Revise Notes Ent Flashcards
Acute Otitis Media
Acute Otitis Media
Pathophysiology
Inflammation of the middle ear, of infectious aetiology
AOM most commonly affects young children (3-36 months peak incidence)
Causes
Bacterial - haemophilus, strep. pneumoniae, moraxella
Viral - RSV, adenovirus
Clinical features
Symptoms
Acute onset of unilateral ear pain
In children this may be suggested by ear tugging, rubbing or general symptoms such as irritability, poor feeding, crying
Examination Findings
Otoscopy: The tympanic membrane appears…
Erythematous, inflamed
Bulging
May have an air-fluid level (if effusion is present)
If there is perforation, there may be discharge in the canal
AOM
Management
NICE advises admitting the following patients:
Severe systemic infection
Suspected complications of AOM (e.g. meningitis/mastoiditis)
Children < 3/12 with fever (T>38)
Consider admitting:
Any patient < 3/12 age
3-6 months with fever of 39 degrees or higher
Antibiotics
Most patients with AOM do not need antibiotics. There is no significant benefit in duration of illness/symptom severity.
Patients who should be considered for antibiotics include the following groups:
Patient is systemically very unwell - offer immediate ABx
Patient < 2 years with bilateral infection or otorrhoea - consider antibiotics (immediate or delayed script)
1st line: Amoxicillin for 5-7 days
Escalation: Co-amoxiclav - if worsening symptoms despite amox.
Pen all: Macrolide - clarithromycin/erythromycin
Chronic suppurative otitis media
Pathophysiology
A complication of AOM in which there is chronic inflammation within the middle ear, resulting in recurrent otorrhoea through a perforated tympanic membrane.
Clinical Features
Symptoms
Otorrhoea for > 2 weeks, often white, yellow or green
Conductive hearing loss
Sometimes tinnitus, aural fullness
NO history of ear pain, fever, systemic illness
There is usually a history of acute otitis media
Otoscopy
Perforated tympanic membrane
Dried discharge or debris in ear canal
Management
Refer to ENT - management typically with aural toilet, topical antibiotics (quinolones - ciprofloxacin) and steroids.
Acute mastoiditis
Pathophysiology
A complication of acute otitis media in which there is an extension of infection into the mastoid air cells.
Clinical Features
Symptoms
Ear pain
Otorrhoea
Worsening hearing loss
Examination Findings
Postauricular erythema, tenderness to palpation, boggy/fluctuance
Pinna can be displaced forward and downwards
Systemic upset - fever, sepsis
Otoscopy - erythematous, bulging tympanic membrane
Management
Emergency admission - IV ABx, may require surgery (e.g. cortical mastoidectomy)
Investigations - CT
References and Further Reading
NICE CKS. Otitis media - acute [May 2023]. Available at URL:
https://cks.nice.org.uk/topics/otitis-media-acute/
NICE CKS. Otitis media - chronic suppurative [July 2022]. Available at URL: https://cks.nice.org.uk/topics/otitis-media-chronic-suppurative/
Labyrinthitis
Pathophysiology
Labyrinthitis describes the inflammation of the labyrinth.
It can be differentiated from vestibular neuronitis by the presence of hearing loss (which is NOT present in VN).
Clinical features
Clinical features
Symptoms:
Vertigo
Hearing loss
Tinnitus
But NOT aural fullness (suggests Meniere’s)
Allergic Rhinitis
Pathophysiology
Exposure of the nasal mucosa to allergens results in IgE mediated inflammation of the nose
Causes
Seasonal allergic rhinitis - occuring at predictable times due to seasonal allergens (e.g. hay fever)
Perennial - seasons throughout the year due to persistent allergens (such as dust mites or animal allergies)
Clinical features
Sneezing
Nasal itching
Rhinorrhoea +/- congestion, post-nasal drip etc.
Frequently associated with allergic conjunctivitis - bilateral itchy eyes, hyperaemic/injected, tearing
History of atopy - asthma/allergies/atopic dermatitis, or FHx.
Management
Manage according to severity - symptoms are considered mild to moderate if they have minimal impact on QOL/ADLs/sleep, severe if they have more significant impact.
Vestibular Neuronitis
Pathophysiology
Inflammation of the vestibular nerve, most commonly occurs following a viral infection.
