Special Senses Flashcards
1
Q
What should IOP (intraocular pressure) be?
A
11-21 mmHg
2
Q
How is IOP measured
A
with a tonometer
force needed to flatten the corneal surface
3
Q
What is ocular HTN
A
raised IOP (>21mmHg) without developing the changes of glaucoma.
4
Q
define the anterior chamber of the eye
A
between the iris and the cornea’s innermost surface, the endothelium.
5
Q
How is aqueous humour made
A
produced by the ciliary bodies
6
Q
Describe the passage of aqueous humour through the anterior chamber
A
made in ciliary body passes posterior to iris, anterior to the lens, and then through pupil flows out via trabecular meshwork then canal of Schlemm then episcleral vessels then systemic venous circulation
also the uveoscleral route:
instead drains into root of iris/ciliary muscle before draining into scleral vascular system
7
Q
What is acute angle closure glaucoma
A
there is a junction between the iris and cornea at the periphery of the anterior chamber = the anterior chamber angle.
the iris can become apposed to the trabecular meshwork and so block off the aqueous drainage.
8
Q
What is the difference between primary and secondary angle closure glaucoma
A
primary = as a consequence of the anatomy of the eye: some people’s angles are naturally very narrow which makes the angle more vulnerable to blocking off. Severe hypermetropes, advanced age, asian
secondary = as a result of forces exerted on the iris either anteriorly or posteriorly (eg, the lens bulging forward as a result of swelling) or blockage, as a result of the trabecular meshwork being blocked by matter such as blood (from a hyphaema), blood vessels (from poorly controlled advanced diabetic eye disease) or proteins (as seen in hypertensive uveitis).
9
Q
Describe the control of aqueous humour production
A
autonomic - adrenergic
alpha 2 - stimulation reduces aqueous production and increases uveoscleral outflow, leading to fall in IOP
beta 2 - stimulation increases aqueous producion adn therefore increases IOP
10
Q
What are the symptoms of acute angle closure glaucoma
A
Pain - this is severe and rapidly progressive.
Blurred vision (rapidly progressing to visual loss).
Coloured haloes around lights.
N+V
11
Q
What situations can precipitate acute angle closure? Why?
A
during a moment of stress or excitement,
whilst watching TV in dim lighting conditions
after topical mydriatics or systemic anticholinergics.
due to pupillary block. - The mid-dilated pupil snags on to the lens, so causing a build-up of aqueous beneath it which further pushes the iris forward, so eventually blocking off the trabecular meshwork.
12
Q
Give some signs of acute angle closure glaucoma
A
generally unwell.
red eye - more marked around the periphery of the cornea.
There is a hazy cornea
non-reactive (or minimally reactive) mid-dilated pupil.
Globe hard on palpation
13
Q
What is the diagnostic criteria for angle closure glaucoma
A
History of at least 2 of:
Ocular pain.
Nausea/vomiting.
History of intermittent blurring of vision with haloes
AND
at least three of the following signs:
IOP greater than 21 mm Hg (clinically this can mean a stony hard pupil).
Conjunctival injection.
Corneal epithelial oedema.
Mid-dilated non-reactive pupil.
Shallow chamber in the presence of occlusion.
14
Q
How is angle closure glaucoma managed pharmacologically
A
give all topical glaucoma medications that are not contra-indicated in the patient, together with intravenous acetazolamide. Patients are lain supine.
Topical agents inlude:
Beta-blockers - eg, timolol, cautioned in asthma.
Steroids - prednisolone 15 every 15 minutes for an hour, then hourly.
Pilocarpine 1-2% (in patients with their natural lens).
Phenylephrine 2.5% (in patients who do not have their own lens).
Acetazolamide is given intravenously (500 mg over 10 minutes) and a further 250 mg slow-release tablet after one hour - check for sulfonamide allergy and sickle cell disease/trait.
Offer systemic analgesia ± antiemetics.
15
Q
Describe the mechanism of action of beta blockers on the eye eg. timolol
A
reduce production of aqueous by ciliary body
16
Q
Describe the mechanism of action of alpha agonists on the eye eg. apraclonidine
A
reduced production of aqueous by ciliary body
increased outflow via uveoscleral tract
17
Q
Describe the mechanism of action of prostaglandin analogues on the eye eg. latanoprost
A
increase uveoscleral outflow
18
Q
Describe the mechanism of action of carbonic anhydrase inhibitors on the eye eg. acetazolamide
A
decrease production aqueous
19
Q
Describe the mechanism of action of parasympathomimetics on the eye eg. pilocarpine
A
increases outflow of aqueous by ciliary muscle contraction, opening trabecular network
20
Q
How is angle closure glaucoma managed surgically
A
Peripheral iridotomy (PI) - this refers to (usually two) holes made in each iris with a laser, usually at around the 11 and 2 o’clock positions. This is to provide a free-flow transit passage for the aqueous. Both eyes are treated, as the fellow eye will be predisposed to an AAC attack too
Surgical iridectomy - this is carried out where PI is not possible.
Lensectomy - one of the few situations where cataract surgery is performed on an urgent basis is when the cataractous lens has swollen to precipitate an attack of AAC. The lens is extracted at the earliest opportunity.
