Ocular Diseases Assoc w/LV Px

Albinism

A congenital condition characterised by lack of pigment. Can be oculocutaneous (skin and eyes) or just ocular. 1 in 20000 of general population. Cat. into Tyrosinase +ve or -ve, -ve has more severe effect on vision 6/60-6/120, +ve better 6/24 which improves over time.

• VF appear full
• Blue irises - transillumination
• Photophobia
• Nystagmus
• Hypoplasia of macula
• High incidence of strab
• Poor stereo
• High refractive error
• SYSTEMIC - white or yellowish hair, eyebrows, eyelashes, pink skin, sensitive to sun damage
• Assoc w/Hermansky-Pudlack syndrome - genetic metabolic disorder

Low vision management involves corrective Rx, aperture control contact lenses, tints, UV protection, magnification for distance and near

Cataracts

The opacification of the crystalline lens, classified according to area affected - ant/post subcapsular, ant/post cortical, equitorial, nuclear. Caused by trauma, metabolism, toxic cause, 2ary to inflammation, drugs, hereditary, age-rel. 95% of those over 65 have some form of lens opacification

• VA varies w/degree and location of opac, most often bilat but asymmetric, nucscler not often assoc w/vision loss - more myopic. Posterior subcap has profound effect on VA especially with small pupil
• VF - ok
• Dull/abnormal ret reflex, refraction more myopic, reduced acuity, increased glare, distortion, monoc diplopia, altered colour perception. Treated by removal

LV management centres around lighting, filters and AR coat for glare and magnification

Diabetes Mellitus (I = juvenile onset, II = adult onset)

Signs and Symptoms are excessive thirst, urination, hunger, fatigue w/weight loss and recurrent infections. DR is the biggest single cause of registered blindness in the UK amongst working age people. Smoking and obesity increase the risk. Type I will tend to show retinopathy within 10 to 12 years, type II after 20. 60% will show some degree of retinopathy.

• VA from 6/6 to total blindness, fluctuates dude to blood sugar level if poorly controlled, lens changes (myopic) and CMO (hyperopic)
• VF - 2ary complications can cause loss - laser burns, retinal detachment, Glaucoma, CMO - macular degen.
• Other complications - accomm insuff, Diplop, Cats, Glau (rubeosis), RD, MD/CMO, decreased corneal sensitivity, neovasc, haemorrhages

LV Vision management - refraction, sunglasses and filters, increased illum, mag/minification, flashlight/torch, non-optical, mobility services support groups.

Glaucoma

Open angle - asymptomatic, closed angle pain, blurred vision, photophobia, halos, nausea, vomiting

• VA generally unaffected until end stage
• VF typically respects horizontal midline, arcuate defects, nasal step. Gradually spreads to periphery and centrally
• Diagnostic testing - ON head, VF, IOP, ant chamb angle

LV management w/magnification, lighting indoors & out, glare control, contrast enhancement, minification, peripheral awareness systems, other professional services

Macular Holes

Round red spots in centre of macula 1/3 to 2/3 DD in size, may have grey halo around it where RD happened. May be caused by trauma, myopia, CMO, inflammation but most are idiopathic.

• VA depending on location 6/9-6/120
• VF full thickness holes = dense central scotoma
• Metamorphopsia and reduced VA

LV management with magnification, eccentric viewing, lighting and filters to increase contrast

Macular Disease

Any degenerative condition affecting the macular area. Eg ARMD, Stargardt's, Best's Disease

• Reduced VA D&N, metamorphopsia, central field loss, reduced colour vision, increased glare and photophobia
• Test w/VF, colour testing (D15 usually shows RG loss), flu angiog

LV management with refraction, magnification, lighting, glare control, non-optical, support groups

Myopic Degeneration

This is excessive stretching and expansion of the posterior segment, with scleral and choroidal thinning.

• VA decreases as condition progresses, may lead to NPL from 2ary complications
• VF varies w/structures involved
• Blurred Dv, flashes/floaters, thinning of RPE, posterior staphyloma, Fuch's spot, Retinal detachment
• Associated syndromes - Down's, Marfan's syndrome, Stickler's Syndrome

LV Management refraction, magnification, lighting and contrast enhancement, glare control and photophobia protection, torch @ night, other professional services

RP

1 in 3000-4000 of the population. Most common in males - autosomal recessive/dominant/x-linked

• VA from 6/6 to NLP
• VF starts in mid-periphery and goes inward and outward
• Nyctalopia, light/dark adaptation affected, attenuated BV, bony spicule pigmentation, waxy disc, posterior subcapsular cataracts, CMO

LV Management - minification, peripheral field awareness, magnification, sunlenses, lighting control, torch at night, genetic counselling

Retinopathy of Prematurity

Abnormal proliferation of retinal blood vessels in premature infants receiving oxygen therapy. About 7% of babies in UK born prematurely.

