Management Flashcards
Environmental Risk factors for myopia:
Low light exposure (dopamine theory)
Low outdoor time <2h/d
Increased near work >45min at 20cm
Urbanisation vs Rural
Increased educational activity
Hx poor distance vision:
Onset: acute indicates inflammation
Describe symptoms: headaches/squinting/glare
Medical history: LEE / medications
Family history: myopia
Ocular discomfort: uveitis/ciliary spasm
Preliminary/screening tests:
D/N VA
Cover test
NPC
Accommodative amplitude (if needed)
Stereoacuity (if needed)
Amsler grid (if needed)
Color vision (young males)
Confrontation of VF (dim/light)
Pupil testing
Motility
Myopia visual impairment risks:
Greater risk with high myopia (>6D)
Retinal detachment/hole/tear
Peripapillary atrophy (atrophy near ON)
Lattice degeneration (pigmented retinal thinning)
Tilted insertion of OD
Tigroid fundus (tessellated colouration from RPE thinning)
Lacquer cracks (break in bruchs membrane)
Fuchs’ spot at macula
Pavingstone degeneration (chorioretinal atrophy)
Posterior staphyloma (scleral stretching)
Loss of choroidal circulation > CNV
Assessing presbyopia:
VA w/pinhole
Near add determined via:
Fused cross-cyl
Push up / Push down
Age expected/Hofstetter’s formula:
18-0.3(age) = expected amplitude
Hyperopia management:
Delay treatment: educate young asymptomatic adults
Partial correction: young Px with symptoms
Full correction w/cycloplegic refraction: child with strabismus
MF soft CLs on myopia control:
Plus power on periphery corrects hyperopic defocus
Misight lenses have 55% reduction in myopia progression
(greater add power > better reduction / worse vision)
Assessing myopia:
VA w/pinhole (expect refractive correction)
NPC / near VA (greater)
Auto-refraction
Refraction/subjective
Fundoscopy w/OCT (myopic retinopathies)
Assessing Hyperopia:
VA w/pinhole (expect refractive correction)
NPC / Near VA (lesser)
Auto-refraction
Cycloplegic subjective/refraction
Fundoscopy w/OCT (crowded ON)
Assessing astigmatism:
VA w/pinhole (expect refractive correction)
Auto-refraction
Refraction/subjective (dots/clock dial)
Keratectomy/Topography
OrthoK:
Hard lens forming neg-pressure on cornea overnight > thickens epithelium in mid periphery (vise-versa central epith) > myopic correction at macula / hyperopic correction at periphery
ROMEO / HM-PRO studies > 50% myopic reduction
Stable Myopia correction:
SV specs/CLs
OrthoK
Surgical correction (flatten cornea):
PRK/LASIK/LASEK/SMILE
Clear lens extraction / replacement
Stellest/DIMS/myosmart:
Lenslets in peripheral lens (<>9mm optical zone) reduces hyperopic defocus
Reduces myopic progression (in dioptres) by 50%
May be combined with atropine if significant progression
Required HT for cataracts:
Onset of vision change: sudden (trauma), range from 4 weeks (PSC), gradual (nuc.)
Ocular hist. (refractive/disease/amblyopia/surj./trauma)
Systemic health: (coronary art./cerebrovascular disease / hypertension / diabetes m. / dementia/arrhythmias/ chronic obstructive pulmonary disease) *conditions on supine position difficulty
Medications: a-antagonists (tamsulosin hydrochloride) lead to surj. Complications (floppy iris syndrome)
Allergies: anaesthetics/anti-inflammatories/antibiotics
HT for visual effect of cataracts:
Reading/distance
Facial recognition
TV watching
Bright/dark
Glare
Day/night driving
Moving in unfamiliar places
Using steps
Employment/housework
Hobbies
Myopia management stats:
4 main options with ~40% myopia slowing
Atropine 0.05%
OrthoK
MF soft CLs
DIMS/Stellest lenses
Atropine:
Muscarinic antagonist for M4 scleral receptor
Causes photophobia, accomodation loss, and rebound on cessation
Cataract general health risk factors:
DM, HT, coronary disease
Smoking, alcohol, obesity, poor nutrition
Corticosteroids, alpha-antagonists (tamsulosin hydrochloride)
Uveitis, eye trauma
Cataract comorbidities:
AMD/diabetic retinopathy: lesser VA improvement, Sx increases disease progression from inflammation
Fuch’s endothelial dystrophy: Sx progresses endo loss
Marfan’s syndrome: Sx may damage weakened zonules
Visual assessment in cataracts:
VA 1/pinhole: dist/near
Contrast sensitivity
Contrast sensitivity under glare (^loss of 0.35 logCS units is significant)
Colour vision (^3.0 LOCS III causes tritan)
