ENT Flashcards
Acute otitis media
Inflammation of the middle ear associated with an effusion, rapid onset of signs and symptoms of an ear infection
Persistent - same episode, persists after management or is worsening
Recurrent - 3 or more within 6 months, 4 or more in the last 12 months
AOM causes
Bacterial - Haemophilus influenzae, Streptococcus pneumoniae
Viral - Adenovirus, Rhinovirus
AOM risk factors
Younger age
Male
Smoking/passive smoking
Frequent contact with children
AOM features
Ear pain
Reduced hearing in the affected ear
Fever
Cough
Sore throat
AOM otoscopy
Tympanic membrane is red, yellow or cloudy
May be bulging with air-fluid level
May have perforation (discharge in ear canal and hole in tympanic membrane)
AOM management
Analgesia and antipyretics (paracetamol, ibuprofen), typically self-limiting and resolves in 3 days (can be up to 1 wk)
If Abx required give 5-7 day course of amoxicillin (clarithromycin or erythromycin if allergic), can give as immediate or back-up if patient becomes systemically unwell or is likely to have complications
AOM complications
Recurrent or persistent infection
Mastoiditis
Hearing loss
Tympanic perforation
Facial nerve paralysis
Labrynthitis
CSOM
Chronic inflammation of the middle ear and mastoid cavity
Presents with recurrent ear discharges through a tympanic perforation for at least 2 weeks
Complication of AOM
CSOM organisms
Pseudomonas aeruginosa
Staphylococcus aureus
Aspergillus species
Candida species
CSOM risk factors
Younger age
Atopy
URTI
AOM
Second-hand smoke
Snoring
CSOM features
Ear discharge for >2 weeks
No ear pain or fever
Hearing loss in affected ear
Hx of AOM
Ear trauma
Glue ear grommets
May have tinnitus or pressure in the ear
CSOM otoscopy
Tympanic membrane perforation
Middle ear inflammation
CSOM examination
Postauricular swelling and tenderness, facial paralysis, vertigo, intracranial involvement
Assess hearing loss and impact on ADL
Exclude otitis externa, foreign body, wax, and neoplasm
CSOM red flags
Indicative of mastoiditis or intracranial infection - headache, nystagmus, vertigo, fever, labrynthitis, facial paralysis, swelling/tenderness behind the ear
CSOM management
Referral to ENT for diagnosis
DO NOT swab or initiate treatment
Advise to keep ear dry and clean with dry cotton wool
Reassure that any hearing loss will likely return to normal after treatment and perforation heals
CSOM complications
Mastoiditis
Meningitis
Facial nerve paresis
Intracranial abscess
Sigmoid sinus thrombosis
OMwE
“glue ear”, characterised by a collection of fluid within the middle ear space, without signs of acute inflammation
OMwE causes
Eustachian tube dysfunction
Adenoidal infection/inflammation
Pressure in the middle ear cannot be regulated so a negative pressure is created, fluid is drawn into the middle ear cavity from the mucous membranes
OMwE risk factors
Bottle fed
Paternal smoking
Atopy
Genetic disorders - mucociliary disorders or craniofacial disorders
OMwE features
Unilateral conductive hearing loss
Tinnitus
Otalgia, sensation of pressure within the ear
Vertigo
OMwE otoscopy
Tympanic membrane retracted
Straw coloured due to the presence of fluid
Dull with loss of light reflex
May see a “bubble” behind the membrane
OMwE management
50% resolve spontaneously, so active surveillance for 3 months
If no resolution:
- non-surgical: hearing aid insertion
- surgical: myringotomy & grommet insertion
Grommet insertion recommended for those with > 3 months bilateral OMwE & hearing level in better ear < 25-30dBHL
Any child with persistent disease and multiple grommet insertion should be considered for potential adenoidectomy
(Certain cases, such as patients with Down syndrome, first line therapy may actually be a hearing aid, as complications from grommet can be common)
OMwE complications
Conductive hearing loss
Speech and language delays in children
Damage to tympanic membrane
Balance problems and clumsiness
Infection secondary to grommets
Tympanosclerosis
OMwE referral
Down’s syndrome or cleft palate
Severe hearing loss
Persistent hearing loss
Structurally abnormal tympanic membrane
Suggestive of cholesteatoma
Dry tympanic perforation
Causes - barotrauma, direct trauma, sudden loud noise
Symptoms - sudden hearing loss, otalgia, tinnitus
Diagnosed on otoscopy
Treatment - most self-limiting, will heal in 6-8 weeks, avoid submerging ear in water, do not put anything in the ear (incl. ear drops), analgesia to reduce pain
Wet tympanic perforation