• VA from 6/6 to NLP
• VF variable depending upon which part of the retina is involved
• High myopia, strabismus, RD, glaucoma, cataract, corneal scarring, glare and photophobia, CVI

LV Management - refraction, magnification, sunlenses, filters, lighting control

Causes of Visual Impairment

Global

• 47.8% Cataract
• 13% other -trauma etc
• 12.5% Glaucoma
• 10.6% AMD
• 3.3% Corneal Opacity
• 4.8% DR
• 3.9% Childhood Blindness
• 3.6% Trachoma
• 0.8% Onchocerciasis

Cataract

• Affects about 16m worldwide
• An IOL costs about 10 dollars

Onchocerciasis

• Control programme in west africa over 11 countries which protected 30m people including children, costs $1 per person

Vit A Deficiency

• Xerophthalmia (dry eyes) causes 350,000 children to become blind per annum
• Prevented by good diet with fruit and veg etc

Diabetes

• 2% of the UK pop are known to have it, 10% will have DR that requires ophthalmological intervention
• Untreated 6-9% of those with prolif. DR would become blind each year
• Affects working age group
• Screening and treatment is expensive

Preventing Blindness Worldwide

• Immunisation
• Nutrition & Education
• Personal Hygiene
• Sanitation
• Training and local medical facilities

Support for the Visually Impaired in the YooKay

• Social work - centre for sensory impaired people provides info, advice, equipment, training, certification/registration eye clinic, technical services & library
• RNIB - charity, provides training and rehab, wide range of non-optical LVAs, braille, talking books, advice & campaign for equal rights eg lobbies for provision of new drugs, computer training, funding/carrying out research
• RNIB training courses - goal to provide VIPs with skills, qualifications and confidence to remain in work or obtain employment. Have learning resource centre with study and library area, classrooms, training rooms, recording studio, interview suite, guide dog facilities, cafe_bar, sports facilities, accommodation
• RNIB talking book service - Annual subs, NVA is
• Royal National College for the blind - skills for independent living, academic studies, GCSE/A-Level/AS Levels/BTEC, GNVQ, AVCE
• Royal Blind School in Edinburgh - day/residential school for pre-, primary and 2ary. Scottish braille press there too
• Talking Newspaper Assoc of UK - local volunteers, local press, weekly editions, national newspapers and magazines, annual subs
• Calibre - adult and children's compact cassette library, 6000 adult and 1000 children's books
• National Library Of The Blind 350,000 braille and Moon books, 13,500 music scores, electronic books
• Playback - Glasgow City Council 1976 centre for sensory impairment, registered charity w/80 volunteers, 46,000 cassettes a month. Magazines, newspapers, tape library and reading service
  

Low Vision Rehabilitation

Psychological barriers to process of rehab

• Concealment - px still pretends vision is fine - the eyes still look normal. They may feel the vision loss is seen as a general cognitive decline by others. They may reduce social contact, stay indoors. Younger px may fear losing their job/loss of independence
• Px refusing LVAs - think new glasses will do it. Equate VI with 'blind' and give up. They may have unrealistic expectations as well as other worries like caring for partner/money etc. Practitioner must explain that aids can be difficult to use but be encouraging and REALISTIC - ie don't give them aids they won't use

Prognostic Factors in Predicting Success w/LVA use

You have to wonder what constitutes successful LVA use/assessment - increased VA/confidence/performance of required tasks? Stuff that can be measured: VA, reading speed/acc, frequency of use of LVA.

• VA Studies - success rates vary consid. depending on criteria. Up to 95% of px achieve improvement
• Quality of life studies - Manchester Low Vision Questionnaire
• Attending LV Clinic - 67% px benefit 'a great deal', 22.8% a little, 10.5% not at all

WRT to a successful predictor of LVA use

• VA - poor, improved VA doesn't necess mean that LVA will be any good
• VF - good, extent and location of remaining field important, restricted field tends to have poor prognosis
• Stability of eye cond - good, better chance of success if stable
• Duration of VI - poor prognosis if recent (loss model)
• Cause of VI - poor, depends more on motivation
• Age - Good, younger = better prognosis
• Education/Intelligence, poor, people w/good intel tend to do better, but it's more fluid intel (ie adaptability to new task)
• Motivation - good. PROBABLY THE MOST IMPORTANT FACTOR! Self img/psychological barriers

Px Prefers

• Simple stuff! High spec adds, hand mags, stand mags, illuminated mags

Non-Optical and Sensory LVAs

These make the best use of residual vision/work via sensory substitution. Non-optical aids include daily living aids, environmental design, lighting and contrast and tints.

