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250 Cards in this Set
- Front
- Back
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History of presenting illness: subnormal vision |
- duration - differnences between eyes - distortion/haloes/floaters of vision - flashing lights - momentary losses of vision - field defects |
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History of visual loss: |
- monocular/binocular - time of event, method of symptom awareness (cover other eye) - change in symptoms/associated symptoms eg flashers and floaters - duration/recovery - visual loss- general, central, associated field, peripheral only, global effect on function |
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Relevant medical history: |
DM, HTN, COPD, dysthyroid eye disease, connective tissue disease, smoking hyperlipidaema |
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Ocular examination: parts of eye |
VA, eyelids and lacrimal apparatus, conunctiva, cornea, ant chamber, IOP, iris, pupils, orbit, visual fields, colour vision, fundus, position of eyes, ocular movements |
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Ocular examination of the cornea: |
Fluorosein staining for epithelial defects/foreign body detection, especially vertical abrasions as a clue for subtarsal foreign bodies - eversion of eyelid required |
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Part of pupil examination: |
Bright room light exam, dim room light exam, direct + consensual light reflex, swinging flash light test for RAPD, accommodation reflex |
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Orbit examination: |
proptosis and enopthalmos |
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Colour vision tested with: |
Ishihara colour chart |
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Fundus examination: |
- Red reflex: media- lens/vitreous - Retina- optic disc (colour, contour, cupping) - General fundus - Macula |
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Position of eyes: |
- cover/uncover - alternate cover test |
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Ocular movements: |
- conjugate ocular movements - convergence |
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Red reflex: a) how b) what |
a) arms length from pt, look through opthalmoscope at the pupil ensuring iris is in focus b) cataracts seen as dark areas in the reflex nb if no red reflex visible- very dense cataract or vitreous haemorrhage |
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Fundoscopy: a) how b)comment on c) retina |
a) dilate pupils with 1% tropicamide, ask pt to look straight ahead, for ant segment focus lens at 10D b) lids, conjunctiva, sclera, cornea, ant chamber- inflammation, hypaema, hypopyon, iris, pupil (roud, regular), lens c) OD- colour, contour, cup, follow vessels outwards + look in direction you want to examine, ask pt to look straight into light to visualise macula |
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Glaucoma fundus findings: |
Cup disc ratio >0.5, ganglion atrophy caused by glaucoma, ISNT rule for optic disc |
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Afferent + efferent pupillary defects: a) APD b) EPD c) RAPD |
a) implies ON problem or a large retinal lesion b) implies a 3rd nerve problem- pupil fails to constrict but ON function normal c)implies partial ON or signifigant retinal damage with some impulses transmitted |
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Pupil examination: pt looking in distance a) inspection for b) testing for APD c) testing for RAPD- marcus gunn pupil d) testing for near response |
a) anisocoria- unequal pupil size - worse in bright or dim light b) Direct +consensual light response- if APD direct response absent but consensual present c) swinging light test- if subtle ON defect bad eye dilates slightly when light shined back onto it d) look for accomadation and miosis |
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Light near dissociation- what |
- normal near reflex (accomadation) - abnormal light reflex |
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Lesions posterior to the optic tract ( occipital lobe) a) light reflex |
a) normal light reflex eg pts with cortical blindness have normal light reflexes |
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RAPD caused by |
Anterior visual pathway pathology |
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3rd nerve palsy pupil abnormalities: |
- pt may have complete ptosis - eye looks down + out - there is EPD - affected pupil is larger than normal (more obvious in bright light) |
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Horner's syndrome- |
- pt may have neck scars - partial ptosis - aparent enopthalmos - affected pupil smaller than normal - anisocoria more pronounced in dark |
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Adie's pupil- |
- young pt - efferent pupillary defect (on direct/consensual testing) + tonic pupil responses - pupil constriction on convergence is slow, but does eventually occur - if pt has associated abnormal tendon reflexes- then they may have Adie's syndrome |
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Argyll- Robertson pupils: |
- pt may be blind from congenital syphilis -pupils small + irregular, sluggish light responses + light near dissociation |
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Traumatic mydriasis |
- facial scars - signs of pupil rupture (irregular pupil margins) |
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Visual fields examination: components of examination |
- ask visual acuity -position 1m away at same eye level as pt - ask if they can see all your face- detect obvious scotomas - test each eye seperatly by covering one eye - count fingers in quadrants - white hat pin - pt looks at tip and identifies colour, ask pt when they first see tip and if disapears - repeat with red pin - test for blind spot |
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Medial rectus: primary action |
Adduction |
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Lateral rectus: primary action |
adduction |
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Superior rectus: a) primary b)secondary c) tertiary |
a) Elevation
b) Intorsion- max in adduction c) Adduction- max in adduction |
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Inferior rectus: a) primary b) secondary c) tertiary |
a) depression- max in abduction b) extorsion max in adduction c) adduction |
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Superior oblique: a) primary b) secondary c) tertiary |
a) intorsion b) depression c) abduction |
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Inferior oblique: a) primary b) secondary c) tertiary |
a) extorsion b) elevation c) abduction |
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Strabismus-manifest squint : what |
-Misalignment of the visual axis due to ocular mm imbalance causes a manifest squint/strabismus -ocular development in infancy aligns eyes so the visual axis of each eye are paralell + foveae are directed at the same object -leads to development of binocular single vision + steropsis (depth perception) |
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Exotropia |
Outwards deviation of affected eye |
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Esotropia |
Inwards deviation of the affected eye |
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Hypertropia |
Upwards deviation of the affected eye |
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Hypotropia |
downwards deviation of the affected eye |
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Cyclotropia |
Wheel rotation of the affected eye |
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Latent squint (heterophoria): |
-Deviation of the eyes only obvious when binocular single vision is dissociated or inhibited by performing an alternate cover test - Binocular vision= ability to appreciate single image of an object as the brain fuses both images - As dissociation of binocular single vision is stopped, eyes revert to their original position - commonly found in normal population, rarely causes symptoms |
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Exophoria |
tendancy for the eyes to wander outwards on dissociation |
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Esophoria |
Tendancy for eyes to wander inwards on dissociation |
