body anyeurysm)
Movement with swallowing (thyroid) or tounge protusion (thyroglossal cyst)
Transillunination with light (cystic hygroma)
What should be looked for when examining a patient with a neck lump to help establish the cause (other than the actual lumps features)
Weight loss (malignancy, hyperthyroid)
ENT infection
Skin pallor and bruising - leukaemia
Focal chest sounds (lung ca)
Clubbing (lung cancer)
Hepatosplenomegaly (leukaemia)
For which patients with a neck lump is a 2 week wait referral warranted?
Unexplained neck lump in over 45s
A persistent neck lump at any age
How urgent is an ultrasound in a patient with a neck lump that is growing in size?
Within 2 weeks if under 25
Within 48hrs if 25+
If suggestive of soft tissue sarcoma requires a 2WW
What bloods might be undertaken in a patient with a neck lump?
Dependent on the suspected cause
FBC and blood film for leukaemia and infection
HIV test
Monospot test or EBV antibodies for infectious mononucleosis
Thyroid function tests for goitre or thyroid nodules
Antinuclear antibodies for systemic lupus erythematosus
Lactate dehydrogenase (LDH) is a very non-specific tumour marker for Hodgkin’s lymphoma
Investigating a neck lump?
Bloods (FBC, blood film, TFTs, HIV, monospot/EBV ab, ANA, LDH)
Imaging (USS first line, CT or MRI, nuclear medicine scan - toxic thyroid nodules, PET scan for metastatic cancer)
Biopsy (FNA, core, incision, removal of lump)
Causes of lymphadenopathy?
REACTIVE: URTI, dental infection, tonsillitis
INFECTED: HIV, TB, EBV
INFLAMMATORY CONDITIONS: SLE, sarcoidosis
MALIGNANCY: lymphoma, leukaemia, metastasis
Which of the cervical lymph nodes, if enlarged, are the most concerning for malignancy?
Supraclavicular lymph nodes
(malignancy of chest of abdomen)
Red flags - lymphadenopathy?
Unexplained - not associated with infection
Persistently enlarged > 3cm diameter
Abnormally shaped (ie oval with length more than double width)
Hard or rubbery
Thethered or fixed to skin or underlying tissues
Associated constitutional symptoms
Lymphadenopathy- infectious mononucleosis
Infectious mononucleosis is a cause of lymphadenopathy. It is caused by infection with the Epstein Barr virus (EBV) and most often affects teenagers and young adults. It is found in the saliva of infected individuals and may be spread by kissing or sharing cups, toothbrushes and other equipment that transmits saliva.
It presents with
Fever
Sore throat
Fatigue
Lymphadenopathy
Mononucleosis can present with an intensely itchy maculopapular rash in response to amoxicillin or cefalosporins.
The first-line investigation is the Monospot test. It is also possible to test for IgM (acute infection) and IgG (immunity) to the Epstein Barr virus.
Management is supportive. Patients should avoid alcohol (risk of liver impairment) and contact sports (risk of splenic rupture).
Key finding in lymph node biopsy in patients with Hodgkin’s lymphoma?
Reed Sternberg cells
What are B symptoms in lymphoma?
Systemic symptoms, including:
Fever
Weight loss
Night sweats
What are lymphomas?
Lymphomas are a group of cancers that affect the lymphocytes inside the lymphatic system.
These cancerous cells proliferate within the lymph nodes and cause the lymph nodes to become abnormally large (lymphadenopathy).
There are two categories of lymphoma: Hodgkin’s lymphoma and non-Hodgkin’s lymphoma.
Hodgkin’s lymphoma is a specific disease and non-Hodgkins lymphoma encompasses all the other lymphomas.
What cells proliferate in lymphoma?
Lymphocytes
What age of patient typically presents with lymphoma
Binomial age distribution
Peak around 20 and 75 years
Lymphadenopathy - lymphoma
Lymphadenopathy is the key presenting symptom.
The enlarged lymph node or nodes might be in the neck, axilla (armpit) or inguinal (groin) region.
They are characteristically non-tender and feel “rubbery”.
Some patients will experience pain in the lymph nodes when they drink alcohol.
What staging system is used for lymphoma?
Ann Arbor staging system
Lymphadenopathy- leukaemia
Leukaemia is the name for cancer of a particular line of the stem cells in the bone marrow. This causes the unregulated production of certain types of blood cells. They can be classified depending on how rapidly they progress (chronic is slow and acute is fast) and the cell line that is affected (myeloid or lymphoid) to make four main types:
Acute myeloid leukaemia
Acute lymphoblastic leukaemia
Chronic myeloid leukaemia
Chronic lymphocytic leukaemia
The presentation of leukaemia is quite non-specific. If leukaemia appears on your list of differentials then get an urgent full blood count. Some typical features are:
Fatigue
Fever
Pallor due to anaemia
Petechiae and abnormal bruising due to thrombocytopenia
Abnormal bleeding
Lymphadenopathy
Hepatosplenomegaly
What is a goitre?