• Self threading needles, liquid level indicators, talking watches, large number telephones or microwaves, 'bump ons' or 'hi marks' and coloured stickers
• READING - making object bigger (large print books/bills/clocks/watches etc), talking watches or books or newspapers, reading stands, typoscopes, good lighting
• WRITING - felt tips, yellow paper, lined paper, writing frames

Braille was developed in 1824 and consists of 3x2 grid pattern of 6 dots giving 63 characters, 26 letters & contractions & punctuation. There are two levels - in grade 1 every word is spelt out and in grade 2 there are approved contractions for stuff like 'and' and 'with'. 20% of those registered blind can use braille. Books are thick and bulky and it isn't good for the elderly due to loss of sensation in their fingertips. It can be generated by a computer.

Moon is another tactile language that was developed in 1847. It was designed for people who previously had sight, featuring curves and lines that are more approximate to actual letters.

Electronic Aids for reading and writing

• CCTV, video magnifiers, head mounted devices
• Computers - scanners, speech synthesis, braille keyboards/printers, PDAs, USB cameras
• Built into OS - Windows has accessibility, Mac OSX has 'universal access' which enlarges icons, arrow, alters contrast and has voice output.
• Screen magnification software eg Zoomtext is also available.

Mobility Aids

• Canes and Sticks
• Electronic Aids (ultrasound, sonar)
• Dogs (see later)
• People (guides)
• Talking Signs
• Built Environment

White Sticks (if has red stripes this indicates px is deaf too)

1. Symbol Cane - lightweight, folds up, indicated px is VI
2. White walking stick - as above but aids support
3. Long Cane - most common. Developed by war vets in US following world war 2. Needs extensive training (+150hrs). Made of lightweight aluminium, held at chest height at 30 degree angle and swung in L to R arc as foot goes forward. Touches ground at end of travel and may have roller on tip
4. Guide Cane - Shorter/stronger than long cane, used as back up for those with residual vision

Trailing

Technique to help locate door, walk in straight line, detect posn of objects in front of the px on the same side of his body as the extended arm. This can provide useful info about everyday objects, obstacles and potential hazards. In familiar environment the px moves close to the wall with knuckles against it using the other hand in front to detect obstacles

Electronic Mobility Aids

• Ultrasonic - ultracane, hand held (miniguide, palmsonar), head mounted (sonic pathfinder), Bat K sonar-cane
• Laser - laser cane which has three beams (ground, waist, up) and alerts with tones and vibration
• GPS - MOBIC (mobility of blind and elderly people interacting with computers), braille note GPS, Trekker

Dogs

Guide dogs for the blind started in 1931. Running cost is 45m pa and they get no Govt funding. The dogs guide the owner and avoid obstacles, stop at kerbs/steps, find doors, road crossings and frequently visited places and lead across roads. The owner is basically responsible for encouraging the dog while directing and informing it.

Guide dog owners have to be over 16, have VI which makes safe independent travel difficult - marked decrease in VA, CS or VF. 43% of guide dog users are totally blind, mainly due to congenital or early onset degenerative disease. RP makes up 18% and optic atrophy 10%. The average age is 53.

Guide Dog Assessment

General Info Visit

• Info on services and training provided

Mobility Assessment

• Medical Status, cause and degree of VI, options (long cane or other, guide dog assess, non guide dog mobility aids)
• Contrainds - sufficient sight, age, dislike of dogs

Guide Dog Assessment

• Instructor assesses appropriate aid/suitability
• Work with dog to determine whether px can walk with it, follow movements, keep control, react etc
• Assessment of home environment

Breeding

1200 guide dogs are bred each year, mostly labs/lab-golden retr. cross. There has been a programme going since the 60s to reduce health probs and regulate supply. The dogs have x-ray health checks and eye exams

