6) ear, eye, nose, skin, throat (ie special senses) Flashcards
OTITIS EXTERNA
- what is it?
- time definition of acute and chronic?
- group of organisms more likely to cause acute?
- group of organisms more likely to cause chronic?
inflammation of external ear canal
Acute = < 3 weeks (aka “Swimmer’s” Ear)
- norm bacterial (norm staph aureus)
Chronic = >3 months
- norm fungal (norm aspergillus)
OTITIS EXTERNA
- age most affected?
- lifestyle risk factors? 3
- medical conditions that are risk factors? 3
age (peaks between 7-12 years)
- Moisture (swimming)
- Trauma (ear clearance w finger/cotton bud)
- Hearing aids
- Wax build up
- DM
- Immunocompromised
OTITIS EXTERNA
- two main initial symptoms? 2
- main finding on examination? 1
- late severe signs/symptoms? 3
MAIN SYMPTOMS
- pruritic/itchy ear
- otalgia (esp on movement of tragus)
O/E
-erythema AND oedema of ear canal + ear
(Also mobile tympanic membrane)
LATE SIGNS
- pre-auricular lymphadenopathy
- discharge
- hearing loss
nb can also get a fever but not common
OTITIS EXTERNA
- possible investigation? 1 (when do?)
- ear hygiene advice?
- medication treatment options? 3
- additional medication to help with symptoms? 1
Can do EAR SWAB (rarely useful unless Sx are persistent/recurrent)
- Olive oil for ear wax
- if swollen/narrow ear canal: can put wick/gauze soaked in sofradex
- Avoid cotton buds!
Mild = TOP Acetic acid spray 2%
Mod = TOP Abx ± Steroids
Nb TOP Abx include neomycin and clioquinol (then TOP steroids have same names as PO/IV ones)
advice SIMPLE ANALGESIA (paracetamol/nsaids)
Nb most resolve within a few days!
OTITIS EXTERNA
- differential diagnosis? (3 common, 3 rarer)
= contact eczema / dermatitis
= impacted ear wax
- foreign body
= perforated otitis media (or chronic secretory OM)
- cholesteatoma
- malignancy (if unresponsive to Mx)
OTITIS EXTERNA
- most common complications? 3
- rare, but serious type of otitis externa? 1
- hearing loss
- narrowed ear canal
- abscess
NECROTIZING (MALIGNANT) OTITIS EXTERNA =immunocompromised its (90% are pseudomonas) -severe pain -exudate + oedema -micro-abscesses -headache +/- facial nerve palsy
Can spread to bone causing osteomyelitis + death
Need urgent admission and ENT referral
IMPACTED EAR WAX:
- most common symptom? 1
- other symptoms? 4
hearing loss = MOST COMMON
- blocked ears / feeling of fullness
- ear discomfort / earache
- tinnitus
- itchiness
nb ?vertigo (although that not confirmed!)
nb can also get cough (dt stimulation of vagus nerve)
IMPACTED EAR WAX:
- main exam to do?
- main DDx? 4
look with otoscope (if impacted, won’t see ear drum)
DDx
- otitis externa (esp if inflammation of external ear)
- foreign bodies (esp in children)
- polyp of ear canal
- osteoma of ear canal
nb can also get rare thing called: keratosis obturans (see pearly white plug of keratin)
EAR WAX:
- when should it be removed? 5
- 1st line management?
- 2nd line management?
- 3rd line management?
If earwax is totally occluding the ear canal AND any of the following are present:
- Hearing loss
- Earache
- Tinnitus
- Vertigo
- Cough suspected to be due to earwax
nb if suspected perforated ear drom, don’t do these things!
1ST LINE
- olive oil or sodium bicarb ear drops for a week
2ND LINE
- ear irrigation
can return and have more drops then more irrigati9on etc but if really can’t clear:
3RD LINE
- refer to ENT for manual removal
nb if recurrent, can have regiular drops and/or irrigation etc (basically whatever works!
always safety net for infection!!
DEAFNESS
- causes of conductive? (4 common, 4 rarer)
- causes of sensorineural? (3 common, 4 rarer)
CONDUCTIVE
= ear wax
= otitis externa
= otitis media
= glue ear
- otosclerosis
- cholesteatoma (see other flashcard)
- foreign body
- perforated tympanic mebrane (eg from trauma)
SENSORINEURAL
= presbycusis
= noise induced hearing loss (NIHL) (60% also have tinnitus)
= congenital (eg Alports)
- meniere’s disease
- acoustic neuroma
- drug ototoxicity
- damage to brain (eg meningitis, multiple sclerosis, infarct)
OTOSCLEROSIS
- what is it?
- main risk factor?
- age of onset?
- two main symptoms?
get replacement of normal bone by vascular spongy bone.
Autosomal dominant - FHx main risk factor!
Onset is usually at 20-40 years
MAIN SYMPTOMS:
- conductive deafness
- tinnitus
nb 10% of patients may have a ‘flamingo tinge’ on tympanic membrane, caused by hyperaemia
GLUE EAR
- what is it?