Causes - infection (otitis media - increased pressure in the middle ear cavity)
Symptoms - sudden hearing loss, otalgia, tinnitus
Otoscopy - diagnostic, will have presence of discharge in the auditory canal (differentiates from dry)
Treatment - antibiotics to treat underlying cause (amoxicillin for AOM)
Mastoiditis
Middle ear and mastoid are the same cavity so otitis media often causes a degree of mastoiditis -> the inflammation within the air cells can progress to necrosis and subperiosteal abscess, causing concern
Mastoiditis features
Tender, boggy, erythematous swelling behind the ear
Can push the pinna forward if left untreated
Otorrhoea, headaches, hearing loss in affected ear
Fever
Mastoiditis otoscopy
Bulging, erythematous tympanic membrane
May have fluid level behind membrane
Discharge may be present
Mastoiditis management
All should be managed in a hospital setting, high-dose broad-spectrum IV antibiotics for at least 1-2 days, followed by oral for 1-2 weeks (typically cephalosporins), analgesia and anti-pyretics
May need myringotomy (drainage of middle ear) as therapeutic or for culture
If subperiosteal abscess is present or severe symptoms with no improvement on IV anitbiotics - immediate mastoidectomy
Vestibular migraine
A migraine accompanied by vertigo, dizziness or balance problems
Vestibular migraine symptoms
Typical migraine symptoms - nausea, vomiting, photophobia, phonophobia (sensitivity to sound), sensitivity to movement, visual disturbances
Associated vestibular symptoms - vertigo, dizziness, balance disturbances
Vestibular migraine causes
Exact causes unknown
Certain triggers - stress, tiredness, hormones, eye strain, tension in neck or shoulders, irregular meals or lack of food, dehydration, caffeine, food additives, bright lights and flickering, loud noises, strong smells
Vestibular migraine diagnosis
At least 5 episodes
Present or past history of migraines
Vestibular symptoms lasting between 5 mins and 72 hrs
Migraine headache or associated symptoms in at least half of the episodes
Vestibular migraine management
Prevention - identify and avoid triggers, antidepressants, beta-blockers and antiepileptic medications
Acute treatment - analgesia, triptan medications, anti-emetics, avoid opiates
Tonsillitis
Inflammation of the palatine tonsils as a result of either a bacterial or viral infection
Tonsillitis aetiology
Viruses – adenovirus and EBV
Bacterial – strep pyogenes (group A strep)
Tonsillitis risk factors
Smoking – second hand from parents or personal smoking in older children
Tonsillitis clinical features
In general last between 5-7 days, symptoms lasting longer than 7 days may be due to glandular fever
Odynophagia
Fever
Reduced oral intake
Halitosis
New onset snoring
SoB
Examination: red, inflamed tonsils, white exudate spots on the tonsils, cervical lymphadenopathy
Centor criteria
Differentiate between bacterial and viral tonsillitis
1) Tonsillar exudate
2) Tender anterior cervical lymphadenopathy or lymphadenitis
3) Fever/history of fever
4) Absence of cough
Score of 3 or more = highly suggestive of bacterial infection
FeverPAIN criteria
Fever (during previous 24 hours)
Purulence
Attend rapidly (within 3 days after onset of symptoms)
Severely inflamed tonsils
No cough/coryza
Score 0-1 = 13-18%, score 2-3 = 34-40%, score 4-5 = 62-65%
Tonsillitis differentials
Quinsy/peritonsillar abscess
Pharyngitis
Glandular fever
Tonsillar malignancy
Epiglottitis
Tonsillitis management
Initial – inpatient admission/not: respiratory compromise, unable to eat or drink, patients not getting better with abx
Antibiotics – 7-10 days of penicillin V
Analgesia
Steroids
Operative treatment
- In one year: 7 or more episodes
- In two years: 5 or more episodes per year
- In three years: 3 or more episodes per year
Tonsillitis complications
Spread of the infection into the peritonsillar space = peritonsillar abscess
Spread into the retropharyngeal/parapharyngeal spaces – requires prolonged IV abx and sometimes surgical drainage
Recurrent tonsillitis
Post streptococcal conditions
Post streptococcal glomerulonephritis – more common in children (6-8), classic triad of hypertension, haematuria and oedema, often proteinuria as well
Rheumatic fever – autoimmune response to GAS which typically affects children aged 5-14, develops 2-5 weeks after the initial infection and causes a variety of symptoms: prolonged fever, anaemia, arthritis & pancarditis
Glandular fever
Caused by EBV
Presents as a sore throat with associated fever and lymphadenopathy
Most common – 1-6 and 18-22