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Hyperphoria |
Tendancy for uypward deviation |
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Hypophoria |
tendancy for downward deviation |
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Cyclophoria |
tendancy for wheel rotation of the eye |
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Manifest squint in a child can lead to: |
Supression - to overcome diplopia brain ignores image from the squinting eye - if image from affected eye is constantly supressed during critical period of visual development, squinting eye becomes amblyopic (lazy) |
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Testing for squint: |
- cover test - performed at 6m + 1/3 m to see if fixation distance affects the squint - performed with or without glasses to determine if refractive correction has any affect on the squint - peformed to light + accomadative target - repeated with and witout any head position pt may adopt |
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Manifest squint causes: |
- primary - secondary: due to loss or impairement of vision - consecutive- following a squint operation |
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Esotropia can be classified as: constant |
- infantile (develop in first 6 months)
- idiopathic (occurs after 6 months of age) - related to accomadation- correction of hypermetropia reduces size of esotropia - but doesn't eliminate - non- accomadative- stress, sensory deprivation, divergence insufficiency |
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Esotropia: intermittent |
- related to accommodation: uncorrected hypermetropia - related to fixation distance: near esotropia |
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Exotropia: |
- primary can be constant or intermittent - more pts present with intermittent rather than constant (constant usually infantile) - manifest or distant/near fixation - secondary exotropia in infants with pathological visual loss from birth |
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Parlaytic squint |
- congenital or acquired from birth - classified according to the underlying cause of limitation of movement (neurogenic, mechanical, myogenic) - neurogenic: palsies of 6,3,4 CN - mechanical: factors that interfere with mm contraction or relaxtion or otherwise prevent free movement of the globe - myogenic: causes directly affecting mm: MG, inflammation, dysthyroid, disease or trauma |
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Conjugate occular movement: |
movements of both eyes in the same direction- versions |
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Disjugate movement |
movements of both eyes in the opposite direction- vergences |
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Ductions |
movements of one eye from the primary position into one of the 8 main positions of gaze |
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Testing smooth pursuit |
Pt watches light as it moves from primary position to one of 8 positions of gaze, observation of corneal reflexes to gauge extent of limitation or overaction |
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Supranuclear motility disorders: result in |
- palsies of conjugate movement (gaze palsies) - no diplopia |
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Internuclear opthalmoplegia: |
- failure of adduction of one or both eyes - convergence retained - abduction nystagmus |
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Possible responses to cover/uncover test: a) uncovered eye moves inwards to fix b) uncovered eye moves outwards to fix c) uncovered eye moves downwards to fix d) uncovered eye moves upwards to fix e) no movement |
a) exotropia b) esotropia c) hypertropia d) hypotropia f) no manifest squint |
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Alternate cover test for detection of latent squint: (90% of population have) a) looking at b) eye moves outwards to fix c) eye moves inwards to fix |
a) movement of covered eye b) esophoria c) exophoria |
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Vertical phorias: a) eye movements b) If right eye starts off in elevated position + moves downwards c) if left eye starts off in elevated position + moves downwards |
a) one eye will move up and one will move down in all cases- specify which eye starts where b) right hyperphoria so left hypophoria c) left hyperphoria so right hypophoria |
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Ocular movement testing: |
- cover uncover test performed in primary position to establish deviation and size in primary position - light is moved from primary position to one of 8 position of gaze - cover uncover test performed comparing result with those in primary position - differences from the primary position will indicate that one or omore of the mm in that particular position of gaze is under-acting, over acting or restricted |
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Path of vision: |
light- cornea- pupil- lens- retina- visual cortex |
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Refractive components of vision: |
- cornea= 40D - lens= 20D - axial length ~22.22mm |
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Define: a) vision b) visual acuity |
a) level of vision that the eye can resolve unaided- smallest line of letter read without optical correction
b) measure of the eye's ability to resolve fine detail with the optimum optical correction in place |
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Accommodation: a) near vision triad b) what is Accommodation? c) how is accomadation carried out? d) presbyopia due to |
a) accomadation, constriction, convergence b) ability of the lens to change shape, resulting in a change in power so images are clearly focused on retine c) ciliary mm contracts, zonules relax, lens become convex d) sclerosis of the crystalline lens resulting in decreased accomadative ability |
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Distance vision tested using: a) what b) from what distance? c) normal VA |
a) Snellen chart b) from 6m away c) 6/6 - young adults/children may be able to read better |
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Near vision: a) componenets of optical system b) measurement of the optical power of a lens or mirror c) emmetropia d) amnetropia |
a) cornea, lens, axial length b) Dioptre (D) c) optically perfect eye d) one or more of the optical parameters are deficient so an optical focusing error occurs |
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Myopia= short-sightedness a) where is light focused b) refractive myopia c) axial myopia |
a) In front of the retina b) effective power of the eye is too strong >60D c) eye is too long >22.22mm, corrected with divergent lenses to spread light rays out and push focus back to retina |
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Hypermetropia: long sightedness a) where is light focused b) refreactive hypermetropia c) axial hypermetropia |
a) behind retina b) effective power of the eye too weak <60D c) eye is too short <22.22mm , corrected with convergent lens so light rays contracted and focused to pull forward onto retina |
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Astigmatism: a) causes what symptoms b) problem in an eye with astigmatism c) correction |
a) blurred or distorted vision b) eye rugby ball shaped instead of football c) convergent or divergent lens + additional lens to correct astigmatic error (cylindrical or toroidal lens) |
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Describing prescriptions: a) -3.0 DS b) +3.00/-0.75 x 180 c) -9.50/-1.25 x 30 |
a) myopic by 3 ds b) hypermetropic by 3 ds, cylindrical myopic lens of 1.25 ds used at 180 degree axis (for astigmatism) c) myopic,mypoic cylinder of 1.25 ds used at axis of 30 degrees |
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Contact lens indication for use: a) visual b) occupational c) cosmetic d) medical e) psychological f) other |
a) anisometropia, high myopia, aphakia, irregular scarring, keratoconus, corneal grafts, refractive surgery failure, theatre, film, armed forces b) theatre, film, armed forces, pro sports c) replace spetacle use, change eye colour, prosthetic lenses d) therapeutic, bandage e) where pt can't accept wearing glasses f) sports, physcial inability to wear glasses |
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Soft contact lenses: a) advantages b) disadvantages |