Slit lamp: retroillumination LOSCI3, comorbidities (glauc)
Tonometry > DFE: comorbidities (AMD)
Pupils: RAPD / compare post-op
LOSC III grading:
Lens opacities classification system
NO: opalescence 0-6
NC: brunescence 0-6
C: cortical 0-5
P: posterior 0-6
Pelli-Robson contrast sensitivity chart:
Most common contrast test:
16 letter triplets (4.9cm high) in decreasing contrast by 0.15 Log CS units (first triplet of 0 Log CS)
0.05 Log CS score for each letter after first triplet
Px 20-50y should have 1.80 Log CS with each eye, older Px should have min 1.65 Log CS (Binocular score should be 0.15 greater)
Cataract PC:
Dist/near vision loss
Hazy/cloudy
Glare
Poor night vision
Contrast loss
Monocular diplopia
Shadowing
Clinical response to cataract:
- Establish visual disability (effect on life)
- Determine effect (glare/blur/colour)
- Diagnose LOSCI3
- Consider comobities (degree of disability attributed to cataract)
- Assess Sx benefit
- Obtain informed consent
Causes of EDE:
MGD
Infrequent blink
Environment
Ectropion / lagopthalmos
CLs via lipid layer loss
Mass lesions
Vit A def.
Defective mucins (infection)
Complications of cat. Sx:
1/200 VA loss
50% PSO by 3y (epith. Lens reminants)
Dislocated IOL
Rupture of capsule
Dislocation of capsule (weak zonules)
Suprachoroidal hemorrhage
^IOP
Cystoid macular oedema (^prostaglandins > vessel leak)
Retinal detachment (^with myopia)
Endophthalmitis (+/- infectious) > blindness 0.04-0.4% by 6w
Cataracts review:
PSC review 6mo
Nuclear review 12mo
Return if notable change
Refer to wait list if severe cataract or Px need to drive
Education on cataracts:
Sx. Improves QoL
Cat will progress
Nothing is lost from defferal
Specs needed after (6 weeks)
Opthal initial and 2 follow-up appt.
Sx. Needs 2 operations on 2 days
Anti inflammatory/microbial drops
Public is free (1-2years)
20min surgery under local anasthesia (blurred)
Unlikely complications
Causes of ADDE:
Sjrogren’s syndrome (autoimmune against exocrine glands)
Lacrimal gland dysfunction: Primary (age/genetics) or secondary (AIDS/Lymphoma)
Lacrimal gland duct obstruction
Alteration in stimulation (reflex block)
Types of MGD:
Primary (age/acne): increased bacterial lipases > meibum cleavage > fatty acid formation > increased melting point > hardening
Secondary: diseases
Cicatrical: hyposecretion from damage / steven-johnson syndrome / allergies
HT for presenting with dry eye:
Onset/duration: acute/chronic
Symptom description: itch/FBS
Triggering factors: AC/stimulants
Medications: anti-histamines
Medical conditions: Sjrogrens
CLs/screen use
Diagnostic tests for DED
Tear stability (TBUT / osmolarity)
Tear production (Schirmers / meniscus)
Ocular surface (staining / ocular surface index)
DED questionaire
Osmolarity (>317mOsm/L)
Phenol red (pH dye on string like schirmers)
Lactoferrin test (lacrimal Gland production)
Meibometry
Impression cytology (goblet population)
Schirmer test:
5mm fold in Whatman filter inserted under lower lid (temporal side), don’t touch cornea/lash
Px closes eyes over filter
Remove paper after 5min
<10mm without anesthesia / <6 with ana. Indicates abnormal
TFBUT:
NaFl instilled with Wratten #12 cobalt filter lens
Px blinks before holding eyes open
Timed appearance of black spots
<10s abnormal, repeated breakup in given area indicates localized surface abnormality
Sodium Fluroescein function:
NaFl peak absorption at 493nm (blue), emits 520(green), instilled via strip (1% drop), viewed via wratten #12 (yellow-green) filter
Hydrophilic (doesn’t pass lipid bilayer epithelium or tight junctions), pools in corneal/conj. Areas of cell loss
Goals of DED management:
Eliminate exacerbating factors
Lubricate ocular surface
Minimize exposure
Restore normal osmolarity
Prevent inflammatory mediator/enzyme production
Improve film stability
Step 3 DEWS management:
Autologous serum drops
Therapeutus CLs (bandage)
Step 1 DEWS management:
Education
Environment change
Modification of topical medications
Ocular lubricants
Lid hygiene / warm compress
Step 2 DEWS management:
Non-pres lubricants
Tea tree oil(Demodex)
Punctal occlusion/moisture chamber
Overnight ointment
Lipiflow
Short term FML
Blepharitis management:
Ant. > lid scrubs decrease bac. Load or 1/3 shampoo
Pos. > warm compress + massage > melts meibum caps and expresses