Glandular fever risk factors
Exchange of saliva – incubation period is around 6 weeks
Blood transfusion
Stem cell and solid organ transplant
Glandular fever clinical features
Sore throat (worst they’ve ever had), snoring & sleep apnoea, swollen neck
Systemic – feverish, headaches, N&V, tired all the time, generalised aches and pains in the muscles and joints
Examination – enlarged inflamed tonsils (often meeting in the middle), significant cervical lymphadenopathy, abdominal tenderness & splenomegaly, hepatomegaly, palatal petechiae
Glandular fever differentials
Tonsilitis – generally shorter-lived and tends to have fewer of the systemic symptoms
Quinsy – tends to be unilateral with swelling predominantly superior to the tonsil
Glandular fever investigations
Routine bloods – FBC (raised lymphocytes), LFTs – elevation of liver enzymes, should resolve in week 5
Monospot test in immunocompetent adults
More specific ELISA based immunoassays and anti-viral capsid antigen IgG
Glandular fever management
Symptomatic relief with paracetamol or ibuprofen
Condition is usually self limiting
Encouraging the person to return to normal activities as soon as possible, exclusion from work or school is not required
Avoid heavy lifting and contact sports for the first month of the illness – reduce the risk of splenic rupture
Advising on ways to limit the spread of the disease – avoid kissing, not sharing eating utensils
Glandular fever complications
Post-viral fatigue
Upper airways obstruction
Splenic rupture
Neutropenia
Immunocompromised people – may result in malignant disease eg. hodgkin’s lymphoma & nasopharyngeal carcinoma
Bell’s palsy
Acute, unilateral facial nerve weakness or paralysis of rapid onset (< 72 hours) and unknown cause
Bell’s palsy clinical features
Rapid onset
Facial muscle weakness involving upper & lower parts of the face -> reduction in movement on the affected side, often with drooping of the eyebrow & corner of the month and loss of nasolabial fold
Ear and postauricular region pain on affected side
Difficulty chewing, dry mouth & changes in taste
Incomplete eye closure, dry eye, eye pain or excessive tearing
Ramsey-hunt syndrome
Caused by VZV
Presents as a unilateral lower motor neurone facial nerve palsy
Painful and tender vesicular rash in the ear canal, pinna and around the ear on affected side
Treatment should be initiated within 72 hours: prednisolone & aciclovir, lubricating eye drops
Bell’s palsy management
Most people make a full recovery within 3-4 months
Important to keep eye lubricated – lubricating eye drops
For people presenting within 72 hours of the onset of symptoms = prednisolone
Antiviral treatments alone are not recommended
Croup
Common respiratory disease that typically occurs in children aged between 6 months and 3 years
Most commonly caused by a virus (parainfluenza virus types 1 or 3)
Croup clinical features
A child with a sudden onset of a seal-like barking cough
Hoarse voice
Symptoms typically worse at night & increase with agitation
Non-specific URT symptoms, progressive upper airway obstruction can result in the development of stridor and respiratory distress
Croup differentials
Bacterial tracheitis – following a viral-like respiratory illness from which the person appears to be recovering then becomes acutely worse
Epiglottitis – preferred posture is sitting upright with head extended, rarely seen since widespread immunisation against haemophilus influenzae B
Foreign body in upper airway
Peritonsillar abscess
Croup management
Single dose of oral dexamethasone to be taken immediately
Advise parents/carers:
- Symptoms usually resolve within 48 hours
- Use paracetamol/ibuprofen for fever/pain
- Fluids regularly
- Take child to hospital if respiratory distress
Acute sinusitis
Inflammation of the paranasal sinuses in the face
Usually triggered by a viral upper respiratory tract infection & defined by symptoms that last less that 12 weeks
Acute sinusitis clinical features
Adults – presence of nasal blockage (obstruction/congestion) or nasal discharge (anterior/posterior nasal drip) with facial pain/pressure and/or reduction of sense of smell
- Other features: altered speech, tenderness, swelling or redness over the cheekbone, cough
Children – presence of nasal blockage or discoloured nasal discharge with facial pain/pressure and/or cough
O/E – inspect and palpate maxillofacial area to elicit swelling and tenderness, performing anterior rhinoscopy
When should you suspect acute bacterial sinusitis?