a) flexible, good initial comfort, larger diameter ensures secure fit, safer for sport, may be used for extended wear b) split easily, depositions from tear, more expensive, dehydrate if left out solution |
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Rigid gas permeable lenses: a) advantages b) disadvantages |
a) fixed shape and durable, good for all day wear, smaller diameter incurs less risk of hypoxia, creates smoother ocular surface, visual result for irregular corneas + high astigmatism, easy to clean, good VA if large astigmatism b) poor initial comfort, smaller diameter so prone to fall out eye |
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Causes of red eye (2 broad terms) |
1) haemorrage 2) congestion |
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Haemorrage: a) subconjunctival b) retrobulbar c) causes |
a) posterior edge of haemorrage is visible, mostly, mostly innocuous, related to bleeding disorders/elderly pts on aspirin/warfarin, may be due to trauma, usually asymptommatic, may track down with gravity b) cannot see posterior border, check eye movements for proptosis- if proptosis- emergency- decreased eye movements, increased pressure, compromised ON function c) iatrogenic, trauma, head injury, skull base fracture |
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Eye congestion: a) localised b) generalised |
a) episcleritis, phlycten b) conjunctivitis keratitis, uveitis, acyte glaucoma |
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Generalized redness: types (2) |
Conjunctival, ciliary/circumcorneal |
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Conjunctival redness: features |
- predominantly in conjunctival fornices - superficial vessels- blacncj with topical vasoconstrictors eg phenylepherine 2.5% - blood flow from periphery towards cornea |
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Conjunctival infection: types and features a) viral b) bacterial c) allergic nb viral + allergic tend to be bilateral |
a) gritty eyes, watery discharge, follicles, raised LNs b) gritty eyes, purulent discharge, raised LN c) itchy eyes, stringy discharge, papillae, no LN |
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Conjunctivitis neonatorum a) commonest worldwide cause b) commonest UK cause |
a) gonorrhoea b) chlamydia |
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Ciliary/ circumcorneal congestion: features |
- deeper vessels - dusky red colour - no blanching - don't move with folds - centrifugal blood flow (towards fornices) |
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Ciliary congestion: causes |
- foreign body - trauma - keratitis: viral, bacterial, immune - uveitis - acute angle closure glaucoma |
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Allergic conjunctivitis: a) symptoms b) course c) treatment |
a) itch/burn, bilateral, seasonal, stringy discharge. lid swelling, papillae, no LN b) self limiting c) opticrom, lodoxamide, steroids |
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Viral conjunctivitis: a) symptoms b) course c) treatment |
a) gritty eyes, bilateral, stress related, watery discharge, lid swelling, follicles, self limiting, LN present b) self limiting c) antiviral, steroid |
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Bacterial: a) symptoms b) course c) treatment |
a) sore, gritty eyes, purulent discharge, may be unilateralm crusting + matting of eyelids b) needs treatment c) antibiotics- topical + systemic |
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Corneal abrasion- circumcorneal redness: a) use what to show b) cause c) treat |
a) flourosene dye (orange)- illuninated with blue light + floreses green b) foreign body underneath eyelid c) pull away eyelid and clean under surface |
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Dendritic ulcer: appearence |
circumcorneal blush, squiggly dendritic ulcer with dye q |
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Corneal abrasions/ulcers: a) causes b) symptoms c) treatment d) ulcers |
a) trauma, infection, exposure b) painful eye, photophobia, 'feeling something is in the eye' c) emperic erythromycin until epithelium reforms d) ulcers more likely to have bacterial infiltrate - treatment with ciprofloxacin + follow up on daily basis |
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Herpetic keratitis a) cause b) presentation c) appearence in slit lamp d) course e) treatment |
a) HSV type 1
b) red injected eye, pain, may be rash near orbit, unilateral in 85% c) dendritic ulcer stains brightly with floroscein d) initial infection involves superficial cornea, but infection reactivates as deeper corneal infection causing scarrig and decreased corneal sensitivity e) topical acyclovir, oral acycolvir + continued prophylactic acyclovir beware to avoid topical steroids as they increase viral replication and cause corneal scarring |
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Pseudommonas ulcers: a) who? b) appearence c) treatment |
a) contact lens wearers b) cover with ciprofloxacin, if bad hrly fortified antibiotics eg vanc |
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Hypopyon a) what |
a) bacteria from ulcer causes toxins to go through cornea to the iris + iris to exude cells + proteins which collect as cells + fibrin in the anterior chamber- sterile pus |
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Uveitis a) what b) signs c) aetiology d) treatment |
a) inflammation of the iris + CB b) keratitic precipitates- deposits of cells at the back of the cornea, constricted pupils, synechiae- adhesions to lens c) usually unknown- disease association with anky spond, RA d) dilate pupil by giving dilating drops + steroids - increases distance between iris and lens to decrease chance of adhesions |
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Acute angle closure glaucoma: a) presenting symptoms b) investigation |
a) headache, nausea, vomiting, reduced vision, halos, circumcorneal injection, corneal haze (oedema), fixed, mid dilated pupil b) measure pressure |
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Acute painless loss of vision: history: |
- previous ocular history - general cardio disease - family history eye disease - drugs - eye drops - symptoms: monocular or binocular - time of event - change in symptoms: flashers/floaters - assoc. symptoms- headache, numbness, dizziness - duration/recovery - visual loss- general, central, field loss, peripheral - global effect on function |
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Monocular causes of acute, painless loss of vision: THINK ANATOMICALLY |
- Acute corneal disease (HSV)- rare to be painless - Anterior chamber haemorrhage - rare- hyphaema - Acute cataracts- lens clouding- hit by lightening - Vitreous haemorrhage - optic neuritis - anterior ischaemic optic neuropathy , ANION - unioccular optic disc swelling due to inflammation/CRVO, neoplasia -optic atrophy - from extensive retinal disease, optic nn compression- blurred disc margin, pericapillary swelling, bulging optic disc - retinal: branch vv oncclusion, central retinal vv occlusion, central retinal aa occlusion, branch retinal aa occlusion, retinal detatchment, macular haemorrage |
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Vitreous haemorrhage: a) causes b) signs c) investigations d) course and treatment |
a) proliferate diabetic retinopathy, retinal tear, posterior vitreous attachment (usually benign in elderly) b) no fundal view, vision down to HM c) B scan to view retina d) Blood can take up to 6 weeks to clear, PRP or vitrectomy if not cleared <3 months, urgent vitrectomy if looks like retinal tear/detatchment |
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Optic neuritis: a) causes b) signs c) treatment |
a) demyelination MS, viral infection/vasculitis (rare) b) decreased VA + colour vision, pain- exacerbated by eye movement, VF: central scotoma, RAPD, OD= normal or swollen- develops to pale retrobulbar neuritis(MS) C) Neurology + high dose corticosteroids |
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anterior optic neuropathy: opthalmic emergency - unilateral may proceed to bilateral a) signs b) types c) causes of types d) treatment |
a) RAPD, swollen disc, cotton wool spots + haemorrhage, altitudanal field loss (1/2 ON affected) b) anterior ischaemic optic neuropathy (AION), Anterior non ischaemic optic neuropathy (ANION) c) AION- temporal arteritis: temporal pain, jaw claudication, scalp tenderness, shoulder pain (pain on combing hair/chewing, ANION- htn, diabetes, atherosclerosis d) AION- urgent ESR+CRP, high dose corticosteriods |