Generalised swelling of the thyroid gland
Causes of goitre?
Graves disease (hyperhtyroidism)
Toxic multinodular goitre (hyperthyroidsm)
Hashimoto’s thyroiditis (hypothyroidism)
Iodine deficiency
Lithium
What are the three salivary gland locations?
Parotid glands
Submandibular glands
Sublingal glands
Why might individual lumps in the thyroid occur?
Benign hyperplastic nodules
Thyroid cysts
Thyroid adenomas (benign tumours that can release excessive thyroid hormone)
Thyroid cancer (papillary or follicular)
Parathyroid tumour
What are the main reasons salivary glands may be enlarged?
Sialolithasis - stones blocking the drainage of the glands
Infection
Tumours (benign or mallignant)
What cells does the carotid body contain and what is their role?
Glomus cells - chemoreceptors that detect the bloods oxygen, CO2 and pH.
Paraganglia - group of glomus cells
What is a paragangliomas? Where do they present and what are there features?
Tumour of the glomus cells of the carotid body.
Usually benign and slow growing.
Painless, pulsatile lump which is mobile laterally (not vertically) with associated bruit found in the anterior triangle of the neck (near the angle of the mandible)
When might a carotid body tumour/paraganglioma cause symptoms?
Compression of the glospharygeal (IX) nerve, vagus nerve (X), acessory nerve (XI) or hypoglosssal (XII) nerve
What might compression of the vagus nerve (e.g. carotid body tumour) result in?
Horners syndrome: Ptosis, miosis, anhidrosis
Compression of which nerve can cause Horner’s syndrome?
Vagus nerve
Triad of symptoms in Horner’s syndrome?
Ptosis
Miosis
Anhidrosis
Characteristic findings on imagine of a paraganglioma (carotid body tumour)
A characteristic finding on imaging investigations is splaying (separating) of the internal and external carotid arteries (lyre sign).
How are paragangliomas (carotid body tumours) mostly treated?
Surgical removal
What are lipomas and how do they appear on examination? How are they managed?
Benign tumours of adipose tissue
Soft
Painless
Mobile
Absence of skin changes
They are typically treated conservatively with reassurance (after excluding other pathology). Alternatively, they can be surgically removed.
Thyroglossal cyst O/E
Midline of neck
Mobile
Non tender
Soft
Fluctuant
Move up and down with movement of the tongue (due to connection between thyroglossal duct and tounge)
Can use USS or CT to confirm diagnosis
How are thyroglossal cysts managed and why?
Surgical removal:
To confirm diagnosis on histology
To prevent infection of the cyst (causing a hot, tender and painful lump)
May recurr after surgical removal
What kind of neck lump moves on toungue protusion?
Thyroglossal cyst
What is a key differential for a thyroglossal cyst (since it occurs at a similar location)
Ectopic thyroid tissue
Why does a thyroglossal cyst occurs?
Thyroid gland starts developing in the fetus at the base of the toungue
It graduall travels down the neck to final position in front the the trachea and beaneath the larynx
It leaves a track behind called the thyroglossal duct which usually regresses but can persist and give rise to a fluid-filled cyst
Why do brachial cysts arise?
Congenital abnormality
Failure of complete second brachial cleft formation
This leaves space surrounded by epitherial tissue in the LATERAL aspect of the neck which can fill with fluid
How do brachial cysts present?
Soft
Round
Cystic swelling
Between angle of the jaw and sternocleidomastoid muscle in the anterior triangle of the neck
Usually after 10 years of age once the cyst becomes noticible or infected
How do brachial cysts present?
Soft
Round
Cystic swelling
Between angle of the jaw and sternocleidomastoid muscle in the anterior triangle of the neck
Usually after 10 years of age once the cyst becomes noticible or infected
How are brachial cysts managed?
Conservative, without any active intervention, where it is not causing problems
Surgical excision where recurrent infections are occurring, there is diagnostic doubt, or it is causing other problems
Round soft non-tender lump just anterior to the SCM presenting in a teenager?
Likely brachial cyst (most commonly originating from the second brachial cleft)
Potential areas of head and neck cancers
Nasal cavity
Paranasal sinuses
Mouth
Salivary gland
Pharynx (throat)
Larynx (epiglottis, supraglottic, vocal cords, glottis and sub glottis)
The HPV vaccine protects against strains 6, 11, 16 and 18. Which of these is most commonly involved in head and neck cancer?
16
Head and neck cancer management?