Symptoms > 10 days
Discoloured/purulent nasal discharge
Severe local pain
Fever > 38
Marked deterioration after an initial milder form of the illness
Elevated ESR/CRP
Acute sinusitis management
Symptoms < 10 days – self-care measures
Symptoms > 10 days with no improvement – consider prescribing a high-dose nasal corticosteroid for 14 days, consider a back-up abx prescription (not necessary)
Chronic sinusitis
Symptoms > 12 weeks with objective evidence of sinonasal inflammation on examination
Chronic sinusitis clinical features
Lasting longer than 12 weeks
Adults – presence of nasal blockage/nasal discharge with facial pain/pressure and/or reduction of the sense of smell
Children – presence of nasal blockage/nasal discharge with facial pain/pressure and/or cough
O/E – evidence of sinonasal inflammation: inspecting and palpating the maxillofacial area, performing anterior rhinoscopy (nasal inflammation, mucosal oedema, mucopurulent nasal discharge)
Chronic sinusitis risk factors
Allergic rhinitis
Asthma
Immunosuppression
Chronic sinusitis management
Inform that chronic sinusitis may last several months
Advise the person – avoid allergic triggers, stop smoking, good dental hygiene, avoid underwater diving
Consider nasal irrigation with saline solution
Consider a course of intranasal corticosteroids for up to 3 months, especially if suspicion of an allergic cause
Weber’s test results
Normal result – patient hears the sound equally in both ears
Sensorineural hearing loss – sound will be louder in the normal ear
Conductive hearing loss – sound will be louder in the affected ear
Rinne’s test results
Normal – AC > BC
Abnormal – BC > AC
- Suggests a conductive cause for the hearing loss
Sensorineural hearing loss causes
Age-related presbycusis
Meniere’s disease
Labyrinthitis
Acoustic neuroma
Neurological conditions – stroke, MS, brain tumours
Medications – loop diuretics, aminoglycoside abx, chemotherapy drugs (cisplatin)
Conductive hearing loss causes
Ear wax
Infection – otitis media or otitis externa
Fluid in the middle ear
Eustachian tube dysfunction
Perforated tympanic membrane
Otosclerosis
Cholesteatoma
Presbycusis
Age-related hearing loss
Type of sensorineural hearing loss that occurs as people get older
Tends to affect high-pitched sounds first and more notably than lower-pitched sounds
Gradual and symmetrical
Presbycusis risk factors
Age
Male gender
Family history
Loud noise exposure (hearing protection should be worn in occupations such as woodworking/construction)
Diabetes
Hypertension
Ototoxic medications
Smoking
Presbycusis presentation
Gradual and insidious hearing loss
Female voices more difficult to understand
May be associated tinnitus
Patients with hearing loss are more likely to develop dementia & treating the hearing loss may reduce the risk
Presbycusis diagnosis
Audiometry
- Sensorineural hearing loss pattern
- Normal/near-normal hearing at lower frequencies
- Worsening hearing loss at higher frequencies
Presbycusis management
Effects cannot be reversed
Optimising the environment eg. reducing the ambient noise during conversations
Hearing aids
Cochlear implants (hearing aids are not sufficient)
Otitis externa
Inflammation of the skin in the external ear
Acute (< 6 weeks) and chronic (> 3 months)
Exposure to water whilst swimming can lead to inflammation in the ear canal, trauma another predisposing factor, removal of ear wax can increase the chances of infection
Otitis externa causes
Bacterial infection
Fungal infection – think in patients that have had multiple courses of topical abx
Eczema
Seborrheic dermatitis
Contact dermatitis
Otitis externa bacterial causes
Pseudomonas aeruginosa – gram-negative aerobic rod-shaped bacteria
Staph aureus
Otitis externa presentation
Ear pain
Discharge
Itchiness
Conductive hearing loss
Examination: erythema and swelling in the canal, tenderness, pus/discharge in the ear canal, lymphadenopathy
Otitis externa diagnosis
Can be made clinically with an examination of the ear canal
Ear swab can be used to identify the causative organisms but not usually required
Otitis externa management
Mild – acetic acid 2%, can also be used prophylactically before and after swimming in patients that are prone to otitis externa
Moderate – topical abx and steroid (eg. neomycin, dexamethasone and acetic acid = otomize)
- Aminoglycosides are potentially ototoxic, therefore essential to exclude a perforated tympanic membrane
Severe – may need oral antibiotics (flucloxacillin or clarithromycin)