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Retinal detatchment: types- 3 - history |
1) Rhegmatogenous- commonest 2) Tractional 3) Exudative - floaters +/- flashing lights, visual field loss (pattern variable depending on amount of retina detatched), RAPD, red reflex abnormality, acuit normal if macula on |
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Rhegmatogenous detatchement: cause |
Retinal tear |
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Tractional retinal detatchment: cause |
Proliferative diabetic retinopathy + scarring- contractile membrane form across the retina (PRP prevents this) |
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Exudative retinal detatchment: causes |
- posterior uveitis - intraocular tumours |
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Retinal detatchment- treatment: |
Vitrectomy: - removes vitreoretinal traction/membranes - closes retina, breaks tear + drainage of subretinal fluid - adheres retine back to RPE |
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Binocular causes of acute painless loss of vision: chiasm |
- pituitary apoplexy: rapidly extending pituitary tumour: can occur without pain, bilateral acute visual loss, bilateral APD |
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Binocular causes of acute painless loss of vision: optic nn causes: |
Papilloedema, optic neuritis- sarcoid, inflitrative, |
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Papilloedema: |
- swollen optic disc due to raised ICP - blurred disc margin |
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Binocular global causes: |
- cortex- calcrine cortex - CVA to visual cortex - homonomous hemianopia - migraine- scotoma |
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Retinal vein occlusion: a) types b) cause c) seen in d) signs e) associations |
a) central retinal vein or tribuitary (branch) retinal vein occlusion b) thrombosis in vessel lumen at arteriovenus crossing points (OD= central) c) middle aged/elderly, BP d) sudden, painless vision loss- can drop to HM, haemorrhage, oedema e) diabetes, HTN, blood dyscrasias, vasculitis, increased IOP, may be RAPD |
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Retinal vein occlusion- COMPLICATION + TX |
- exclude treatable causes- prevent - Treatment is of complications: - Macula oedema: laser treatment or ozurdex (decreases inflammation, oedema + thickening of the retina) - neovascularisation: laser of ischaemic areas of the retina - neovascular glaucoma (Rubeotic): laser (PRP) + surgery- painful blind eye may need removal |
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Retinal arterial occlusion: what |
- leads to more severe vision loss than vv occlusion - embolisation= commonest cause- from carotid aa- cholesterol/calcified plaques/fibrinoplatelet material - stationary emobli decrease blood supply to an area of the retina |
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Amaurosis fugax- what |
- emboli pass through retinal vascular system causing transient visual loss |
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Signs of central retinal aa occlusion: |
- cherry red spot, - attenuated (thin) aa's - pallor of macula - cotton wool spots - >6 weeks cherry red pallor receeds + optic disc pallor occurs - emboli in retinal aa - carotid bruits - VA: Counting fingers - RAPD- change not noticable if not affecting macula - Prodromal events: 'shutter coming down' |
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Retinal aa occlusion: treatment |
- asesss CV risk factors: HTN, diabetes, IHD, PVD, smoker, consider giant cell arteriritis- esr - Investigations: doppler scan of carotid, TIA referral 20% risk of stroke in 2 weeks, consider aspirin - no treatment - rebreathe in paper bag to dilate blood vessels, occular massage, paracentesis to decrease IOP |
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Floater and flashers- causes: |
- ageing vitreous humour becomes more liquid + peels away from the retina causing posterior vitreous detatchment (PVD) - Traction of retina- tear - Rhegmatogenous RD - Floaters: vitreous opacities, haemorrhage or pigment - |
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Macular haemorrhage: a) causes b) history c) examination d) ix e) associations |
a) AMD, diabetic retinopathy, macroenuerysm, b) distortion of vision, scotoma c) variable acuity, no RAPD, full peripheral field, central haemorrhage on fundoscopy, signs of primary disease d) BO e) use of viagra- valsava maculopathy- occurs during intercourse |
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Conditions in which the optic disc is swollen: |
- optic neuritis - papilloedema- bilateral -malignant HTN - arteritic HTN - Non arteritic AION |
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OPtic neuritis: a) presentation b) signs c) signs d) risk of |
a) blurred vision, decreased central vision, retrobulbar pain especially on eye movement + globe tenderness, swollen disc + blurred margin, b) RAPD, red desaturation, central scotoma c) increased risk in MS- send for MRI d) Developing demyelination |
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Papilloedema a) what b) symptoms c) signs |
a) bilateral swelling due to raised IOP b) headaches, transient blurring of vision, swollen OD, splinter haemorrhages @ disc margin, exudates, cotton wool spots + retinal folds - changes bilateral c) enalrged blind spot, if ICP not corrected optic atrophy = gradual progressive field loss, irreversible |
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CN 3 Palsy: a) innervates b) presentation c) causes (2) and pupil involvement |
a) IO, MR, IR, SR, LPS, Pupil b) eye looks down and out, severe ptosis +/- blown pupil depending on cause c) surgical- aneurysms/trauma- affects pupillary fibers- blown pupil medical- HTN, diabetes- spares pupil |
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CN4 palsy- a) affects b) appearence |
a) superior orbital affected- intorsion - eye unable to look down and in b) on looking ahead, slightly raised, on looking to opposite side up + in |
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CN6 palsy: a) what |
a) Lateral rectus- abduction b) eye drifts medially due to pull of MR mm |
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CN7 palsy- bell's palsy a) what b) symptoms |
a) facial nn palsy- mm of facial expression, orbicularis oris= eye closure b) unable to close eye on affected side leading to corneal dryness, exposure keratitis, corneal ulceration - test corneal sensation |
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Pupil responses: a) sympathetic response b) parasympathetic response |
a) pupil dilates- fight or flight- mydriasis b) pupil constricts- miosis |
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Light reflex: 4 neurones 1) 2) 3) 4) |
1) Sensory- retina to PTN, nasal retina- fibers decussate to contralateral PTN, temporal retina- fibers re,ain ipsilateral 2) PTN to EWN- each PTn connects to both EWN- direct and consensual pupillary reflexes 3) EWN to coliary ganglion - parasymp through CN 3 4) Post ganglionic motor- leave ciliary ganglion and pass in short ciliary nn to innervate sphincter pupillae |
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Near reflex: a) what triad b) pathway |
a) accomadation, miosis, convergence b) same as lightL 3rd nn- ciliary ganglion- short ciliary nn- influences from frontal and occiptial nn's |
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Adie's pupil a) who b) what c) presentation d) other signs |
a) young adults b) post viral denervation of post ganglionic supply to sphincter pupillae + ciliary mm, 80% unilateral c) large, irregular pupil, direct pupil reflex sluggish or absent, consensual response slow/absent, near reflex present but slow redilatation, vermiform movements of pupil border d) may show slow tendon reflexes |
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Horner's syndrome: a) presentation b) causes |
a) miosis due to unapposed action of sphincter pupillae, mild ptosis of 1-2mm and weakening of muller's mm, reduced ipsilateral sweating (only if lesion is below sup cervical ganglion) b) first order neurones- brainstem disease, spinal cord tumour, diabetic autonomic neurpathy. second order neurones- pancoast tumour, carotid aortic aneurysm, neck dissections. third order neurones- cluster headaches, ICA dissection, cavernous sinus mass |