- age of peak onset?
- main presenting symptom?
Effectively chronic otitis media with effusion (aka secretory otitis media)
age 2-7 (normally around 2)
symptom:
= conductive HEARING LOSS (often picked up as inattention, language delay at school!)
nb can also present as behavioural problems or balance problems
PRESBYCUSIS:
- cause?
- conductive or sensorineural hearing loss?
- bilateral or unilateral?
- what do patients often complain of?
AGE-RELATED
BILATERAL
SENSORINEURAL hearing loss
Patients may describe difficulty following conversations
Audiometry shows bilateral HIGH-FREQUENCY hearing loss
MENIERE’S DISEASE
- age at presentation?
- four main symptoms? (which norm most prominent?)
- how long do episodes last?
- what clinical test is positive?
middle-aged adults
recurrent episodes of:
- vertigo (most prominent)
- tinnitus
- hearing loss (sensorineural)
- sensation of fullness or pressure (in one or both ears)
episodes last minutes to hours!
ROMBERG test is positive (close eyes and fall)
nb may also have nystagmus!
ACOUSTIC NEUROMA
- aka?
- which cranial nerves affected? 3 (and what symptoms does this then give?)
- diagnostic investigation? 1
aka vestibular schwannoma
(actually more accurate as is a benign tumour of the schwann cells surrounding the vestibular nerve)
cranial nerve EIGHT
- hearing loss (sensorineural)
- vertigo
- tinnitus
cranial nerve FIVE
- absent corneal reflex (IMPORTANT SIGN!)
(can also get trigeminal neuralgia)
cranial nerve SEVEN
- facial palsy (less common)
diagnosis = MRI cerebello-pontine angle
(nb also norm do audiometry too to quantify hearing loss)
ALWAYS refer to ENT surgeons if suspect! (they will manage conservatively or with microsurgery)
nb Bilateral acoustic neuromas are seen in neurofibromatosis type 2
Which common drugs are potentially ototoxic? 5
- gentamicin (and other amino glycosides - anything ending in MYCIN)
- furosemide
- aspirin (and some other nsaids)
- quinine
- some cytotoxics (eg cisplatin and carboplatin)
HEARING LOSS
- first clinical exam to do?
- two clinical tests to do to determine if conductive or sensorineural? (which is which and what does a ‘positive’ test for each mean?)
- when are these tests NOT useful?
OTOSCOPY (see if you can visualise any wax or middle ear effusions etc)
RHINNES TEST
= put tuning fork next to ear then on mastoid
- if air conduction (AC) > bone conduction (BC) then it is positive (means either normal hearing or sensorineural hearing loss)
- if BC >AC then is negative (means conductive hearing loss in that ear)
WEBBERS TEST
= put tuning fork on mid forehead
- lateralises to midline: normal hearing OR bilateral disease (conductive or sensorineural)
- lateralises to AFFECTED ear in CONDUCTIVE hearing loss
- lateralises to UNAFFECTED ear in SENORINEURAL hearing loss
NOT useful if bilateral or mixed hearing loss!!
HEARING LOSS
- after otoscopy + rinnes + webers tests, what is next line investigation? 1
- other investigation to consider if unsure of cause? 1
- what to do if suddent unilateral hearing loss?
AUDIOMETRY (refer for)
- in all pts to quantify hearing loss
consider imagine (eg CT if unsure of cause - esp if conductive)
refer to ENT urgently if sudden unilateral hearing loss!
HEARING LOSS
- management option for people with moderate-severe sensorineural hearing loss? 1
- if patients are deaf from birth, other management option? 1
Pathology excluded & Patients 50-80 years old? –
refer for HEARING AID (or “assess & fit”) appointments
- nb can also give to younger pts
deaf patients can have COCHLEAR IMPLANTS
nb for conductive hearing loss you treat the cause - eg gromits for glue ear, surgery for any mass
VERTIGO:
- what is it?
- most important causes? 6
- other rarer causes? 4
Vertigo may be defined as the false sensation that the body or environment is moving
= viral labyrinthitis
= vestibular neuronitis
= BPPV
= meniere’s
= vertebrobasilar ischaemia
= acoustic neuroma
- posterior circulation stroke
- trauma
- multiple sclerosis
- ototoxicity e.g. gentamicin
For each of these causes of vertigo:
- viral labyrinthitis
- vestibular neuronitis
- BPPV
- meniere’s
- vertebrobasilar ischaemia
- acoustic neuroma
describe:
1) speed of onset? (and if any preceeding events)
2) what triggers vertigo attacks? (+ how long last)
3) any associated hearing loss or tinnitus? (and any other associated symptoms)
VIRAL LABYRINTHITIS
1) SUDDEN onset (following recent viral infection)
2) no recognised trigger
3) HEARING may be affected, incl tinnitus (also get NAUSEA and vomiting!)