Management will be guided by the multidisciplinary team (MDT). It will be dependent on the location, stage and individual patient factors.
Staging usually involves the TNM staging system, grading the tumour, node involvement and metastases.
Treatment may involve any combination of:
Chemotherapy
Radiotherapy
Surgery
Targeted cancer drugs (i.e., monoclonal antibodies)
Palliative care
Cetuximab is an example of a monoclonal antibody used in treating squamous cell carcinomas of the head and neck. It may also be used to treat bowel cancer. It targets epidermal growth factor receptor, blocking the activation of this receptor and inhibiting the growth and metastasis of the tumour.
What is cetuximab and how can it treat SCC?
Cetuximab is an example of a monoclonal antibody used in treating squamous cell carcinomas of the head and neck. It may also be used to treat bowel cancer. It targets epidermal growth factor receptor, blocking the activation of this receptor and inhibiting the growth and metastasis of the tumour.
What is glossitis?
Glossitis refers to an inflamed tongue. The tongue becomes red, sore and swollen. The papillae of the tongue atrophy (shrink), giving the tongue a smooth appearance. It is sometimes described as “beefy”.
Causes of glossitis?
Iron deficiency anaemia
B12 deficiency
Folate deficiency
Coeliac disease
Injury or irritant exposure
What is angioedema and what are the top three causes?
Angioedema refers to fluid accumulating in the tissues, resulting in swelling. It can affect a number of areas, such as the limbs, face and lips. It can affect the tongue, causing the tongue to swell.
The three top causes of angioedema to remember for exams are:
Allergic reactions
ACE inhibitors
C1 esterase inhibitor deficiency (hereditary angioedema)
Angioodema
Glossitis
What is oral candisasis?
Oral candidiasis is also called oral thrush.
It refers to an overgrowth of candida albicans, a type of fungus, in the mouth. This results in white spots or patches that coat the surface of the tongue and palate.
Causes of oral candidiasis?
Inhaled corticosteroids (particularly with poor technique, not using a spacer and not rinsing with water afterwards)
Antibiotics (disrupt the normal bacterial flora giving candida a chance to thrive)
Diabetes
Immunodeficiency (consider HIV)
Smoking
Management of oral candidiasis?
Miconazole gel
Nystatin suspension
Fluconazole tablets (in severe or recurrent cases)
What is geographic tongue?
Inflammatory condition where patches of epithelium and papillae of the tongue are lost.
Patches are irregular shaped (resembelling a map)
The condition tends to relapse and remit, with episodes of the abnormal tongue appearance that can last days to weeks before resolving or changing. The cause of these changes is not known.
Geographic tongue is a benign condition and does not cause any harmful effects. It does not usually require any treatment. Symptoms such as discomfort or burning are sometimes treated with topical steroids or antihistamines.
Geographic tongue
What might geographic tongue be associated with?
Geographic tongue often occurs without any associations. However, it can be related to:
Stress and mental illness
Psoriasis
Atopy (asthma, hayfever and eczema)
Diabetes
What might geographic tongue be associated with?
Geographic tongue often occurs without any associations. However, it can be related to:
Stress and mental illness
Psoriasis
Atopy (asthma, hayfever and eczema)
Diabetes
What is a strawberry tongue and what are the key causes?
A strawberry tongue appearance occurs when the tongue becomes swollen and red, and the papillae become enlarged, white and prominent.
The two key causes of a strawberry tongue to remember are:
Scarlet fever
Kawasaki disease
Strawberry tongue
What causes black hairy tongue and how is it managed?
Black hairy tongue results from decreased shedding (exfoliation) of keratin from the tongue’s surface.
The papillae elongate and take on the appearance of hairs.
Bacteria and food cause the dark pigmentation.
This gives the appearance of black hair on the tongue.
Patients may also report sticky saliva and a metallic taste.
Black hairy tongue may be due to dehydration, a dry mouth, poor oral hygiene and smoking.
Management involves ensuring adequate hydration, gentle brushing of the tongue and stopping smoking.
Black hairy tongue results from decreased shedding (exfoliation) of keratin from the tongue’s surface.
The papillae elongate and take on the appearance of hairs.
Bacteria and food cause the dark pigmentation.
This gives the appearance of black hair on the tongue.
Patients may also report sticky saliva and a metallic taste.
What is Leukoplakia
White patches on mouth (tongue/buccal mucosa)
Why might leukoplakia require a biopsy?
It is a precancerous condition, meaning it increases the risk of squamous cell carcinoma of the mouth.
They may require a biopsy to exclude abnormal cells (dysplasia) or cancer.
How is leukoplakia managed?
Management involves stopping smoking, reducing alcohol intake, close monitoring and potentially laser removal or surgical excision.