Makin the dog guide

• Puppy walking at 6 weeks old w/volunteer walkers who teach dog to ignore distractions or other dogs, walk on LHS and in straight line, centre of pavement, and stand and wait at kerb. 75% of puppies can do this, the other 25% are killed. No not really they are used as dogs for therapy, for the disabled, RAF, Customs & Excise, Prisons etc
• At 10-12 weeks the clever dogs go to a training centre where a proper dog trainer becomes involved, dog is fitted with harness and does tasks in busier environment etc
• At 3 months advanced training starts and dog is tailored to individ. needs

Pairing

Priority system. At 5 months dog attached to owner then 3-4 weeks intensive training, px taught to take care of dog. The owner pays a nominal 50p for the dog and the dog actually costs 35000 over its lifetime

Working

Continuing support is provided, with regular health checks, food/vet bills, third party insurance. Most dogs work 7-8 yrs. Guide dogs are allowed anywhere thanks to disability discrimination act 1995

Retiring

This is caused by health problems, increased mistakes, loss of concentration, slower walking speed, loss of confidence. The dog can stay with the owner as a pet or be rehoused.

Environmental Design

Simple things

• TV away from windows
• Sit close to TV/blackboard
• Location of reading lights
• At one side of teacher/TV if hemianopic px
• Colour schemes - Light paint on walls, dark round doors, lighter door with contrasting handle, dark flooring, hard flooring - for the sound, contrasting skirting boards for stairs

Architectural Design

• Features to aid VIPs eg lighting contrast
• Wide/sliding doors
• Auditory indicators eg in lifts
• Handrails
• Enclosed Staircases
• Tactile elements like on floors
• Avoid stuff like glass doors
  

LV: Lighting

Lighting

The goal of lightning is to provide adequate lighting in the appropriate places without any glare

• General lighting - there should be an even distribution of light with extra for hazardous areas. Ceilings and walls should be light coloured and non-reflective. Patients should face away from the window in daylight to avoid glare
• Local lighting - take into account inverse square law and also cosine law (put paper as close to 90 degrees to light source as possible to get maximum illuminance
• NB 60yr old needs 3 times the illumination of a 20 yr old due to senile miosis, media opacities and loss of neurons

Glare

• Discomfort Glare - subjective visual discomfort - px feels visually uncomfortable or fatigued. VA not affected by glare and discomfort relieved by tints. EG In uveitis, ocular albinism, cone-rod dystrophy, RP. Can be measured by getting patient to adjust light to a certain level of unpleasantness. No clinical relevance tho
• Disability Glare - Loss of retinal image contrast as a result of intraocular light scatter or stray light. This reduces visual performance. The degree of glare depends on the angle between the task and the glare source & the relative luminance
• Media opacs lead to IO light scatter and veiling luminance across retinal image and a reduction in contrast. Eg ageing, cataract, pos. chamber IOL, PCO, Keratoconus, Corneal Oedema, RK, vit opac

Disability glare can be measured objectively - px viewing an acuity/low contrast chart under controlled lighting conditions. This allows for simulation of everyday situations like flu overhead lighting, sunlight on cloudy day etc. Optom measures VA while shining penlight into pxs eye at a fixed distance and angle (eg 10cm and 30 degrees). Drop in VA of 2 lines or more indicates a significant degree of glare.

Reducing Disability Glare

• Environmental control, task lighting, avoidance of shiny surfaces, tints to reduce retinal illuminance, visors and hats
• People who may benefit from tint - media opac, albino, RP, Cone dystrophies, aniridia (though cone dystrophy may be better), corneal dystrophies, diabetics, uveitis
• Prescribe tints wrt subjective comfort or objective w/low contrast charts vs high contrast charts, varying illumination.

CIBSE Recommended levels for normally sighted px
(in lux)

• Living Room 50, Sewing/Sustained Reading 300, Kitchen 300, Hall/Stairs 150, Bathroom 50, Bedroom 50.
• 50-100% increase in those figures if you're over 65
• 5 times to 10 times increase if you're a VIP. Usually compromise w/1000 lux, adjustable

Bulbz

• Fluorescent is best. Gives poor colour rendering because usually at discreet wavelength but this is irrelevant in a low vision context.
• Discharge tube can be folded to give more compact bulb
• 9w or 11w, high efficacy
• Stays cool even after prolonged application
• NB Px can use any light source and it will not affect the way they read
  

Real Image/Transverse Magnification

M = SIZE OF IMG (on screen) / SIZE OF ORIGINAL OBJECT

CCTV is the most common way of producing this kinda magnification. It's aberration free (with magnification edge of magnifier view = rubbish) but the resolution of the screen determines image quality. Up to 70x mag is possible but usually about 30x is limit. The magnification is variable with a zoom control in a way that just ain't possible with an optical aid. This means if the px requires a change in magnification it remains useful. It has variable camera/task and eye/screen distances so allows for more normal viewing and extended reading. Reading speed is about the same though. Contrast etc is variable too.

