ophthalmology Flashcards
what is acute angle closure glaucoma
rapid rise in intraocular pressure due to sudden obstruction to the flow of aqueous humor within the eye
obstruction from iris pushed or pulled forward so obstructs the trabecular network
pressure leads to compression of the optic nerve and visual loss
risk factors of acute angle closure glaucoma
family history older age female ethnicity - Chinese anatomy - long sighted
symptoms of acute angle closure glaucoma
blurred vision /halo around lights
headache (not relived by analgesia)
vomiting
watering eyes
red eye
fixed mid-dilated pupil
globe hard to touch
corneal oedema - cloudy cornea
investigations for acute angle closure gluacoma
measure intra-ocular pressure (digital or tonometry)
gonioscopy by ophthalmology to assess angle
management of acute angle closure glaucoma
pilocarpine eye drops
acetaxolamide to reduce production of aqueous humour
analgesia +/- antiemetic
laser iridotomy - make hole in iris to re-establish drainage
chemical eye injuries
can produce extensive damage to ocular surface and anterior segment leaidng to visual impairment and disfigurement
severity of chemical eye injuries depends on
toxicity of the chemical
how long in contact with eye
depth of penetration
area of involvement
symptoms of chemical eye injury
severe pain
epiphora (excessive eye watering)
blepharospasm
reduced visual acuity
investigations for chemical eye injury
pH of the eye
management of chemical eye injurys
irrigation topical anaesthetic topical antibiotic cycloplegic agents for comfort lubricating eye drops steroid drops may need surgical treatment
irrigation in chemical eye injurys
remove offending substance and restore physiologic pH
penetrating eye injury
injuries that penetrate the eye but not through (no exit wound)
full thickness rupture of the cornea and/or sclera
risk factors for penetrating eye injury
risk behaviour men 30s home and workplace failure to wear eye protection
symptoms of penetrating eye injury
pain double vision foreign body sensation blurred vision subconjunctival haemorrhage, peaked pupil., hyphema, iris deformities, lens distruption, virteous haemorrhage, retinal tears
conjunctivitis
inflammation of the conjunctiva
causes of conjunctivitis
infectious bacterial
infectious viral
noninfectious (allergic)
pathophysiology of conjunctivitis
infection inflammation
dilatation of conjunctival vessels
conjunctival hyperemia and oedema
inflammatory discharge
risk factors of conjunctivits
exposure to causative AGENT, immunocompromised state and atopy
contact lens wear
presentation of conjunctivits
itching eye + redness and purulent discharge (if bacterial) - unilateral
unaffected vision
eyelid oedema, chemosis, excessive lacrimation
discharge in conjunctivitis: bacterial gonococcal viral allergic nonallergic
bacterial = purulent, white/yellow/green gonococcal = hyperpurulent, profuse viral = watery, stringy allergic = watery, mucoid nonallergic = mucoid
management of conjunctivitis
- in general
- allergic
- chlamydia
- bacterial
ocular lubricant drops/ophthalmic ointment
allergic conjunctivitis = antihistamine drops
systemic therapy to eradicate chlamydia infection
bacterial conjunctivitis = topical antibiotics
corneal ulcers
inflammatory condition of the cornea = open corneal sore
many causes - bacterial, fungi, viruses, protozoa
risk factors for corneal ulcers
improper contact lens use corneal abrasions eye burns xerophthalmia (dry eyes) eyelid disors steroid eye drops vitamin A deficiency
presentation of corneal ulcers
red eye severe pain soreness discharge (tearing, pus) eyelid swelling blurred vision vision loss photophobia
investigations for corneal uclers
slit lamp
fluorescein dye - ulcer margins
herpes simplex ulcers - typical dendritic/geographic pattern
history + decreased visual acuity
management of corneal ulcers
meds -
antimicrobial eye drops,
analgesic for pain control
steroid eye drops (after infection irradiation to reduce swelling and prevent scarring)
surgery - corneal transplantation to reduce damaged cornea if scarring decreases vision
giant cell arteritis
inflammation of the lining of the arteries in head
causes of giant cell arteritis
inflammation of artery walls –> swelling –> narrowing of vessels –> reduced O2/nutrient supply
genetic and environmental factors increase suseptibility to inflammation
risk factors for giant cell arteritis
age 70-80 women 2x more white northern european or scandinavian polymyalgia rheumatica family history
presentation of giant cell arteritis
unilateral head pain/tenderness - affecting temples
scalp tenderness
jaw pain when chew or open wide
fever, fatigue, unintended weight loss
vision loss or double vision
sudden permanent loss of vision in one eye
giant cell arteritis is related to
polymyalgia rheumatica
complications of giant cell arteritis
blindness
aortic aneurysm
stroke