Leukoplakia
What is erythroplakia/eythroleukoplakia and why does it require management?
Erythroplakia is similar to leukoplakia (white patches on tongue/bucal mucosa), except the lesions are red.
Erythroleukoplakia refers to lesions that are a mixture of red and white.
Both erythroplakia and erythroleukoplakia are associated with a high risk of squamous cell carcinoma and should be referred urgently to exclude cancer.
Erythroplakia/erythroplasia
What is lichen planus and what patterns does it appear in?
Lichen planus is an autoimmune condition that causes localised chronic inflammation of the skin. The skin has shiny, purplish, flat-topped raised areas with white lines across the surface called Wickham’s striae. It usually occurs in patients over 45 and is more common in women.
Lichen planus can also affect the mucosal membranes, including the mouth. Often it only affects the mouth.
In the mouth, it can take three patterns:
Reticular
Erosive
Plaque
Lichen planus
Lichen planus - reticular pattern
A reticular pattern involves a net-like web of white lines called Wickham’s striae.
Lichen plannus reticular pattern (Wickham’s striae)
Lichen planus - erosive lesions
Erosive lesions are where the surface layer of the mucosa is eroded, leaving bright red and sore areas of mucosa.
Erosive lichen planus
Lichen planus - plaque pattern
Plaques are larger continuous areas of white mucosa.
Oral lichen planus plaque pattern
Management of oral lichen planus
Smoking cessation
Good oral hygiene
Topical steroids
What is gingivitis and how does it present?
Gum inflammation
Swollen gums
Bleeding after burshing
Halitosis (bad breath)
What might gingivitis lead to?
Periodontitis refers to severe and chronic inflammation of the gums and the tissues that support the teeth. This often leads to loss of teeth.
Acute necrotising ulcerative gingivitis is a rapid onset of more severe inflammation in the gums. It presents similarly to gingivitis, however, it is painful. Anaerobic bacteria usually cause this.
Risk factors for gingivitis?
Palque build up - inadequete brushing
Smoking
Diabetes
Malnutrition
Stress
What is plaque?
Bacteria live in plaque, damaging the teeth and gums. Hardened plaque is called tartar.
Gingivitis management?
Good oral hygiene
Stopping smoking
Dental hygienist treatment to remove plaque and tartar
Chlorhexidine mouth wash
Antibiotics for acute necrotising ulcerative gingivitis (e.g., metronidazole)
Dental surgery if required
What is gingivits and what causes it?
Gingival hyperplasia refers to abnormal growth of the gums. The gums are notably enlarged around the teeth.
Possible causes of gingival hyperplasia include:
Gingivitis
Pregnancy
Vitamin C deficiency (scurvy)
Acute myeloid leukaemia
Medications, particularly calcium channel blockers, phenytoin and ciclosporin
Relations of the submandibular gland
Two parts, superficial and deep to the posterior boarder of the mylohiod in a U shaped pattern.
Superficial part: in the digastric triangle, partially deep to the maindible, covered superficially by the plasmyta and the skin
Deep part: between myohyoid and the hypoglossus
Duct runs from deep part and is crossed by the lingual nerve
Hypoglossal nerve runs deep to the gland
Cervical branch of the facial nerve runs superfically to the gland
Removal of which gland might result in damage to the cervical branch of the facial nerve?
Submandibular (cervical branch runs superfically to gland)
What nerve damage might occur during removal of the submandibular gland?
Lingual
Hypoglossal
Cervical branch of CN7
Muscular contents of the posterior triangle
Inferior belly of omohyoid muscle crosses SCM to anterior triangle
A number of vertebral muscles (covered by prevertebral fascia) form the floor of the posterior triangle:
Splenius capitis
Levator scapulae
Anterior, middle and posterior scalenes
Vascular contents of the posterior triangle
External jugular vein (superficially) after crossing SCM
Within the posterior triangle, the external jugular vein pierces the investing layer of fascia and empties into the subclavian vein.
Anatomical clinical relevance of external juglar vein
The external jugular vein has a relatively superficial course down the neck, leaving it vulnerable to damage.
If it is severed, in an injury such as a knife slash, its lumen is held open – this is due to the thick layer of investing fascia
Air will be drawn into the vein, producing cyanosis, and can stop blood flow through the right atrium. This is a medical emergency, managed by the application of pressure to the wound – stopping the bleeding, and the entry of air.
The transverse cervical and suprascapular veins also lie in the posterior triangle
The subclavian, transverse cervical and suprascapular veins are accompanied by their respective arteries in the posterior triangle.
Nerve contents of the posterior triangle
Accessory nerve (XI) crosses the posterior triangle in an oblique, inferoposterior direction, within the investing layer of fascia. It lies relatively superficial in the posterior triangle, leaving it vulnerable to injury.