Punctal occlusion:
Temporary plugs: dissolve in 2w
Prolonged: removed in 6m (risks granuloma)
Permenant occlusion: opthal for cautery
Anti-inflammatory treatment of DED:
Fluromethalone alcohol/acetate (FML/Flarex): 0.1% qid > 1week with lubricants
Topical ciclosporin (cequa/ikervis): 0.05% bid for ADDE, reduces T-cell inflammation (requires oxford grading scale = 4)
Topical lifitegrast (Xiidra 5%): lymphocyte function-associated antigen (LFA-1) antagonist, blocks LFA-1 on lymphocytes from intercellular adhesion molecule-1 (ICAM-1) on epith.
Uncommon DED treatments:
Manuka honey
Systemic tetracyclines: alters meibum for rosacea/bleph.
Omega 3 fatty acid supp.: decreases inflammation systematically
CLs: occlusive GP scleral CLs provide saline reservoir
Lacrisert: plastic insert placed in lower lid to hold artificial tears
Palpebral tarsorrhaphy: stich lids closer together
Anisocoria Hx:
Symptoms: droopy lids, double vision, headache
Onset: acute/traumatic
General health: DM/HT
Medications: tamulosin / apraclonidine (glauc)
PERRLA examination (first test):
Pupils Equal Round Reactive to Light (direct/consensual) and Accommodative
1. Direct response: light activates ipsilateral EW > ipsilateral constriction
2. Consensual: light activates ipsilateral EW > contralateral EW activation > contraction
Accommodative: Near response triad > visual cortex / pupillomotor Centre in midbrain response
RAPD examination (second test):
Swinging flash test for Relative Afferent Pupil Defect.
No RAPD: equal constriction W/O radiation excluding Hippus
Mild: affected pupil constricts and redilates
Moderate: affected pupil does not change, then dilates
Severe: immediate dilation of affected pupil
Lack of consensual response is not RAPD, only examine pupil with light shown on it
Clinical tests for anisocoria:
VA w/pinhole
IOP: ^AACG / low in horners
Motility: CN3
Ptosis: horner/CN3
Slit lamp: adies/injury/AACG
Fundoscopy: DM/HT > CN3
Pupil assessment
Assessing anisocoria greater in light:
Greater in light > parasym. Loss > CN3 palsy / adies
0.1% pilocarpine > great constriction of affect pupil in early adies (<2w) from Ach upregulation
1% pilocarpine > constriction of CN3 palsy
Faliure to constrict > pharmacological/atrophic mydriasis
Assessing anisocoria greater in dark:
Greater in dark > sym. Loss > horners/aberrant regen (CN3/adies)
0.5% apreclonidine > pupil dilation of affected eye. Requires 1w post onset for a1 upregulation
1% hydroxyamphetamine > dilation of affected eye if 1/2 order neuron lesion (release of 3rd neuron noradrenaline)
Red eye Hx:
Onset: acute/chronic
Uni/bilateral: allergic
Constant/intermittant: causative
Pain description: itch
Vision affect: corneal
Discharge type: water/mucoid
Light sensitivity: corneal
Previous episodes: viral
Risk factors: CLs, allergies, trauma
Types of discharge in conjunctivitis:
Watery (viral/acute allergic): serous exudate / tears
Mucoid (chronic allergic / DED): mucoid from inflamed goblet cell
Mucopurulent (chlamydial / bacterial): mucoid and pus (leukocytes)
Purulent (gonococcal): pus
Red eye clinical tests:
VA w/pinhole: Corneal involved
Motility: orbital cellulitis
Pupils: AACG/Uveitis (synechiae)
Tonometry: AACG
Slit lamp:
- Lids: Bleph/Trachiasis
- Conj: papillae/follicles, hyperemia, discharge, membranes
- Cornea: infiltrates
AC: flare cells/hypopyon
Fungal keratitis treatment:
Ophthal referal
Topical natamycin 5% per 30min /24h > per hour / 24h > qid for months
Paired BS antibiotics prevent co-infection
Cycloplegics to reduce ciliary spasm
Never steroids (increase fungal replication)
Chronic bacterial conjunctivitis management:
Lid hygiene regime
Chloramphenicol .5% qid 1w
Acute bacterial conjuntivitis management:
Self limiting (3w)
Chloramphenicol .5% qid 1w to slightly reduce symptoms
Hyperacute bacterial conjuntivitis management:
GP referral for systemic tetracycline/erythromycin
Untreated > cornea ulceration > endophthalmitis
Trachoma treatment:
Initial infection > self limiting
Recurrent > single dose of azithromycin 20mg/kg up to 1g
Management of CL hypoxia:
Discontinuation of CLs until corneal oedema/surface is healed
Lubricating drops for symptoms / healing
Refit with higher Dk/t lenses / change CL regieme
EKC management:
Self limiting 1-3w.