investigations of giant cell arteritis
reduced pulse and hard cord like feel and appearance of temporal arteires on examination
blood tests - ESR and CRP
imaging - USS, MRA, PET
biopsy of temporal atery
management of giant cell arteritis
high dose corticosteroids for one to 2 years (lower dose)
methotrexate
keep an eye on bone density, prescribe calcium and vit D supplements
retinal detachment
emergency situ where retina pulls away from its normal position - separating from layer of blood vessels
types of retinal detachment
rhegmatogenous - hole or tear allowing fluid out
traction - scar tissue on retina surface
exudative - fluid accumulates, no whole or tear
risk factors for retinal detachment
aging prev retinal detachment in one ey family history extreme near sightedness prev eye surgery prev eye injury prev eye disease or disorder
presentation of retinal detachment
painless but warning signs include::
- sudden appearance of many floaters
- photopsia (flashes of light)
- blurred vision
- gradually reduced peripheral vision
- curtain like shadow over visual feild
investigations for retinal detachment
retinal examination -look for tears
USS - look for bleeding
management of retinal detachment
before detached - laser surgeyr and cryopexy to secure retina down
after detached - pneumatic retinopexy + cryopexy, scleral buckling or vitrectomy
vitrectomy
draining and replacing fluid in the eye
orbital cellulitis
infection of the fat and muscles around the eye - affecting the eyelids, eyebrows and cheeks
causes of orbital cellulitis
children - often bacterial sinus infection in beginning
more in <7yo
risk factors for orbital cellulitis
recent URTI sinus infection younger foreign bodies in orbit trauma immunosuppression systemic infection dental infection
presentation of orbital cellulitis
painful swelling in upper and lower eyelid bulging eyes decreased vision pain when moving eye fever generally ill feeling difficult eye movements, perhaps double vision shiny, red or purple eyelid
investigations of orbital cellulitis
bloods - FBC, blood culture and spinal tap
xray of sinuses, CT or MRI of sinuses and orbit, culture of eye and nose drainage, throat culture
management of orbital cellulitis
intravenous antibiotics
surgeyr to drain abscess ir relieve pressure
meibomian cyst
chalazion
= sterile inflammatory granuloma caused by obstruction of sebaceous gland
cause of meibomian cyst
obsturction of meibomian gland can cause to enlarge and rupture
triggers inflammatory reaction against lipid content
risk factors for meibomian cysts
pregnant women with
- chronic belpharitis
- seborrheic dermaittis
- rosacea
- pregnancy
- diabetes mellitus
- elevated cholesterol
- chronic hordeola (styes)
presentation of meibomian cyst
firm, painless, localised eyelid swellings that develop over several weeks
more common in upper than lower eyelid
unilateral
management of meibomian cyst
warm compres 10-15min + masage 5 times a dya
urgent referral if malignancy suspected
refer to ophthalmologist if vision affected, discomfort or cosmetic issues
blepharitis
chronic condition - inflammation of the eyelids
affects both eyes
when oil glands at the base of eyelashes get clogged = irritation and redness
causes/risk factors of blepharitis
seborrhoeic dermatitis infection clogged or malfunctioning oil glands in eyelids rosacea allergies eyelash mites or lice dry eyes
presentation of blepharitis
watery, red eyes gritty, uring or stinging sensation in the eyes eyelids appear greasy itchy eyelids flaking of skin around the eyes crusted eyelashes sensitivity to light blurred vision improving when blinking
investigaitons for belpharitis
examination of the eye
swabbing skin for testing
management of blepharitis
fight infection - eyedrops, creams etc
inflammation - steorid eyedrops
immune systen - cyclosporine (symptom relief)
treat underlying cause
clean eyes daily, lubricate eyes, control dandruff and mites
cataract
clouding of the normally clear lens of the eye
protein and fibres in lens break down and clump together –> clouding the lens –> cataract scatters and blocks the light as it passes –> blurred vision
causes of cataract
aging injury inherited genetic disorders eye conditions, past surgery or diabetes long term steroid use
risk factors of cataract
older diabetes excessive exposure to sunlight smoking obesity high blood pressure prev eye injury or inflammation prev eye surgeyr prolonged use of corticosteroid meds drinking excessive alcohol
presentation of cataract
clouded, blurred vision or dim vision increasing difficulty with vision at night sensitivity to light and glare need for brighter light for reading and other activities seeing halos and lights frequent changes in eyeglasses fading or yellowing of colours double vision in a single eye both eyes
investigations for cataract
visual acuity test
slit lamp examination
retinal exam
applanation tonometry