The cervical plexus forms within the muscles of the floor of the posterior triangle. A major branch of this plexus is the phrenic nerve, which arises from the anterior divisions of spinal nerves C3-C5. It descends down the neck, within the prevertebral fascia, to innervate the diaphragm.
Other branches of the cervical plexus innervate the vertebral muscles, and provide cutaneous innervation to parts of the neck and scalp.
The trunks of the brachial plexus also cross the floor of the posterior triangle.
Nerve point of the neck
For anaesthesia of the neck area, a cervical plexus block can be used.
Local anaesthetic is injected along the posterior border of sternocleidomastoid at the junction of its superior and middle thirds.
This junction is where the cutaneous branches of the cervical plexus emerge, known as the nerve point of the neck.
Subdivisions of the posterior triangle
The omohyoid muscle splits the posterior triangle of the neck into two:
The larger, superior part is termed the occipital triangle.
The inferior triangle is known as the subclavian triangle and contains the distal portion of the subclavian artery. It is also known as the omoclavicular or supraclavicular triangle.
Where would a parotid gland tumour cause a lump?
Neck mass anterior to the ear
How might a parotid gland cancer present?
Lump anterior to ear
Palpable lymph nodes in neck
Facial nerve palsy (drooling, face droop, etc)
What would an acessory nerve plasy cause?
Shoulder drop
Freys syndrome
Freys syndrome is a rare neurological disorder resulting from damage to or near the parotid glands responsible for making saliva, and from damage to the auriculotemporal nerve often from surgery.
Risks of thryoid surgery on a hyperthryoid patient
High risk of bleeding
Thyrotoxic storm
Risk of thyroid surgery on a euthyroid patient?
Hypothyroidism
Damage to parathyroid glands - hypoparathyroidism and hypocalcemia
RLN damage
Bleeding infection
Course of the recurrent laryngeal nerve
The nerves branch off the vagus nerves in the neck
Left side loops under the aortic arch
The right loops under the right subclavian artery
Both then pass upawrds to supply the larygeal muscles passing deep to the cricothyroid joint
What are aphthous ulcers?
Aphthous ulcers are very common, small, painful ulcers of the mucosa in the mouth. They have a well-circumscribed, punched-out, white appearance.
Apthous ulcers
Why might apthous ulcers occur?
Aphthous ulcers commonly occur in otherwise healthy people, with no underlying cause. They may be triggered by emotional or physical stress, trauma to the mucosa or particular foods.
They may also be an indication of underlying conditions, notably:
Inflammatory bowel disease (Crohn’s disease and ulcerative colitis)
Coeliac disease
Behçet disease
Vitamin deficiency (e.g., iron, B12, folate and vitamin D)
HIV
Management of aphthous ulcers?
Aphthous ulcers usually heal within 2 weeks. Manageable ulcers do not require any intervention.
Topical treatments can be used to treat symptoms, including:
Choline salicylate (e.g., Bonjela)
Benzydamine (e.g., Difflam spray)
Lidocaine
Topical corticosteroids can be used in more severe ulcers. These may reduce the duration and severity of symptoms. Options include:
Hydrocortisone buccal tablets applied to the lesion
Betamethasone soluble tablets applied to the lesion
Beclomethasone inhaler sprayed directly onto the lesion
The NICE guidelines on suspected cancer (updated January 2021) recommend a two week wait referral in patients with “unexplained ulceration” lasting over 3 weeks.
Facial nerve pathway
The facial nerve exits the brainstem at the cerebellopontine angle. On its journey to the face, it passes through the temporal bone and parotid gland.
It then divides into five branches that supply different areas of the face:
Temporal
Zygomatic
Buccal
Marginal mandibular
Cervical
Motor function of the facial nerve?
Muscles of facial expression
Stapedius
Posterior digastric, stylohyoid and platysma muscles in the neck
Sensory function of the facial nerve?
Anterior 2/3 of the tongue
Parasympathetic function of the facial nerve
Submandibular and salivary glands
Lacrimal glands
Significance of distinguishing between and upper and lower motor neuron facial nerve palsy?
It is essential to make this distinction because, in a patient with a new-onset upper motor neurone facial nerve palsy, you should be referring immediately with a suspected stroke.
In contrast, patients with a lower motor neurone facial nerve palsy can be managed with less urgency.
How to differntiate between an upper and lower motor neuron palsy of the facial nerve
Each side of the forehead has upper motor neurone innervation by both sides of the brain. However, each side of the forehead only has lower motor neurone innervation from one side of the brain.
In an upper motor neurone lesion, the forehead will be spared, and the patient can move their forehead on the affected side.
In a lower motor neurone lesion, the forehead will NOT be spared, and the patient cannot move their forehead on the affected side.