21
Q
Give some complications of angle closure glaucoma
A
permanent loss of vision,
repetition of the acute attack,
attack in the fellow eye
central retinal artery or vein occlusion
22
Q
Give some risk factors for open angle glaucoma
A
age >65 Family history Race - it is three to four times more common in Afro-Caribbean people Ocular hypertension myopia (short-sightedness) retinal disease (eg, central retinal vein occlusion, retinal detachment and retinitis pigmentosa) Diabetes a systemic hypertension
23
Q
Describe briefly the pathophysiology of open angle glaucoma
A
The primary problem in glaucoma is disease of the optic nerve.
there is a progressive loss of retinal ganglion cells and their axons. (optic neuropathy)
associated with a raised IOP
flow is reduced through the trabecular meshwork
24
Q
How does open angle glaucoma present?
A
most people are asymptomatic, because initial visual loss is to peripheral vision and the field of vision is covered by the other eye,
patients do not notice visual loss until severe and permanent damage has occurred, often impacting on central (foveal) vision.
Open-angle glaucoma may be detected on checking the IOPs and visual fields of those with affected relatives.
Suspicion may arise if abnormal discs, IOPs or visual fields are noted.
25
How is the eye examined for potential open angle glaucoma
Gonioscopy - used to measure the angle between the cornea and the iris
Corneal thickness - this influences the IOP reading. If it is thicker than usual, it will take greater force to indent the cornea and an erroneously high reading will be obtained.
Tonometry
Optic disc examination - this is a direct marker of disease progression. Optic disc damage is assessed by looking at the cup:disc ratio: normal is 0.3, although it can be up to 0.7 in some normal people: Glaucoma is suggested by an increase in cupping with time, rather than by cupping alone.
Visual fields
26
Hoe is the cupping of the optic disc measured?
```
cup = bright bit in middle
disc = dark bit around it
```
cup radius:disc radius
increased = more than 0.3
27
Do I need to inform the DVLA if my patient has glaucoma
The onus is on the patient to inform the DVLA (and it is important to document that you have advised them of this).
It is the DVLA (and approved opticians) who will assess the visual fields and decide whether a patient can continue to drive.
If you are concerned that the patient should not drive and has not told the DVLA (despite your clear advice to do so), it may be appropriate to inform the DVLA medical advisors
28
What treatments are available for open angle glaucoma
drugs to reduce IOP - beta blockers, alpha agonists, sympathomimetics, carbonic anhydrase inhibitors, miotics
laser - Argon laser trabeculoplasty (ALT) (lasering to the trabecular meshwork in the iridocorneal angle, so enhancing aqueous outflow), Selective laser trabeculoplasty (SLT)
surgery - trabeculectomy, artificial shunt, canaloplasty
29
What is AMD
age-related macular degeneration
changes, which occur in the central area of the retina (macula) in people aged 55 years and above.
without any other obvious precipitating cause,
30
What are the key findings on examination of the retina in AMD
drusen
dry - hypo/hyperpigmentation of RPE, geographic atropy
wet - neovascularisation
31
What are drusen
lipid and protein deposits beneath the RPE in AMD
32
How is the severity of AMD classified
No AMD: none or a few small drusen.
Early AMD: multiple small or a few intermediate drusen +/- abnormalities of the RPE.
Intermediate AMD: extensive intermediate or one or more large drusen +/- GA not involving the fovea.
Advanced AMD: GA involving the fovea +/- any features of wet AMD.
33
What are the risk factors for AMD
smoking
age
FH/genetics
cardiovascular
obesity
34
What are the symptoms of AMD
may be no symptoms at first if only one eye is affected! - other eye compensates
Painless deterioration or blurring of central vision, typically in a person aged 55 or more.
Metamorphopsia — distortion of vision, where straight lines (such as window blinds) appear crooked, wavy or bent.
Scotoma — the person may describe a black or grey patch affecting their central field of vision.
Light glare.
Loss of (or decreased) contrast sensitivity (the ability to discern between different shades).
Size or colour of objects appearing different with each eye.
Abnormal dark adaptation (difficulty adjusting from bright to dim lighting).
Photopsia — a perception of flickering or flashing lights.
Visual hallucinations (Charles Bonnet syndrome).
35
Give some differences in the presentation of dry and wet AMD
dry:
gradual visual deterioration
difficulty with reading, initially with the smallest sizes of print and then later with larger print.
wet:
visual deterioration can develop quickly.
central vision blurring and distortion
A person may suddenly become unable to read, drive, and see fine detail such as facial expressions and features.
36
Give some differentials for AMD
```
refractive error
cataracts
open angle glaucoma
retinal detachment
amaurosis fugax
diabetic maculopathy
```
37
What investigations should be done in AMD
test visual acuity
Amsler grid - distortion
slit lamp
38
What management is needed for dry AMD
urgent referral within one week to specialist services
no specific treatment
stop smoking - reduces risk of progression
multivitamins if intermediate or advanced - reduces risk of progression
visual rehabilitation
treat other visual problems to make vision as good as possible
39
What management can be given for wet AMD. Why does it work and how is it given
anti-VEGF
VEGF acts as a proangiogenic growth factor and stimulates permeability of blood vessels
given by intravitreal injections one a month for 3 months. continued if beneficial
in most people it stops progression. in a few it even improves vision!
