ENT Flashcards
referred ear pain
As a result of the large amount of nerves passing nearby the ear it is possible for stimuli residing within the sensory net of cranial nerves V, VII, IX, X and upper C2 and C3 can potentially cause pain in the ear.
Rinne and Weber hearing test
Rinne test - conduction hearing loss (bone conduction is greater than air conduction)
sensorineural hearing loss will test NORMAL for this (bone louder than air)
Webers test - tests for sensorineural hearing loss (will be loudest in NORMAL ear)
and conductive hearing loss (will be loudest in AFFECTED ear)
normal should be heard equally
acute otitis media (AOM)
Background:
Most common in children ages <4
Complications include recurrence of infection, hearing loss, tympanic membrane perforation, mastoiditis, intracranial abscess, sinus thrombosis and facial nerve paralysis
Pathology:
Acute inflammation in the middle ear (cochlear, vestibular apparatus and nerves) associated with effusion and rapid onset of ear infection presentation
Bacteria can enter from the back of the throat through the eustachian tube
Viral causes are often preceded by a viral upper respiratory tract infection
Aetiology:
Viruses and bacteria (most commonly strep. Pneumoniae, H/ influenza, moraxella catarrhalis)
AOM risk factors and presentation
Risk factors: Passive smoke Daycare or nursery Formula feeding Craniofacial abnormalities
Presentation:
Earache
Rubbing or holding the ears
Fever, crying, poor feeding, restlessness, cough or rhinorrhea, clinginess
Tympanic membrane is distinctly red, yellow or cloudy and may be bulging
Ear discharge (if perforated)
Balance issues and vertigo is vestibular system affected
AOM Ix and management
Investigation/diagnosis:
Ear examination
vitals
Management:
Many cases resolve spontaneously within a few days (95% cases)
Pain and fever - paracetamol or ibuprofen
Encourage regular fluids
Antibiotics for those who are systemically unwell, have presentation of more serious illness/condition or who are high risk of complications (clinical judgement)
First line 5-7 days of amoxicillin (clarithromycin for erythromycin for allergy or pregnancy)
Presenting with severe systemic infection, suspected complications (meningitis, mastoiditis, intracranial abscess etc.) or children <3 YO with temperature of >38 degree C need hospitalisation
Safety net to come back if worsening or persisting longer than 48 hours if antibiotics prescribed
otitis externa
Otitis externa/swimmer’s ear:
Background:
Acute (<3 weeks)
Chronic (>3months)
Very common and more than 1% of people will be diagnosed with the conditions each year
Affects all ages but incidence peaks between ages 7-12
Complications can include abscess, inflammation of tympanic membrane, malignant otitis
Pathology:
Inflammation of the external ear canal +/- infection
Aetiology:
Bacterial infection
Disturbing/damaging cell lining of the ear canal e.g. excessive cotton bud use or hot tubs causing inflammation
otitis externa risk factors and presentation
Risk factors:
Diabetes or radiotherapy to the head/neck increase the risk of malignant otitis
Presentation:
Ear pain, itching, discharge and hearing loss
Swollen, red or eczematous ear canal and/or external ear
Usually systemically well and not bothered by infection
Ear may leak fluids, look wet and crusty and may smell
Screen for red flags - fever, swelling or hot to touch beyond ear, regional LAP, hearing loss
otitis externa Ix and Mx
Investigation/diagnosis:
History/clinical diagnosis
Ear examination
Ear swab for persistent or recurrent symptoms
Management:
Paracetamol or ibuprofen (codeine for severe pain) analgesia
Topical preparation (Otomize spray) containing dexamethasone, antibacterial spray. Also can use steroid eye drops for simple otitis externa cases. Use for 7 days but up to 14 if symptoms persist, 2-3 drops 3-4x daily. Tilt ear up and back (or back and down if child <3 years), press tragus and keep head tilted to the side for a few moments to help keep fluid in the ear
Topical acetic acid for 1 week
Topical antibiotics for mod-severe cases - clioquinol
Antibiotic ear drops (otomize CI in TM perforation - use gentamicin with no steroid)
Oral antibiotics only in severe infection or those at high risk of severe infection (diabetes, immunocompromised, systemic signs of infection) - amoxicillin.
Surgery to repair tympanic membrane, ossicles, remove cholaestoma etc.
General advice to keep ears clean, dry, avoid using cotton buds, moisturising any eczema etc.
Follow up recommended for those with severe otitis externa, chronic OE, diabetes or are immunocompromised
Suspected ,malignant otitis - urgent admission
cerumen impaction
Pathology:
Earwax is a normal physiological substance made from dead flattened cells, cerumen (waxy substance), sebum and various foreign substances
It cleans, lubricates and protects the lining of the ear canal, trapping dirt, dust and hair and repelling water. It is acidic and normally coats the walls of the ear canal, inhibiting growth of bacteria and fungi
It is normally spontaneously removed from the ear via natural jaw movement. If this is inadequate or disrupted then the wax is retained in the canal and may become impacted
Aetiology:
Inadequate or disrupted clearing of earwax from ear canal
cerumen impaction presentation, Ix
Presentation: Reduced hearing Feeling of blocked ear or irritation Found incidentally on hearing aid assessment Tinnitus
Investigation/diagnosis:
Clinical history
Ear examination
cerumen impaction management and referrals
Should remove the ear wax if: person is symptomatic, tympanic membrane is obscured or person wears a hearing aid and impression is needed for a mould or the wax is causing the hearing aid to whistle
Ear drops (olive oil) for 3-5 days BD initially to soften wax (CI for suspected eardrum perforation)
Consider ear irrigation if symptoms persist (must have olive oil for at least 5 days BD before irrigation)
Referral to ENT:
Chronic perforation of eardrum
Past history of ear surgery
Foreign body in ear canal
Used ear drops but not successful and irrigation is CI
Unsuccessful irrigation
Had multiple attempts to remove impacted earwax including combination of treatments
Persistent symptoms despite resolution of impaction
mastoiditis
Background:
Serious infection, more common in children
Most people recover quickly with no complications if diagnosed and treated promptly
Pathology:
Inflammation of the mastoid bone behind the ear
Aetiology:
Can occur secondary to otitis media or externa so always important to palpate the mastoid bone behind the ear for every ear assessment - causes pain or is swollen
mastoiditis presentation, Ix and Mx
Presentation:
Earache (persistent and throbbing)
Creamy, often profuse ear discharge
History of increasing deafness
Pyrexial and unwell
Marked tenderness over mastoid antrum
Pinna may be pushed down and forward due to swelling in post-auricular region
Tympanic membrane either red and bulging or perforated (if neither of these it is NOT mastoiditis)
Rinne test negative and Weber’s test positive for conductive hearing loss (sound loudest in affected ear)
Investigation/diagnosis: Vitals - temperature, BP, oxygen Ear examination Mastoid palpation Rinne and Weber’s test
Management:
Same day referral to ENT
tonsilitis
Background:
Very common presentation in children and adults
Self limiting condition often resolving within 3 days in 40% of people and within 1 week in 85% of cases
Pathology:
Inflammation of the tonsils +/- an infection
Aetiology:
Viral or bacterial infection (streptococcal most commonly)
tonsillitis presentation and Ix
Viral - runny nose, cough, feeling generally unwell, earache
Bacterial - isolated sore throat, smelly breath, not eating or drinking well, feeling generally unwell
Ix:
throat examination
centor score
fever pain score
centor score (tonsillitis)
each scores 1 pt (max 4). Score of <2 is low risk and score of 3 or 4 thought to be associated with 32-56% likelihood of isolating strep infection
tonsillar exudate,
tender anterior cervical LAP or lymphadenitis,
history of fever >38 degrees,
absence of cough
fever pain score (tonsillitis)
each scores 1 pt. <2 thought to be more likely a viral cause. Score of 3 considers delayed antibiotic script. 4 or 5 prescribe antibiotics are likelihood of bacterial infection is higher
Fever during last 24 hours Purulence Attend rapidly within 3 days onset Inflammation of tonsils No cough or coryza (inflammation of mucous membranes in the nose)
management of tonsillitis
Viral - document, reassure that it should self resolve within the next few days/one week and to come back if this is not the case or they begin to show systemic symptoms (high fever etc). Paracetamol or ibuprofen for analgesia
Difflam spray for soothing throat inflammation (not routinely prescribed)
Corsodyl mouthwash (daily wash for long term OR acute bacterial wash for use during infection ONLY as can stain teeth), regular fluids, small amounts of regular foods that are easy to swallow (ice cream, soups)
Consider delayed antibiotic prescription for more vulnerable patients without severe symptoms and feverpain score of 2 or 3 (phenoxymethylpenicillin - penicillin V - first line for 10 days, clarithromycin for allergy, erythromycin for pregnancy with allergy). Treated for 10 days to reduce risk of recurrence.