Cold compress / lubricants (comfort)
Topical cortico. (flarex 0.1% qid) for corneal subepithelial infiltrates
VKC management:
Topical lubricants w/systemic anti-histamines
Topical anti-histamine Levocabastine 0.05% QID
mast cell stabilliser Lodoxamide0.1% QID
Cortico. If severe
Usually resolves after 50 years of age
SAC/PAC management:
Topical lubricants w/systemic anti-histamines
Topical anti-histamine/mast cell stabilliser (zaditen) if severe
GPC symptoms and management:
Itching, hyperemia, sup. And inf. Tarsal papillae, mucoid
Secondary cases can have increased mucoid/debris on CL w/loss of CL tolerance (symptoms worse following removal)
* Avoid allergen, topical anti histamines/mast cell stabilisers/steroids/NSAIDs
Secondary > remove stimulus, change cleaning regime, topical treatment (no steroids)/
AKC management:
Topical lubricants w/systemic anti-histamines
Topical anti-histamine/mast cell stabilliser (zaditen)
Cortico. If severe
Signs of keratits:
Hyperemia: prostaglandins
Corneal oedema: prostaglandin > endothelial pump dysf.
Discharge: watery(CN 5)/mucoid(bacterial)
Pain: severe/increasing (infection)
Epithelial defect: immune infiltrate/epith. Apoptosis
AC reaction: hypopyon(infective) / inflammatory mediators (sterile)
CL keratopathy staining:
Scattered dots: Dot toxicity
Superior (epith. Arcuate) lesion: tight lid hyopxia (SEALs)
Diffuse spread: CL overwear
3/9 ‘oclock: RGP poor size
Management of bacterial keratitis:
Fluoroquinolone mono w/ciprofloxacin ointment 0.3%
Q10m for first hour > qhour for 24h > review > qhour for 24h > q2hour
Unresponsive/complex > microbe culture > dual therapy
Clinical testing for keratitis:
VA w/pinhole
Pupils: sluggish response
Slit lamp: conj. Hyperemia/corneal defect/AC response
Tonometry
Acanthamoeba treatment:
Cease CLs and see ophthal.