40
Give some examples of anti-VEGF meds
ranibizumab
| aflibercept
41
What causes diabetic retinopathy
microvascular occlusion leads to retinal ischaemia. leads to formation of AV shunts and neovascularisation
leakage from vessels leads to intraretinal haemorrhage and oedema
42
What are the key features of DR on visualisation of the retina
Microaneurysms
Hard exudates - precipitates of lipoproteins
Haemorrhages
Cotton wool spots - build-up of axonal debris due to poor axonal metabolism at the margins of ischaemic infarcts.
Neovascularisation
43
Define the stages of diabetic retinopathy
Background (mild) non-proliferative DR: at least one microaneurysm.
Moderate non-proliferative DR: microaneurysms or intraretinal haemorrhages ± cotton wool spots, venous beading, intraretinal microvascular abnormalities (IRMAs).
Severe to very severe non-proliferative DR (sometimes referred to as pre-proliferative disease), as above: blot haemorrhages and microaneurysms in 4 quadrants
venous beading in at least 2 quadrants
IRMA in at least 1 quadrant
Non-high-risk proliferative DR: new vessels on the disc (NVD) - or within one disc diameter of it or new vessels elsewhere (NVE).
High-risk proliferative DR: large NVD or NVE (defined by comparing to the optic disc surface area) or presence of pre-retinal haemorrhage. In advanced disease, there may also be an accompanying retinal detachment.
44
Define the stages of diabetic maculopathy
Focal or diffuse macular oedema: areas of leakage which may be well circumscribed or diffuse.
Ischaemic maculopathy: the clinical appearance may be relatively normal but the visual acuity has dropped and ischaemia is seen on fluorescein angiography.
Clinically significant macular oedema (CSMO): there may be thickening of the retina and hard exudates which, when found within a specific distance of the fovea or when found to be above a certain size, define CSMO.
45
What are the risk factors for DR
poor glycaemic control
HTN
renal disease
pregnancy - may cause fast progression
46
What might a patient with DR notice about their vision
asymptomatic
painless gradual deterioration of central vision
dark painless floaters - due to haemorrhages
47
How should a patient with DR be examined
acuity test
slit lamp
dilated fundal photographs
48
Describe the screening program for diabetic retinopathy
visual acuity and fundal photography at diagnosis of T1/T2DM
retested every year
starts at 12 years old
49
What symptoms in a patient with DR would require an emergency review?
Sudden loss of vision.
Rubeosis iridis (formation of abnormal blood vessels on the anterior iris).
Pre-retinal or vitreous haemorrhage.
Retinal detachment
50
State primary prevention methods for DR
```
glycaemic control - <7%
blood pressure control <140/90 (<130 if DR established)
lipid control
smoking cessation
balanced diet
```
51
When might treatment be offered in DR
no clear cut lines
| proliferative or maculopathy can be offered treatment
52
What treatments are available for DR
laser treatment
intravitreal corticosteroids
anti-VEGF
surgery - vitrectomy if intravitreal bleed
53
What does laser treatment for DR help with
induces regression of new blood vessels
reduces central macular thickening
arrests progression, but does not restore sight
54
What are some causes of sudden painless loss of vision
```
retinal artery occlusion
retinal vein occlusion
retinal detachment
vitreous haemorrhage
ischaemic optic neuropathy
```
55
Describe how retinal vein occlusion leads to the loss of vision
vein occluded due to formation of thrombus, external compression or disease of vein wall
leads to ischaemic damage to retina
VEGF leads to neovascularisation and haemorrhages
56
What is the difference between branch retinal vein occlusion (BRVO) and central retinal vein occlusion
branch - more common. only part of retina affected
central - can be non-ischaemic or ischaemic. affects whole of retina
57
What are the symptoms of BRVO
unilateral painless loss of vision
metamorphopsia - linear objects look curvy or rounded.
visual field defects
58
What is found on examination in BRVO
vascular dilatation
tortuosity of vessels
haemorrhages in one area
no RAPD
59
What is the management of BRVO
urgent r/v with opthalmologist
panretinal photocoagulation laser treatment if macular oedema or neovascularisation
triamciolone
60
What are the risk factors for retinal vein occlusion
```
age
HTN
hyperlipidaemia
diabetes
smoking
obesity
raised IOP
sarcoidosis
hyperviscosity
thrombophilia
```
61
What is the diffrence between non-ischaemic and ischaemic CRVO in terms of outcome
```
non-ischaemic = milder and more common. most resolve fully.
ischaemic = severe. can end up with painful eye and severe visual impairment
```
62
What are the symptoms of CRVO
sudden unilateral painless loss of vusion or blurred vision
| often on waking
63
What is found on examination of CRVO
non-ischaemic - mild or absent RAPD, dot blot and flame haemorrhages everywhere
ischaemic - severe visual impairment, marked RAPD, disc oedema, haemorrhages!