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Argyll Robertson Pupil: a) cause b) presentation |
a) tertiary neurosyphilis b) Accomadation reflex present, pupillary reflex absent - neither constricts in bright lighgt, both constrict on accomadation, light near dissociation |
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Traumatic mydriasis a) what b) signs |
a) dialted pupil b) facial scars, signs of pupil rupture + irregular margins |
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Proptosis: a) what b) direction c) measurement of severity d) pseudoproptosis e) causes |
a) abnormal protrusion of the globe b) intraconal or extraconal c) Hertel's exopthalmometer d) patients with high myopia (bigger globe than normal), usually have contralateral enopathlmos e) thryoid eye disease, tumours, inflammation, infection |
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Enopthalmus a) what b) causes |
a) condition in which bone is recessed within the orbit b) small globes, structual bone abnormalities (blow out fracture), atrophy or orbital content (irradiation, scleroderma) |
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Opthalmoplegia: a) what b) causes |
a) restriction or disability of the ocular mm b) tumour, restrictive myopathy (TED, myositis), ocular motor nerve lesions, trauma (blow out fractures) |
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Causes of decreased VA: |
- Corneal exposure - ON compression - choroidal folds |
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Dynamic properies: a) increased venous pressure- causes b) pulsation-causes |
a) TED, vascular anomalies b) AV communication (bruit), defect in orbital roof= CSF pulsation (no bruit) nb bruit is a sign of a carotid cavernous fistula |
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Opticociliary shunt: a) what b) causes |
a) blood is shunted from central retinal circulation to pericapillary choroidal circulation when there is obstruction to a normal drainage channel b) ON/orbital tumours that compress intraorbital ON- optic sheath meningioma, ON glioma, cavernous haemangioma |
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Thyroid eye disease: clinical manifestations- |
- eyelid retraction/lag, - periorbital oedema, - exopthalmus (proptosis)- in 1/3- permenant in 70% - diplopia in 5-10% - compression of the ON - rare - exposure keratopahty- cornea exposed due to inability to close eyelid |
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TED: Soft tissue involvement |
- eyelid erythema - conjunctival injection -chemosis -swelling of the caruncle - eyelid oedema |
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Von Graefe's sign= lid lag |
seen when pt follows moving target from superior to inferior position |
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TED-Optic neuropathy: a) affects b) investigations |
a) 5% of pts b) perform a CT, visual acuity, colour vision, pupillary reaction, visual fields, fundoscopy |
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TED restrictive myopathy: a) clinically presents as b) processes c) muscle most commonly involved |
a) diplopia b) oedema + fibrosis c) inferior rectus |
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Orbital cellulitis: a) what b) presentation c) orbital signs d)complications |
a) infection behind the orbital septum, usually secondary to ethmoiditis
b) severe malaise, fever, orbital signs c) severe oedema and redness, proptosis: usually lateral and down, painful opthalmoplegia, optic nn dysfunction if advanced d) optic neuropathy, raised IOP, retinal vasculature occlusion, intracranial- meningitis, brain abscess, cavernous sinus thrombosis |
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orbital cellulitis: management |
Pre-treatment: hospital admission, systemic antibiotic therapy, monitor optical nn function Post-treatment: indications for surgery- antibiotic resistance, orbiral/subperiosteal abscess, optic neuropathy |
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Idiopathic orbital inflammatory disease (IOID): a) what b) Presentation c) Clinical course |
a) Pseudotumour- non neoplastic, non infectious orbital lesions b) Age: 20-50yrs, severe abrupt + painful onset, unilateral, periorbital swelling, chemosis, proptosis, opthalmoplegia c) Early spontaneous resolution without sequalae- no treatment, prolonged intermittent activity + eventual remission - steroids, radiotherapy, cytotoxics (anti-inflammatory), severe prolonged activity - causes a 'frozen orbit' - opthalmoplegia + ptosis |
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Orbital varices: |
- congenital enlargements of pre=existing venous channels - usually unilateral - may bleed or become thrombosed |
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Isolated orbital varices: |
- intermittent proptosis-stimulated by valsalva manouvre - non-pulstile, no bruit |
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Direct carotid cavernous fistula: |
- defect in intracavernous part of internal carotid -> rapid flow shunt - ptosis, chemosis, conjunctival injection - pulsatile proptosis, audible bruit + thrill- can be abolished by ipsilateral carotid compression - fundoscopy: retinal venous congestion + haemorrhages -causes: spontaneous rupture in HTN females, head trauma - raised IOP |
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Indirect carotid cavernous fistula: |
- Indirect communication between meningeal branches of internal carotid or external carotids + cavernous venous sinuses - low velocity shunt - causes: congenital malformations, spontaneous rupture - presentation: dilated episcleral vessels, raised IOP + wide pulsation, occasional opthalmoplegia, mild proptosis |
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Encehaloceoele: a) what b) types c) presentation |
a) herniation of intracranial contents through congenital skull defect b) meningocele (only dura), meningoencapholocele (meninges + brain tissue)- anterior or posterior c) Proptosis- caused by CSF pulsation (no bruit) |
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Orbital tumours: a) vascular b) lacrimal gland c) neural tumours d) miscellaneous |
a) capillary haemangioma, cavernous haemangioma b) pleomorphic adenoma, lacrimal gland carcinomas c) optic nn glioma, optic nn sheath meningioma d) miscellanous tumours- metastases, invasion from sinuses |
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Capillary haemangioma: a) what b) presentation c) course |
a) most common orbital tumour in children b) 30% at birth, 100% at 6 months, most commonly in superior anterior orbit, may enlarge on coughing/straining, associated 'strawberry naevus' common c) grows in first year, resoultion in 70% by age 7yrs |
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Capillary haemangioma: a) systemic associations b) treatment |
a) High output cardia failure, Kasahach Merrit syndrome, Maffuci syndrome b) steroid injections (for superficial component), systemic steroids, local resection (difficult) |
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Cavernous haemangiomas: a) what b) who c) presentation d) tx |
a) most common benign orbital tumour in adults, located just behind the globe b) female proponderance ~70%, presents in 4th-5th decade, slowly progressive axial proptosis, may cause choroidal folds c) surgical excision |
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Pleopmorphic lacrimal gland adenoma: a) presents b) on MRI |
a) 4th-5th decade, painless, slow growing, smooth mass in lacrimal fossa, inferonasal globe displacement, posterior extension may cause proptosis and opthalmoplegia b) smooth outline, excavation of lacrimal gland fossa |
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Lacrimal gland carcinomas: a) presentation b) management c) prognosis |
a) 45h-5th decade, painful fast growing mass in lacrimal fossa, inferonasal globe displacement, posterior extension may cause proptosis + opthalmoplegia + episcleral congestion, trigmeinal hypoaesthesia in 25% b) biopsy, radical surgery + radiotherapy c) very poor prognosis |
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Optic nn glioma: |
a) young girls, associated with NF1 b) gradually progressive proptosis, optic atrophy, presents at end of first decade with visual loss c) observation (no growth, good vision, good cosmesis), excision (poor vision, poor cosmesis), radiotherapy (intracranial extension) |