Components

• Camera
• Light Source
• X-Y Platform
• Monitor screen (bigger screen = larger FOV - only 4 characters required for reading but up to 15 required for optimum page navigation)
• With the most common design (PORTABLE CCTV) each component is fixed and mounted vertically 'in line', working space is fixed or limited, all the controls are together so easier to set up. Also it's more portable duh.
• Can also add 2nd camera for distance

Advantages

• Zoom on magnification - overall view at low mag then increase for detail
• Adjustable mag if vision changes
• Monochrome/colour monitor allows for real life colour or different combinations
• Contrast reversal 0 >50% of px prefer white on black as it reduces scatter in media opacities
• Reading duration much increased but speed the same
• Binocular viewing from a normal distance
• More psychologically acceptable than a magnifier? Just looks like a computer if it's a kid@school
• Good if Parkinsons or something prevents optical aid usage
• Good if px has extensive vfd. Easier to adapt to steady eye strategy with it
• Split screen for simultaneous tasks

Disadvantages

• Expensive & need continuing service & repair
• Persistence of image on phosphor if CRT style screen
• Requires more practice than optical aids (15-20 sessions of daily practice)
• Bulky/obtrusive/difficult to move around - would need one for home and one for work
• Control posns often better for right handed
• Depth of field is limited (probs with thick books)

A head mounted device works in basically the same way. There are also TV readers which attach to the px's TV. The users of EVE aids are usually young & motivated. Px w/ VA>6/90 seem to gain little benefit from their use (mainly for reading, filling in forms, school tasks and viewing photos.

As regards to obtaining the visual aid, optical aids are usually provided by the HES - free to any px on permenant loan. There's no general formal scheme for electronic aids - they are bought privately. A registered VIP doesn't pay the VAT. Local charities or 'electronic aids for the blind' also supply but most are bought privately. They are available to use in libraries.

Tapermag

• Real image magnifier consisting of a bundle of transparent glass optical fibres
• Each fibre is narrow at the end which rests on the text and expands towards the top edge. The magnification is mainly real image magnification with a bit of relative distance magnification (the image is closer to the eye than the reading material)
• Aberration free but has a limited range of magnification (2.1-2.3x mag)
• Expensive compared to plus lens magnifiers.

LV: Visual Field Loss

This is broken down into central/peripheral field loss, with central always being associated with poor acuity.

Peripheral field loss can be caused by glaucoma or retinitis pigmentosa gradually over many years or sometimes cerebrovascular accident which causes homonymous hemianopia which is usually sudden onset due to a stroke or some other acute vascular lesion in the brain. That too can have a gradual onset if due to a tumour. Remember that any patient that has lost peripheral vision has lost rod cells so will have poor night vision.

Functional Effects

• A central field of 10 degrees or less significantly impairs mobility. When looking into the distance px isn't aware of the layout of his surroundings so bumps into things
• w/Intermediate vision it's difficult to get the whole task into view at the same time (TV/Computer) and finding objects on a cluttered desk is difficult
• w/reading px doesn't has trouble seeing ends of lines and starts of new ones

Other effects of hemianopia causing brain lesion

• Hemiplegia - difficult to posn/grip magnifier and/or task
• Loss of higher visual functions - agnosia (eg face recognition), alexia (reading)
• Oculomotor problems - squints, decomp phoria
• Personality/behaviour/attention change (drug induced maybe?)

Field Enhancement For Sighting

Reverse telescopes are used for tunnel vision but NOT hemianopia. They use magnification of less than 1 to fit more information into the available field. Acuity reduces in proportion. There's also something called an amorphic lens with minifies in the horizontal plane only, expanding the field in the area where it will be most useful while also preserving acuity. It is beneficial for scanning, finding things, viewing TV etc. They are fairly rare in the UK but are actually legal for driving in the US.