NEVER prescribe amoxicillin (because you can never tell the difference clinically between glandular fever and tonsillitis, amoxicillin can cause nasty rash with glandular fever)
pharyngitis and presentation
Background:
Very common presentation in children and adults
Self limiting condition often resolving within 3 days in 40% of people and within 1 week in 85% of cases
Pathology:
Inflammation of the oropharynx
Aetiology:
Viral infection most commonly
Bacterial infection
Presentation:
Localised more just to the oropharynx less the tonsils
redness, skin changes, swelling
pharyngitis Ix and Mx
Investigation/diagnosis:
Throat examination
Management:
Symptoms control only using paracetamol/ibuprofen
Corsodyl mouthwash (daily mouthwash for long term OR for infection ONLY used during acute infection or can stain teeth)
Good fluid intake and small regular meals (soups, ice cream)
NO ABX NEEDED
infectious mononucleosis
glandular fever:
Background:
Self limiting illness
Spread via contact with saliva (especially kissing - AKA kissing virus), sharing cups, toothbrushes etc.
Can take up to 6 weeks to present with symptoms
Most common in young adults and teens
Have lifelong immunity post-infection
Complications can include damaged spleen, rash, jaundice, malaise and depression
Pathology:
Viral infection
Aetiology:
Epstein-Barr virus
glandular fever presentation
Symptoms occur for a week or so then settle over the next week Sore throat Swollen glands and tonsils Flu like symptoms Malaise and fatigue Swelling around the eyes Splenomegaly (temporary) Asymptomatic (subclinical infection common in children and >40 YO)
glandular fever Ix and Mx
Investigation/diagnosis: Clinical history Throat examination Lymph node examination Vitals - temperature Bloods - epstein-barr viral antibody
Management:
Encourage good fluid intake, small easy to swallow foods
Do not share contaminated items with household persons, avoid kissing and close bodily contact with others while symptomatic
Paracetamol or ibuprofen for fever and analgesia
Avoid drinking alcohol this will worsen symptoms
approach to looking at the throat
Is there any erythema? Where is it located?
Can you see the tonsils? Are they enlarged? Bilaterally or unilaterally?
Is there exudate?
Is the uvula central or deviated?
quinsy
peritonsillar abscess:
Background:
The bad boy of throat infections
Predominantly common in teenagers and young adults
Complications - necrotising fasciitis, mediastinitis, pericarditis, pleural effusions, airway compromise, aspiration, haemorrhage after tonsillectomy, recurrence of peritonsillar abscess
Pathology: Weber glands (salivary glands immediately above the tonsillar area in soft palate) are thought to play a minor role in clearing trapped debris from the tonsillar area. An infection resulting in trapped pus and abscess formation. Tissue necrosis and scarring and obstruction of the ducts draining the glands causing swelling.
Aetiology:
Secondary to acute tonsillitis, progresses to peritonsillitis and results in formation of a peritonsillar abscess or can arise from primary infection
Usually caused by strep. Pyogenes (group A strep) or staph. Aureus and H. influenzae
quinsy presentation
Unilateral tonsil swelling Fever Drooling Foul smelling breath Painful to swallow Trismus (difficulty opening the mouth) Altered voice (hot potato voice) due to pharyngeal oedema and trismus Earache on affected side (referred pain) Neck stiffness symptoms Headaches and general malaise Displaced uvula Severe - airway compromise or spontaneous rupture leading to aspiration
quinsy Ix and Mx
Investigation/diagnosis: Clinical diagnosis Throat examination Vitals - temperature CT scan for atypical presentations (inferior pole abscess) or high risk for drainage procedure (bleeding disorders etc) or to guide drainage in difficult cases Culture of pus/throat swab
Management:
Refer same day to hospital/ENT surgery for surgical intervention
IV fluids for dehydration
Analgesia
IV antibiotics of penicillin, cephalosporins, amoxicillin + clavulanic acid and clindamycin or metronidazole + penicillin depending on cultures
IV Igs (rare)
Single dose IV steroids may help reduce inflammation
Surgery - if conservative management is not successful, needle aspiration and drainage (USS guided if needed). Interval tonsillectomy if there is a background of chronic or recurrent tonsillitis
parotitis
Background:
The most commonly affected salivary gland affected by inflammation
Pathology:
Inflammation of the parotid glands (one or both)
Aetiology:
Tumours
Viral - mumps
Obstruction (stones or thickened saliva - more risk on hot days)
Sarcoidosis - Heerfordt’s syndrome (sarcoidosis with parotid enlargement, fever, anterior uveitis and facial nerve palsy)
Bacterial infection
HIV related lymphocytic infiltration
parotitis presentation and Mx
Swelling of parotid glands (uni or bilateral)
Loss of jaw angle (parotid swelling)
Accessory lobe may swell causing lump anterior to the ear
Displaced ipsilateral tonsils
Mx
Investigate and manage underlying cause
Mumps - self limiting, supportive treatment only
Salivary gland blockage (stone or thickened saliva) - drink lots of water, eat lemon, sherbert etc. to stimulate salivation and encourage flushing out of blockage
Acute suppurative infection - antibiotics and incision and drainage for abscess
Salivary flow encouragement using warm compress, sialogogues (lemon drops, gum, vitamin C lozenges), hydration, salivary gland massage and good oral hygiene
Chronic infections - duct obstruction by stone or structure needs removal, gland decision for recurrent or severe problems.
parotitis investigations
Investigation/diagnosis:
Bloods - FBC, inflammatory markers, U+Es, blood cultures, viral serology and salivary antibody testing, HIV screen
Pus swabs for culture and sensitivities
Sialography
USS
CT/MRI to exclude neoplasm
Fine needle aspiration or incisional biopsy if malignancy suspected
throat/gland examination:
Inspect deep lobe through the mouth
Ask patient to clench teeth to allow palpation of masseter - feel parotid across anterior border of masseter muscle
Inspect orifice of duct in the mouth opposite second upper molar by retracting teeth with spatula
Pressure on parotid gland may cause pus extrusion from orifice
Examine facial nerve for weakness or asymmetry (malignancy)
Vertigo
Background:
A type of dizziness referring to a false sensation that oneself or the surroundings are moving or spinning, usually accompanied by nausea and loss of balance
It is a mismatch between vestibular, visual and somatosensory systems
Can be classified into central or peripheral vertigo based on the cause
Majority of cases seen are viral or benign positional vertigo
Prevalence of vertigo and dizziness in those aged 60+ reaches 30%
Pathology:
Varies depending on cause
Aetiology:
Central - cerebral cortex, cerebellum, brain stem pathology e.g. cerebrovascular disease, migraine, MS, acoustic neuroma, diplopia and alcohol intoxication
Peripheral - vestibular labyrinth, semicircular canals or vestibular nerve pathology e.g. viral labyrinthitis, vestibular neuritis, benign paroxysmal positional vertigo (BPPV), meniere’s disease, motion sickness, ramsay hunt syndrome (herpes zoster)
Vertigo presentation
Feeling of rotatory or spinning symptoms
Symptoms of underlying cause..
Ear symptoms - hearing loss, ear discharge, tinnitus, history of recent URTI or ear infection
Neurological - headache, diplopia, visual disturbance, dysarthria or dysphagia, paraesthesia, muscle weakness or ataxia
Autonomic symptoms - N+V, sweating, palpitations
Migraine aura - visual or olfactory symptoms
History of recent head trauma may indicate BPPV
Anxiety and depression can aggravate vertigo
Acute intoxication with alcohol
Nystagmus common in acute vertigo
Vertigo investigations
Full Neurological examination (Romberg’s test)
Ear examination
Eye examination
Dix-hallpike maneuvers - used to confirm BPPV
Head impulse test - determine if cause of vertigo is peripheral or central (not sensitive)
Unterberger’s test - identifies damage to one of the labyrinths. Patients should march on the spot for 30 seconds with eyes closed, observing for lateral rotation. Rotate to the AFFECTED labyrinth side.
Audiometry - cochlear function
Electronystagmography, calorimetry and brain-stem evoked responses - Vestibular function
CT/MRI
EEG - epilepsy
Lumbar puncture - MS
Syphilis serology
Vertigo management
Identify and treat underlying cause
Explain and reassure for anxiety related exacerbations
Advise not to drive while dizzy or likely to experience an episode (DVLA states those liable to sudden attacks should stop driving)
Advise them to inform their employer if it poses a risk in the workplace (ladders, heavy machinery, driving etc)
Discuss risk of falling in the home
Consider symptomatic drug management for one week (must stop 48 before seeing a specialist) - prochlorperazine, cinnarizine, cyclizine or promethazine
Leaflets and support advice on chronic dizziness, rehabilitation
vertigo referrals
Referrals:
Severe N+V, inability to tolerate fluids, symptomatic drug treatment needs hospitalisation
Very sudden onset vertigo not provoked by positional change and is persistent refer urgently to neurologist or balance specialist (ENT)
Central neurological presentation e.g. new headache, gait disturbance, truncal ataxia refer urgently to neurologist
Acute deafness without typical features of Meniere’s diseases refer urgently to ENT
Undetermined cause refer to balance specialist (ENT) urgency dependent on clinical presentation
Bengin paroxysmal positional vertigo BPPV
Background:
Most common cause of vertigo (illusion of movement)
Can affect any age but is common around age 50
Younger people may develop BPPV as a consequence of head trauma
Women are twice as affected as men
Pathology:
Otoliths become detached from the macula (utricle-based receptor for detecting head position and movement) into the semicircular canals (posterior most commonly, inferior and then anterior rarely).