Clinical features
Vertigo
Vertigo is often severe, and begins suddenly
Vertigo is constant, even when head is still - but usually worsened by movement/changes in head position
This helps to differentiate from episodic vertigo such as BPPV (<1 min), MD (20mins+-24hrs)
Symptoms usually settle over a few days, and return to normal within 1-2 months
Other symptoms:
Imbalance, falls
Does NOT feature hearing loss ( labyrinthitis does - this is a key differentiating factor)
Does NOT cause tinnitus ( Meniere’s disease does)
There is often a history of a recent viral illness, e.g. URTI/flu-like illness
Examination findings
Fine horizontal nystagmus
Management
For rapid relief of severe vertigo/N&V - buccal/IM prochlorperazine (or cyclizine)
If symptoms less severe - short course (up to 3/7) of PO prochlorperazine/AH (cyclizine)
Meniere’s Disease
Pathophysiology
Meniere’s disease is an inner ear disorder of uncertain aetiology
There is an association with endolymphatic hydrops (swelling of the membranous labyrinth),
which results from an imbalance in the production and reabsorption of endolymph within the inner ear.
Clinical features
Meniere’s is characterised by
Episodic vertigo
Spontaneous +/- N&V
Episodes last at least 20 minutes (and no longer than 24hs)
Fluctuating sensorineural hearing loss
Roaring tinnitus
A sensation of aural fullness - the feeling of ‘pressure’ within the affected ear - often precedes a vertigo attack
Symptoms are most commonly unilateral
Management
Patients with suspected MD should be referred to ENT for confirmation of diagnosis
For the relief of vertigo, nausea & vomiting:
Prochlorperazine or antihistamine (e.g. cyclizine) for up to 7 days
If rapid relief of symptoms is required (e.g. severe symptoms):
Buccal/IM prochlorperazine (or IM cyclizine)
Prophylaxis:
Consider a trial of betahistine to reduce frequency/severity of episodes
Benign Paroxysmal Positional Vertigo
Pathophysiology
BPPV is caused by the movement of debris/crystals within the semicircular canals of the inner ear.
Movement of the head results in movement of the calcium carbonate crystals, which causes the endolymph to move and induces the spinning/rotational sensation of vertigo.
Clinical features
Most commonly presents between the ages of 50-70 yrs, women > men,
with recurrent episodes of transient vertigo - the room/surroundings spinning.
Vertigo is triggered by head movements/changes in position - classically when the person rolls over in bed or bends over.
Episodes of vertigo are usually short, lasting < 1-2 minutes
Hearing and tinnitus are NOT features of BPPV
Examination findings:
Dix-hallpike manoeuvre positive - provokes vertigo and nystagmus
Management
1st line: Epley manoeuvre
Suggest Brandt-Daroff rehabilitation exercises
NICE suggests that symptomatic drug treatment is of limited benefit for patients with BPPV
Assessment of vertigo - Red flags
Red flag symptoms may suggest a central cause of vertigo (e.g. POCS) and require urgent brain imaging. They include:
An isolated episode of persistent vertigo (lasting > 24rs), with sudden onset.
Associated headache
Acute deafness (and not consistent with Meniere’s)
Not provoked/altered by change in position (e.g. normal head impulse test)
Abnormal gait/ataxia
Neurological signs identified o/e inc. CN abnormalities/sensory changes or weakness.
Vertigo
Vertigo is a symptom which describes the sensation of the ‘room spinning’ or the (rotational) movement of one’s surroundings, in the absence of any true physical movement.
Causes of vertigo include
Central: Pathology within the brainstem/cerebellum
Posterior circulation stroke
Vestibular migraine
Intracranial tumours
MS
Peripheral: Typically an issue within the inner ear
ENT - BPPV, Meniere’s, vestibular neuronitis/labyrinthitis
Sore Throat
Background
Sore throats are most commonly the result of an URTI with inflammation of the throat mucosa.
Presentations include:
Acute pharyngitis - inflammation of the mucosa of the oropharynx
Tonsillitis
Assessment
The FeverPAIN or Centor criteria are recommended to determine the risk of group A streptococcal infection, and therefore the requirement for antibiotics.
Symptoms suggestive of strep: Scarlet fever rash, T>38.5, exudate, LN, no cough
FeverPain - 1 for each of the following:
Fever
P - Purulence (exudate on tonsils/pharynx)
A - Attend within 3/7 of symptom onset
I - Inflamed tonsils
N - No cough/coryzal symptoms
Centor criteria - 1 for each of:
C - cervical LN
E - exudate on tonsils
N - no cough
T - temperature >38
Sore throat
Urti
Mng
Management
Withhold DMARDs and carbimazole whilst awaiting result of a FBC
Antibiotics:
FeverPAIN score of 4 or 5, or Centor score of 3 or 4 - antibiotics
1st line: Phenoxymethylpenicillin
Pen all: Clarithromycin (erythromycin if pregnant)
Peritonsillar Abscess (Quinsy)
Most common in children aged 2-5yrs
Often occurs as a complication of streptococcal tonsillitis
Clinical features
Systemic upset - fever, SIRS
Sore throat, neck pain
Trismus, muffed ‘hot potato voice’
Uvular deviation away from the quinsy
Hallitosis
Management
Admit - IV antibiotics
Needle aspiration/incision & drainage
Glandular fever (Infectious mononucleosis)
Pathophysiology
Cause: Ebstein-Barr virus (EBV) 90% (others - CMV/HIV/toxoplasmosis)
Spread: Salivary - kissing/sharing food/drink
Following acute infection, EBV persists lifelong in a low-grade replicative, carrier state.