64
What is a RAPD and how is it seen
relative afferent pupillary defect
if left eye affected:
light shone in right eye, both pupils constrict
light shone in left eye, both pupils dilate
light shone in right eye, both pupils constrict
65
What can cause a retinal artery occlusion
most commonly:
embolism - from AF or carotids
vasoobliteration
vascular compression
66
Where is the occlusion in CRAO? What defect does this cause?
in the central retinal artery before it branches as it emerges from the optic nerve
affects whole of retina
macula can be preserved due to blood supply from choroid
67
What is found on examination in CRAO
```
unilateral acute painless loss of vision
history of amaurosis fugax
RAPD
pale retina
attenuation of vessel
```
68
What systemic examination needs to be done in CRAO
pulse - AF
BP
carotid bruits
heart murmurs
69
What is the management of CRAO
nothing is proven to improve!
firm ocular massage
reduce IOP
dilation of artery
also: reduce RF, carotid endarterctomy, low vision aid clinics, notify DVLA
70
What is branch retinal artery occlusion
only one branch of the retinal artery affected
| leads to segmental loss of vision
71
What is retinal detachment
separation of inner neurosensory retina from underlying RPE (retinal pigment epithelium)
therefore fluid can accumulate in the subretinal spae
72
What types of retinal detachment are there
rhegmatogenous
exudative
tractional
73
Describe the cause of rhegmatogenous retinal detachment
```
age related shrinking of vitreous leads to posterior vitreous detachment
causes traction on retina
retinal tear
fluid vitreous seeps under retina
leads to detachment
```
74
Describe the cause of exudative retinal detachment
leakage of fluid into subretinal space due to inflammation or malignancy
75
Describe the cause of tractional retinal detachment
abnormal vasculature (eg due to proliferative diabetic retinopathy) leads to contraction of vitreous, so retina is pulled away. there is no retinal break.
76
What are the symptoms of retinal detachment
floaters and flashes
sudden onset painless progressive visual loss
dark curtain or shadow starts peripherally and moves centrally
77
What is found on examination in retinal detachment
RAPD
altered red reflex - grey/folded appearance
reduced acuity - if macula involved
visual field defects
can see the detached retina on fundal examination
78
What is the management of retinal detachment
URGENT if macula on as sight can be preserved.
cryotherapy/laser photocoagulation for retinal ters and holes
surgery toclose any retinal tears or holes, reduce vitreous traction, and reattach the retina: vitrectomy, Scleral buckling, Pneumatic retinopexy
79
What is a vitreous haemorrhage
bleeding into the vitreous humour
80
What are the most common causes of vitreous haemorrhage
proliferatve diabetic retinopathy
posterior vitreous detachment
ocular trauma
81
What are the symptoms of vitreous haemorrhage
sudden painless visual loss or haze
red hue
floaters
worse in the morning - due to blood settling on the macula during sleep
82
What is giant cell arteritis
also known as temporal arteritis
medium and large vessel vasculitis
granulomatous inflammation of extracranial branches of carotid artery and opthalmic artery
83
Which disease is associated with giant cell arteritis
polymylagia rheumatica - bilateral upper arm stiffness, aching, and tenderness; pelvic girdle pain
84
What are the risk factors for GCA
european
>50
genetics
85
What are the symptoms of GCA
```
temporal headache
myalgia
malaise
fever
scalp tenderness
intermittent jaw claudication
sudden painless loss of vision in eye
double vision
visual field defects
```
86
What can be seen on fundoscopy in GCA if the eye is affected
pallor and oedema of optic disc
cotton wool spots
small haemorrhages
87
What can be felt on examination of the temporal artery in GCA
prominent
beaded
tender on palpation
pulseless
88
What investigations should be done in GCA
ESR FBC LFT
| biopsy of temporal artery
89
What are the likely blood test results in GCA
raised ESR >50
normocytic normochromic anaemia
raised platelets
raised ALP
90
What is seen on biopsy in GCA
predominance of mononuclear cell infiltration or granulomatous inflammation, usually with multinucleated giant cells.
91
What is the management of GCA
urgent referral to specialist
40mg prednisolone PO
60mg if jaw claudiation
IV methyprednisolone if eye involvement
low dose aspirin + PPI
92
What is the long term management of GCA
reduced steroids gradually, check response
consider osteoporosis prophyaxis
blue steroid card
monitor symptoms and ESR/CRP, and blood pressure and glucose every 3m
93
What is a cataract
an opacity (cloudy area) that forms within the lens of an eye which can reduce the transparency of the lens
opacity is due to deposition of aggregated proteins or yellow/brown pigment of ageing
94
State the different locations of cataracts
Nuclear cataracts - in the central (nuclear) part of the lens.
Cortical cataracts - in the outer (cortical) layer of the lens.
Subcapsular cataracts -directly under the lens capsule and can be anterior or posterior.