You can differentiate between an upper and lower motor neurone lesion by asking the patient to raise their eyebrows. If they can raise both eyebrows and wrinkle both sides of the forehead, the patient has an upper motor neurone lesion. If the eyebrow on the affected side cannot be raised and the forehead remains smooth, the patient has a lower motor neurone lesion.
Facial nerve palsy - UMN causes
Unilateral upper motor neurone lesions occur in:
Cerebrovascular accidents (strokes)
Tumours
Bilateral upper motor neurone lesions are rare. They may occur in:
Pseudobulbar palsies
Motor neurone disease
Facial nerve plasy - LMN causes
Bells plasy
Ramsy hunt syndrome
Infection
Trauma
Tumour
Systemic disease
What is Bell’s Palsy and how is it managed?
Bell’s palsy is a relatively common condition. It is idiopathic, meaning there is no apparent cause. It presents as a unilateral lower motor neurone facial nerve palsy. The majority of patients fully recover over several weeks, but recovery may take up to 12 months. A third are left with some residual weakness.
If patients present within 72 hours of developing symptoms, NICE clinical knowledge summaries (updated 2019) recommend considering prednisolone as treatment, either:
50mg for 10 days
60mg for 5 days followed by a 5-day reducing regime of 10mg a day
Patients also require lubricating eye drops to prevent the eye on the affected side from drying out and being damaged. If they develop pain in the eye, they need an ophthalmology review for exposure keratopathy. The eye can be taped closed at night.
What is Ramsay Hunt syndrome, how does it present and how is it managed?
Ramsay-Hunt syndrome is caused by the varicella zoster virus (VZV). It presents as a unilateral lower motor neurone facial nerve palsy. Patients stereotypically have a painful and tender vesicular rash in the ear canal, pinna and around the ear on the affected side. This rash can extend to the anterior two-thirds of the tongue and hard palate.
Treatment should ideally be initiated within 72 hours. Treatment is with:
Prednisolone
Aciclovir
Patients also require lubricating eye drops.
Systemic diseases that might cause a lower motor neurone facial nerve palsy
Diabetes
Sarcoidosis
Leukaemia
MS
Gulliane Barre syndrome
Infections that might cause a lower motor neurone facial nerve palsy
Otitis media
Mallignant otits externa
HIV
Lyme disease
VZV
Tumours that might cause a lower motor neurone facial nerve palsy?
Acoustic neuroma
Parotid tumour
Cholesteoma
Trauma that might cause a lower motor neurone facial nerve palsy
Direct trauma
Damage during surgery
Base of skull fracture
Within what timeframe of presentation, do NICE recommend considering prednisolone as treatment for Bells Palsy?
72 hours
What is the thyroid gland?
The thyroid gland is located at the base of the neck.
It is a highly vascular structure responsible for controlling the basal metabolic rate of the body through the production of thyroxine and triiodothyronine hormones.
Vasculature of the thyroid
The arterial supply to the thyroid is from the superior and inferior thyroid arteries.
Venous drainage of the thyroid is via the superior, middle, and inferior thyroid veins
What nerve is of greatest significance during thyroid surgery and why?
The recurrent laryngeal nerves are intimately associated with the thyroid gland running in the tracheo-oesophageal groove and are at risk during surgery. They supply the muscles of the larynx (except cricothyroid) and sensation below the vocal cords. Injury causes vocal cord palsy with associated hoarseness and can also give problems with airway obstruction if the nerves on both sides are injured.
When might the parathyroid glands be at risk during ENT surgery
The parathyroid glands are also closely related to the thyroid gland. They are involved in calcium haemostasis and can be accidentally removed or damaged during surgery leading to hypocalcaemia. This is normally only a problem when both sides of the thyroid have been operated on. i.e. total or completion thyroidectomy
Most important investigations in a patient presenting with a thyroid lump?
TFTs
FNA
If there is any diagnostic doubt a hemithyroidectomy should be carried out to give definitive histology. Lumpectomies are not done on the thyroid because if it is a malignant nodule this will not give adequate margins on the mass and it would also make further surgery very difficult due to scarring and put the recurrent laryngeal nerve at an unacceptably high risk
How are follicular adenoma and follicular carcinoma of the thyroid managed and why are they managed the same way?
Both managed with total hemithyroidectomy as CANNOT differentiate between the two on FNA, sent for definitive histology
Non-neoplastic thyroid nodules?
Single nodule – colloid, cystic
Multinodular goitre
These are common and if they show typical features on
ultrasound do not necessary require fine needle aspiration. Any
dominant nodule should have an FNA.