Most common in patients aged 15-24 yrs
Clinical features
Symptoms
Prodromal symptoms - myalgia, malaise, fatigue, sweats
Non-specific rash (classically triggered after treatment of sore throat with amoxicillin)
Pyrexia
Severely sore throat
Examination findings
Lymphadenopathy - classically bilateral posterior cervical LN
Enlarged tonsils - may come together in the midline, covered in white exudate “whitewash”
Palpable splenomegaly
RUQ tenderness or sometimes hepatomegaly
Mild-moderate symptoms, or mild persistent symptoms:
1st Line - Either:
PRN intranasal antihistamine (azelastine) OR
PRN non-sedating oral antihistamine (cetirizine/loratadine)
Moderate-severe symptoms, or failure of 1st line treatments
Regular intranasal coricosteroid during period of allergen exposure (e.g. spring/summer for hayfever) - mometasone furoate, fluticasone propionate
Further management
Persistent symptoms despite IN steroid..
Nasal congestion - short-term nasal decongestant - xylometazoline for 1 week
Watery rhinorrhoea - IN anticholinergic (ipratropium bromide)
Nasal itching/sneezing - REGULAR PO antihistamine, or combination intranasal steroid/antihistamine
For very severe symptoms, significantly affecting QOL - low dose prednisolone for 3-10 days.
Bell’s Palsy & Ramsay Hunt
Bell’s Palsy
Pathophysiology
An acute, unilateral lower motor neurone facial nerve palsy resulting in facial weakness/paralysis.
Aetiology unclear, possibly viral
Clinical features
Rapid onset of facial muscle weakness
Unilateral and involves upper and lower parts of the face, with resultant facial droop
50% of patients complain of pain in the ear and postauricular region
LMN pathology – facial paralysis with forehead involvement (LMN).
Other symptoms include postauricular pain, dry eyes, reduced taste
Management
1st Line: Prednisolone 50-60mg OD for 10 days
Eye care - lubricating eye drops and tape eye close at bedtime if required.
Antivirals alone are not recommended. There may be ‘a small benefit’ when used in combination with steroids - NICE advises specialist advice.
References and Further Reading
NICE CKS: Management of Bell’s Palsy [2019]. Available at URL: https://cks.nice.org.uk/topics/bells-palsy/
Ramsay Hunt Syndrome
Pathophysiology
Infection of the geniculate ganglion by varicella zoster virus resulting in a lower motor neuron facial nerve palsy, with accompanying zoster oticus (vesicular ear rash).
Clinical features
Symptoms
Facial droop - acute LMN facial nerve palsy - involves muscles of the forehead
Ear pain
A painful, erythematous vesicular rash (zoster oticus) within the ear canal and mucuous membrane of the oropharnyx
SNHL, tinnitus, vertigo, hyperacusis - if vestibulocochlear nerve involvement
Preceding flu-like illness
Loss of taste on anterior 2/3rds tongue
Management
1st line: Antivirals (aciclovir, valaciclovir, famciclovir) AND steroids (prednisolone 60 mg OD 5/7)
Cerumen
Background
Cerumen (earwax) is produced in the external auditory canal. Accumulated cerumen within the canal can become impacted and lead to conductive hearing loss.
Clinical Features
History of use of cotton buds, hearing aids, earplugs
Hearing loss is the most common complaint
Feeling of fullness in ears, earache, tinnitus
Otoscopy: Accumulation of earwax, can be adherent to tympanic membrane, occlusion of canal by cerumen
Management
Softening of wax to aid removal
Ear drops - sodium bicarbonate 5%, olive oil QDS for 5 days
If continued symptoms - consider ear irrigation or microsuction
Cholesteatoma
Pathophysiology
An abnormal collection of keratinocytes, and squamous epithelium in the middle ear.
Cholesteatomas are expanding and invasive, and cause damage to structures within the middle ear.
If untreated, this can lead to problems with hearing/balance.
They can also become infected.
Can be congenital (epidermal cysts) but usually develop later in life (acquired) due to eustachian tube dysfunction.
Clinical features
Symptoms
Recurrent foul-smelling, purulent discharge (which doesn’t respond to treatment with ABx)
Hearing loss
Tinnitus
Dizziness, loss of balance if left untreated
Otoscopy
Discharge within canal, crust in upper TM, perforation.
Management
Refer all cases of suspected cholesteatoma to ENT - require CT imaging and audiology assessment
Management - surgical removal
Admit if vertigo or CN7 palsy, complications such as meningitis/IC abscess.