Detached otoliths may continue to move after movement ceases resulting in vertigo sensation of ongoing movement with other sensory inputs
BPPV cause and risk factors
Aetiology: Mostly idiopathic Heady injury Spontaneous degeneration of labyrinth Post-viral illness (viral neuritis) Complication of stapes surgery Chronic middle ear disease
Risk factors: Increasing age (40-60 most commonly) Women (2:1 ratio) Meniere’s disease Anxiety disorders Migraine - particularly in children
BPPV presentation
Vertigo provoked by head movements (rolling over in bed, lying down, sitting up, leaning forward, turning head to side etc.)
Symptoms are worse when head is tilted to one particular side
Sudden onset and lasting 20-30 seconds with rapid resolution if head is kept still
Brief latent period of 5-20 seconds between head movement and vertigo symptoms
Nausea (vomiting is rare)
Symptoms worse in the mornings
Light-headedness lasting several minutes or hours
BPPV investigations
Detailed history
Ear examination
Cranial nerve examination
Dix-hallpike test - confirms posterior canal BPPV
CT/MRI for diagnostic uncertainty
HINTS exam - head impulse test, nystagmus type and skew
BPPV management
Advise symptoms are usually self limiting over several weeks but may recur
Advise getting out of bed slowly and reducing head movements
Offer period of observation or immediate treatment (Epley’s manoeuvre or Brandt-Daroff exercises)
Advise against driving whilst dizzy or if provoked attack is likely (DVLA must be notified if person is liable to sudden and unprovoked or unpredicted episodes of disabling giddiness)
Follow up in four weeks to assess resolution of symptoms
Referral to specialist if Epley’s manoeuvre cannot be done in primary care, has been performed and repeated without success, uncertain diagnosis, symptoms have not resolved in four weeks or there are three or more recurrences of vertigo
Epleys manoeuvre
Most widely used repositioning manoeuvre for BPPV
Aims to move otoliths back into utricles from posterior semicircular canals.
Sit patient upright on couch with head turned to 45 degrees to the affected side (positive from Dix-Hallpike test)
Place hands on either side of the patients head and guide patient to lie down with head dependent 30 degrees over the edge (same as Dix-Hallpike)
Rotate head to 90 degrees opposite side with patients face upwards and head remaining dependent
Roll patient onto their side whilst holding their head in this position then rotate the head so it is facing downwards (tell patient to look at the ground)
Sit patient up sideways while maintaining head rotation
Simultaneously rotate the head centrally (should be no nystagmus now and otoliths should be repositioned)
Each position should be maintained until full symptom resolution and nystagmus has been achieved for at least 30 seconds
Symptoms can resolve quickly after treatment but full recover ycan take days-weeks
If not settled within a week diagnosis of BPPV is likely, consider repeating manoeuvre
Can be taught to be self-performed at home for patients
Brandt-Daroff exercises
Series of home exercises to loosen and disperse inner ear debris
Not as effective as Epley’s
Sit on side of the bed with head rotated 45 degrees
Close eyes
Quickly lie down to opposite side until head touches the bed, nose up, lateral occiput resting on the bed
Stay in position for 30 seconds then sit up
Turn head to other side and repeat
One session should include 6 repetitions to each side repeated 3 times daily until vertigo free for at least 2 consecutive days
Labyrinthitis and vestibular neuritis
Background:
Vestibular neuritis - confirmed cases where only the vestibular nerve is involved and is a common cause of vertigo. Peak onset of 40-50 YOs
Labrynthitis - the vestibular nerve and labyrinth are affected, also a cause of vertigo but less common than vestibular neuritis. Most commonly viral, between the ages of 30-60 years.
Pathology:
Vestibular neuropathy from herpes simplex most commonly affects the superior division of the nerve (longer than the inferior division and travels through a bony passage so is more vulnerable to swelling or ischaemic effects)
Labyrinthitis is caused by inflammation of the membranous labyrinth and damage to the vestibular and auditory end organs. Hearing loss is always present to some degree due to cochlear involvement
labyrinthitis and vestibular neuritis causes and risk factors
Aetiology:
Vestibular neuropathy is caused by reactivation of latent type 1 herpes simplex virus in the vestibular ganglion or can be caused by autoimmune and microvascular ischaemic insults
Labyrinthitis is caused by viral infection and URTI most commonly. Bacterial is a dangerous disorder, can also be associated with systemic disease
Risk factors: Female (2:1) Viral infection Chronic suppurative and acute otitis media Cholesteatoma Meningitis Inner ear malformations
Labyrinthitis presentation
Detailed history Sudden onset severe vertigo Not triggered by movement but may be exacerbated by movement N+V Hearing loss and tinnitus (with labyrinthitis but NEVER vestibular neuritis) can be uni or bilateral Preceding URTI symptoms Otalgia suggests herpes zoster Nystagmus Positive head impulse test
labyrinthitis and vestibular neuritis investigations
Ear examination
Cranial nerve exam
Gait assessment
HINTS examination - Head impulse test, Nystagmus Type and Skew
Swab of ear effusions if present
CT/MRI
Vestibular function tests - caloric testing, electronystagmogram and vestibular evoked myogenic potentials
labyrinthitis and vestibular neuritis management
Sudden onset unilateral hearing loss - refer to ENT urgently as may indicate acute ischaemia of labyrinth or brainstem
Safety net to seek medical attention for worsening symptoms, neurological symptoms (diplopia, slurred speech, gait disturbance etc)
Reassure patient this can usually be managed at home, lie still during attacks with eyes closed, encourage activity as soon as possible after to speed up development of vestibular compensation
Prochlorperazine or antihistamines for vertigo, N+V symptoms taken for the most minimal time possible
Labyrinthitis may need surgical management depending on cause (effusion, mastoiditis, cholesteatoma)
Vestibular rehabilitation exercises
Falls risk assessment
meniere’s disease and risk factors
Background:
Uncommon condition roughly 1:1000-1:2000
Disorder of the inner ear
Pathology:
Increased pressure within the endolymphatic system resulting in a swelling of the membranous labyrinth of the inner ear
Aetiology:
Changed in fluid volume in the labyrinth due to increased pressure within the endolymphatic system
Risk factors: Autoimmune conditions Family history Metabolic disturbances of sodium and potassium levels in inner ear Migraine Viral infections Head trauma
meniere’s disease presentation and Ix
Vertigo
Fluctuating hearing loss
Tinnitus
Typical attack begins with cochlear symptoms, followed by vertigo
Investigations/diagnosis:
Clinical diagnosis (rule out red flags for brainstem stroke)
Examination to rule out other vertigo causes (Dix-Hallpike manoeuvre)
Audiometry to assess hearing loss (sensorineural loss)
Balance test - ENG or video nystagmography
Bloods - eGFR, glucose, U+Es, FBC, CRP, ESR, TFTs
acute episodes of vertigo should be differentiated from non-rotatory dizziness
Meniere’s disease management
Lifestyle intervention - diet control Trial of betahistines Medical ablation (aminoglycoside) Pressure pulse treatment (provide positive pressure through pulse generator into ear canal) Psychological management for symptoms
Acute attack: Lie down on firm surface Avoid spinning drinks (causes vomiting) Cinnarizine, promethazine or cyclizine Oral steroid or intratympanic injections effective for acute and chronic symptoms
epistaxis
Background:
Most common ENT emergency, usually minor and self limiting
Anterior bleeding is most common (90% cases),
Posterior bleeding is in around 10% of cases, common in more elderly patients and often more severe
Pathology:
Anterior - bleeding occurs in the anterior septal area supplied by Keisselback’s plexus in Little’s area
Posterior - Usually arises from posterior nasal cavity at the following sites: behind posterior part of middle turbinate or posterior superior roof of the nasal cavity, supplied by the sphenopalatine artery
epistaxis causes and risk factors
Aetiology Trauma Chronic sinusitis Irritants (smoke, drugs) Drugs - topical corticosteroids Rhinitis Vascular malformation (telangiectasia) Neoplastic cause
Risk factors:
Hot, dry climates (causes skin to dry and crack)
Deviated nasal septum altering airflow pattern causing dryness
Colds and allergies (inflammation)
Medical causes - kidney failure, thrombocytopenia, hypertension, hemophilia
Alcohol
Drugs - anticoagulants, NSAIDs
epistaxis presentation and Ix
Presentation:
Anterior bleeding - clinically apparent bleeding from the nose, usually unilateral
Posterior - blood running into the throat or from both nostrils (bilateral)
History of recent trauma, HTN, bleeding disorders
Medications - aspirin, clopidogrel, warfarin, etc
Nasopharyngeal carcinoma - often unilateral epistaxis
Investigations/diagnosis:
Vitals - BP, pulse, temp, oxygen
ABCDE (airway, haemodynamic stability)
Bloods - FBC, G+S, cross-match, coagulation studies
epistaxis management
Sit upright, tilt torso forward with mouth open
Stabilise and maintain airway patency
Pinch cartilaginous part of nose firmly and gold for 10-15 mins
If bleeding stops with first air - topical anaesthetic may be used for 10 days (naseptin - CI in allergy to neomycin, peanut, soya)
If not - consider nasal cautery if bleeding point can be seen or nasal packing (nasal tampons, inflatable pack, ribbon gauze with vaseline for 1-3 days) if this is ineffective or bleeding point cannot be seen.