management of cataract
regular eye exams quit smoking manage other health problems sunglasses reduce alcohol surgery
open angle glaucoma
drainage from cornea and iris remains open but trabecular meshwork is partially blocked
intraocular pressure increase
damage to optic nerve
risk factors of open angle glaucoma
high intraocular pressure >60yo black, Asian, Hispanic family history diabetes, heart disease, HTN, sickle cell anaemia cornea thin in centre extreme vision (near/far) prev eye surgery corticosteroids - espec. eye drops
clinical presentation of open angle glaucoma
patchy blind spots in peripheral or central vision, freq bilateral
tunnel vision in lateral stages
if untreaded = blindness
investigations of open angle glaucoma
measure intraocular pressure (tonometry)
test optic nerve damage
check for areas of vision loss (visual feild loss)
measure corneal thickness
inspect drainage angle
treatment of open angle glaucoma
lower intraocular pressure - prostaglandin eyedrops, beta blockers eyedrops, alpha adrenergic agonist eyedrops, carbonic anhydrase inhbitor eyedrops, rho kinase inhibitor, miotic or cholinergic agents
srugery - laser therapy, filtering surgery, drainage tubes, minimally invasive glaucoma surgery
macular degenration
age related damage to the macula
2 types - wet and dry
dry macular degernation
dry = macula gets thinner with age - progressive and develops over several years - no treatment
wet macular degernation
abnormal blood vessels grow in the back of the eye and damage macula - treatment available
risk factors of macular degeneration
family hsitory
>55yo
caucasian
smoke
presentation of macular degeneration - early, intermediate and late
early dry AMD - no symptoms
intermediate dry AMD - either no symptoms or mild blurriness in central vision, trouble seeing in low light
later AMD (wet or dry type - straight lines look wavy or crooked, blurry area near centre of vision, blank spots appear and blurry area enlarges, colours seem less bright, trouble seeing in low light
investigations of macular degeneration
eye exam
optical coherence tomography - pictures of inside of eye
management of macular degeneration
prevention - stop smoking, exercise, maintain good BP and cholesteral
treatment - vitamins and minerals to prevent further degeneration, anti VEGF drugs to inject into eye (if wet AMD), photodynamic therapy - injections and laser treatment
causes of red eye
acute close angle glaucoma penetrating/perforating eye injury chemical eye injury conjunctivitis corneal ulcers corneal abrasion corneal foreign body uveitis episcleritis and scleritis
neurological conditons thar may present with ocular signs
cranial nerve palsy’s - CN III, IV and VI
horners syndrome
papilloedema
causes of acute/subacute vision loss
giant cell arteritis retinal detatchment amaurosis fugax posterior vitreous detachment vitreous haemorrhage vaascular occlusion of retinal circulation retinal artery occlusion retinal vein occlusion optic neuritis
cuases of gradual loss of vision
cataract
open angle glaucoma
macular degeneration
refractive issues- myopia/hypermetropia/presbyopia
oculoplastics/eyelid conditopns
orbital cellulitis meibomian cyst aka chalazion blepharitis dry eyes blocked nasolacrimal duct skin cancer of the eyelid
paediatric eye conditions
amblyopia
squints
congenital/paediatric cataracts
inherited diseases
inherited paediatric eye diseases
retinitis pigmentosa
petinoblastoma
keratoconus
general medical conditons affecting the eye
diabetes
hyeprtension
thyroid eye disease
define corneal abrasion
superficial scratch to the cornea
what increases risk of corneal abrasion
dry or weak cornea wearing contact lenses working in settings with eye hazards sports w eye injuries bells palsy - lid closure
presentation of corneal abrasion
pain gritty feeling in the eye tearing redness sensitivity to the light headache
if left untreated corneal abrasion can become
corneal ulcer
investigations of corneal abrasion
fluorescein drops to highlight imperfections in cornea
initial management of corneal abasion - patient
rinse eye - water/saline
blinking
pull upper lid over lower
treatment of corneal abrasion
not deep - antibiotic ointment singular dose and pain relief
deep - dilating drop to relax eye and ease pain, antibitoic ointment 1 week, eye pad, pain releif and rest
red flag symptoms for corneal abrasion
sudden pain in eye of injury, often on waking in morning
watering and sensitivity to light
blurred vision
define corneal foreign body
object in eye that should not be there
either conjunctival, corneal, subtarsal (under eyelid)
presentation of corneal foreign body
foreign body entering eye through wind blowing/hgh velocity etc
unilateral
ocular irritation, red eye, watering, blurred vision
investigations for corneal foreign body
slit lamp examination or torch examination
evert eye lids to check for subtarsal FB
fluorescein staining