95
What is the difference between a congenital and developmental cataract
congenital = at birth or <1yr
| developmental - after infancy
96
What are the risk factors for cataracts
DM
systemic steroids
smoking
```
ageing
trauma
atopic dermatitis
UVB exposure
malnutrition
```
97
What are the risk factors for congenital cataracts
```
heriditary
rubella
VZV
CMV
HSV
Down's syndrome
Edward's syndrome
```
98
What are the symptoms of cataracts
```
gradual and painless reduction in visual acuity.
gradual difficulty in:
Reading.
Recognizing faces.
Watching television.
```
glare (difficulty seeing in the presence of bright light).
Gradual reduction in perception of colour intensity.
Frequent changes of spectacle prescription caused by refractive changes due to cataracts developing.
Double vision in one eye (monocular diplopia).
99
What are the signs of cataracts
reduction in acuity
opacity visible in lens
dark defects in red reflex
100
What are the signs of a congenital cataract
```
opacity visible in lens
dark defects in red reflex
white/grey pupil
nystagmus
strabismus
sensitivity to light
```
101
How are cataracts managed?
surgery!
| extracapsular lens extraction and phacoemulsification of lens
102
What is strabismus?
misalignment of the visual axes - both eyes are not directed at an object at the same time.
103
What is the difference between a manifest and latent squint
A manifest squint (a 'tropia'): present when the eyes are open and being used so that when one eye views the object of interest, the other eye is deviated.
A latent squint (a 'phoria'): a squint that is present only when the use of the two eyes together is interrupted ('dissociated'). For example, by covering one eye.
104
What is the difference between an esotropia and an exotropia
esotropia = convergent squint, towards midline
exotropia = divergent squint, away from midline
105
What is the difference between a concomitant and an incomitant squint
concomitant = direction of gaze does not alter size of the deviation
incomitant = direction of gaze does affect the size, or indeed presence, of the squint. due to paralysis of ocular muscles
106
What are the potential causes of strabismus
```
idiopathic
refractive errots
retinoblastoma
amblyopia
cerebral palsy
CN palsies
```
107
What is amblyopia
decrease of vision arising from dysfunctional processing of visual information
due to degradation of the retinal image during a sensitive period of visual development.
108
What can cause amblyopia
strabismus (squint) results in amblyopia because the images at the fovea are different.
bilateral moderate-to-high refractive errors
differences in refraction cause one image to be more blurred than the other, leading to amblyopia on that side.
uncorrected astigmatism in one eye
deprivation or physical obstruction of the image (for example, by a cataract or marked ptosis
109
How can a manifest squint be detected on examination
cover test
look at object.
cover unaffected eye
affected eye moves to look at object
110
How can a latent squint be detected on examination
cover uncover test
look at object
cover the affected eye for 3 secs
uncover eye and look for movement
affected eye will move back to look at object if latent squint
111
What examination should be done when assessing a aquint
cover/uncover
red reflex
eye movement - concomitant or incomitant
acuity test
112
How is strabismus managed
corrective glasses
occlusion or penalisation therapy of good eye - encourages use of ambliopic eye
surgery to correct
113
What is acute otitis media
presence of inflammation in the middle ear,
| associated with an effusion and accompanied by the rapid onset of symptoms and signs of an ear infection
114
What causes acute otitis media
```
Bacteria:
Haemophilus influenzae,
Streptococcus pneumoniae,
Moraxella catarrhalis
Streptococcus pyogenes
```
```
Viral:
respiratory syncytial virus (RSV),
rhinovirus,
adenovirus,
influenza virus,
parainfluenza virus
```
115
What are the symptoms of acute otitis media
Acute onset
earache.
holding, tugging, or rubbing of the ear
non-specific: fever, crying, poor feeding, restlessness, behavioural changes, cough, or rhinorrhoea.
116
What are the signs on examination of acute otitis media
red, yellow, or cloudy tympanic membrane.
bulging of the tympanic membrane, with loss of normal landmarks
an air-fluid level behind the tympanic membrane (indicates effusion)
Perforation of the tympanic membrane and/or discharge in the external auditory canal.
117
How is acute otitis media managed
adequate pain relief
if antibiotics required:
5–7 day course of amoxicillin.
118
When are antibiotics required for acute otitis media
otorrhoea - discharge from ear
| <2 years with bilateral infection
119
What are some potential complications of acute otitis media
Persistent otitis media with effusion.
Recurrence of infection.
Hearing loss (usually conductive and temporary).
Tympanic membrane perforation.
Labyrinthitis.
Rarely, mastoiditis, meningitis, intracranial abscess, sinus thrombosis, and facial nerve paralysis.
120
What is otitis media with effusion
collection of fluid within the middle ear space without signs of acute inflammation.
121
What are the symptoms of otitis media with effusion
Hearing loss causing:
Mishearing,
difficulty with communication in a group,
listening to the TV at excessively high volumes
needing things to be repeated.
Lack of concentration, withdrawal.
Impaired speech and language development.
Impaired school progress.
Mild intermittent ear pain with fullness or popping.
There may be a history of recurrent ear infection, upper respiratory tract infections or nasal obstruction.
122
What are the causes of otitis media with effusion in children
Impaired eustachian tube function causing poor aeration of the middle ear.
Low-grade viral or bacterial infection.
Persistent local inflammatory reaction.
Adenoidal infection or hypertrophy.