Benign thyroid neoplasams
Adenoma - mainly follicular
Malignant thyroid neoplasms
o Papillary adenocarcinoma – 70% - Often seen in younger patients, or where there is a history of irradiation of the neck.
o Follicular carcinoma – 20% - It has a preponderance to metastasis to the bones and lungs.
o Medullary carcinoma – 5% - This is a neoplasm of the calcitonin regulating C-cells. It is typically seen in multiple endocrine neoplasia, and therefore screening of other organs involved in MEN syndromes is required. There is a genetic component.
o Anaplastic carcinoma - ~5% - Typically seen in older patients. This has a poor prognosis and by the time of diagnosis the prognosis if often a matter of weeks to months.
Management of non neoplastic thyroid nodules
Conservative –these can be managed conservatively unless there is diagnostic uncertainty
Surgery
o For compressive symptoms, cosmesis or patient preference.
o Should aim to restrict surgery to hemithyroidectomy due to the increased morbidity from a total thyroidectomy and the need for lifelong thyroxine replacement.
Management of neoplastic thyroid nodules?
Adenomas – require no further treatment after diagnostic hemithyroidectomy
Carcinoma
o Surgery
Total Thyroidectomy for papillary, follicular and medullary carcinoma
Anaplastic disease is normally too far advanced for curative surgery
o Radio-iodine therapy
For papillary and follicular carcinoma after surgery
General complications of thyroid surgery?
Post-operative haemorrhage
Airway obstruction
o Secondary to haemorrhage
o Secondary to bilateral vocal cord palsy
Vocal cord palsy
Hypocalcaemia
Anatomy of the parotid gland?
The parotid gland is a serious salivary gland located anterior to the pinna and lateral to the ramus of the mandible.
The gland is split into deep and superficial lobes by the facial nerve which passes through the gland.
The majority of the gland lies superficial to the
facial nerve.
Facial palsy is one of the most serious risks from parotid surgery and can also be caused by a parotid malignancy
Parotid gland neoplasams
80% of salivary gland neoplasms occur in the parotid gland.
80% of parotid neoplasms are benign in nature.
80% of benign parotid neoplasms are pleomorphic adenomas.
In which salivary gland are tumours most common?
Parotid gland
In which salivary gland is infection most common?
Submandibular gland
Submandibular gland anatomy
The submandibular gland is located inferior to the body of the mandible and superior to
the digastric muscle. It’s duct opens into the mouth close to the frenulum of the tongue.
The hypoglossal and lingual nerves run medial to the gland and are at risk during
submandibular gland surgery. Unlike the parotid gland, the submandibular gland has
mixed mucous and serous secretions.
The sublingual glands are entirely mucous and are
located where?
In the floor of the mouth
What proporiton of neoplasms arising from the submandibular gland are malignant?
50% of neoplasms occurring in the submandibular gland are malignant
WHen might an abscess in the submandibular gland typically arise?
Submandibular abscesses may develop following sialolithiasis or
sialadenitis
In which salivary gland are most neoplasms mallignant?
Sublingual (80%)
What is sialadenitis caused by?
Acute sialadenitis may be viral or bacterial. Bacterial disease is typically due to
staphylococcal infection and is typically seen in dehydrated or immunocompromised
individuals. Viral disease is caused by a range of viruses including:
1. Paramyxovirus – Mumps
2. Coxsackievirus
3. Echovirus
4. HIV
Chronic sialadenitis is rare, and sometimes seen in TB, sarcoidosis, HIV, and syphilis.
What is sialadenitis?
Sialadenitis is the inflammation and enlargement of one or several major salivary glands.
In which salivary gland are stones most common?
Submandibular
How might you investigate sialolithiasis?
Ultrasound
or sialogram
When is sialolithasis most painful?
During meals
Management of sialolithiasis?
Conservative
o most will settle conservatively
o analgesia
o hydration
o sialogogues
Endoscopy
Radiological removal
Surgery
o Intraoral removal of palpable stones
o Removal of salivary gland
Potential complications of sialolithasis?
Sialadenitis
Abscess formation
Sjögren’s Syndrome
This is an autoimmune disease causing lymphocytic infiltration into the ductal tissue of
secretary glands.
It classically presents with dry eyes and dry mouth and patients may have enlarged salivary glands.
Patients are at increased risk of developing lymphoma.
The disease may be primary:
Xerostomia and xerophthalmia without connective tissue abnormality.
Or secondary:
As primary disease, with connective tissue disease, most commonly rheumatoid
arthritis.
Diagnosis is made from the history, examination, some specific autoantibodies and a
biopsy of minor salivary glands on the inner lip
Thyroid lump 2ww referrals red flags
Cervical lymphadenopathy
slow-onset and persistent pain,
voice changes,
family history,
or rapidly enlarging masses.