siedels test for penetrating globe injury
siedels test
looks for fluprescein stained aqueous running down ocular surface if eye penetrated
= penetrating globe injury
management of corneal foreign body
removal of FB - (loose can be irrigated with saline, conjunctival removed by sterile cotton bud, corneal needs referral to ophthal and removal using green needle with slit lamp)
7 days topical chloramphenical post removal
uevitis
eye inflammation affecting the uvea = iris, ciliary body and choroid
causes of uevitis
autoimmune or inflammatory disroder e.g. sarcoidosis, SLR, crohns, akylosing spondylitis
infection - cat scratch disease, herpes, syphilis, toxoplasmosis, tuberculosis
medication side effect
eye injury or surgery
cancer- lymphoma
risk factor for difficult to control uevitis
smoking
presentation of uevitis
eye redness, pain, light sensitivity, blurred vision, floaters, decreased vision
symptoms sudden and get worse quickly
investigations of uevitis
assessment of vision and response to light
tonometry
slit lamp examination
fundoscopy
management of uevitis
drugs that reduce inflammation - corticosteroids drugs to control spasms and relieve pain drugs to fight bacteria or viruses immunosuppressants surgery - vitrectomy
define episcleritis
idiopathic inflammation of the superficial episcleral layer of the eye.
relatively common, benign and self limiting
define scleritis
autoimmune dysrefulation causing inflammation of the whole thickness of the sclera
with ocular complications
requiring systemic treatment
presentation of episcleritis vs scleritis
episcleritis = acute onset, mild pain, redness and irritation
scleritis - subacute onset of severe pain with eye movement, blurred vision, vision loss and photophobia
examination of episcleritis vs scleritis
episcleritis = mobile vessels, blanch with phenylephrine drops, reddish hue
scleritis = adherent vessels, not blanching with phenylephrine drops, bluish, hue, slit lamp reveals nodules, scleral thinning and corneal changes, systemic inflammation
episcleritis management
self limiting normally
can consider topical steroids in refractory cases
treatment of scleritis
systemic steroids/NSAIDS/topical antibiotics
what is posterior vitreous detachment (PVD)?
when vitreous gel separates from the retina - normal part of ageing
how does PVD occur?
vitreous gel becomes liquird and condenes due to age
eventually cannot fill entire vitreous cavity, hence gel separates from retina
sometimes abnormal adhesion occurs between vitreous gel and retina = tear in retina or retinal blood vessel
presentation of PVD
Floaters
flashes
symptoms become less intense over several weeks
investigations of PVD
optical coherence tomography or ocular ultrasound
management of PVD
no specific treatment needed since symptoms subside in 3 months
complications are rare but serious
vitrectomy surgery to remove floaters if persist
what is vitreous haemorrhage
bleeding into the vitreous humour - from blood vessels at back of eye
caused by trauma or fragility of vessels
causes of vitreous haemorrhage
bleeding from abnormal blood vessels - metastatic disease, diabetic eye disease, macular degeneration, retinal vein occlusion, Sickle cell disease
bleeding from tears in retina from PVD
trauma to eye
risk factors for vitreous haemorrhage
diabetes >60 smoking HTN high risk activities
presentation of vitreous haemorrhage
mild floaters and haziness to complete vision loss
painless
comes on quickly
unilateral
red tint to vision
investigations for vitreous haemorrhage
slit lamp examination to see if blood in vitreous
ultrasound if cant see source of bleeding
angiogram to look at abnormal blood vessels
CT if suspected penetrating injury
management of vitreous haemorrhage
find source of bleeding
stop bleeding - lazer treatment, avoid exercise
repair damage to retina to prevent permanent vision loss
vitrectomy if vitreous obscures view and prevents treatment
retinal artery occlusion
blockage of retinal artery - carrying oxygen to nerve cells at back of eye = severe vision loss
causes of retinal artery occlusion
embolus
thrombolus
presentation of retinal artery occlusion
sudden painless loss of vision in one eye
- CRAO (central retinal artery occlusion) = severe loss of vision
- BRAO (branch retinal artery occlusion) = loss of section of vision, may go unnoticed
investigations for retinal artery occlusion
dilated eye examination shows cherry red spot
centre of macula appears red with surrounding retina pale
fluorescein angiography shows delay in retinal artery filling
optical coherence tomography shows swelling in inner layers of retina which atrophy over time and
management of retinal artery occlusion
hyperventilation to dilate retinal arteries allowing clot to dislodge
paracentesis to lower intraocular pressure to dislodge embolus
lowering intraocular pressure with medication
ocular massage with thumb to dislodge clot