VESTIBULAR NEURONITIS
1) recurrent attacks (following recent viral infection)
2) no recognised trigger
3) NO hearing loss (distinguishes from above! - as only affects vestibular nerve!) (also get nausea and vomiting)
BENIGN PAROXYSMAL POSITIONAL VERTIGO (BPPV`)
1) Gradual onset
2) triggered by change in head position (each episode lasts 10-20 seconds)
3) NO hearing loss or tinnitus (may get some nausea)
MENIERE’S
1) gradual onset recurrent episodes
2) no trigger although exacerbated by movement, episodes lasts minutes to hours
3) associated with hearing loss, tinnitius and fullness/pressure in ears
VERTEBROBASILAR ISCHAEMIA
1) elderly patients
2) vertigo on EXTENSION of neck
3) no associated symptoms
ACOUSTIC NEUROMA
1) gradual onset
2) no known trigger
3) associated with hearing loss, vertigo, tinnitus (and absent corneal reflex!)
LABYRINTHITIS
- how to distinguish from vestibular neuronitis? 1
- three groups of causes? (which is by far most common?)
- average age at presentation?
get hearing loss +/- tinnitus as well as vertigo (in vestibular neuronitis only the vestibular nerve is affected so only get vertigo + nausea)
LABYRINTHISITIS CAUSES
- VIRAL (by far most common!)
- bacterial (have pus, more unwell)
- systemic infection (obs are off)
viral is normally secondary to a recent URTI or herpes!
average age of presentation is 40-60
LABYRINTHITIS
- Main symptom? (describe onset and severity)
- associated symptoms? 3
- clinical sign on examination? other sign you may see?
- possible prodrome?
VERTIGO
- not triggered by movement (but is exacerbated by it!)
- SUDDEN onset
- is incapacitating
- nausea and vomiting (frequent!)
+/- hearing loss
+/- tinnitus
see spontaneous (norm horizontal) nystagmus
other sign = Gait disturbance (fall/lean towards affected side)
(normally fine sitting)
nb may also see abnormality on inspection of the external ear canal and the tympanic membrane e.g. vesicles in herpes simplex infection
POSSIBLE PRODROME
- Viral Prodrome (coryza etc)
- Rhinorrhoea + Fever
HINTS exam
- what used to differentiate between?
- describe each section and findings?
used to distinguish between a central cause of vertigo (eg stroke) from a peripheral cause (eg labyrinthitis or vestibular neuronitis)
1) Head Impulse test
= (test for peripheral vestibular function)
- Fix pt. gaze straight ahead/at your nose. Rapidly turn pts. head 10-20° to one side and then reset back to face you.
NORMAL = patient holds fixed gaze w/ head movement.
ABNORMAL = saccades present i.e. patients eyes have to flick back to your nose (GET IF PERIPHERAL)
2) Nystagmus Type
- Ask pt. to look left & right to discern whether nystagmus (indicated by the fast phase of movement) is unidirectional & consistent nystagmus = POSITIVE (sign of peripheral cause)
- Nystagmus that changes on position i.e. fast phase to left when looking left and vice versa indicates a central cause (e.g. Stroke/TIA)
3) Skew
- Cover/uncover each eye in turn & note any skew – typically vertical skew. Movement = central causes of vertigo.
SO an abnormal head impulse test, unidirectional nystagmus and no vertical skew are sensitive markers of PERIPHERAL CAUSES of vertigo
LABBYRINTHITIS:
- how is diagnosis normally made?
- investigations to consider if diagnosis is uncertain or suspect more sinister cause? 6
Diagnosis is largely CLINICAL (ie based on hx and exam)
nb glucose is helpful in excluding hypoglycaemia.
in most patients with suspected viral labyrinthitis, no other investigation is necessary
OTHER
- pure tone audiometry (to assess hearing loss)
- FBC + blood culture (if systemic infection suspected)
- culture and sensitivity testing (if any middle ear effusion)
- temporal bone CT scan (if suspecting mastoiditis or cholesteatoma)
- MRI scan (can rule out causes such as suppurative labyrinthitis or central causes of vertigo)
- vestibular function testing (may be helpful in difficult cases and/or determining prognosis)
VIRAL LABYRINTHITIS:
- when to refer urgently to ENT?
- prognosis?
- advice to patients? 2
- medication to prescribe? 1
Emergency admission + see ENT specialist if sudden onset U/L hearing loss
prognosis for viral labyrinthitis: Good. Benign & self-limiting. Majority of cases take several days to few weeks to resolve completely
ADVICE
- Avoid driving/operating machinery
- During acute attacks, lie still w/ eyes closed
Medication: PROCHLORPERAZINE for dizziness
(nb this is a 1st gen anti-psychotic - so can haveEPSEs with it!)
Benign paroxysmal positional vertigo (BPPV)
- average age of onset?
- triggers?
- how long episode last for?
- what manouvere is positive? 1
- what manouvere is performed to treat? 1
55 years = average onset
vertigo triggered by change in head position (e.g. rolling over in bed or gazing upwards)
nb may be associated with nausea
each episode typically lasts 10-20 seconds
positive Dix-Hallpike manoeuvre
nb usually resolves spontaneously after a few weeks to months
Symptomatic relief may be gained by:
- EPLEY manoeuvre (successful in around 80% of cases)
nb can also teach the patient exercises they can do themselves at home, termed vestibular rehabilitation, for example Brandt-Daroff exercises
nb Medication is often prescribed (e.g. Betahistine) but it tends to be of limited value
CHOLESTEATOMA
- what is it?