Ear wick may be used if canal is very swollen & treatment with ear drops/sprays will be difficult (left there for a period of time and then removed when swelling settles)
Fungal infections – can be treated with clotrimazole
Malignant otitis externa
Severe and potentially life-threatening form of otitis externa
Infection spreads to the bones surrounding the ear canal and skull -> osteomyelitis of the temporal bone of the skull
Underlying risk factors – diabetes, immunosuppressant medications, HIV
Symptoms – persistent headache, severe pain and fever
Granulation tissue at the junction between the bone and cartilage in the ear canal is a key finding
Emergency management – admission under ENT, IV abx, imaging to assess extent of infection
Complications – facial nerve damage and palsy, other CN involvement, meningitis, intracranial thrombosis, death
Meniere’s disease
Long-term inner ear disorder that causes recurrent attacks of vertigo, symptoms of hearing loss, tinnitus & feeling of fullness
Meniere’s disease pathophysiology
Associated with the excessive build-up of endolymph in the labyrinth of the inner ear, causing an increased pressure and disrupting the sensory signals
Increased pressure of the endolymph = endolymphatic hydrops
Meniere’s disease presentation
40-50 years old, presenting with unilateral episodes of vertigo, hearing loss and tinnitus
Vertigo – comes in episodes, can come in clusters over several weeks followed by prolonged periods without vertigo symptoms, not triggered by movement or posture
Hearing loss – fluctuates (associated with vertigo attacks) then gradually becomes more permanent, sensorineural hearing loss, generally unilateral & affects low frequencies first
Tinnitus – occurs with episodes of vertigo before eventually becoming more permanent, usually unilateral
Other – fullness in the ear, unexplained falls without loss of consciousness, imbalance
Spontaneous nystagmus can be seen during an acute attack (usually in one direction)
Meniere’s disease diagnosis
Clinical, based on signs and symptoms
Made by an ENT specialist
Need an audiology assessment to evaluate hearing loss
Meniere’s disease management
Acute attacks – prochlorperazine, antihistamines (cyclizine, cinnarizine and promethazine)
Prophylaxis – betahistine
BPPV
Common cause of recurrent episodes of vertigo triggered by head movement
Peripheral cause of vertigo (problems is located in the inner ear)
BPPV presentation
Variety of head movements can trigger attacks of vertigo
Symptoms settles after around 20-60 seconds and patients are asymptomatic between attacks
Often episodes occur over several weeks and then resolve but can reoccur weeks or months later
Do NOT cause hearing loss/tinnitus
BPPV pathophysiology
Crystals of calcium carbonate that become displaced into the semicircular canals
Occurs most often in the posterior semi-circular canal
Crystals disrupt the normal flow of endolymph through the canals, confusing the vestibular system
Head movement creats the flow of endolymph in the canals, triggering episodes of vertigo
Dix-hallpike manoeuvre
Can be used to diagnose BPPV
1) Patient sits upright on a flat examination couch with their head turned 45 degrees to one side
2) Support the patient’s head to stay in the 45 degree position while rapidly lowering the patient backwards until their head is hanging off the end of the couch, extended 20-30 degrees
3) Hold the patient’s head still, turned 45 degrees to one side and extended 20-30 degrees below the level of the couch
4) Watch the eyes closely for 30-60 seconds, looking for nystagmus, repeat the test with the head turned 45 degrees in the other direction
Will trigger rotational nystagmus (towards the affected ear) and symptoms of vertigo
Epley manoeuvre
Can be used to treat BPPV, idea is to move the crystals in the semi circular canal into a position that does not disrupt endolymph flow
1) Have patient go from an upright position with their head rotated 45 degrees (to the affected side) down to a lying position with their head extended off the end of the bed, still rotated 45 degrees
2) Rotate the patient’s head 90 degrees past the central position
3) Have the patient roll onto their side so their head rotates a further 90 degrees in the same direction
4) Have the patient sit up sideways with the legs off the side of the couch
5) Position the head in the central position with the neck flexed 45 degrees, with the chin towards the chest
6) At each stage, support the patient’s head in place for 30 seconds & wait for any nystagmus/dizziness to settle