`retinal vein occlusion
when blood clot blocks the vein so blood cannot drain from retina leading to haemorrhage and leakage of fluid from blocked blood vessels
CRVO vs BRVO
central retinal vein occlusion = blcokage to main retinal vein
BRANCH retinal vein occlusion = blockage of one of the smaller branch veins
risk factors of retinal vein occlusion
diabetes, HTN, hypercholesterolaemia
clinical presentation of retinal vein occlusion
causes vision loss due to macular oedema, neovascularisation, neovascular glaucoma
painless vision loss or blurring - gets worse over hrs-days
complete visio loss almost immediately sometimes
investigations of retinal vein occlusion
OCT
ophthalmoscopy
flurescein angiography
management of retinal vein occlusion
cant unblock veins but treat problems related to the occlusion
- VEGF
- intravitreal injection of corticosteroid drugs
- focal laser therapy
- pan retinal photocoagulation therapy
optic neuritis
infalmmation of the optic nerve
causes of optic neuritis
not always clear
infection
MS
risk factors for optic neuritis
MS
high altitudes
caucasian
clinical presentation of optic neuritis
diminished vision trouble distinguishing colours blurry vision inability to see out of one eye abnormal reaction of pupil to light pain in eye on movement
investigations of optic neuritis
examination response to direct light visual acuity MRI brain ability to differentiate colour fundocsopy
management of optic enuritis
can resolve my itself
breif course of steorids injected into vein to improve inflammation and swelling
dry eyes
common condition when tears arent able to provide adequate lubrication to eyes
tear instability leads to inflammation and damage to surface of the eyes
causes of dry eyes
decreased tear production - aging, medical conditions, medications, corneal nerve desensivity
increased tear evaporation - blocked meibomian glands
risk factors for dry eyes
older
women
low vit A or omega 3
wearing contact lenses or having refractive surgery
presentation of dry eyes
stinging, burning or scratchy sensation of eyes stringy mucus sensitivity to light eye redness diffculty wearing contact lenses difficulty night time driving watery eyes blurred vision or eye fatigue
investigations of dry eyes
eye exam blotting strips to measure tears tear quality test tear osmolarity test tear samples for markers of dry eyes = matrix metalloproteinase-9 or decreased lactoferrin
treatment of dry eyes
medications - antibiotics, eyedrops for inflammation, eye inserts (artificial tears), tear stimulaters (choinergics), eye drops from own blood
closing tear ducts to reduce tear loss
using speicial contact lenses
unblocking oil glands - warm compresses
using light therapy and eye lid massage
blocked nasolacrimal duct
means tears cannot drain normally = watery, irritated eyes
causes of blocked nasolacrimal duct
Congenital blockage
Age-related changes
Infection or inflammation
Injury or trauma
Tumor
Eyedrops
Cancer treatment
presentation of bloocked nasolacrimal duct
excessive tearing redness of white of eye recurrent eye infection or inflammation painful swelling near the inside corner of eye crusting of eyelids mucus or pus discharge from lids blurred vision
investigations of blocked nasolacrimal duct
tear drianage test
irrigation and probing
eye imaging - XRAY, CT, MRI to find location of blockage
treatment of blocked nasolacrimal duct
medications to fight infection - antibiotic eyedrips watch and wait or massafe dilation, probing and flushing stenting or intubation balloon catheter dilation
most common types of eye lid cancer
basal cell carcinoma - lower eyelid, pale skin
squamous cell carcinoma - sun exposure, more aggressive and metastatic
melanoma - deepest layer of epidermis, most serious
presentation of eyelid cancer
change in appearance of eyelid eyelid swelling/thickening chronic infection non healing eyelid ulceration spreading, colourless mass
treatment of eyelid cancer
surgery, eye removal, radiation therapy, chemotherapy
types of diabetic retinopathy
early diabetic retinopathy/non-proliferating diabetic retinopathy
advanced diabetic retinopathy
early diabetic reitnopathy
new blood vessels arent proliferating walls of vessel in retina weaken larger vessels dilate and become irregular leads to oedema of reitna (macula) can affect vision
advanced diabetic retinopathy
progresses from earlt
damaged blood vessels close off = growth of abnormal blood vessels which are fragile and leak into vitreous fluid
scar tissue from growth of new blood vessels can cause retinal detachment
can cause glaucoma
risk factors for diabetic retinopathy
duration of DM poor control of DM high BP smoking pregnancy
presentation of diabetic retinopathy
spots or dark strings floating in vision
blurred vision
dark or empty areas of vision
vision loss
complications of diabetic retinopathy
vitreous haemorrhage
retinal detachment