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Optic nn sheath meningioma: |
a) typically affects middle aged women b) gradual visual loss, proptosis c) Dependant on clinical pattern: observation (slow growing tumours), excision (aggressive tumours + poor vision), radiotherapy (slow growing tumours, good vision) |
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Optic metastases from primary sites- |
breast, bronchus, prostate, skin melanoma, GI tract, kidney |
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Cataracts= |
any opacity within the lens |
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Cataracts- aetiology |
- age related - traumatic - metabolic - toxic: maternal infection (toxoplasmosis) - maternal infection - maternal drug ingestion - hereditary |
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Cataracts- types + features from history: |
- Posterior subcapsular: trouble with bright lights/oncoming headlights, reading vision affected more than distance vision - Nuclear sclerotic cataracts: myopic shift, increased need for glasses - cortical cataract: opacities assume radial spoke like configuration |
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Traumatic cataracts: |
- penetrating eye injury- direct damage to lens - blunt injury- iris pigmented onto lens - vossius ring - glass blowers cataract- infrared radiation affects anterior lens capsule - electric shock - ionising radiation |
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Cataracts: metabolic: |
Diabetes (age related or true diabetic) Galactosaemia mannosidosis fabry's disease Lowe's Wilson's disease Hypocalcaemic syndrome |
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Cataracts- toxic: |
corticosteroids- systemic/topical - post subcapsular chlorpromazine chemotherapy |
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Cataracts- secondary complicated |
- anterior uveitis - hereditary retinal degenerations- retinitis pigmentosa, gyrate atrophy, stickler's syndrome - high myopia -glaucomflecken- ant subcapsular |
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Cataracts: maternal infection + drugs |
- rubellla - toxoplasmosis -CMV -drugs: thalidomide, corticosteroids |
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Causes of presenile cataracts: |
-dystrophia myotonica -atopic dermatitis |
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Cataracts classification according to stage of development: |
- immature: not involving whole lens - mature: cortex totally opaque - hypermature: lens has become smaller, wrinkled lens capsule due to leakage of water out lens |
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Cataracts- management: |
- degree of disability - pt opinion - best corrected visual acuity - coexisting ocular pathology (MD, advanced glaucoma) -general health -age of pt not contraindication to surgery - no need to wait until cataracts matures |
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Cataracts biometry: |
calculation of required intraocular lens power |
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Phacoemulsifcation: procedure |
- standard surgery performed in UK - small incision: 2.5-3.5mm performed - anterior lens capsule peeled in circular way - use of high frequenct phaco probe to fragment and aspirate the nucleus- breaks into 4 quads + each removed seperately - cortex aspirated - viscoelastic injected to make space for IOL - foldable IOL made of acrylic + silicone is inserted through the wound which unfolds in the lens capsule bag |
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Adavantages of phaco: |
- small incision, fast recovery- 6/6 next day - good refractive results, little astigmatism - quick operation |
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Complications of cataracts surgery: |
- posterior capsule opacification - 20-40% - vitreous loss - retinal detatchment - endopthalmitis |
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AMD: Symptoms |
Drusen mottled atrophic macular geographical atrophy gradual loss of central vision difficulty recognising faces wet- profound central visual loss distortion of straight lines/doorways/reading print |
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Dry AMD: |
Druse, RPE atrophy, gradual photorecptor loss, gradual visual loss |
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Wet (exudative) AMD: |
-Choroidal neovasculature membrane- grows into the retine and causes sudden visual deterioration and distortion pigment epithelium detatchement- can lead to retintal detatchment and scarring |
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Risk factors- AMD: |
smoking, cardio disease (HTN, hyperlipidaemia), low blood antioxidant levels |
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AMD- invgestigations: |
visual acuity, amsler grid, reading speed (decreased), contrast sensitivity, fundus photos, fundus fluorescein angiography, indocyanine green aniography, optical coherence tomography |
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AMD- management dry: |
High dose antioxidants + vitamins + minerals, management ot risk factors, Amsler grid for monitoring, provision of visual aids |
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AMD- Wet- management- pharmacological: |
Ranibizumab (Lucentis)- blocks all anti-vegf isoforms, maintains vision in 95%, Pegaptanib sodium (Macugen), Avastin, Aflibercept
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AMD-Wet management: non pharma |
PDT- Visudyne injected + activated by non thermal light to cause endothelial damage to CNV, thrombus formation and occlusion of vessels- treatment every 3 months Surgery- vitrectomy + submacular excision of CNV- replacement and rotation of macular Combination- PDT+ Anti-VEGF |
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AMD-rehab: |
Registration as visually impaired, LVA- visit and dialogue, support group and societies |
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General ocular manifestations of diabetes: |
- EOM palsy - stroke - retinal vascular occlusions -cataracts - DR - maculopathy - diabetics 25X more likely to become blind - incidence of DR realted to duration of DM |
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DR- risk factors: |
- Poor DM control - hyperlipidaemia -renal impairement -HTN - age -smoking - duration of DM - acceleration of DR in pregnancy |
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Features of diabetic retinopathy: |
-microanuerysms - retinal haemorrahages: dot, blot, flame, preretinal - exudates- at junction between normal and oedematous macula - cotton woold spots- debris from damaged neurones - venous changes: looping + beading of vv/venules |
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Staging NPDR: |
RO=none, R1-mild= anurysms, retinal haemorrage, exudates, cotton wool spots R2-mod= severe haemorrhages (20/quad), IRMA, venous beading, cotton wool spots R2-SEVERE: 4-2-1 Rule: Severe haem in 4 quads, venous beading in 2, IRMA in 1 |
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Staging PDR: |
R3: Mild to mod- new vessel growth at OD- NVD, new vessels everywhere (NVE) R4=Severe PDR: NVD>1/3 OD size, NVD + preretinal/vitreous haemorrhage, NVE>1/2 OD size + preretinal/vitreous haemorrhage, look out for new vessels at iris (rubeotic glaucoma) |
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Diabetic maculopathy: |
- extensive capillary leakage causes macula oedema - focal oedema is caused by microaneurysms= circinate - Ischaemic maculopathy- macula appears normal, decreased VA, investigation with FFA shows capillary non perfusion at fovea |
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Vision loss in PDR: |
-Vitreous haemorrhage - retinal detatchement - fibrovascular proliferation in front of macula - rubeotic glaucoma - macular oedema/ischaemia involving central macula - loss of peripheral visual field due to ischaemia/laser treatment loss in NPDR due to oedema/ischaemia |
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DR management: general |
- control diabetes and other risk factors - laser photocoag -pharma: Anti-VEGF, anti-permeability agents -vitrectomy |
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Laser photocoagulation-DR: |
-focal laser for focal leaks - grid laser- for diffuse macula oedema - pan retinal photocoagulation: PRP- targets thousands of spots around peripheral retina + destroys ischaemic retina to decrease angiogenic stimulus |