Cocktail of polyhexamethylene biguanide (PHMB) 0.02% with brolene 0.15% tapered from hourly>quaterly from 2-6 months
FML contradicted until infection is controlled
HSK treatment:
Self limiting in 3w
Live virus (dendritic/geographic):
Topical aciclovir 3% 5/d for 10d
Assisted with topical lubricants
AC reaction can be assisted with cycloplegics
If corneal toxicity at risk > oral acyclovir 400mg 5/d for 10d w/specialist refferal
Metaherpetic / neuroprophic:
Topical lubricants per hour
HZO symptoms and treatment:
Punctate epith. Keratitis
Skin rash (nose)
Aciclovir 800mg 5/day for 10d
GPC management:
Removal of stimulus (CLs) for 1 month > monitor
Severe cases > topical mast cell-stabiliasers/anti-histamines
If returning to CLs change cleaning solution/regieme, decrease wear time
Management of CL related toxic/allergic conjuntivitis:
Immediate CL cessation
Frequent non-preserved topical lubricants
Refit with daily CLs and non-preservative cleaning agent (hydrogen peroxide)
Management of 3/9’ staining:
Px education on correct wear and reducing forceful blinking
Topical lubricants reduce peripheral desiccation
Refit CLs with thinner edges / better diameter
CLPU/CNPU management:
Immediate cessation of CLs
Sterile lesion doesnt need therapeutic management > 24h BS antibiotic (fluroquinolone Ciprofloxacin) if too similar to bac keratitis or disrupted epith. w/infiltrates
Management of CL associated dry eye:
Lubricants and DED management (MGD)
Refit with higher Dk/t lenses / change CL regieme
Tight lens syndrome management:
Immediate cessation of CLs
Topical lubricant aid healing
Chlorsig if epithelium disturbed
Refit CLs with RGP / change regieme
Frequent lubricants when resuming CLs for hydration
CLARE management:
Immediate CL cessation > self resolves by 1w
No therapeutic management required as is sterile inflammation > 48h BS antibiotic (fluroquinolone Ciprofloxacin) if too similar to bac keratits or disrupted epith. w/infiltrates
Viral keratits clinical testing:
VA w/pinhole
Slit lamp: vessicles, corneal staining, infiltrates, AC
Corneal sensitivity
Pupils: sluggish
Fundoscopy
Tonometry
Scrape: debribe/culture
HSK dendritic ulcer management:
Self limiting 3w Review daily
Treatment initiated to minimise scarring
3% aciclovir ointment 5/d for 2w(or 3d post re-epithelialisation)
Cycloplegic for pain relief / ciliary spasm (when AC related)
Unresponsive > scrape/culture
Lack of re-repithelisation > toxicity/neurotrophic keratophy
Oral acyclovir 400mg 5/d for 10d to avoid epithelial toxicity (GP ref)
HSK geographic ulcer management:
Aciclovir 3% 5/d until re-epithelilised
Monitor for toxicity /co-infection signs > oral aciclovir / opthal ref
Lack of re-repithelisation > toxicity/neurotrophic keratophy
Oral acyclovir 400mg 5/d for 10d to avoid epithelial toxicity (GP ref)
Metaherpectic / neurotrophic ulcer management:
Opthal refferal w/ scrape / culture
Non-preservative lubricants every hour
HSK deeper infection management:
Opthal refferal
Epith. > 3% acyclovir ointment 5/d
Stromal/AC > prednisolone Forte 1% per 2/h (monitor rapid viral replication)
Trabeculitis/steroid response > b-blocker/a-agonist glaucoma medication
After resolution oral acyclovir 400mg 3/d reduces recurrence by 50% (HEDS)
VZV reactivation management:
GP referal
Oral acyclovir 800mg 5/d for 10d
Should initiate within 72h > later will still be benificial
Classifications of TED:
[NO SPECS]
No symptoms
Only signs (lid retraction)
Soft tissue involved
Proptosis
EOM involvement
Corneal involvement
Sight loss
Management of HZO:
Epithelial: oral aciclovir 800mg 5/d for 10d w/pres-free lubricants
Nummular stromal: FML qid, 400mg aciclovir 3/d
Disciform stromal / keratouveitis: Predneferin forte 1% per 2h, 400mg aciclovir 3/d, anti-glaucoma, cycloplegics
Hx graves disease:
Vision loss: mono/binocular, intermittant?
Diplopia
Eye strain/uncomfortable
Dry/sore/gritty eyes
Soft tissue swelling around eyes?