glaucoma
blindness
investigations of diabetic reitnopathy
fundoscopy
intravenous fluorescein angiogram
optical coherence tomography
management of diabetic retinopathy
retinal screening
control diabetes
if advanced - vascular endothelial growth factor inhibitors injected into vitreous, macular oedema treated with ranibixumab, photocoagulation to stop leakage of blood and fluid, panretinal photocoagulation to shrink blood vessels, vitrectomy
what is thyroid eye disease
autoimmune disorder characterised by lymphocyte infiltrate of the orbit causing muscle and fatty tissues to become inflamed
in extremes can cause compartment syndrome, compromsing optic nerve and signigicant proptosis may compromise cornea= urgent orbital decompression
presentation of TED
proptosis (bluging eyes)
red, swollen or retracted eyelids
corneal irritation
extraocular muscle compression and inflammation = diplopia/restricted eyemovement
optic nerve compromise = vision loss, blurred vision, reduced colour vision
investigations of TED
TFT - but can be euthyroid with evidence of TED (past hyperthyroid)
management of TED
symptomatic management during active disease - ocular lubricatns, prisms for diplopia, good thyroid hormone control
if evidence of optic nerve compression or residual symptoms - orbital decompression (surgery)
life style = stop smoking, selenium supplements
causes of CN III palsy
aneurysm - posterior communicating artery = PAINFUL
vasculitis = mononeuritis in diabetes and hypertension
pathology near cavernous sinus in sof or orbit
clinical presentation of CNIII palsy
DOWN AND OUT
ptosis
dilated pupil - pupil involvement = bad
pain = aneurysm
ipsilateral to side of lesion
investigations for cranial nerve palsys
MRI or CT to determine cause
full CN exam
management of CN III palsy
surgery if tumor or aneurysm to releive pressure on nerve and promote healing
eliminate double vision and improvement eye alignment - vision therapy, patching one eye, prism lenses, eye muscle surgery, eyelid surgery to correct ptosis
CNIV palsy causes
trauma affecting orbit (longest cranial nerve so vulnerable to damage)
vasculiitis (DM, HTN)
congenital
tumor
presentation of CNIV palsy
incomplete depression in adducted position
torsion of eye in orbit
compensatory head tilt towards shoulder
ipsilateral bhypertrophy and excyclotorsion
double vision when try to read book
CNVI palsy cause
vasculitis (DM HTN)
high intracranial pressure
presentation of CNVI palsy
double vision when look to side of lesion
inturning of eye and double vision in primary position
compensatory head turning to the right
no abduction in the eye
causes of horners syndrome
damage to sympathetic nervous system pathway
first order, second order and third order neurons
things causing damage to first order neurons (hypothalamus to spinal cord)
Stroke
Tumour
Diseases causing loss of myelin
Neck trauma
Cyst or cavity in spinal colum (syingomyelia)
things causing damage to second order neurons (spinal column to neck)
Lung cancer
Tumour of the meylin sheath (schwannoma)
Damage to aorta
Surgery in chest cavity
Traumatic injury
things causing damage to third order neurons (side of neck to facial skin and muscles of iris and eyelid)
Dmaage to carotid artery along side of neck
Damage to jugular vein
Tumour or infection near base of skull
Migraines
Cluster headache
presentation of horners syndrome
miosis, ptosis and anhydrosis
cause of papilloedema
optic disc swelling secondary to elevated intracranial pressure
presentation of papilloedema
raised ICP symptoms - headache, nausea, vomiting
chronicity, blurring of vision and loss of visual feild
transient eppisodes of visual loss
diplopia if VI crannial nerve palsy
myopia
nearsightedness
- near objects = clear, far = blurry
focus image in front of retina
causes of myopia
long eyeball
cornea over curved
causes of hypermetropia
short eyeball
cornea too little curved
hypermetropia
long sightedness
distances = clear, close = blurry
focuses images behind the retina
presbyopia
gradual loss of eyes ability to focus on nearby objects
cause of presbyopia
hardening of the lens with aging,
less flexible and no longer changes shape to focus on close images
risk factors for presbyopia
age
DM, MS, CVD
drugs
presentation of presbyopia
hold reading material far away
blurred vision at normal reading distance
eyestrain or headahces after reading or doing close up work
management of myopia
concave lenses
laser eye surgery
management of hypermyopia
convex lenses
laser eye surgery
treatment of presbyopia
eyeglasses contacts refractive surgery to change cornea shape corneal implants corneal inlays
amblyopia
lazy eye
reduced vision in one eye caused by abnormal visual development early in life
causes of amblyopia
muscle imbalance (stabrismus ambylopia)
refractive differences
deprivation - problem with one eye such as cataract
risk factors for ambylopia
premature birth