Admit person to hospital if nasal pack has been inserted in primary care
Monitor vitals and haemodynamic stability, correct with IV fluids if needed
Review of medications - especially anticoagulants
Anterior bleeding in CVD, imapred coagulation or platelet dysfunction: Topical vasoconstrictors (lidocaine) Chemical cautery with silver nitrate stick applied to bleeding point for 5-10 seconds If fails: nasal packing or electrocautery
Posterior bleeding:
Refer to otolaryngologist, head and neck specialists
Inflatable balloons or posterior packs with cotton gauze +/- GA
Topical antibiotic ointments if packing left in for >48 hours
After care:
Bleeding stopped: recommend for 24 hours where practical they avoid activities which may increase the risk of re-bleeding including: blowing/picking nose, heavy lifting, strenuous exercise, lying flat, drinking alcohol or hot drinks
Advise if re-bleeding then apply first aid again, if this fails they should seek urgent medical advice
chronic otitis externa management
Chronic otitis externa:
If fungal infection is suspected - clotrimazole or other antifungal prep used. 7-14 days T/QDS.
Irritation suspected - prescribe corticosteroid prep
Unknown cause - topical corticosteroid without antibiotic, can prescribe acetic acid spray alongside
Inadequate response - continue steroid but reduce strength
Still no response - consider trial of antifungal drug e.g. clotrimazole
sinusitis
Background:
Rhinosinusitis - inflammation of the nose and sinuses
Acute - severe, duration of 1-3 weeks; self limiting shows complete resolution within 12 weeks of onset
Chronic - persistent, may last several weeks to months >12weeks
Pathology:
four sinuses: frontal, ethmoid, maxillary and sphenoid (deep)
Inflammation and infection in paranasal sinuses typically resulting in blockage of the sinus orifices
Oedema of nasal tissues and thickening of normal mucus, impairing sinus drainage and infection can ensue
causes of sinusitis
Acute - usually preceded by coryza viral infection
Chronic - Initially triggered by acute infection then complicated by underlying pathology (allergy) affecting the lining of the membranes of the nose and sinuses
Infection - viral and bacterial
Irritants - air pollution, smoke, chemicals
Allergies
Anatomical issues - narrowing of nasal cavity from trauma or development resulting in mucus build up
presentation of acute and chronic sinusitis
Acute: Severe facial pain/pressure around the cheeks, eyes, forehead Nasal discharge (usually dark green) Swelling High fever Toothache
Chronic: Nasal obstruction Headache Nasal discharge Low grade fever Anosmia Facial discomfort Halitosis
Ix and management of acute and chronic sinusitis
Investigation/diagnosis:
Clinical diagnosis
MRI/CT
Management:
Acute:
Saline douching, steaming with vapour rubs
Decongestant nasal sprays (can cause refractory sinusitis if used for more than one week)
Antibiotics (must wait until at least 2 weeks of infection as most cases are viral), first line penicillin V 500mg QDS or amoxicillin TDS
2nd line co-amoxiclav 625mg TDS (covers more spectrum if penicillin doesn’t improve)
Allergy to penicillin; doxycycline 200mg/100mg OD or clarithromycin/erythromycin 500mg BD for 5 days
Chronic:
Steroid nasal sprays to reduce inflammation (mometasone, fluticasone, avamys)
Antihistamines for allergies
Nasal endoscopy used to improve patency of sinus orifices (last resort for failed medical management)
allergic rhinitis
Background:
IgE mediated inflammatory disorder of the nose which occurs when the nasal mucosa becomes exposed and sensitised to allergens
Nasal blood vessels and tissues swell, usually due to an allergen such as pollen, leading to a narrowing of the nasal passages
Pathology:
Inhalation of allergens, triggering release of histamines and other inflammatory mediators (leukotrienes, prostaglandins etc.)
If prolonged or had previous reaction, T cells develop and also initiate immune response
Mast cells in tissues can be broken down by rubbing the nose or eyes resulting in further release of inflammatory mediators making symptoms worse
These act on cells, nerve endings and blood vessels resulting in increased mucus secretion and leading to hayfever symptoms
allergic rhinitis classifications and risk factors
Classifications:
Seasonal: cyclical annual symptoms in response to seasonal allergen i.e hayfever, triggered by grass and tree pollens
Perennial: constant symptoms, allergens from house dust mites, animal dander
Intermittent: symptoms 4 days a week and >4 consecutive weeks from house dust mites
risk factors:
family history
atopy conditions
allergic rhinitis presentation and investigations
Itchy nose, ears, throat and eyes Sneezing (sternutation) Rhinorrhea Lacrimation Nasal congestion Postnasal drip causing cough Snoring Mouth breathing Halitosis (chronic) Oral allergy syndrome due to cross-reaction, may suffer throat irritation when eating certain foods
Investigation/diagnosis:
Clinical history - occupation, home, pets, family history, atopy (triggers), severity/impact, type, persistence, location of symptoms
Allergenic testing - skin prick testing, RAST test
allergic rhinitis management
Self management: saline irrigation, allergen avoidance, washing bedding at high temps, eliminating exposure to animals, occupational irritants etc
Medication:
Blocked nose: steroidal nasal spray (fluticasone or beclomethasone if severe)
Itchy or watery eyes: eye drops (sodium cromoglycate eye drops), antihistamine tablets or syrups or eye drops (Loratidine or cetirizine for mild/mod symptoms)
Itchy or runny nose: antihistamine tablets/syrups or nasal sprays (loratadine, cetirizine tablets or nasal sprays - Azelastine nasal spray for mild/mod symptoms or non-drowsy tablet e.g. loratadine)
Moderate to severe symptoms: regular use of steroidal nasal spray (mometasone, fluticasone furoate) typically dosed one spray TWICE daily into each nostril.
Severe/chronic:
Fexofenadine 120mg chronic rhinitis
Montelukast - asthmatic pts
Prednisolone short course if severe
Immunotherapies:
Subcut or sublingual therapy for those with exposure allergen symptoms, confirmed IgE sensitivity and persistent symptoms (expose them to increasing doses to develop immunological tolerance) periodically over 3 years. Done in clinical setting in case of severe symptoms
Anti IgE licensed for severe allergic asthmatics
allergic rhinitis referrals
Red flags - unilateral symptoms, blood stained nasal discharge, recurrent epistaxis, nasal pain
Nasal obstruction +/- structural abnormality
Allergy clinic referral if treatment optimised and failed for immunotherapies
nasal decongestants, nasal spray technique and nasal drop technique
A sympathomimetics, they bind to a and a adrenergic receptors (GPCRs) in the nasal mucosa, causing vasoconstriction, and thus opening the nasal passage
Xylometazoline, pseudoephedrine and phenylephrine act as sympathomimetics
They are often included in over the counter preparations purchased through pharmacies, but are sometimes also prescribed. They are cautioned in those with hypertension as they raise blood pressure.
Stated in the BNF: Pseudoephedrine is ‘less suitable for prescribing’ i.e. a drug the formulary committee believe should ideally not be prescribed
Nasal spray technique
Shake the container well and look down (chin on chest)
Using the right hand for the left nostril, put the nozzle just inside the nose aiming for the outside wall.
Squeeze once or twice in different directions, while breathing in gently through the nose. Do not sniff.
Change hands, then repeat for the other nostril.
Nasal drop technique
Gently blow the nose to try and clear it.
Shake the container well.
Tilt the head backwards.
Place the drops in the nostril (squeeze the container gently if necessary).
Keep the head tilted and sniff gently to let the drops penetrate.