123
What are the signs of otitis media with effusion
Opacification of the drum (other than due to scarring).
There are usually no signs of inflammation or discharge on examination.
Loss of the light reflex, or a more diffused light reflex.
Indrawn, retracted, or concave drum.
Presence of bubbles or fluid level.
Yellow or amber colour change to the drum.
conductive hearing loss
124
What can cause otitis media with effusion in adults
unilateral is suspicious!!!
Due to Eustachian tube dysfunction or blockage:
Severe sinusitits
Severe or chronic allergy
Severe nasal septal deviation
enlarged tonsils and adenoids
A nasopharyngeal tumour near Eustachian tube openings.
Radiation to the head and neck following cancer treatments.
Secondary inflammation from allergic rhinitis.
Frequent upper respiratory infection.
Trauma (usually barotrauma - eg, after a dive or flight).
125
What are the management options for otitis media with effusion
watch and wait - most spontaneously resolve
surgery - grommets, adenoidectomy if recurrent upper respiratory tract symptoms
hearing aids
126
Which children is surgical management of otitis media with effusion recommended for
Persistent bilateral OME lasting three or more months.
A hearing loss in the best ear of 25-30 dB or worse
Children with better hearing but who have social, educational or developmental difficulties may exceptionally also benefit from surgical treatment.
127
Which conditions increase the risk of otitis media with effusion
Cleft palate (causing impaired function of the eustachian tube).
Down's syndrome (impaired immunity and mucosal abnormality increasing susceptibility to infection).
Primary ciliary dyskinesia.
Allergic rhinitis.
128
What is chronic suppurative otitis media (CSOM)
a chronic inflammation of the middle ear and mastoid cavity, which presents with recurrent ear discharges (otorrhoea) through a tympanic perforation
occurs when persistent tympanic membrane perforation leads to recurrent middle ear infection and chronic inflammation.
129
What are the most common causes of CSOM
```
Pseudomonas aeruginosa (most common).
Staphylococcus aureus.
Proteus species.
Aspergillus species.
Candida albicans.
```
130
What are the symptoms of CSOM
Ear discharge persisting for more than 2 weeks, without ear pain or fever.
Hearing loss in the affected ear.
Tinnitus and/or a sensation of pressure in the ear may also be present.
A history of acute otitis media (AOM), ear trauma, or glue ear and grommet insertion
A history of allergy, atopy, and/or upper respiratory tract infection.
131
What is seen on examination in CSOM
perforated tympanic membrane
oedematous external auditory canal
discharge - fetid, purulent and cheese-like or clear and serous.
Granulation tissue is often seen in the medial canal or middle ear space.
The middle ear mucosa seen through the perforation may be oedematous or even polypoid, pale, or erythematous.
132
How is CSOM managed
An appropriate antibiotic, usually given topically.
Regular intensive aural toilet (microsuction) to remove debris.
Control of granulation tissue - topical steroids
surgery if cholesteatoma present
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What are the potential complications of CSOM
Intratemporal complications include:
Petrositis
Facial paralysis
Labyrinthitis
Intracranial complications include:
Lateral sinus thrombophlebitis
Meningitis
Intracranial abscess
Sequelae include:
Hearing loss
Tympanosclerosis
134
What is a cholesteatoma
abnormal sac of keratinizing squamous epithelium and accumulation of keratin within the middle ear or mastoid air cell spaces
can become infected and also erode neighbouring structures
135
Which areas can be affected by a cholesteatoma
```
incus
stapes.
facial nerve,
cochlea,
semi-circular canals,
mastoid bone
roof of the middle ear
```
136
Describe the pathophysiology causing a cholesteatoma
chronic negative middle-ear pressure due to a dysfunction of the Eustachian tube causes the tympanic membrane to be 'sucked back' and retract.
As this process continues, there is erosion of part of the tympanic membrane producing a slowly expanding defect.
A pocket lined by squamous, non-keratinising epithelium is thus formed.
137
What are the symptoms of cholesteatoma
progressive conductive hearing loss
vertigo
headache
facial nerve palsy
138
What can be seen on examination of a cholesteatoma
A deep retraction pocket in the tympanic membrane, with or without granulation tissue and skin debris.
A crust-like lesion, often yellow or brown in colour, usually in the upper part of the tympanic membrane
often surrounded by pus, and sometimes associated with a perforation of the adjacent tympanic membrane.
139
What investigations need to be done in choleastoma
CT head - to assess extent of lesion and bony defects
140
What is the management of cholesteatoma
surgery to remove it
141
What is BPPV
benign paroxysmal positional vertigo
| a disorder of the inner ear characterized by repeated episodes of positional vertigo
142
What causes BPPV
loose calcium carbonate debris (otoconia) in the semi-circular canals of the inner ear (canalithiasis).
When the head moves, otoconia move in the semi-circular canals, causing motion of the fluid of the inner ear (endolymph) which induces the symptom of vertigo
143
What are the symptoms of B dependent ear with the vertical component towaPPV
Symptoms are brought on by specific movements and positions of the head relative to gravity
Vertigo <1 minute, precipitated by positional change
asymptomatic between attacks.