small size at birth
family history of lazy eye
developmental disabilities
presentation of ambylopia
eye wanders inwards or outwards eyes dont appear to work together poor depth perception squinting or shutting an eye head tilting
treatment of amblyopai
corrective eywear eyepatches bangerter filter glasses eyedrop (temp blur vision) surgery activity based treatments
squint/strabismus
misalignment of the visual axis
causes of squint
refractive errors
causes of poor acuity in one or both eyes
neurodevelopmental conditions
management of squinty
glasses to correct refractive error
occlusion or penalization therapy to treat amblyopia
surgery to correct misalignment
congenital/paediatric cataracts
congenital clouding of lens
risk factors for congenital cataracts
infection before or soon after birth
family history
premature
management of congenital cataracts
referral to ophthal and removal 6-8 weeks of age
put in flexible palstic artifical lens instead
will need contacts or glasses to help focus
retinitis pigmentosa
inherited degenerative disease involving breakdown and loss of cells in the retina
slowly affects retina and causes loss of night and side vision
inherited
retinoblastoma
eye cancer that begins in retina affecting young children
= poor vision eye redness, swelling of eye, higher risk of other cancers
inherited
keratoconus
occurs when cornea thins and gradually bulges outwards into cone
presentation of keratoconus
blurred vision sensitivity to light and glare frequent changes to prescription sudden worsenign or clouding of vision both eyes 10-25 yo slow progression 10 years
Presentation of retinoblastoma
white colour in pupil when light shone on it eyes appear to look in diff directions poor vision eye redness eye swelling
presentation of retinitis pigmentosa
early stages = night blindness and progressive loss of visual feild
late stages = more loss of visual field = tunnel vision
preseptal vs orbital cellulitis ocular motility
preseptal cellulitis has intact ocular motility
orbital cellulitis has restricted ocular motility and has pain on eye movement
orbital cellulitis management
urgent admission and imaging (ct)
IV antibiotics
surgical draINAGE
untreated = 40% mortality - intracranial infection and cavernous sinus thrombosis
giant cell arteritis
life threatening inflammation of medium and large vessels
immediate systemic steroids and refer to rheumatology
symptoms of giant cell arteritis
new onset headache jaw claudication constitutional symptoms PMR visual symptoms fever limb claudication
acute 3rd nerve palsy
outcomes and causes
life threatening - aneurysm (PCA which ruptures in 2/3 untreated cases = 50% fatal)
microvascular
tumour
demyelination
vasculitis
painless, sponataneous bleeding
no treatment
if recurrent check clotting, FBC, BP
remember base of skull if history of trauma
refer if- proptosed, pulsatile, painful or poor vision
subjunctival haemorrhage
Common! Normally strep. Pneumoniae, H. influenzae or staph. Aureus/epidermis
Signs/Symptoms:
• Bilateral (usually)
• Mucopurulent or purulent (if +++ consider Gonococcal)
• FB sensation (burning / stinging)
• No photophobia
• Lids and conjunctiva may be oedematous
Investigations:
• ? Swab
Treatment:
Topical abx e.g. Chloramphenicol QDS 5-7
bacterial conjunctivitis
conjunctival follicles
viral e.g. chlamydial
‘grains of rice’ appearance
hyperplastic lymphoid tissue
most prominent in fornices
conjunctival papillae
allergic or bacterial
velvety cone shaped elevations
hyperplastic epithelium with vascular tuft
most prominent in palpebral and limbal conjunctiva
Symptoms/Signs: Bilateral Watery (no discharge) Soreness, FB sensation No photophobia
Examination:
Conjunctiva is often intensely hyperaemic
May be associated: Follicles, Haemorrhages Inflammatory membranes Lymphadenopathy (esp.preauricular node)
Aetiology is normally adenoviral ?recent URTI
No treatment needed but advice as very contagious (note topical antivirals if herpes)
viral conjunctivitis
Signs/Symptoms: Itch Bilateral Watery discharge Chemosis (oedema) Papillae ?Hayfever, atopy, family history
Treatment: Cold compress Reduce/remove allergen Antihistamines NSAIDS Mast cell stabilizers Topical corticosteroids ?immunosuppression
allergic conjunctivitis
Normally idiopathic (rarely RA, Polyarteritis nodosa, SLE, IBD, Sarcoid, GPA, Herpes Zoster, Syphilis)
Signs/Symptoms: Often asymptomatic Mild tearing/irritation Tender to touch Localised or diffuse
Treatment: Self limiting but can last for months Lubricants NSAIDs Sometimes steroids Phenylephrine drops?
episcleritis
Deeper layers affected
Signs/Symptoms:
Much more painful – intense boring pain in eye, worse on eye movement
Ocular tenderness
Watering and photophobia
More commonly has medical associations (Note RA and scleromalacia perforans)
Does NOT blanche with vasoconstrictors such as phenylephrine
Can be localised, diffuse or nodular.
