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
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
Impacted ear wax (cerumen)
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
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)
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).
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
Type B tympanogram
Type C tympanogram
Suggests ET tube dysfunction
The peak of the tracing has negative pressure
What do nasal polyps look like?
Nasal polyps appear as round pale grey/yellow growths on the mucosal wall.
Nasal polyp
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
Paranasal sinus anatomy
Structures of importance: lamina papracea forming the medial wall of the orbit, anterior cranial fossa, internal catorid artery
Investigating allergic rhinosinusitis?
Skin prick tests (SPT) for specific allergens
RAST blood tests if SPT not possible
What causes ‘saddle nose deformity’ (obvious step in nose)
Nasal septal haematoma left untreated leading to erosion of the septal cartillage
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)
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 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 imagaing is this and what does it show?
Barium swallow
Pharangeal pouch
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.
Quinsy (peritonsilar abscess)
What are the three salivary gland locations?
Parotid glands
Submandibular glands
Sublingal glands
Compression of which nerve can cause Horner’s syndrome?
Vagus nerve
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).
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”.
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 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 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
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.
Leukoplakia
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
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.
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.
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
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.
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
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.