The px can also use a hand held minus lens which acts as if it's the -ve objective lens of a reverse telescope (the +ve eyepiece is the user's accommodation/bifocal). The higher power the lens, the bigger the field but smaller the acuity. Calculating the magnification uses the same telescopic eq as before M = -Fe/Fo where Fe is the accomm/add giving

M = 1 /(1-dFo)

Optimum lens diam = d x alpha (fov in degrees) / 60

Convex mirrors can be used in kitchen/hallway etc to detect people, open doors etc. Those ones that you see when you're in a different country going round a corner in the metro station. At the tube too actually come to think of it.

Field Enhancement For Mobility

There are various systems. First of all there's a hemianopia mirror which can be fixed or clipped onto existing specs. It projects objects from the missing field into the intact part of the patient's retina. This does create a blind spot where the mirror is blocking the normal view, but that area is seen by the other eye. It's again a convex mirror to expand the field and can be tinted to help distinguish direct and reflected images. Also it can be made semi reflecting so the view isn't totally obscured. Hemianopia mirrors aren't used very often.

A prism system is good for sufferers of RP and px w/bitemporal hemianopia w/<20degrees field and acuity better than 6/30. Stick on fresnel prism on the side of the lens closest to the defect base TOWARDS DEFECT with as much power as poss (15-30dioptres). Looking straight ahead the view is not affected. The problems with this system are the jump at the prism apex, the corresponding prism scotoma, and poor vision through the fresnel prism meaning you have to turn your head fully to critically examine the object. A fair bit of training is required. The prism should be placed in line with the edge of the pupil or limbus or at the edge of the measured field - 1mm on the spec lens is about equal to two degrees of field. You can assess this subjectively by moving a card across the lens until the px just notices it, then getting them to walk around a bit to make sure it isn't noticed.

Normally the prisms are fitted binocularly. Monocular is also possible, with the prism split vertically so the patient views through the centre of it. 30-40diop prism gets 20 degrees of field expansion and the patient never views through the prism so image degredation is not noticed. This requires little/no training and there isn't a prism scotoma. Other methods include full aperture (last resort) and InWave which is a field expanding channel lens. Also if you can't see the whole tv as part of your visual loss you could maybe just move the TV further away.

MANAGEMENT OF CENTRAL FIELD LOSS

Central field loss is a relatively common condition (ARMD, macular holes, CSR, Cystoid Macular Oedema, Toxic Maculopathies) and very disabling. It causes acuity loss impairing reading and face recognition, distortion, photostress, photophobia, depth perception problems, Charles Bonnet Syndrome. If the field loss is unilateral then the patient will usually just tend to ignore the worse eye and may not even realise the condition is present at first. Central field loss is only a problem if bilateral. As the fovea is involved acuity goes way down and images formed away from the fovea make the eye 're-foveate'. If viewing with one eye or suffering BCFL then the patient could be aware of a blank patch covering the object of regard if fixating centrally. Patient may use PRL just off the edge of the scotoma. Level of acuity there can be calculated. The available treatment methods are EV training, prism relocation and surgery.

Px w/central field loss

• Has a variety of magnifiers but can't really tell difference between them. Improvement with magnifier is less than expected and often reaches a plateau
  
• Has equal problems viewing newspaper headlines as small print
• Can read single letters or short words but can't even attempt long ones.

Eccentric Viewing

• This is heavily biased towards reading tasks. EV direction must be identified then practice w/SES commences
• Keep eye still & move text. This is easier than trying to refixate with an eccentric location on the retina. Also a good way of using a magnifier
• Treatment required a lot of follow-up visits/patience and is not often done
• First you have to locate the PRL with a scanning laser ophthalmoscope/video fundus camera, then use amsler grid, central field screeners etc and practice EV for faces, TV, looking at watch
• Lots of practice sessions are required - px uses printed sheets which get progressively more difficult - longer words, smaller letters, more words to a line. Should be done five minutes at a time a couple of times a day, warning px that they will feel very tired and improve slowly but there can be a great improvement over time
• Start with high power magnifier/small print or reading specs and bigger. May need to make magnifier less powerful as patient gets better

EV Training in Glasgow

• Px enters training programme after assessment @ GCU/Gartnavel/RAH
• LVA assessment by optoms with H&S, Refraction, mapping of scotoma, assessment of magnification needs using an Rx or hyperocular lens, assessment of suitability then referral
• Training - initial meeting, 1hr/week for 5 to 8 weeks, 5-10mins daily practice
• Trained using ZoomText, AceReader pro, lighting, typoscopes, hyperoculars, variety of texts
• Technique - use correct magnification, single eye technique, steady eye strategy, PRL, fixate on first letter or word them move text.