Treatment:
Frequent steroids, refer to ophthalmology.
scleritis
70% Idiopathic but can be:
Systemic associations: Sarcoid, AS, IBD, Reiter’s, Psoriatic arthritis, Behcets)
Infection
Trauma
Post-op
Masquerade (retinal detachment, retinoblastoma, lymphoma)
Signs/Symptoms: Pain/ache Photophobia Perilimbal conjunctival injection Blurred vision ?Miotic pupil AC flare/calls, KPs, hypopyon, Posterior synechiae
Treatment:
Topical steroids and mydriatic/cycloplegics
Investigate if recurrent or atypical
anterior uveitis
Signs/Symtoms: Unilateral (trigeminal nerve distribution) Painful ?Hutchinson sign Eye not always involved in V1 HZ
Treatment:
Oral antivirals e.g. acyclovir PO 5x per day for 10/7.
herpes zoster ophthalmicus
hutchinsons sign
Hutchinson’s pupil, an unresponsive and enlarged pupil on the side of an intracranial mass
Most commonly:
Bacterial (Staph, strep, pseudomonas)
Viral (Herpes simplex and zoster)
Often associated CL use or trauma but may be secondary to lid/conjunctival disease
Signs/Symptoms: Ocular pain Watering and discharge (bacterial) Decreased vision Photophobia Visible lesion – note size/shape and staining
Treatment: Intensive antibiotics e.g. levofloxacin, exocin. Anti-virals Mydriatics (steroids?) Avoid CL use
microbial keratitis - inflammation of the cornea
Signs/Symptoms:
Extreme pain in orbit and head, ?worse when reading/in reduced light
Nausea, vomiting, abdominal pain
Vision loss
Injected eye
Hazy, oedematous cornea
Pupil often oval, non-reactive and mid dilated
?History of narrow angles ?FH ?Hypermetrope ?Pseudophakic
Treatment:
Urgent referral!
Pain relief +/- anti-emetics as required
Diamox 500mg IV, pilo 2% stat, timolo 0.25%, iopidine 0.5% stat, pred forte, lie supine, analgesia and antiemetic, ?PI ?admit ?diode
acute angle closure gluacoma
Intra-ocular inflammation and progressive vitritis
Infective vs sterile
85% exogenous
Surgery (?complicated/prolonged), FBs, Penetrating injury, Injections
15% endogenous
Eg haematogenous spread
Mortality of 4%
Timeframe:
1-2/7 = toxic reaction
<6/52 = bacterial (normally 7-14 days)
>6/52 = chronic, 90% are propionibacterium acnes.
Refer urgent for tap and inject
endophthalmitis
ocular emergencies that may lead to blindness
acute angle closure glaucoma penetrating/perforating eye injury orbital cellulitis giant cell arteritis chemical injuries
acute neurological conditions that may present with ocular signs
painful third nerve palsy
painful horners syndrome
the red eye
conjunctivitis - all causes corneal ulcers acute angle closure glaucoma uveitis episcleritis/scleritis
trauma
corneal abrasion
foreign bodies
chemical injuries
blunt/penetrating injury
drusen spots
found in macular degeneration
found in choroid naevi - benign
HLA B27
ankylosing spondylitis
how does diabetes affect the eye - pathphysiology
cant use up sugars due to hyperglycaemia
water comes into blood vessels
weakens walls of blood vessels (leaky)
therefore affects end blood vessels first - feet and eyes
flames
retinal arteries weak = bleed and leak
cotton wool spots
reitnopathy - parts of retna die off due to ischamia - diabetes
makes new blood vessels - immature and week leading to more bleeding
VEGF
Treatment of diabetic retinopathy with neovascularisation
anti VEGF injections
esotropia vs exotropia
eso = eyes point inwards
exo = eyes point outwarda
latent squint
phoria
mulberry sign on retina
astrocytic hamartoma
endopthalmitis
Endophthalmitis is infection inside the globe and most commonly occurs after surgery (although rarely endogenous infections can seed to the eye).