Brandt-daroff exercises
Can be performed by the patient at home to improve the symptoms of BPPV
Involve sitting on the end of a bed and lying sideways, from one side to the other, whilst rotating the head slightly to face the ceiling
Exercises are repeated several times a day until symptoms improve
Vestibular neuronitis
Inflammation of the vestibular nerve
Usually attributed to a viral infection
Vestibular neuronitis pathophysiology
Inflammation of the vestibular nerve, viral infection may trigger this
Distorts the signals travelling from the vestibular system to the brain, confusing the signal required to sense movements of the head
Results in episodes of vertigo where the brain thinks the head is moving when it is not
Vestibular neuronitis presentation
Acute onset of vertigo
May be history of a recent viral URTI
Most severe for the first few days, initially vertigo constant, after which it is triggered or worsened by head movement; associated with:
- N&V
- Balance problems
NO loss of hearing
Head impulse test
Can be used to diagnose peripheral causes of vertigo, resulting from problems with the vestibular system
1) Patient sitting upright and fixing gaze on examiner’s nose
2) Holds the patient’s head and rapidly jerks it 10-20 degrees in one direction while the patient continues looking at the examiner’s nose
3) Head is slowly moved back to the centre before repeating in the opposite direction
Eyes will saccade (rapidly move back and forth) as they eventually fix back on the examiner
Will be normal if patient has no current symptoms/central cause of vertigo
Vestibular neuronitis management
Prochlorperazine
Antihistamines (eg. cyclizine, cinnarizine and promethazine)
Symptomatic treatment can be used for up to 3 days, more extended use may slow down recovery
Referral if symptoms do not improve after 1 week/resolve after 6 weeks -> may require further investigation or vestibular rehabilitation therapy
Labyrinthitis
Inflammation of the bony labyrinth of the inner ear, including the semi circular canals, vestibule & cochlea
Usually attributed to a viral URTI
Rarely – can be caused by a bacterial infection, secondary to otitis media/meningitis
Labyrinthitis presentation
Acute onset vertigo
Hearing loss
Tinnitus
May have symptoms of causative virus – cough, sore throat and blocked nose
Labyrinthitis diagnosis
Clinical diagnosis
Head impulse test
Labyrinthitis management
Supportive care and short-term use of medication to suppress the symptoms
Prochlorperazine
Antihistamines
Abx for bacterial labyrinthitis
Rarely have lasting symptoms (but can have permanent hearing loss -> more common after bacterial labyrinthitis, particularly associated with meningitis)
Cholesteatoma
Abnormal collection of squamous epithelial cells in the middle ear
Non-cancerous but can invade local tissues and nerves and erode the bones of the middle ear
Can predispose to significant infections
Cholesteatoma pathophysiology
Negative pressure in the middle ear (caused by eustachian tube dysfunction) causes a pocket of the tympanic membrane to retract into the middle ear
Small area of the tympanic membrane gets sucked inwards
Squamous epithelial cells of this pocked continue to proliferate and grow into the surrounding space, bones and tissues
Can damage the ossicles resulting in permanent hearing loss
Cholesteatoma presentation
Foul discharge from the ear
Unilateral conductive hearing loss
Further symptoms – infection, pain, vertigo and facial nerve palsy
Otoscopy – abnormal bild-up of whitish debris or crust in the upper tympanic membrane
Cholesteatoma management
CT head can be used to confirm the diagnosis and plan for surgery
Surgical removal of the cholesteatoma
Nasal polyps
Growths of the mucosa that occur in the nasal cavity or sinuses
Often associated with inflammation, particularly with chronic rhinitis
Grow slowly and gradually obstruct the nasal passage
Unilateral polyps – red flag and should raise suspicions of tumours
Nasal polyps associations
Chronic rhinitis/sinusitis
Asthma
Samter’s triad – nasal polyps, asthma & aspirin intolerance/allergy
CF
Eosinophilic granulomatosis with polyangiitis (churg-strauss syndrome)
Nasal polyps management
Unilateral polyps should be referred for specialist assessment to exclude malignancy
Medical management – intranasal topical steroid drops or spray
Surgical treatment where medical management fails
- Intranasal polypectomy – polyps are visible close to the nostrils
- Endoscopic nasal polypectomy – where polyps are further in the nose or the sinuses