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Pharma-DR: |
-Anti-VEGF: ranibizumab,pegaptanib sodium -Triamcinolone: anitpermeability + anti inflammatory, injected intravitreally - dexamathasone implant for 4-6 months - fluocinolone implant- 2yrs |
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Vitrectomy: indications |
persistant vitreous haemorrhage/retinal fibrosis/tractional retinal detatchment if threatening macula or non response to PRP |
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Aquesous pathway: |
-Produced: ciliary body in posterior chamber- moves forward round lens + flows through pupil to the anterior chamber - Anterior chamber fills- aqueous spreads outwards in irido-corneal angle - aq. exits eye through trabecular meshwork into canal of schlemm + returns to blood circulation |
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IOP's: |
Normal> 50yrs= 15.5mmhg 5% population >21.1mmHg nb some people get damage from pressure in normal range |
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Glaucoma- risk factors: |
Family history, black race, raised IOP, myopia, age |
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Open angle glaucoma- WHAT: |
- Degeneration of the trabecular meshwork filter causing aqueous back up + chronically elevated eye pressure - atrophy of the ganglion nerve in the retina causes gradual vision loss - optic disc cupping, visual field defects, tunnel vision, blindness |
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Glaucoma- presentation: |
- asymptommatic until almost blind - 30-40% fibers lost before visual field defect, 90% before symptommatic |
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Glaucoma- inestigations: |
- IOP: Goldmass tonometry using slit lamp or tonopen, force needed to flatten cornea equated to IOP - Optic disc: cup + colour + position of blood vessels- cup disc ration: ISNT rule, optic haemorrages overlying OD rim - Visual field analysis- using humphrey gold standard- central vision spared |
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Glaucoma- pattern of visual field loss: |
- loss of superior visual field- 2nd blind spot - scotoma forms around blind spot in arcuate fashion + brain fills in the gaps - temporal vision preserved - ND- disease doesn't cross midline - IOP>30- Blind in 3yrs -IOP 25-30- blind in 6yrs -IOP 21-25- blind in 15yrs |
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Primary open angle glauma: treatments |
- Prostaglandin agonists- latanoprost - Beta-blockers- timolol - Alpha adrenergic agonists- apraclonidine, brimonidine - topical carbonic anhydrase inhibitors - dorzolamide, brinzolamide - miotics- pilocarpine - systemic carbonic anhydrase inhibitors- acetazolamide, diamox |
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Primary open angle glaucoma- surgery: |
- Argon laser trabeculoplasty - trabeculectomy |
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Acute angle closure glaucoma: a) symptoms b) signs c) risk factors d) treatment |
a) pain, blurred vision, nausea and vomiting b) corneal oedema, red eye, halos round lights, fixed mid dilated pupil , shallow anterior chamber, eye appears hard on prodding, hard to see iris due to oedema c) hypermetropia, family history- eye size and shape, asians d) pilocarpine (miotic) every 5 mins, acetazolamide, trabeculotomy nb treat unaffected eye prophylactically |
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Acute angle closure glaucoma- pathogenesis: |
- lens grows bigger with age + small anterior segment - iris gets closer to trabecular meshwork - at critical point iris blocks trabecular meshwork + aqueous build up in posterior chamber, raising pressure and causing damage to the retina |
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Acute angle closure glaucoma- prodrome: |
- pain in evening - halos round lights - when pt sleep iris constricts and pain relieved - more pain in bright light (mydriasis) - symptoms may persist for a few days before acute attack |
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Rubeotic glaucoma: a) causes b) patho c) symptoms d) signs |
a) central retinal vein occlusion, diabetic retinopathy b) ischaemia- release of vasoproliferative factors- new blood vessels grow on surface and periphary of iris- cross trabecular meshwork- scar tissue occurs- contraction and closing of angle causing secondary increase IOP c) pain, decreased vision d) red eye, corneal oedema, rubeosis (blood vessels on iris), pupil distortion, if left to continue duller corneal light reflex |
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Amblyopia |
-Decreased vision in one or both eyes with no evidence of strucual abnormality -VA difference > 2 lines - causes: lack if visual stimulation during critical period of visual development - stimulus deprivation- cataracts, ptosis - Anisomotropic- difference between refractive error between 2 eyes, 1DT is signif difference - Strabismic (squint)- suppression |
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Amblyopia: management |
- If treated in critical period (<7yrs) can be reversed -occulsion if the good eye by patch, beware of inducing occlusion amblyopia |
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Binocular vision- 3 processes: |
-simulatenaeous perception (of an image in each eye) - fusion - Stereopsis (3D depth) |
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Strabismus (squint): manifest |
- directional deviation of one eye so visual axis is not aligned - diagnoes on cover uncover - binocular vision not possible as axis not aligned - consequences= diplopia or suppression -diplopia - occurs if onset of manifest squint >7rs - suppression-image from squinting eye is suppressed, no double vision- occurs if onset <7rs |
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Strabismus management- convergent squint: |
- convex (+) lenses - hypermetropia - relax eye outwards - relax accomadation |
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Strabismus management: divergent squint: |
- concave lenses (-) -myopia -relax eye inwards - helps induce accomadation |
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Strabismus surgery: |
- on EOM to straighten eyes/make them look straighter -give pt back binocular vision -improve cosmesis - combined strengthening/weakening procedure on antag/agonist mm - horizontal strbismus: MR/LR - vertical strabismus: IR/SR/SO/IO |
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Visual acuity: |
- needs to be tested uniocularly or amblyopia won't be detected - crowded tests: pts with amblyopia have 'crowding' can ident single letters well but struggle to identify more letters in a line |
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Testing children's VA: |
- Qualitative assesement: fixing + following, reaching for toys - Quantitative assesement: for monitoring visual development + quantifying any increase/decrease in VA |
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Preferential looking |
- babies - black and white square wave grating against a grey background - gratings of decreasing width- harder to see - child looks towards gratings if seen |
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Cardiff cards (measured in snellen equivalent): |
- for young pre verbal chilren - 40cm test distance - pics in black and white against a grey background on top/bottom - pics composed of thinner lines each time - child looks towards pics if seen |
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Kays pictures: |
- for young verbal children -3m test distance - 4 pics in line surrounded by box= crowded - child names pics |
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LogMAR crowded/uncrowded: |
- crowded= 4 letters in a lin surrounded by a box - uncrowded= single letters - for children familiar with letters/shapes -3m test distance - child can name/match letters |
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Bailey lovey- 4m test distance: |
- for all pts who can name letters - 4m test distance |
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Snellen VA: |
-6m test distance - unequal distance between letter + lines of the letters - recorded as a fraction - numerator = 6 (test distance) -denominator= line they can read - +/- depending on hypermetropia (+)/myopia (-) |
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LogMAR VA: |