Prism Relocation

• Px fixating centrally - target imaged at scotoma. Need to find correct prism power and direction to place image on optimum PRL
• Do this by testing monocularly, using trial lenses for distance Rx and reading add for 20cm (can vary from +4.00 to +7.00 depending on px), putting prism in rotatable part of trial frame and getting px to rotate to find clearest vision on reading chart. If no improvement change prism power. When prism found try +/-0.50 power changes
• Prescribe - EG found N8 RE w/+6.00 & 4D at 90 and N24 LE w/+6.50 and 6D@150 then give +6.00 and 4D @90 both eyes.
• Reports suggest up is most common base direction
• Evidence for this working is scattered and unreliable, one study w/placebos found little difference
• Could argue that prism relocation has no theoretical basis - can't the px just refixate?

Surgical Treatment Options

• Macular Translocation Surgery
• w/wet AMD - detach and rotate retina, rotate globe in opposite direction.
• Still in research phase

Causes of central field loss

• AMD
• Best's Disease
• Stargardt's Disease
• Achromatopsia
• Cone dystrophies

Causes of peripheral field loss

• RP
• Strokes - hemianopia
• Chorioretinitis
• Glaucoma
• Aniridia
• Marfan's
• Ret det
• Leber's Amaurosis
• ON disorders eg optic atrophy
• Optic dysplasia and hypoplasia
  

More Common CL Complications

When there's staining in an area around the periphery of the lens it's likely to be one of two things. It could be lens binding which is more common in extended wear lenses, lenses that are too tight or px working in a dry atmosphere. It could also result from damage to the lens from fingernails/getting trapped in the case.

If there are particles visible underneath the lens it's often tear film debris. This is common in the sort of patient that just plonks their lenses in straight away in the morning. The debris will be visible under the slit lamp and will appear to be squashed down by the lens. If the debris is sleep debris then the patient isn't likely to notice it, but makeup has a more granular structure that will cause the lens to become uncomfortable. Mucin balls can be found under extended wear lenses - this is tear debris rolled into a ball by the movement of the lens.

CLPC

Symptoms include itchiness which worsens on removal of the lens. Also reduced wearing time. CLPC is a type IV delayed hypersensitivity reaction. There is a type I element too - the histamine response causing the itchiness.

CL wear should be discontinued for a good length of time - a guideline used = the efron grade of the CLPC x 2 = the number of months to discontinue wear.. EG grade 2 = discontinue for 4 months, assessing again 2 months in. Lens type should also be changed - dailies so that there are no further problems with denatured proteins. Also the lenses are thinner which minimises the mechanical action on the lids. You should expect improvement of at least 1 grade after a couple of months.

Mast cell stabilisers and anti=histamines can be used in the meantime to reduce symptoms as well as cold compresses. Some optoms actually just fit dailies straight away but if the CLPC is grade 2 or more that ain't going to work.

Flat Fitting RGP

Central abrasion that could ulcerate. Refit with steeper lens. The patient could wear the flat lens while the other lens is on order but

• minimise wearing time/wear specs when poss
• come straight back to practice if red eye/painful/blurry vision

Chronic Hypoxia corn neovasc

• Due to overwear, tight fit, lower H20 content lens
• Response = increase O2 transmission w/ultrathin lens/higher H20 content lens (NB consider whether PX will be able to wear higher water content lens in office with AC)

Steep Fitting RGP - Air Bubble?

• Could result in blinking w/froth + areas of dryness
• Fit flatter

Microcysts/Vacuoles

• Reversed light path = microcyst, unreversed = vacuole.
• Grade by counting numbers

Foreign Body

• Stromal diffusion of flu indicates deep!
• Give chloramphenicol every 2hrs for 12 hrs then 4x/day
• NB you have to take lenses out to put drops in, will px comply?
• See px in 24hrs, improvement? If not up dosage again or refer to hospital
• Check that foreign body isn't still around - slit lamp, under lids
• Need to work out cause, gardening accident? Could be something that could be avoided in the future
  

Glaucoma Care by Optoms in Bristol

This was another really good lecture! There was a HUGE amount of info in it that I can't hope to replicate here. Go back to the actual notes and read read read.