Repeat for the other nostril, if required.
oral thrush
Background:
Colonisation of oral mucocutaneous layer by candida resulting in pseudomembrane (white plaque)
Pathology:
Candida can be a normal part of the gut and vaginal flora
Compromised immune defences or break down in mucosal membranes can cause infections of candida strains over colonising
Aetiology:
Candida albicans is the most cultured species
Sometimes candida glabrata, C. krusei and C. tropicalis
oral thrush risk factors
Very young or elderly Immunocompromised Medications - ICS inhalers Impaired salivary function/dental prosthesis/poor dentition Endocrine disorders Smoking Poor diet/nutritional deficiencies Trauma
oral thrush presentations
Pseudomembranous candidiasis (oral thrush) - patches of curd like, white or yellowish plaques that occur anywhere (particularly cheeks, gyms, palate and tongue)
Erythematous candidiasis (atrophic oral candidiasis) - soreness and erythema, particularly on the palate and dorsum of the tongue. Filiform papillae disappear and dorsum appears smooth
Denture stomatitis - erythema, rarely sore, in the denture bearing area
Angular cheilitis - erythema, fissuring, soreness at angles of the mouth
Hyperplastic oral candidiasis (plaque like oral candidiasis) - nodular forms or white plaques on cheek, tongue, not easily removed
Median rhomboid glossitis - central, erythematous, demarcated area of papillary atrophy of the tongue along the posterior midline
All cases - can impair speech, feeding, failure to thrive, dry mouth, globus sensation, dysphagia or odynophagia if severe.
oral thrush Ix
Microscopy, sensitivities and culture swabs
Tongue scraping - remove white plaques to reveal a red base
Clinical diagnosis
Bloods - FBC, HbA1C, glucose, TFTs for recurrent or chronic cases
Swab or biopsy - underlying cause
oral thrush management
Children <16 YOs:
Topical antifungal 1st line oral miconazole gel for 7 days, 2nd line oral nystatin suspension for 7 days
Good dental hygiene, particularly with ICS use
Consider paediatric advice if extensive or unresponsive
Adults >16 YOs:
Topical antifungal 1st line oral miconazole gel for 7 days, 2nd line oral nystatin suspension for 7 days
Oral antifungal fluconazole 50mg OD for 7 days (extend to 14 days if not completely resolved)
Good dental hygiene particularly if ICS use or dentures
Smoking cessation
Consider referral to oral/maxillofacial surgeon if extensive or unresponsive after 14 days
Immunosuppressed patients:
Seek specialist advice prior to treatment if person is taking ciclosporin or oral tacrolimus or receiving chemotherapy
Consider extended fluconazole course or increase to 100mg dose OD
Lower threshold for bloods/drug monitoring
HIV: PO fluconazole 100mg for 7 days, provided the person is otherwise well and not taking prophylactic antimycotic treatment. Seek specialist advice before starting treatment.
Nasal polyps and risk factors
Background:
Swelling in the lining of the nose usually due to inflammation
Can occur at any site in the nasal cavity or paranasal sinuses but most commonly seen in the clefts of the middle meatus (lateral wall) and a significant proportion arise from the ethmoid sinus
Pathology:
Growth of tissue/cells forming lumps/masses throughout the
nasal cavity
Aetiology:
Unknown, thought to be chronic inflammation may trigger polyp formation
Risk factors: Male (2:1) Late onset asthma Aspirin intolerance in adults Cystic fibrosis
nasal polyps presentation
History of recurring acute or chronic sinusitis Symptoms depend on size of the polyp Nasal airway obstruction Nasal discharge - watery, green may suggest infection, unilateral, blood tinged suggests tumour, foreign body, nose picking, misapplication of nasal spray Rhinorrhea Sneezing Postnasal drainage Dull headaches Snoring and obstructive sleep symptoms Hyposmia or anosmia and reduced taste Examination - yellowish gray structures, singular or multiple grape like lesions, NOT sensitive to palpation, usually bilateral Widened nasal bridge
nasal polyps Ix and referrals
Investigation/diagnosis:
Rhinoscopy (rigid or flexible) to confirm diagnosis, exclude infection or red flags
CT scans for those with failing medical therapy or with atypical or severe disease
Refer:
Polyp diagnosis uncertain
Unilateral polyps (malignancy) 2WW
Children with polyps (cystic fibrosis)
nasal polyps management
1st line intranasal topical steroid (mometasone, fluticasone, beclomethasone, triamcinolone in each nostril) - avoid BD beclomethasone in children
AVOID with untreated fungal, bacterial or viral nasal infections, after recurrent nasal surgery or trauma (unless specialist advised) or with pulmonary TB
Review for associated or underlying conditions - asthma and aspirin sensitivities
Antihistamines if allergic rhinitis present
Nasal douching with saline combined with medical management
Leukotriene receptor antagonists
Systemic corticosteroids short course, consider injection by specialist
Surgical management - functional endoscopic sinus surgery (FESS) to restore nasal function, reserved for last resort but there is an argument for early intervention to reduce exposure to adverse effects of medical management
chronic otitis media
Pathology:
Persistent infection of inflammation of the middle ear
Can result in formation of polyps or tympanic membrane perforations as well as destruction of ossicles, causing conductive hearing loss
Can lead to cholesteatoma formation
Aetiology:
Recurrent acute otitis media
Blockage of the eustachian tube
Flare ups after infections or water entering the ear
chronic otitis media presentation, Ix and Mx
Presentation:
Each discharge
Hearing loss
Persistent or recurrent acute otitis media symptoms or flares
Investigation:
Ear examination
CT/MRI for cholesteatoma, polyps, structural damage etc.
Management:
Keep water out of the ear, clean and dry all drainage
Antibiotic ear drops
Oral antibiotics
Surgery to repair tympanic membrane, ossicles, remove cholaestoma etc.
hearing impairment
Background:
Can be congenital or acquired
Conductive hearing loss (CHL) - problem in the outer or middle ear
Sensorineural hearing loss (SNHL) - problem in the inner ear, CN VIII, auditory pathways or auditory cortex (sensory - cochlea, inner ear and neural - CN VIII, pathway, cortex)
Pathology:
Depends on underlying cause
Aetiology/risk factors:
External ear - trauma, cerumen
Middle ear - trauma, fluid
Inner ear - trauma, infection, meniere’s disease
Auditory pathway - viral infection or tumours
Congenital - maternal rubella or cytomegalovirus infection during pregnancy, genetic deafness (autosomal recessive or dominant), associated syndrome such as Down’s syndrome
Perinatal - prematurity or hypoxia during/after birth
Infancy - jaundice, meningitis and encephalitis, otitis media or glue ear and chemotherapy
hearing impairment presentation and Ix
Presentation:
Reported hearing loss from patient or parent
Ignoring calls or sounds
Children - Frustration or bad behaviour, poor speech and language development, poor school performance
Investigations/diagnosis:
Ear examination - exclude wax or acute infections
UK newborn hearing screening programme (NHSP) testing hearing in all neonates
Hearing assessment - whisper test, Rinne - Weber tests,
Audiometry tests - pure tone audiometry (standard), speech audiometry and acoustic impedance audiometry (tympanometry)
hearing loss/impairment management
Children: MDT referral, speech and language therapy, educational psychology, ENT specialist, hearing aids for children with retained hearing and sign language ]
First time presentation - exclude acute causes (wax, infections), refer for investigations and management
Educate on support available, sign language, leaflets on hearing loss and support groups
Idiopathic sudden sensorineural hearing loss - consider steroid
Hearing aids
Assistive listening devices - personal loops, communicators, TV amplifiers, telephone devices, smoke alarms, doorbell sensors etc. (direct to the social services, fire service, access to work or disabled student allowance etc.)
hearing impairment referrals
Refer anyone to ENT with: unilateral hearing loss, fluctuating hearing loss not associated with URTI, hyperacusis (intolerance to everyday sounds), persistent tinnitus unilateral, pulsatile or significantly changing/causing distress, vertigo that has not resolved or is recurrent, hearing loss not age related
Refer with hearing loss after initial treatment of earwax to ENT with: partial/complete obstruction of external canal preventing examination, pain affecting ear for >1 week or not responding to Tx, history of discharge, abnormal appearance (inflammation, polyps, perforated ED, swelling, blood etc., or a middle ear effusion in absence or persisting after URTI
Sudden or rapid hearing loss - refer those with hearing loss over <3 days within the past 30 days immediately (24 hours) to the ENT or emergency department. Refer those with sudden hearing loss >30 days OR if hearing loss worsens rapidly over period of 4-90 days ago urgently (within 2 weeks) to ENT/audiovestibular medicine service
Acquired unilateral hearing loss and altered sensations/facial droop to ENT or stroke referral immediately (24 hours)
Adults who are immunocompromised and have otalgia (eacharche) with otorrhea (discharge) not responding to Tx within 72 hours to ENT immediately
whisper test
General assessment to start hearing exam
Standing 60cm from patients hear
Whispering numbers in one ear whilst blocking the other
Ask patient to repeat the numbers
audiometry tests
Measures softest, least audible sound (quantitative) in decibels (db) and frequency in hertz Hz
PTA pure tone audiometry is standard testing
Speech audiometry - patient is asked to repeat words, presented via headphones used to predict if hearing aids would help
Acoustic impedance audiometry (Tympanometry): acoustic signal reflected back by the ™, giving a compliance curve. Useful in glue ear assessment
Audiogram - plots frequency on x axis from low to high pitch, then volume on Y axis from low to high db. Each ear bone and air conduction is tested and plotted (X - left AC, ] - left BC, O - right AC, [ - right BC)
In normal hearing all readings will be between 0-20dbs at the top of the chart
In those with sensorineural HL both air and bone will be >20dbs plotted below 20db line on the chart. May be uni or bilateral
In those with conductive hearing loss, BC will be normal but air conduction will be >20db, plotted below the 20 db line on the chart
In those with mixed hearing loss both air and bone conduction will be >20dbs but there will be a difference of >15dbs between the BC > AC
barotrauma pathology, risk factors and presentation
Pathology/cause:
When the eustachian tube (ET) is occluded, the middle ear pressure cannot be equalised during descent in an aircraft or diving so causes damage
Risk factors:
URTI
Conditions inhibiting function of the eustachian tube
Presentation:
Severe pain as drum becomes indrawn/pressure does not equalise
Transudation or bleeding into the middle ear
Perforation of tympanic membrane
Tinnitus
Vertigo
Deafness and hearing loss
barotrauma Ix, Mx and prevention
Investigations/diagnosis:
Clinical diagnosis
Management:
Assurance and education of preventative measures and of symptoms (tinnitus, pain etc.)