Bilateral sensioneural hearing loss causes
Causes of bilateral sensorineural hearing loss include genetic diseases such as Charcot-Marie-Tooth disease, congenital rubella syndrome, presbycusis and ototoxicity at varying frequency range
What is Schwartze sign and what might it suggest
Patients with a positive Schwartze sign may be more likely to have sensorineural (cochlear) otosclerosis. [5] [6] The finding of a reddish discoloration in a patient with hearing loss may suggest otosclerosis, especially of the sensorineural (cochlear) area
The identification of an indurated ulcer involving the lateral tongue in a patient with a long-term smoking history should be considered what until proven otherwise
SCC
Examination in patient presenting with facial nerve palsy
Movement of the facial muscles
Otoscopy
Palpation of the parotid gland and neck
detailed examination of the external auditory canal and tympanic membrane
Facial nerve and parotid gland
The facial nerve demarcates superficial and deep lobes
From, where does the facial nerve arise
The facial nerve arises from the skull base via the stylomastoid foramen.
What is Xerostomia and when might it occur
Xerostomia (dry mouth) represents a common sequelae following radiotherapy for parotid, oral cavity and oropharyngeal cancers. It is also a recognised side effect from medications including, but not limited to, diuretics, beta blockers, tricyclic antidepressants, antihistamines, anticonvulsants and antipsychotics.
Structures passing through the parenchyma of the parotid gland
External carotid artery
Retromandibular vein
Facial nerve
How is the severity of OSAH or OSAS graded?
The apnoea hypopnoea index (AHI) is the number of apnoeas (stopping breathing) or hypopnoeas (reduced airflow during breathing) recorded during the sleep study per hour of sleep. It is generally expressed as the number of events per hour. Based on the AHI, the severity of OSA is classified as follows:
None/Minimal: AHI < 5 per hour
Mild: AHI ≥ 5, but < 15 per hour
Moderate: AHI ≥ 15, but < 30 per hour
Severe: AHI ≥ 30 per hour
What conditions does OSA increase the risk o f
Hypertension
Depression
Ischaemic heart disease
Accidents
Diabetes
Management of broken nose
Book the patient for an ENT clinic appointment within 7-10 days
Managing primary haemorrhage following thyroid surgery
Apply high flow oxygen via face-mask and remove surgical clips/sutures
Wwat cancer accounts for up to 99% of cancers arising from the upper aerodigestive tract.
SCC
What type of laryngeal carcinoma has the best prognosis
Glottic tumours have the best prognosis
Associations with recurrent laryngeal nerve palsy
Thyroid surgery
Aortic aneurysm repair
Carcinoma of the oesophagus
Carcinoma of the bronchus
Polio
Ludwig’s angina
Ludwig’s angina is a form of severe, diffuse cellulitis with bilateral involvement of the submandibular space. Signs may include diffuse, bilateral submandibular and sublingual swelling. Oropharyngeal examination typically reveals elevation of the floor of mouth and posterior displacement of the tongue, creating the potential for a airway compromise. Ludwig’s angina therefore, represents a medical emergency. Temporising measures may include a nasopharyngeal airway. Oropharyngeal intubation is often extremely challenging due to retrograde tongue displacement. In extremis and in the presence of imminent, life-threatening airway obstruction, an emergency tracheostomy is indicated.
What structure is MOST at risk when performing external cervical incision and drainage of the submandibular space?
Marginal mandibular nerve- a branch of the facial nerve
Tonsilar SCC is associated with what infection
Tonsilar SCC is associated with HPV infection
Which part of the TM should be visualised to r/o cholesteotoma
In patients with chronic or recurrent ear discharge, ensure the attic is visualised to exclude cholesteatoma
What type of nystagmus is indicative of a positive Dix-Hallpike manoeuvre
Rotatory nystagmus is indicative of a positive Dix-Hallpike manoeuvre
What distinguishes vestibular neuronitis from labyrinthitis
Unaffected hearing distinguishes vestibular neuronitis from labyrinthitis
What is seen in the fluid of a brachial cyst
A biopsy is performed and reveals cholesterol crystals in the fluid extracted.
What is the main side-effect of using topical decongestants for prolonged periods?
After using topical decongestants for prolonged periods increasing doses are needed to provide the same effect, a phenomenon known as tachyphylaxis.
What cranial nerves are affected in vestibular schwannomas?
Cranial nerves V, VII and VIII are affected in vestibular schwannomas
Pure tone audiogram in NIHL
Pure tone audiogram shows that bone and air conduction in both ears are poor at lower volumes (below 25dB) and within 10 dB of one another
Can prochlorperazine be used to treat vestibular neuronitis?
Prochlorperazine may be useful in the acute phase of vestibular neuronitis, but should be stopped after a few days as it delays recovery by interfering with central compensatory mechanisms