Systemic changes: energy, mood, heat intolerance, rashes, palpatations
Sjogrens syndrome diagnosis:
Unanesthetised schirmers <5mm
Rose bengal score >4
Salivary flow <1.5ml by 15m
Auto-antibodies anti-Ro(SSA) or anti-La (SSB)
Histopathology > high lymphocytes in mucosa
Oral symptoms
Ocular symptoms
Classification requires 3/4 objective or 4/6 total
MG testing and management:
Unable to upgaze for 1min > EOM/LPS loss
Ptosis improves after 2min icepack (acetylcholinesterase inhibition)
Requires ophthal as is life threatening
TED clinical tests:
VA: DED/ON compression
Pupils: RAPD ON compression
Motility: limited / uncomfortable
Red cap desaturation: ON compression
Slit lamp: Blink/lagopthalmos, SLK, NaFl asses exposure keratopathy
Exopthalmometry
Fundoscopy: ON assessment
VFT: ON compression
Quantifying proptosis:
Exophthalmometer measures ent. Protrusion from orbit
Ruler placed on lateral orbit margin
21-23mm mild, 24-27 moderate, >28 severe
Sjogrens syndrome managment:
Follows DEWS2
Manage symptoms
Lubricant gels/ointment, punctal plugs
Therapeutic ciclosporin/liftegrast/steroids
Immunosuppressive therapy
ERM management:
Mild (<6/12): monitor for spontaneous ERM seperation
Symptomatic / (>6/12): epiretinal peel w/vitrectomy
Trypan blue stain 0.15%, silicon oil/gas replacement
75% ^VA, 25% unchanged, 2% VA loss, 75% cataract in 2y
ERM can regrow
TED management:
Opthal refferal AND PERSCRIBE PRISM LENSES
Topical lubericants, anti-inflammatories
Nocturnal lid taping (lagopthalmos)
Systemic glucocorticoids 60mg/d (reduce ON compression)
Surgical orbit decompression, correction of fibrotic muscles
CSR management:
Self resolves 95% in few months *rarely retains slight metamorphopsia
Change lifestyle
Chronic(5%)/recurrent(40%) require photodynamic therapy or anti-VEGF
AMD HT:
Onset: acute/chronic
Location: central/peripheral
Uni/Bilateral: asymmetrical
Progression: worsening
QOL impact: work/hobbies
LEE
Risk factors: FOH, Smoker, HT, Cholesterol
Headaches, peripheral neuropathy (rule out other causes of sudden vision loss)
Managing macula hole:
VA
Macula assessment on fundoscopy
Amsler grid > enlarged central spot / central metamorphopsia/scotoma
OCT
Regular monitoring 3-12mo > vitrectomy
HT maculopathies:
Mono/binocular
Duration/progression: ERM/mac hole slow (years), CSCR fast (days)
Metamorphosia: describe wriggly/wine glass
Change of colour in affected area: CSCR
Impact/severity: near/far tasks
Systemic health/medications: DM/HT
POH: CSCR recurrance
FOH: AMD/Bests disease
Clinical test for maculopathies:
VA: imapct? Record for future comparisons
Refraction/near ADD: hyperopic shift CSCR
Slit lamp: lenticular changes, angles
IOP > DFE: extent of pathology
Amsler grid: describe visual defect / monitor
OCT
Amsler grid:
Qualitative 10(deg) in place of 10-2
Screens mac. Oedema, drusen, CNV, hole/traction
Viewed 30cm, each 5mm square subtends 1(deg)
Note missing area (scotoma), or warping
FFA tools:
Sodium fluroescein: water soluble dye, peak excitation 490nm (blue), emits 520nm (yellow/green)
Yellow/green filter (530nm) blocks blue reflection
80% dye binds serum protein (unbound > renal/hepatic met. Removed by 36h)
AMD clinical tests:
VA: change/progression
Refraction: can VA improve
Pupils: severe asymmetrical > RAPD
Slit lamp: Ant. Examination
Tonometry > DFE: drusen size, RPE change, GA, CNV
OCT/OCT-A: type/severity, progression
Dry AMD treatment:
Monitor early stages > OCT, amsler, follow-ups
Px education
AREDS based “macu-vision plus” supps.
Cease smoking, HT/cholesterol control, BMI reduction
Refer to royal society of the blind
AREDs supplements:
Vit C 500mg, Vit E 400UI, zinc 80mg, Lutin 10mg, zeaxanthin 2mg
Exudative AMD treatment:
Anti-VEGF is standard
Photodynamic/photocoagulation damage retina even with laser activated drugs
Bevacizumab:
Monoclonal antibody against VEGF-A, originally systemic treatment
No significant difference in clinical efficiancy
Australia Lucentis is cheaper now (under PBS)
Electrophysiological testing:
Evaluate RPE / retina function
International Society for Clinical Electrophysiology of Vision developed guide for:
Full-field/Pattern/Multifocal electroretinogram (ERG/PERG/mfERG)
Electrooculogram (EOG)
Cortical-derived visual evoked potential (VEP)
RP clinical tests:
VA
Refraction and BCVA
Slit lamp: associated findings (cataracts)
Tonometry > DFE
OCT: macula structure
VFT/Amsler: Macula assesment
30-2 VFT: peripheral assesment
RP management:
Ophthal reff. > electrophysiological/genetic testing
Low Vision Service reff. > Royal society of the blind > visual aids (service dogs, counselling, employment)
Retinal dystrophy management:
Ophthal refferal > Electrooculography / Electroretinography / gene testing
Genetic counselling (family)
Low vision aids (dogs)
Gene therapy for RPE65 can improve prognosis