- risk factors? (age plus another 3)
- main two features? 2
a non-cancerous growth of squamous epithelium that is ‘trapped’ within the skull base causing local destruction
presents in childhood
- congenital (epithelium trapped in bone during embryogenesis)
- cleft palate (causing eustacian tube dysfunction)
- tympanic membrane trauma (norm secondary to otitis media)
main two features:
1) PROGRESSIVE unilateral conductive hearing loss
2) Painless PURULENT FOUL smelling discharge (otorrhea) – frequent + unremitting
nb depending on size, can also get:
- vertigo
- facial nerve palsy
- cerebellopontine angle syndrome
CHOLESTEATOMA
- what see on otoscopy? 1
- management? 1
Otoscopy
- ‘attic crust’ - seen in the uppermost part of the ear drum (with drum retraction or perforation)
Management
- patients are referred to ENT for surgical removal
RAMSAY HUNT SYNDROME
- what is it? (incl where affected)
- first symptom?
- subsequent symptoms? 3
- medical management? 2
aka herpes zoster oticus
is reactivation of VZV in CN7 (ie shinges in facial nerve)
1st) AURICULAR PAIN
other symptoms
- facial nerve palsy
- vesicular rash (around ear and tongue)
- vertigo + tinnitus
Mx
- PO aciclovir
- steroids
Difference between primary and secondary otalgia?
causes of primary otalgia? (3 common 2 rarer)
causes of secondary otalgia? (4 common, 3 rarer)
primary otalgia is pain orginiting from pathology in the ear
- secondary is when pts feel pain in the ear but this is actually referred from somewhere else
PRIMARY OTALGIA = infection (commonest!) = trauma + foreign bodies = impacted ear wax - ramsay hunt syndrome - otologic neoplasms
SECONDARY OTALGIA = dental inflammation / infection = temporomandibular joint disorders (pain worse w chewing) = trigeminal neuralgia = temporal arteritis - head + neck cancers - eagle's syndrome
Nb Eagle’s syndrome is a condition associated with the elongation of the styloid process or calcification of the stylohyoid ligament, clinically characterised by throat and neck pain, radiating into the ear.
ALWAYS find a cause for otalgia!!! - don’t just treat with analgesia! - if not resolving with eg Abx for suspected infection, refer to ENT
RED FLAGS in history of OTALGIA
- ear symptom? 1
- eye symptoms? 2
- other symptoms? 5
- past medical history? 2
- progressive or sudden hearing loss
- loss of vision (temporal arteritis)
- black spots in vision
- dysphagia
- odynophagia
- dysphonia
- hamoptysis
(head + neck Ca) - weight loss
- immunosuppressed
- diabetes
(rapidly proggressing infection)
describe what each of these words are describing in the eye:
- conjunctiva
- iris
- sclera
- pupil
- cornea
- anterior chamber
CONJUNCTIVA
- thin layer of tissue that covers whole eye EXCEPT cornea
IRIS
- coloured bit of the eye
SCLERA
- white of eye
PUPIL
- black bit
CORNEA
- transparent tiny lens that covers iris, pupil and anterior chamber (conjunctiva doesn’t cover this bit!)
ANTERIOR CHAMBER
- front part of the eye between the cornea and the iris
nb posterior chamber is between iris and lense (then aqueous chamber if actually in main part of your eyeball)
RED EYE findings in these conditions: - acute angle closure glaucoma - anterior uveitis (iritis) - scleritis - conjunctivitis - subconjunctival haemorrhage
1) brief hx / risk factors?
2) appearance of conjunctiva?
3) appearance of iris?
4) appearance of pupil?
5) appearance of cornea?
6) appearance of anterior chamber?
7) intraocular pressure?
ACUTE ANGLE CLOSURE GLAUCOMA = elderly, long-sited pt, sudden pain in/behind eye, reduced visual acuity, halos 2) conjunctiva: injected 3) iris: injected 4) pupil: FIXED MID-DILATED (can be oval) 5) cornea: steamy/hazy 6) anterior chamber: very shallow 7) intraocular pressure: very high!