Treat underlying cause
Follow up for cause resolution - URTI within 1-2 weeks, effusions clear spontaneously and most perforations heal within 6-8 weeks.
Prevention
Avoid flying, diving with URTI or otitis media
Decongestants (nasal) Xylometazoline q 20 mins, pseudoephedrine
Repeated yawns, swallows/jaw movements or valsalva manoeuvres to open the ET
Inflating an otovent device
tympanic membrane perforation
Background:
Divided into two groups based on location of perforation
Marginal - involving the annulus (outer ring), typically more complex with slower healing rates and can result in cholesteatoma formation
Central - does not involve the annulus
Pathology:
Rupture or perforation in the eardrum
Increased risk of infection - AOM
Aetiology/risk factors: Otitis media Direct trauma (cotton buds included) Explosion Acoustic trauma (very loud noise) Barotrauma Surgery (iatrogenic rupture)
TM perforation presentation, Ix
Hearing loss, generally, the larger the perforation the greater the hearing loss
Based on underlying pathology - pain, discharge, itching, fever, tinnitus
Cholesteatoma - retraction in pars flaccida/attic area causing attic perforation
Investigation/diagnosis:
Clinical history
Ear examination (otoscopy) - note size and location of perforation
TM perforation management
Most heal within a few weeks of rupture without treatment within 6-8 weeks (90% children within one month)
Antibiotic drops if infection is suspected
Treating underlying cause e.g. cholesteatoma
It it does not heal spontaneously - surgery to close the tear or hole (myringoplasty/tympanoplasty)
Pinna pathology
Mainly cartilaginous therefore infection (perichondritis) in injuries such as burns, insect bites, piercings is challenging to treat and needs vigorous antibiotic treatment due to the naturally ischaemic tissue
Pinna haematoma from blunt trauma required aspiration and firm packing, complications include secondary infection and ischaemic necrosis then fibrosis (cauliflower ear)
ear foreign bodies
Common in children <5 YO and adults with learning difficulties
Organic FBs (seeds etc.) may swell and cause inflammation
Button batteries (hearing aids) require urgent removal
Method of removal includes syringing, suction, glue, gum etc.
cholesteatoma overview
Background:
Complications - facial paralysis, chronic infection, swelling, meningitis, brain abscess,
Pathology:
Benign skin growth in the middle ear behind the tympanic membrane
Often develops as a cyst the sheds layers of old skin, as these dead skin cells accumulate they may destroy bone of the middle ear, affecting hearing, balance and function of facial muscles due to the close proximity of the facial nerve to the middle ear
Aetiology:
Congenital defect
Repeated middle ear infections
Poorly functioning eustachian tube due to chronic ear infection, sinus infection, colds and allergies causing a partial vacuum in the middle ear which can pull the eardrum and cause a cyst
Presentation: Foul smelling fluid discharge Pressure within ear and discomfort Earache Hearing loss Vertigo Facial muscle paralysis
Investigation:
Ear examination
CT scan
Management:
Surgically removing the mass
Antibiotic regimen in lead up to surgery to treat infection, reduce inflammation and help drain the ear
Nasopharyngeal and oral cancer red flags
Oropharynx:
Persistent sore throat
Lump in mouth or throat
Pain in ear
Hypopharynx:
Dysphagia
Ear pain
Hoarse voice
Nasopharynx:
Lump in the neck
Nasal obstruction
Hoarseness
Other: Hemoptysis Halitosis Trismus (lock-jaw) suggests involvement of pterygoid muscles Weight loss
oral and nasopharyngeal tumours
Background:
Pharyngeal cancer is relatively uncommon in UK
Oropharyngeal cancer is uncommon and typically affects those aged 40-70
Increasing incidence of HPV-related SCC while tobacco-related SCC of the oropharynx is decreasing
Nasopharyngeal carcinoma is endemic in asia and is associated with the Epstein-Barr virus (EBV)
Pathology:
90% of all oropharyngeal tumours are SCC originating in the epithelial cells lining the throat
Other tumours include adenocarcinomas, lymphomas, sarcomas, melanomas
Precancerous lesions include leukoplakia, erythroplakia and mixed erythroleukoplakia
Aetiology: Can be HPV related Tobacco related Viral infection - Epstein-Barr related Risk factors: More common in South Asian background Indian origin
oral and nasopharyngeal cancer presentations
Painless swelling, lump or growth in the neck >3 weeks Hearing loss (unilateral usually) Tinnitus Fluid/discharge from ears Blocked nose (unilateral) Blood stained discharge from nose Epistaxis Headaches Cranial nerve involvement - diplopia and numbness of face (CN II-VI or IX-XII) Numbness in the face Dysphagia Voice changes/hoarseness Weight loss LAP in neck Advanced disease - metastases to skull, bone, lung and liver
Oral and nasopharyngeal cancer Ix
Bloods - FBC, LFTs
CXR - pulmonary metastases
Biopsy for diagnosis
CT/MRI for staging and management planning
Full head and neck examination including mouth - masses, patches, skin changes, LAP
Cranial nerve examination
oral and nasopharyngeal cancer management and referrals
Management:
Surgery +/- radio and chemotherapy
Palliative chemo and radiotherapy for inoperable or extensive cases
5 year survival rates are overall >40% but depend on stage presenting at.
Risk of recurrence is strongly dependent on site and stage of original disease
25% of recurrences are asymptomatic therefore close follow up should be given within the first 3 years with imaging, endoscopic exploration under anesthesia
60% have recurrence within 2 years and 80% by 3 years
Referrals:
Urgent 2WW referral for those with unexplained oral cavity ulceration lasting >3 weeks OR persistent and unexplained lump in the neck
Consider urgent 2WW referral to dentist with unexplained lump on lip or in oral cavity OR red/red and white patches in oral cavity consistent with erythroplakia or erythroleukoplakia (a dentist should also consider 2WW referral for these)
hairy leukoplakia overview
Results from infection with Epstein-Barr virus (EBV)
Once infected with EBV it remains in the body for life, normally dormant
If immune system is compromised (especially from HIV/AIDS) it can reactivate leading to hairy leukoplakia
White patches on the side of the tongue with ‘hairy’ appearance
Not likely to result in mouth cancers and usually does not need removal
May be given antiviral medications to prevent growth of patches
Topical ointments (retinoic acid) can reduce patch size
oral leukoplakia
Background:
Precancerous condition with thick, white or greyish patches forming usually inside the mouth
Mild - usually harmless and often self-resolving
More serious cases can be linked to oral cancers and must be promptly treated
Regular dental care can help prevent recurrences
Pathology:
Unknown but can develop into a cancerous lesion
Aetiology/Risk Factors:
Unknown - primarily linked to tobacco use
Smoking is primary cause but can be from trauma to the cheeks, rough, uneven teeth, dentures, inflammatory conditions and long-term alcohol use
oral leukoplakia presentation and Ix
Presentation:
Occurs on mucosal tissue, such as the mouth, gums, under tongue or lips most commonly.
May take several weeks to develop
Rarely painful
White-greyish patches inside the mouth that cannot be wiped away
Irregular or flat textured
Thick, hard, raised surface
Hairy or fuzzy (hairy leukoplakia)
Can appear with red lesions which are more likely to show malignant changes
Investigation/diagnosis:
Clinical examination
Biopsy to confirm
HIV screening
oral leukoplakia Mx and prevention
Management:
Reassurance that most patches improve on their own and need no treatment
Patient education as to risk of oropharyngeal cancers
Avoid any triggers such as smoking, poorly fitted dentures etc. (address any dental issues via dentist referral)
If biopsy comes back positive for cancers - excision of patch
Prevention:
Smoking cessation
Reduce alcohol intake
Antioxidant rich foods such as spinach, carrots helping deactivate irritants that may cause patches
erythroplakia
Background:
Fiery red patch that cannot be characterised clinically or pathologically as any other definable lesion
Much higher risk of becoming malignant than other oral precancerous lesions.