N+V
Light-headedness and imbalance - can persist for longer than the vertigo episode.
no hearing loss of tinnitus
144
What test should be done on examination in BPPV?
How is this done?
Dix- Hallpike manoeuvre
Ask the person to keep their eyes open throughout the manoeuvre and to look straight ahead.
Ask the person to sit upright on the couch with their head turned 45 degrees to one side.
From this position, lie the person down rapidly (over 2 seconds), supporting their head and neck, until their head is extended 20–30 degrees over the end of the couch with the chin pointing slightly upwards and the test ear downwards. Support the head to maintain this position for at least 30 seconds.
Observe their eyes closely for up to 30 seconds for the development of nystagmus. If nystagmus is present, maintain the position for its duration (maximum 2 minutes if persistent) and note its duration, type, direction, and latency.
Support the head in position and slowly sit the person up.
Repeat with the head rotated 45 degrees to the other side.
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What is found on Dix-Hallpike manoeuvre in BPPV
vertigo
+
torsional (rotatory) upbeating nystagmus (the upper pole of the eye beats towards the dependent ear with the vertical component towards the forehead when looking straight ahead).
Left ear BPPV has a clockwise torsional nystagmus, right ear BPPV nystagmus rotates anti-clockwise.
There is a latent period (usually of 5 to 20 seconds) between completing the manoeuvre and onset of vertigo and nystagmus.
146
How is BPPV managed
watch and wait - spontaenous resolution
Epley manoeuvre
147
How is the epley manoeuvre performed
Stand at the side or behind the person to guide head movements.
Maintain each head position for at least 30 seconds. If vertigo continues, wait until it has subsided.
Start with the person sitting upright with their head turned 45 degrees to the affected side, then lie them back (with their head still turned 45 degrees) until the head is dependent 30 degrees over the edge of the couch (as if performing the Dix-Hallpike manoeuvre). Wait for at least 30 seconds. Then:
With the face upwards, but still tilted backwards by 30 degrees, rotate the head through 90 degrees to the opposite side.
Hold the head in this position for about 20 seconds and ask the person to roll onto the same side as they are facing.
Rotate the person's head so that they are facing obliquely downward with their nose 45 degrees below the horizontal.
Sit the person up sideways while the head remains rotated and tilted to the side.
Rotate the head to the central position and move the chin downwards by 45 degrees.
148
What causes Meniere's disease
idiopathic!
abnormal endolymph production and/or absorption is associated with Meniere's disease
The volume of endolymph in the membranous labyrinth increases and the volume of perilymph filling the bony labyrinth and around the membranous labyrinth decreases (endolymphatic hydrops)
149
What are the symptoms of Meniere's disease
spontaneous vertigo, described as spinning or rocking, N+V
Unsteadiness can persist for several days after the acute attack of vertigo.
Tinnitus, usually described as 'roaring'. Initially, this appears during attacks, but later becomes permanent and may significantly affect quality of life.
Fluctuating sensorineural hearing loss, initially in low frequencies (usually unilateral). Eventually, as the disease progresses, hearing loss becomes permanent and does not fluctuate.
Aural fullness (a sensation of pressure in the ear, or ear discomfort), which often occurs in advance of a vertigo attack — may also be present during the episode.
150
Describe an acute attack of Meniere's disease
May be preceded by a change in tinnitus, increased hearing loss, or a sensation of aural fullness shortly before the onset of vertigo.
Are present for at least 20 minutes, but typically last a few hours (no more than 24 hours).
Can occur in clusters over a few weeks, although months or years of remission can also occur.
Can involve mainly aural symptoms, predominantly vertigo, or both.
151
What might be seen on examination in Meniere's disease
fall over on Romberg's test
unable to walk heel to toe in a straight line.
If asked to march on the spot with their eyes closed, the person may be unable to maintain their position and will turn to the affected side (Unterberger's test).
unidirectional, horizontal-torsional nystagmus may be seen during an episode of vertigo
152
How is Meniere's disease managed?
Alleviate acute attacks - prochlorperazine, cinnarizine, cyclizine, or promethazine toreduce N+V
Reduce severity and frequency of attacks - Low-salt diet and avoiding caffeine, chocolate, alcohol and tobacco are often advised. trial of betahistine (initially 16 mg three times a day) to reduce the frequency and severity of attacks.
Improve hearing and reduce the impact of tinnitus - Hearing aids, masking devices
153
What is the difference between vestibular neuronitis and labyrinthitis
'vestibular neuritis' = only the vestibular nerve is involved,
'labyrinthitis' the vestibular nerve and the labyrinth are affected.
154
What can cause vestibular neuronitis
inflammation due to reactivation of HSV type 1
autoimmune
microvascular ischemic insults
155
What are the symptoms of vestibular neuronitis
VERTIGO
Rotational vertigo occurs spontaneously, may be sudden, develop on waking, or may worsen over the course of the day.
It is exacerbated by changes of head position, but is initially constant even when the head is still. (not triggered by movement)
Acute symptoms usually settle in a few days and gradual recovery occurs over 2–6 weeks.
N+V - often with malaise, pallor, and sweating.