ANTERIOR UVEITIS (iritis)
= HLA-B27: ank spond, RA, reactive arthritis, sarcoid etc, photophobia, deep boring pain - worse with acomodation
2) conjuctiva: injection most marked around cornea (ie red ring around iris)
3) iris: injected
4) pupil: SMALL +/- irregular shape(dt adhesions)
5) cornea: NAD
6) anterior chamber: TURGID (CELLS! = HYPERPYON)
7) IOP: NAD
SCLERITIS = half have rheum diseases, pain - esp on eye movement 2) conjunctiva: injection, is most marked around cornea (ie red ring around iris - nb similar to iritis) - also has BLUISH HUE 3) iris: ?? 4) pupil: NAD 5) cornea: NAD 6) anterior chamber: NAD 7) IOP: NAD
CONJUNCTIVITIS = norm bilateral, bacterial, viral or allergic 2) conjuntiva: injected (greatest towards medial and lateral corners of eyes), discharge (purulent if bacterial) 3) NAD 4) NAD 5) NAD 6) NAD 7) NAD
SUBCONJUNCTIVAL HAEMORRHAGE = norm secondary to valsalva manouvere, HTN, bleeding disorders, trauma, haemorrhagic fevers 2) bright red area of sclera 3) NAD 4) NAD 5) NAD 6) NAD 7) NAD
Initial management of each of these causes of red eye:
- acute angle closure glaucoma? 2
- anterior uveitis? 2
- scleritis? 1
- conjunctivitis? 1
- subconjunctival haemorrhage? 1
which would you refer to opthalmology?
ACUTE ANGLE CLOSURE GLAUCOMA - IV acetazolamide (500mg) - Pilocarpine eye drops (after 1 hr) (see specific flashcard for more info) = refer ASAP
ANTERIOR UVEITIS (iritis)
- steroid eye drops (eg pred)
- atropine eye drop
= refer ASAP
SCLERITIS
- oral NSAIDs is 1st line
= refer ASAP
CONJUNCTIVITIS
- depends on cause (antihistamine for allergic, consider chloramphenicol if bacterial)
= no referral needed
SUBCONJUNCTIVAL HAEMORRHAGE
- none, resolves spontaneously - check BP and if on anticoags
= refer (only if traumatic cause)
ACUTE ANGLE CLOSURE GLAUCOMA:
- pathophysiology? (ie what causes the raised intra-ocular pressure)
pupil dilates -> iris pushes against lense -> aqueous can’t drain from posterior to anterior chamber -> trabecular meshwork also blocked -> aqueous cannot drain from anterior chamber -> RAISED intraocular pressure
this is sight threatening as the raised IOP can -> death of optic nerve
nb normally aqueous humoour is produced by ciliary bodies in posterior chamber then moves to anterior chamber where it is drained in the trabecular meshwork
nb vitreous humour is is in the deeper part of the eye - different to aqueous humour)
ACUTE ANGLE CLOSURE GLAUCOMA:
- age generally affected?
- long or short-sighted people more at risk?
- medications that increase risk?
- what is normally the acute trigger?
generally elderly (also asians at higher risk)
long-sighted at higher risk (hyperopia) - dt shallow anterior chamber
nb you get more long-sighted as you age!!
drugs which can increase likelihood:
- sympathomimetics
- anticholinergics
^both dilate pupil!!
acute trigger is normally low light (eg in evening) as pupil dilates!
nb can also get it secondary to a traumatic haemorrhage (which pushes the posterior chamber anteriorly)
ACUTE ANGLE CLOSURE GLAUCOMA:
- classic prodrome symptom? 1
- main local symptom? 1
- other local symptom? 1
- systemic symptoms? 3
HALOES / rainbows around lights!!
constant aching pain develops RAPIDLY around one eye
- reduced vision
- pain radiates to forehead (headache)
- nausea and vomiting
- abdo pain
ACUTE ANGLE CLOSURE GLAUCOMA, findings on exam / SLIT LAMP:
- visual acuity?
- conjunctiva/sclera?
- iris?
- pupil?
- cornea?
- anterior chamber?
- intraocular pressure?
reduced visual acuity
perilimbal conjunctival injection (ie closest to the iris/cornea)
iris injected
pupil FIXED (ie not responsive to light) MID-DILATED
HAZY cornea (also hard on palpation)
anterior chamber: shallow but NO cells (how differentiate from anterior uveitis)
raised IOP
ACUTE ANGLE CLOSURE GLAUCOMA:
- who to refer to? how urgently?
- nursing management? 2
- two medications to give to treat? 2 (incl route)
- two medications to treat symptoms? 2
- definitive treatment provided by opthalmologists? 1
opthalmologist! - SUPER URGENT! (even OOH)
- lie patient on back (no pillows)
- DON’T put on eye mask or dim light (this will dilate pupil more, making worse!)
1) IV ACETAZOLAMIDE (500mg)
- this works by reducing aqueous secretions
2) PILOCARPINE EYE DROPS (after 1 hr)
- parasympathetic -> constricts pupil which opens trabecular meshwork, allowing drainage
nb can also give betablockers (if not CI) topically (timolol eye drops!)
ALSO PRESCRIBE
- oromorph
- ondasetron
DEFINITIVE MANAGEMENT: Peripheral iridectomy (laser or surgery) – do once IOP is controlled, involves removing iris segment at 12 oclock B/L to allow aqueous flow
DDx for ACUTE RED EYE (with normal lids)
- inflammatory/autoimmune? 3
- infectious? 2
- secondary to foreign bodies? 2
- other? 2
what is the most common cause?