Pathology:
Unknown
Aetiology:
Unknown but strongly associated with drinking alcohol and smoking
Risk factors: Smoking Alcohol Increasing age Men
erythroplakia presentation and Ix
Presentation:
Smooth, velvety granular or nodular lesions with well defined margins adjacent to normal mucosa
Often on the soft palate, floor of the mouth, ventral surface of the tongue, retromolar area
Rarely multiple patches and rarely extensive areas
Soft on palpation unless indurated (invasive carcinoma)
Investigation/diagnosis:
Clinical examination
Biopsy to confirm
History to establish risk factors
erythroplakia Mx
Oral erythroplakia focuses on prevention of malignant transformation and early detection of occult malignancy
Patient education of the condition and chance of malignancy
Advise of smoking cessation/alcohol reduction, encourage a diet rich in vegetables and fruits
Suspicious lesions should be excised surgically or via laser removal
Recurrence rates and development of malignancy are high so needs long-term follow ups
laryngeal and hypo pharyngeal cancers
Background:
Laryngeal and hypopharyngeal cancers present very similarly and are often treated the same
Rarely diagnosed <40 YOs (usually 60+)
Pathology:
Hypopharynx sits at the low end of the pharynx, immediately behind the larynx connecting the mouth and back of the nose to the trachea
Aetiology:
Multifactorial
Risk factors:
Smoking
Alcohol intake
Diet low in fruit and vegetables
laryngeal and hypo pharyngeal cancer presentation and Ix
Presentation: Chronic hoarseness is the most common early symptom Pain Dysphagia Lump in neck Sore throat Earache Persistent cough Breathlessness, aspiration, hemoptysis, fatigue, weakness or weight loss (B symptoms)
Investigation/diagnosis:
Ix are not recommended for primary care as they can delay diagnosis
CXR for hoarseness/breathlessness symptoms to check for pulmonary cancer, refer to head and neck cancers if this is clear
Refer all those with hoarseness for >3 weeks for CXR
Flexible laryngoscopy
FNA biopsy diagnostic
CT/MRI/PET-CT scanning for staging
Examination under general anaesthesia for palpation and direct laryngoscopy with biopsy
laryngeal and hypo pharyngeal cancer management and referrals
Management:
Hypopharynx - radiotherapy to remove cancerous cells if in early stages
Advanced - surgery to remove parts or all of the larynx, hypopharynx or radiotherapy and chemotherapy
Laryngeal red flags:
Urgent referral 2WW for those aged >45 with persistent unexplained hoarseness >3 weeks OR unexplained lump in the neck
nasopharyngeal cancer
Background:
Often presents with non-specific symptoms resulting in a late presentation/diagnosis
Prevalent malignancy in Southeast Asia, Alaska, Greenland and Tunisia
Relatively uncommon in western countries
Peak incidence in 30-40 and 50-60 years
3 main types: all types are treated in the same way Keratinising SCC: keratin within cancer cells Non keratinising SCC: most common type Basaloid SCC (rare) Other types (rare) include adenocarcinomas, lymphoma, melanomas and sarcomas etc.
Pathology:
May be well differentiated, moderate or undifferentiated
Undifferentiated is most common and is strongly associated with EBV infection
Aetiology:
Multifactorial cause
Risk factors: Male (2:1) Origin from Southeast Asia, Alaska, Greenland and Tunisia EBV exposure Heavy alcohol intake
nasopharyngeal cancer Ix, Mx and prognosis
Investigation/diagnosis:
Biopsy is diagnostic (FNA useful)
Skull XRs/CT/MRI/PET scan for staging and management plans
EBV screening (PCR)
Management:
External beam radiation therapy is primary therapy for untreated nasopharyngeal carcinoma
Chemotherapy +/- radiotherapy
Salvage nasopharyngectomy and neck dissection for persistent or recurrent carcinomas +/- chemo/radiotherapy
Palliative care for terminal/multiple distant metastases
Follow up/monitoring - thorough examination of the head/neck for risk of recurrence, surveillance of TFTs, pituitary function, dental checks, oral hygiene monitoring, jaw exercises (avoid trismus), cranial nerve functions and evaluate systemic complaints to identify distant metastases
Prognosis:
Some have long, protracted course and some patients can live for many years
5 year survival rate is roughly 80%, however 20-30% of patients finally progress with distant metastases and/or local/regional recurrence
Nasal and sinus cancer
Background:
Rare cancer affecting men aged >40
Pathology:
Cancerous mutations
Aetiology:
Multifactorial
Risk factors: Male >40 YOs Exposure to dusts, cloth fibres, nickel, chromium and formaldehyde Smoking HPV infection
nasal and sinus cancer presentation
Persistent blocked nose (unilateral) Epistaxis Decreased smell Rhinorrhea Post-nasal drip Pain or numbness of the face (upper cheeks) Swollen neck glands Diplopia Watery eyes Pain or pressure unilaterally in ears Persistent lump on the face, nose, roof of the mouth
nasal and sinus cancers Ix and Mx
Investigation: Nasoendoscopy Panendoscopy Biopsy to confirm Head and neck examination Cranial nerve examination CT/MRI/PET scan for staging and planning management
Management: 2WW referral for persistent unexplained unilateral symptoms, masses in face or neck, weight loss Reassurance and providing information of support groups Surgery to remove tumours Radiotherapy Chemotherapy Smoking cessation MDT follow ups and management 5 years survival rate is around 50%
Aphthous ulcers
Background:
Oral ulcers can be acute or chronic, localised or diffuse
One of the most common oral problems in primary care
Canker sores - clearly defined, painful, shallow, round/oval ulcers not associated with systemic disease, non-infective
Pathology:
Loss of mucosal layer within the mouth
Aetiology:
Local trauma (most common) - dentures, braces, sharp or broken teeth, cheek or tongue biting
Chemical injury - aspirin, NSAIDs, bisphosphonates, improperly cleaned/rinsed dentures
Thermal injury - hot foods/liquids often on the tongue or palate
Systemic causes - autoimmune conditions, dermatoses (lichen planus, erythema multiforme), inflammatory conditions (IBD, reactive arthritis)
aphthous ulcers risk factors and presentation
Risk factors: Women <40 YOs Non-smokers White British ethnicity Higher socio-economic status Family history Stress Food sensitivities Hormonal changes (pregnancy - tend to improve)
Presentation:
Clearly defined, painful, shallow, round/oval ulcers
Symptoms of underlying conditions
No associated symptoms
Triggers/timings of ulcers - after certain foods/drinks/time of month etc.
aphthous ulcers Mx
Management:
Heals within 10 days usually with removal of cause
Ix underlying causes and treat as needed
Mouthwashes - saline (half teaspoon of salt in warm water) use PRN DO NOT SWALLOW, antiseptic mouthwashes for secondary bacterial infections
Topical corticosteroids as dissolvable tablets, outhwashes, pastes, inhaler sprays most effective in prodromal phase of ulcers (beclometasone inhaler 50-100mcg BD (warn of oral thrush)
Local analgesics - lidocaine, lozenges, sprays, systemic analgesics if needed
Antiinflammatories - benzydamine and flurbiprofen mouthwashes, sprays etc.
Orabase available OTC
Low dose oral doxycycline 20mg BD for 3 months for periodontitis
Aphthous ulcers Ix and referrals
Investigation/diagnosis:
Extensive history to determine cause and triggers
Mouth examination (check for LAP)
Bloods - FBC, ESR, ferritin, folate, B12)
Referral:
2WW for unexplained ulceration lasting >2 weeks
2WW for red/red or white patch in oral cavity consistent with erythroplakia or erythroleukoplakia
Refer urgently for unexplained red/white patches that are painful, swollen or bleeding
Refer routinely for unexplained red/white patches that are not painful, swollen or bleeding, frequently disabling recurrent aphthous ulceration that cannot be controlled or suspected underlying cause needing specialist management
laryngitis and risk factors
Background:
Acute <3 weeks
Chronic >3 weeks
Pathology:
Inflammation of the larynx
Aetiology:
Most commonly from viral infections but can be bacterial, fungal, trumatic (coughing, screaming/loud singing, habitual throat clearing)
Chronic - reflux, allergies, trauma, autoimmune diseases, smoking
Risk factors: Smoking RTIs GORD Allergies Autoimmune diseases
laryngitis presentation and Ix
Presentation: Hoarse or breathy voice Pain or discomfort anteriorly in the neck Symptoms of URTI - cough, rhinitis Dysphagia Globus pharyngeus Continual throat clearing Myalgia Fever Fatigue and malaise
Chronic - underlying cause symptoms/history of conditions or medication use, history of intubation or surgery to the throat, neck trauma etc.