- Recorded as decimal -0.0=6/6 -0.6=6/24 -1.0=6/60 - odd letters recorded as 0.04 (6/6-2), 0.56 (6/24 +2), 0.98 (6/60+1) - 4m test distance - equal visual demand at each level of VA - logarithmic progression of letter size + distances between the letter and each line |
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Visual acuity on snellen + LogMAR charts: a) normal b) defective c) better than normal |
a) 6/6Sn OR 0.0 LogMAR b) 6/60 Sn or 1.0 LogMAR c) 6/5 Sn or -0.1 LogMAR |
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Concommitant stabismus: a) what b) who |
a) squint that remains the same size and direction in all positions of gaze b) most children |
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Incomittant strabismus: |
a) squint that changes in different positions of gaze b) due to EOM imbalance |
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3rd nerve palsy: a) appearence b) causes |
a) down + out, ptosis, pupil dilatation if pupil involved b) surgical (anurysm, tumour)- pupil involved as parasympathetic fibers on outside, medical (DM, HTN)- pupils not involved, doesn't affect parasymp fibers |
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4th nerve palsy: a) appeasrence b) patient c) causes |
a) subtle hypertropia of affected eye b) pt tilts head, dipolopia on reading c) 4th nerve has long course- affected by many things: vasculitic, trauma, congenital, tumour |
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6th nerve palsy: a) affects b) causes |
a)LR b) esotropia - eye deviated inwards- bigger at distance compared to near c) DM, HTN, particularly affected by increased IOP |
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Aetiology of cranial nerve palsies\; |
- trauma - SOL- vascular abnormality: anuerysm, carotid cavernous fistula, subdural haematoma - microvascular- common >50yrs, HTN/DM, pupil sparing 3rd nn palsy - inflammatory process- viral eg herpes zooster, meningitis, Tolosa hunt syndrome (inflammation of cavernous sinus) - infection - inner ear infection + CN6 palsy- Gradenigo's syndrome common in children, Herpes Zooster opthalmicus - involves first division of the trigeminal nerve - demyelination - optic neuritis |
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Other causes of motility defects: |
- blow out fractures -thyroid eye disease - myogenic conditons eg myasthenia gravis - ptosis most common - symptoms worse when fatigued - tumour/inflammation/disease of EOM- rhabdomyosarcoma, orbital myositis, disease (chronic progressive external opthalmoplegia) |
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Management of diplopis: |
- prisms- join up diplopic images - occlusion- cover one eye to block diplopic image - surgery |
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Low vision devices for children: |
- bar magnifier, - done 'bright' magnifier, - bifocal spectacles with high adds for reading, - distance binoculars, - distance monoculars, |
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Low vision devices for adults: |
- Hand magnifiers -Stand magnifiers - illuminated HM/SM - high reading adds- strong reading glasses - binoculars/monoculars - spectacle mounted devices |
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Low vision devices: |
-Electronic devices - CCTV - Compact devices - Softwear for PCs - Voice activated devices - screen/scanner readers - braille keyboards |
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General referal GOS 18: WHO + WHAT |
-relay of information from optomoterist to GP or hospital - signs of injury, disease or abnormality and treatment or further investigation required or unsatisfactory level of VA even with corrective lenses - Information: screening + monitoring of diabetics and patients with glaucoma - optometrist can administer whatever services are deemed in pts best interest in an emergency situation |
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GOS 18: Form |
- Section 1 completed by optometrist: pt details, sight test details and acuities, disc appearence, IOPS, visual fields, points of interest - Section 2 by GP: Relevant clinical and social history, BP, urinanalysis and provisional diagnosis |
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Definition of visual impairment: |
- A person who is sustantially and permenantly handicapped by defective vision caused through congenital defect, illness or injury - VA 3/60 to 6/60 - up to 6/24 with moderate field contraction va 6/18 or better if severe field loss (advanced glaucoma, retinitis pigmentosa, hemianopia) |
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Definition of severe visual impairement: |
- A person so blind that they are unable to perform work for which sight is essential (blind) - VA <3/60 - VA 3/60 TO 6/60 with constricted fields loss - VA 6/60 to 6/24 but very constricted fields |
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Letter of visual impairment: LVI |
- use by optometrists/ clinicians outside the hospital - given to pts with signifigant difficulties to help seek advice from a council with social services responsibilities - SS provide information on the services available - information: lives alone, additional carer responsibilities, mobiltiy, key concerns, age, prefered method of contact for further advice |
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Referal of visual impairement: RVI |
- used to allow pts to access SS help without blind registration |
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Certificate of visual impairement: CVI
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- certificate of a person as sight impaired/severely sight impaired/blind - advice to pts - registration is voluntary -may access finance benefits - implies 'disabled' under the DD act - council SS have a legal duty - drivers must contact DVLA |
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CVI parts: |
- part 1: by opthalmologost - part 2 other relevant factors - part 3: consent to registration |
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Ocular trauma- investigations: |
-chemical injury-pH -orbital injury- orthoptic assesement, CT scan - penetrating eye injury- xray for intraocular foreign body, CT,US |
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Ocular injury can be: |
- perforating: breach in ocular coats - non-perforating: contusional, blunt injury |
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Corneal foreign body: a) history b) examination |
a) grinding injury b) metallic foreign body on cronea +/- rust ring, anterior uveitis nb beware of hammering metal- may be intraocular foreign body - check with xray |
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Chemical injury: a) appearence |
a) loss of corneal clarity + lustre- dull, opaque appearance, scarring b) flouscien dye- indicates loss of epithelium - serious, determine if acid of alkaline- alkaline is more severe, check pH of both eyes c) saline irrigation, topical antibiotics- artythromycin ointment, oral vit c to decrease ulceration, topical steroid, topical mydriatic drops to constrict pupil to improve photophobia, artifical tears for ocular lubrication |
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Blunt trauma: a) presentation b) treatment |
a) subconunctival haemorrhage +/- periorbital oedema, hyphaema (could result in acute angle closure glaucoma) b) topical steroids, mydriatic agent |
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Subluxation/dislocation of the lens: |
- ruptured lens zonules - shadow seen over red reflex - consider retinal surgery |
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Retinal detatchment: |
- grey retina protruding forward - OD out of focus - surgical intervention required |
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Blow-out fracture: a) what b) symptoms c) investigation |
a) punch trauma, external pressure to globe , increased presure in orbital cavity, fracture of orbital floor into maxiallary sinus b) restriction of eye movements, inferior rectus can be trapped, periorbital swelling, associated ocular damage nb in children there may not be periorbital swelling c) Xray looks for opacification of maxillary sinuses, CT is definitive diagnosis |
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Trap door fracture= emergency |
trapped inferior rectus can result in ischaemia, fibrosis and contraction of mm -> quick release required |