INFLAM / AUTOIMMUNE
- anterior uveitis / iritis
- scleritis
- episcleritis
- allergic conjunctivitis
INFECTIOUS
- viral conjuctivitis
- bacterial conjuctivitis
SECONDARY TO FOREIGN BODIES
- corneal abrasions / foreign bodies
- bacterial or fungal keratitis / corneal ulcer (almost always secondary to contact lenses!)
OTHER
- acute angle closure glaucome
- subconjuctival haemorrhage
nb subconjunctival haemorrhage can be caused by: trauma, straining (coughing, sneezing, vomiting, Valsalva), conjunctivitis, chronic health conditions (diabetes, hypertension), and coagulopathy
CONJUNCTIVITIS is COMMONEST cause of acute red eye!
CONJUNCTIVITIS
- how is the appearance described?
- three main types?
‘BILATERAL generalised conunctival injection’
nb injections tend to be more peripheral
nb conjunctivitis = most common cause of acute red eye
- bacterial
- viral
- allergic
nb all three very common
CONJUCTIVITIS
- symptoms? 4
- how to distinguish clinically from viral and bacterial causes? 1
- additional feaqtures of allergic conjunctivitis? 2
‘uncomfortable’, gritty eyes (rather than painful)
- erythema of conjunctiva
- watery eyes
- itchy eyes
viral more ‘itchy’ and watery discharge while bacterial is more ‘sticky’ with a more purulent discharge (clinically hard to tell the difference between)
allergic
- eyelid swelling +/- conjunctival oedema
- history of other atopic disease
Management of allergic conjunctivitis:
- advice to patient?
- medication options? 2
use a cold compress
PO antihistamines
OR
TOP anti-histamines e.g. Emedastine or olopatadine
Nb can also have steroid drops if really bad - but these would be started by opthalmologist
BACTERIAL CONJUNCTIVITIS:
- 1st line management option? 1
- norm prognosis without this management?
- which groups of patients always given to? (3 clinical, 2 occupational)
CHLORAMPHENICOL eye drops (or fusidic acid)
controversial - most BACTERIAL infections resolve within 5 days without treatment
(can give delayed prescription)
ALWAYS GIVE Abx to:
- purulent, painful, red
- dry eyes / known eye disease
- contact lense user
- care / ICU / nursery workers
- children at nursery
BACTERIAL CONJUNCTIVITIS
- what to suspect and do if pt fails treatment?
- which group of patients should you refer to opthalmologist straight away?
suspect could be gonococcal or chlamydial cause!
DO EYE SWABS!! and refer to opthalm
refer NEONATES to opthalm straight away as most likely to be chlamydia/gonococcal from mothers birth canal
Three most common causative organisms for BACTERIAL conjunctivitis? 3 (other 2 rarer causes?)
commonest VIRAL cause of conjunctivitis? 1
BACTERIAL = strep pneumoniae = staph aureus = H. influenzae - gonococcal - chlamydial
VIRAL
= adenovirus (80%)
^very contagious!!
what normally preceedes a viral conjunctivitis?
How long do viral conjucntivits symptom s take to go away? when should you refer someone?
URTI norm preceeds (or contact with someone with conjunctivitis - eg in home)
1-2 weeks (but can be as long as 6 weeks!) - refer at 6 weeks
what can often preceede a bacterial conjunctivitis? 2
Otitis media or LRTI
FOREIGN BODY IN EYE:
- symptoms common for all? 5 (conjunctiva abrasian, corneal abrasian and penetrating injury)
- symptom that makes corneal involvement and/or penetrating injury more likely? 1
nb this is just symptoms, do signs on different flashcard
= red eye
= watery eye
= painful eye
= sensation of foreign body in eye
= blurred vision (nb degree of loss of visual acuity doesn’t correlate with severity)
(nb foreign body on cornea is more painful than on sclera)
PHOTOPHOBIA (always suggests corneal involvement, superficial or deep)
EYE INJURY
- sign likely to see in all? 1
- bedside investigation to look for abrasions? 1
- RED FLAG signs for penetrating corneal injury? 5
Conjunctival or ciliary injection (ALL)
FLUROSCEIN STAIN (appears green under blue light if any epithelial damage)
RED FLAGS
- distorted iris / pupil (or globe)
- air bubbles under cornea
- leaking humour
- hyphaema (blood level in iris) -BAD SIGN!
- subconjunctival haemorrhage (only if massive and hx of trauma!)
nb see many of these with eyes alone - but can use a slit lamp too (but norm would just refer to opthalm to do this if unsure!)
SHOULD ALWAY EVERT EYELIDS to look for abrasians / foreign bodies
nb also loss of red reflex (loose in blood in vitreous or large retinal detachment)
Test to do to see if aqueous humour is leaking from eye:
- name?
- what it involves?
Seidel’s test
= 10% Fluorescein (dark orange)
check if aqueous fluid is leaking (treat as open globe injury)
Who to refer to opthalmology urgently following occular trauma / foreign body?
- all high-velocity injuries caused by sharp objects
- chemical inj.
- FBs
- ↓visual acuity
- large abrasion (>60% cornea)
- corneal opacity
- rust ring
- distorted pupil
- retinal damage
- deep laceration of orbit etc.