Investigation/diagnosis: Examination of throat and neck (masses, LAP, epiglottitis etc.) Swabs if exudate present and culture Laryngoscopy Bloods - FBC, serology for autoimmune markers, syphilis and TB screening Lateral XR of neck CT/MRI Barium swallow with contrast
laryngitis management and referrals
Acute:
Reassurance most cases are mild and self limiting
Vocal hygiene - resting voice, avoiding smoking, chewing sugar free gum, drinking lots of fluids, reducing caffeine, lepsips, hot teas etc.
Antibiotics for persistent fever >48 hours, purulent sputum, associated immunodeficiency
Chronic:
Voice hygiene
Voice therapy (speech therapist)
Treat underlying conditions and causes
Referrals:
Refer those with hoarse voice/change to voice for >3 weeks to laryngoscopy 2WW
Refer those with signs of immediate/emergency obstruction to A&E immediately/secondary care
Urgent referral considered for those with recent surgery to neck, intubation, radiotherapy, history of smoking, weight loss, mass in neck, professional voice user (singer etc.), otalgia, dysphagia, signs of systemic illness
oral herpes simplex
Background:
1% of primary care consultations result from cold sores
56-85% of people have serological evidence of HSV-1 by early adulthood
20-40% of young adults who are seropositive for HSV-1 have recurrent cold sores
Recurrences are typically between 2-6 times a year
Pathology:
Transmission via viral shedding into saliva, direct contact with saliva while asymptomatic but more so when symptomatic
Shedding occurs up to 60 hours after symptoms onset
Aetiology/Risk factors:
Factors triggering recurrence - immunosuppression, URTI, fatigue, stress, physical trauma, sun exposure, menstruation, obesity
oral herpes simplex presentation and Ix
Presentation:
Blisters around the mouth
Recurrent oral ulceration on or around the lips (cold sores)
Primary infection - most often in infancy or childhood, may not be symptomatic most commonly present as vesicles and ulcers on the tongue, lips, gums, palate, painful, not able to swallow, drooling, dehydration is common. Associated fever, LAP, halitosis, lethargy, irritability and loss of appetite
Herpetic whitlow may occur with spread to fingers
Recurrent infection - most commonly cold sores, tend to be unilateral, same location recurring 2-3 times per year. On lips, skin around the mouth, chin, nose, begin as erythematous areas that swell into papules, then vesicles, then ulcers over 1-3 days. Ulcers crust over and skin returns to normal within 2 weeks.
Prodromal symptoms - tingling, pain, itching 6-24 hours before lesions appear
Investigation/diagnosis:
Clinical diagnosis
Viral culture GOLD STANDARD
Management of oral herpes simplex
Reassurance and patient education as to how to reduce spreading (avoid kissing while symptomatic, don’t touch lesions, wash hands with soap regularly, do not share lipsticks, avoid oral sex with lesions, do NOT need to exclude children from school) and that lesions heal without scarring by themselves within 2 weeks
Advise of prodromal period being the most effective time to apply Topical antivirals - acyclovir - helps resolution within 7-10 days (oral antivirals for immunocompromised patients)
Local analgesic such as choline salicylate gel (CI in <16YOs due to Reye’s syndrome) or lidocaine gel
Paracetamol or ibuprofen for symptoms relief
Laser therapy decreases pain and reduces the number of recurrences, particularly useful for elderly patients due to low frequency of side effects.
epiglottitis
Background:
Life threatening emergency, now rare due to vaccination programme in children
Previously most common in young children but now can be more prevalent in adults due to vaccination
Pathology:
Inflammation and swelling of the epiglottis due to presence of an infection
Can completely obscure the airways within hours of symptoms developing
Aetiology:
Typically H. influenzae type B
Risk factors:
Unvaccinated young children
epiglottitis presentation and Ix
Presentation: Sore throat Stridor Drooling Tripod position, sat forward with hands on knees using accessory muscles to assist breathing High fever Difficulty or painful swallowing Muffled voice Scared and quiet child Septic and unwell Sternal recession and accessory muscle use
Investigation/diagnosis:
ABCDE approach
Lateral XR of neck - characteristic “thumb sign” confirms diagnosis showing swollen and oedematous epiglottis and excludes foreign body
epiglottitis management
Reassure and comfort patient, avoid examinations where possible
Alert senior paediatrician and anaesthetist
Secure airway (intubation not needed in most cases but must be available)
Tracheostomy if airway closes completely and transfer to ICU
IV antibiotics (ceftriaxone)
Steroids (dexamethasone)
Common complication - epiglottic abscess which is also life threatening, monitor for this and treat promptly
Sialadentitis
Background:
Inflammation of a salivary gland, most commonly the parotid gland (parotitis)
Can be acute, chronic, infective or autoimmune related
Sialolithiasis refers to dilation of a duct due to stones or strictures
Sialadenosis refers to non-neoplastic non-inflammatory swelling with acinar hypertrophy and ductal atrophy
Pathology:
Three pairs of major salivary glands: parotid, submandibular and sublingual. There are also a large number of minor salivary glands distributed widely throughout the oral mucosa, palate, uvula, mouth, tongue, paranasal sinuses etc.
Inflammation of any one of these glands causes tenderness, swelling and can lead to secondary infection if chronic
Aetiology:
Parotitis - viral (mumps), stones, tumours, Sjogren’s syndrome, sarcoidosis, bacterial infection, HIV related infiltration
Submandibular - stones, tumours, sjogren’s syndrome
Minor glands - mucoceles, tumours
Sialadentitis presentation
Swelling uni/bilaterally around gland
Submandibular - swelling beneath and anterior to angle of the jaw, presence of inflammation or pus or visible impacted stone when lifting the tongue to the roof of the mouth
Sublingual - swelling on floor of the mouth
Examination of the facial nerve - facial weakness or asymmetry is suggestive of malignancy
Sign of underlying cause - dry mouth (Sjorgren’s)
Fever, unwell
Difficulty talking and swallowing
Sialadentitis Ix and Mx
Investigation/diagnosis: Bloods - FBC, inflammatory markers, U+Es, cultures, viral serology, HIV screening Salivary antibody testing Pus swab for culture Sialography USS CT/MRI FNA and biopsy for suspected malignancy
Management:
Identify and treat underlying cause
Bacterial Infection - antibiotics, incision and drainage for abcesses
Viral infections - supportive
Stone or strictures - conservative measures promoting salivation to flush out or surgical removal
dental abscess and RFs
Background:
Two main types: periapical and periodontal
Periapical - starts in the centre of the tooth, most common type
Periodontal - starts in supporting structures of the teeth such as the periodontium (between tooth and gums)
Pathology:
Collection of pus within a tooth or nearby structure
Aetiology:
Bacterial infection
Periapical - usually a result of complication of tooth decay
Periodontium - usually a complication of gum disease, periodontal disease where the gums begin to detach from the tooth slightly, allowing pockets to form which may be filled with pus if bacterial infection is present.
Risk factors:
Poor dental hygiene
Gum disease
Dental abscess presentation, Ix and Mx
Presentation: Toothache (severe, throbbing) Gum swelling and tenderness Facial swelling, erythema Affected tooth may be tender or become loose Fever Malaise Jaw spasms (severe)
Investigation/diagnosis:
Oral examination
Vital signs
Management:
Referral to dentist for Ix and Mx same day referral
Incision and drainage of abscess
GP - Cannot prescribe analgesia for infection, may prescribe antibiotics but only if diagnosis is clear to help relieve symptoms
Take simple analgesia for pain OTC
Acoustic neuroma
Background:
8% of all intracranial tumours and 80% of those arising at the cerebellopontine angle (CPA)
Arising from the CPA are usually later presenting (can grow as big as 4cm before symptoms) while those from the internal auditory canal present with symptoms much earlier
Pathology:
Tumours of the vestibulocochlear nerve (CN VIII) arising from Schwann cells of nerve sheath
Most arise from the vestibular portion of the nerve, typically benign and slow growing
Risk factors:
Neurofibromas
High dose ionising radiation of the head and neck
acoustic neuroma presentation, Ix and Mx
Presentation:
Any unilateral sensorineural hearing loss should be treated as an acoustic neuroma until proven otherwise
Unilateral hearing loss or tinnitus
Impaired facial sensation
Balance problems without explanation
Earache (Otalgia)
Hydrocephalus, visual loss and persistent headache, decreased consciousness - severe brainstem compression
Investigation/diagnosis: Any unilateral sensorineural hearing loss should be treated as an acoustic neuroma until proven otherwise Audiology MRI GOLD STANDARD CT
Management:
Microsurgery
Radiotherapy and observation
Small neuroma with good hearing - watch and wait