Balance - unsteady and veer to the affected side.
NO hearing loss and tinnitus
Recent viral illness.
156
What are the symptoms of labyrinthitis
VERTIGO
Rotational vertigo occurs spontaneously, may be sudden, develop on waking, or may worsen over the course of the day.
It is exacerbated by changes of head position, but is initially constant even when the head is still. (not triggered by movement)
N+V
hearing loss - unilateral or bilateral, mild or profound.
tinnitus
157
Which diagnoses need to be considered in acute onset of vertigo
```
BPPV
Vestibular neuronitis and labyrinthitis
Meniere's disease.
vestibular ototoxicity, (for example drug-related damage),
Migraine
Stroke and transient ischaemic attack,
cerebellar tumour,
acoustic neuroma,
multiple sclerosis
```
158
What are the signs on examination of vestibular neuronitis
Nystagmus - fine horizontal but may be mixed horizontal-torsional with the fast phase away from the affected ear.
head impulse test
Skew test
159
How are vestibular neuronitis and labyrinthis managed?
symptoms will usually settle over several weeks, even if no treatment is given.
Advise that bed rest may be necessary if symptoms are particularly severe during the acute phase, but that activity should be resumed as soon as possible
Prochlorperazine or antihistamines for vertigo, nausea and vomiting
do not drive if dizzy, or if they are likely to experience an episode of vertigo while driving.
160
What is the difference between localised and diffuse otitis externa
Localized otitis externa — folliculitis (infection of a hair follicle) that can progress to become a furuncle (boil) in the ear canal.
Diffuse otitis externa — is widespread inflammation of the skin and subdermis of the external ear canal, which can extend to the external ear and the tympanic membrane
161
What is the difference between acute and chronic otitis externa
Acute if it has lasted for 3 weeks or less.
| Chronic if it has lasted for longer than 3 months.
162
What is malignant otitis externa
also known as necrotizing otitis.
an aggressive infection that predominantly affects people who are immunocompromised, or have diabetes mellitus, or the elderly.
spreads into mastoid and temporal bones
163
What can cause localised otitis externa
infection of a hair root by Staphylococcus aureus.
164
What can cause diffuse otitis externa
Bacterial infection:
Pseudomonas aeruginosa
Staphylococcus aureus
Fungal infections
Aspergillus species,
Candida albicans.
Seborrhoeic dermatitis — this may affect the ears in isolation, or be associated with one or more of the following: dandruff, eyebrow scaling, blepharitis, or facial redness and scaling.
Contact dermatitis - irritant or allergic
Trauma — caused by scratching, aggressive cleaning, ear syringing, foreign objects in the ear, and the use of cotton buds, hearing aids or ear plugs.
Environmental factors — high temperature and/or high humidity, perspiration, swimming (especially in polluted water
165
What causes chronic otitis externa
```
Allergic contact dermatitis.
Irritant contact dermatitis.
Seborrhoeic dermatitis.
Fungal infection
Bacterial infection
```
166
What are the symptoms of otitis externa
Itch
Severe ear pain, disproportionate to the size of the lesion
Pain made worse when the tragus or pinna is moved, or when an otoscope is inserted
Tenderness on moving the jaw
Tender regional lymphadenitis
Sudden relief of pain if the furuncle in localized otitis externa bursts
Loss of hearing if there is sufficient swelling to occlude the ear canal
167
What are the symptoms of chronic otitis externa
Constant itch in the ear.
Mild discomfort.
Pain, if present, is usually mild.
168
What are the symptoms of malignant otitis externa
Pain and headache, more severe than clinical signs would suggest.
Vertigo.
Profound hearing loss.
169
What is seen on examination in acute, chronic and malignant otitis externa
The ear canal or external ear, or both, are red, swollen, or eczematous with shedding of the scaly skin.
Swelling in the ear canal is typical of an early presentation of localized otitis externa; later the swelling has a white or yellow centre filled with pus;
Discharge (serous or purulent) may be present in the ear canal.
Inflamed eardrum, which may be difficult to visualize if the ear canal is narrowed or filled with debris
if chronic:
Lack of earwax in the external ear canal.
Dry hypertrophic skin
Pain on manipulation of the external ear canal and auricle.
if malignant:
Granulation tissue at bone–cartilage junction of ear canal; exposed bone in the ear canal.
Facial nerve palsy (drooping face on the side of the lesion).
Temperature over 39°C.
170
How is acute localised otitis externa managed
Analgesia
Antibiotic - oral flucloxacillin for 7 days if spreads to pinna, neck, or face, systemic infection or increased risk of severe infection (such as diabetes mellitus, or compromised immunity).
171
How is diffuse otitis externa managed
analgesia
| topical steroid and/or Abx 7-14 days
172
How is chronic otitis externa managed
If fungal infection:
topical antifungal preparation eg. Clotrimazole 1% solution or Clioquinol and a corticosteroid (for example Locorten–Vioform®).
If irritant, or allergic dermatitis:
avoid contact with the irritant or allergen
topical corticosteroid.
If no cause is evident:
7-day course of a topical corticosteroid
Consider co-prescribing an acetic acid spray.