BASICALLY REFER ANYTHING that is worse than a simple, small corneal abrasion with no foreign
Management of:
- corneal abrasion? 2
- additional management of corneal foreign body (non-penetrating)? 2
ie inaddition to above
CORNEAL ABRASION
- TOP anaesthetics
- TOP chloramphincol (fusidic acid if pregnant)
IF foreign body, ALSO:
- remove FB under TOP anaesthetic
- irrigate eye with water
(then do as above!)
Management of penetrating corneal injury:
- what NOT to do? 1
- who to refer to? 1
- how to protect eye in meantime? 1
- medication to give in ED? 1
Do NOT touch, manipulate or pad the eye
REFER IMMEDIATELY
Give rigid eye shield to protect eye and refer immediately
Give TETANUS shot
CORNEAL ULCER
- main risk factor?
- causative group of organisms?
- do you need to refer to opthalmology?
CONTACT LENSE WEARERS
can be bacterial (commonest), viral (norm HSV) or rarely fungal
YES - REFER URGENTLY!
CORNEAL ULCER
- often initial symptom?
- later symptoms? 4
may start with a ‘foreign body sensation’
then
- photophobia
- blurred vision
- discharge
- pain
CORNEAL ULCER
- signs on exam? 3
- additional bedside investigation? 1 (and what does it show?)
- severe conjunctival injection
- discharge
- eyelid swelling
corneal ulceration demonstrated by fluorescein stain
CORNEAL ULCER
- who manages?
- investigation they will do? why?
- management options? 2
opthalmologists manage
slit lamp - to determine if bacterial or vioral ulcer (look different)
- TOP chloramphenicol (or other Abx)
OR - TOP acyclovir
^depending on cause identified!
CATARACTS
- pathophysiology?
- risk factors? (2 demographic, 2 lifestyle, 2 conditions, 1 med)
nb this excludes for con genital
gradual deposiotion of opaque protein deposits onto lense
- increased age
- female
- smoking
- UV exposure
- diabetes mellitus
- inflammatory eye disease
- corticosteroids
CONGENITAL CATARACTS
- infections that can cause? 5
- other condition associated with? 1
TORCH
- toxoplasmosis
- other (VZV, syphillis, HIV)
- rubella
- CMV
- herpes simplex
down’s yndrome
nb can also get idiopathic congenital cataracts
ADULT-ONSET CATARACTS
- speed of onset?
- describe the loss of vision that occurs? (ie what goes first)
- associated symptoms? 2
GRADUAL (see nb below)
PAINLESS blurred vision, slowly -> loss of vision (esp if bilateral)
nb often both eyes but norm one worse than other
- trouble with nocturnal vision
- difficulty reading (↓Acuity)
- failure to recognise faces
- problems watching TV / see colour less clearly
= DAZZLE / GLARE (esp in sunlight or lights whilst driving at night - “is like driving with a dirty windscreen at night/bright light”)
= HALOES (around bright lights)
nb normal gradual onset ‘nuclear’ cataracts - but can get posterior sub-capsular cataracts which progress faster (norm secondary to STEROIDS)
CONGENITAL CATARACTS
- test to pick up?
- signs if missed? 3
- how quickly do you need to operate to reduce adverse effects? 1
RED REFLEX (absent in congenital cataracts and retinoblastoma) - part of newborn check!
if missed may notice:
- squint
- amblyopia (lazy eye)
- nystagmus
need to operate fast (ideally within 4 weeks) or seeing part of brain won’t develop properly!
CATARACTS
- findings on fundoscopy? 2
- investigation for definitive diagnosis?
red light reflex
- present if early
- absent if late
Lens appears brown or white if bright light shone
refer to opthamlmologist (routine) for slit lamp diagnosis if considering surgery
CATARACTS:
- conservative lifestyle changes? 2 (to prevent getting worse)
- are they allowed to drive?
- definitive management? 1 (when do? 2)
- stop smoking
- wear sunglasses
surgery is only cure
- operate on one eye at a time
can only drive if:
- In daylight be able to read a number plate at a distance of 20m
- Visual acuity must be at least Snellen 6/12 with both eyes open (or in the only eye if monocular)
^if worse than this - must inform DVLA and not drive!
operate if:
- QoL↓
- unable to read number plate @ 20m
ALWAYS DIOCUMENT VISUAL ACUITY (on any referral!)
Definition of:
- meibomian cyst (aka chalazion)
- stye (aka hordeolum)
how do they both present? (signs/symptoms)
two main differences in presentation? 2
MEIBOMIAN CYST - aka chalazion - blocked meibomian gland (norm hydrates eye) -> cyst - NON-infective = NOT tender (may be painful initially) = HARD on palpation
STYE - aka hordeolum - infected meibomian gland (internal) or lash follicle (external) = INFECTIVE (basically a mini abscess) = SOFTER on palpation
BOTH
- single lump on eyelid
- can get watering and slightly red eye
nb both can have a yellowy centre - but stye often more pronounced
nb if whole eyelid swollen, more likely blepharitis (although may have a stye on top of this)
Risk factors for STYE? (3 local conditions, 2 systemic conditions)
= chronic blepharitis
- rosacea
- seborrhoeic dermatitis
- pregnancy
- diabetes mellitus
nb most people who get one don’t have any reisk factors
How diagnosis of stye and meibomian cyst made?
when to refer to opthalmology? 2
clinical diagnosis
- EVERT the eyelid to see an internal stye!!
REFER IF:
- visual disturbance
- associated peri-orbital or orbital cellullitis
also if suspect it is actually a BCC
Management of STYE
- what should patients NOT do? 3
- conservative management? 1
- prognosis?
- other management options in primary care? 2
- when to consider topical antibiotics? 1
DON’T
- attempt to puncture / pop the stye
- wear eye make up until gone
- use contact lenses until gone
DO
- use warm compresses (5-10 mins 2-4 times a day until resolves)
(nb can also use OTC oral analgesias)
nb same advice for meibomian cyst
PROGNOSIS: SLEF-LIMITING (resolve in 1-2 weeks)
if painful external stye, can:
- pluck eyelash from infected follicle
- incision and drainage
only prescribe TOP antibiotic if clinical features of concurrent conjunctivitis (copious muco-purulent discharge)
(obvs if associated peri-orbital / orbital cellulitis then give PO/IV Abx for this)
DIABETIC RETINOPATHY features indicating: - background retinopathy? 1 - maculopathy? 1 - pre-proliferative retinopathy? 2 - proliferative retinopathy? 1
which cause reduced visual acuity?
BACKGROUND RETINOPATHY
- at least one micro-aneurysm (MA - ‘dots and blots’)
MACULOPATHY
- basically anything on the macula (OEDEMA most common, also: ischaemia, haemorrhages)
- can get reduced visual acuity
PRE-PROLIFERATVE
- ‘cotton wall spots’ (aka soft exudates)
- hard exudates
(nb in addition to dots and blots)
PROLIFERATIVE
- new vessel formation (wispy red noodles, often next to ischaemic areas)
- get reduced visual acuity!
nb maculopathy is seperate to other stages - each other stage can occur with or without maculopathy
nb it is actually much more confusion than this with categorisation etc but just learn this!
DIABETIC RETINOPATHY
- how often are people with diabetes screened for it?
- what can do in primary care to control / slow progression? 4
every year!
really important as don’t have any symptoms until far down! - and can stop getting worse but is not reversible!
- nb if get haemorrhages, these can present as painless floaters!
- good glycaemic control
- good HTN control
- good lipid control (diet + statins)
- stop smoking
Aside from diabetic retinopathy, what other eye conditions are people with diabetes at risk of? 2
- cataracts
- glaucoma
(nb also high risk for hypertensive retinopathy too!)
DIABETIC RETINOPATHY:
- management options in secondary care? 4
LASER TREATEMENT
- to obliterate new vessel growth
- slows progression but does not improve visual acuity
INRAVITREAL STEROIDS
ANTI-VASCULAR ENDOTHELIAL GROWTH FACTORS
-end in mab
SURGERY
- may need vitrectomy if have an intravitreal bleed
HYPERTENSIVE RETINOPATHY features of: - grade 1? 2 - grade 2? 2 - grade 3? 3 - grade 4? 1
possible symptoms? 2 (when do these occur?)
GRADE 1
- increased tortuosity (nb normal in small peripheral vessels)
- narrowing (dt deposits)
GRADE 2
- silver/copper wiring
- AV nipping
GRADE 3
- cotton wool spots (ischaemic areas)
- hard exudates
- flame/splinter bleeds
GRADE 4
- papilloedema
SYMPTOMS
- blurred vision
- visual field defects
OCCUR LATE in disease!!
Management of hypertensive retinopathy:
- mainstay? 1
- options if severe? 3
Treat primarily by CONTROLLING BP (meds and lifestyle)
for retinal edema, sometimes:
- laser
- intravitreal steroid injection - injeciton of antivascular endothelial growth factor drugs
ACUTE ANTERIOR UVEITIS:
- aka?
- pathophysiology?
- what conditions is it associated with? 10
- other main risk factor?
aka IRITIS
inflammation of the iris (coloured part of eye) and anterior chamber
HLA-B27 conditions:
- ankylosing spondylitis
- reactive arthritis
- JIA
- IBD (both)
- bechet’s disease (mouth and genital ulcers)
- psoriasis/psoriatic arthritis
- sarcoidosis
- MS
also
- HIV
- TB
other: POST EYE SURGERY infection/inflammation
ACUTE ANTERIOR UVEITIS
- aka? 1
- symptoms? 4
- main DDx to rule out? 1
aka IRITIS
PAINFUL (deep ‘boring’, worse with accomodation) and RED eye
- PHOTOPHOBIA (hurts when pupuil constricts)
- BLURRED VISION
nb may also have a headache and feel systemically unwell (also ask about PMHx/joints)
need to RULE OUT ACUTE GLAUCOMA (presents very similarly)
- obv also all other causes of acute red eye…