It's probably good to summarise glaucoma again. Hammer it in like. It's a variety of diseases with a common denominator - ACQUIRED PROGRESSIVE OPTIC NEUROPATHY. If it's untreated/unsufficiently treated it will lead to progressive loss of visual function. There are a variety of different causes and so a variety of different types/diagnoses. Let's categorise::::

• Open-Angle without ocular or systemic disorders - POAG, Normal Tension Glaucoma
• Angle closure without known ocular/systemic disorders - pupillary block glaucoma, combined mechanism glaucoma
• Developmental glaucomas - congenital, glaucomas assoc w/oc/systemic anomalies, 2ary glaucomas in childhood
• Glaucomas assoc w/oc/sys disorders - assoc w/disorders of endothelium, iris & cil body (pigmentary), lens, retina/choroid/vitreous, assoc w/intraocular tumours, elevated episcleral venous pressure, inflammation, steroid induced glaucoma, ocular trauma, haemorrhage, following intraoc surgery

Chronic Open Angle Glaucoma - Glau w/out ocular/systemic associations

• Epidemiology - onset from 35yr onwards, prevalence 2% (relatively common)
• Risk Factors - major ones are IOP and age, moderates are race and family history, minor are vasculopathy, vasospasm and lot central corneal thickness
• Subdivs - high pressure type (POAG), normal pressure type (Normal Tension Glau)
• Definition - multifactorial glaucoma w/characteristic progressive atrophy of ON head (not exactly sure of cause)
• Cause(s) - mechanical, vascular, autoimmune?
• Heredity - mostly unknown, few genes identified
• IOP Elevation - variety of angle degenerative changes
• Symptoms - none til advanced
• Signs - Physiological open angle, acquired disc/RNFL signs, VF signs
• Course - usually slowly progressive
• Visual prognosis is good cf age, how bad it is when first detected

Why should optoms take a greater involvement in glaucoma care?

• Causes blindness & visual morbidity
• Has substantial impact on the current NHS HES resources
• Optoms are already part of the pathway doing 95% of the glaucoma related referrals
• They have many of the tools/skills to equip them for an extended role
• The new prescribing legislation for optoms can be applied to glaucoma management
• College Glaucoma Higher Qualifications have been established
• NICE Glaucoma guidance is on the way
• The DoH trials of alternative glaucoma pathways have recently been completed
• International critical mass of glaucoma specialist optometrists

In 2004 'supplementary prescribers' were defined and in 2009 'independent prescribers'. Sup. prescribing extends the role of the prescriber to make better use of their knowledge and skills and is suitable for optometric co-management.

The Upcoming Clinical Challenge

Glaucoma is currently the second most common cause of CVI certifications. It has a better prognosis if treated in the disease's earlier stages. Early glaucoma is hard to identify. It's a chronic condition that requires lifelong review and is dominated by medical treatment. Obviously there is a public health issue as a significant proportion of cases may remain undetected.

The population of the UK is growing and ageing. There is expected to be a 12% growth in numbers and 8% shift towards the higher glaucoma prevalence age bracket (over 65 years). Life expectancy is also increasing (2002 women age 84, 2020 88) which obviously means more people having their glaucoma review. In summary, more people will be requiring more appointments for a longer period. Maths suggests that there'll be an extra 390,000 appts required per year by 2031 and current increases in ophthalmologist training are unlikely to meet this demand.

The Bristol Shared Care Scheme

Included peoples were glaucoma suspects, ocular hypertensives, stable/early/moderate POAG, PXF, Pigmentary Glau, px who can perform vf examinations, VA of 6/18 or better both eyes. People who are excluded - unstable glau, normal tension, 2ary glaus, narrow angle glau, any other existing ocular pathology, advanced VF loss and best corrected VA of 6/18 or less.

There was a study from 1993-1997 which showed that the optom and HES measurements were equally reliable and outcomes were comparable after two years of review. Px were more satisfied with having the check done at the local optom presumably because it was closer/easier to get to. The full cost of the assessments was cheaper if everyone was done at the hospital though. So after this study the scheme wasn't introduced. There was increased involvement of in house optoms within the Bristol eye hospital though

ARMD Referral - Is It Wet Or Dry?

Good guest lectures this week! Man yeah! This one was to refer/not to refer. Wet Vs Dry. There ain't no helping dry at this point. Wet can be helped by that lucentis thing that everyone reads about in the paper and gets all excited about. Lucentis inhibits VEGF-A which plays a critical role in the formation of new vessels which are responsible for the leakages.

Anyhoo, the RPE is critical in AMD. Drusen form in the RPE. Drusen are of course waste products of reactions in the retina that haven't been removed properly. They pile up in bulges. They have nothing to do with leaking blood vessels. In summary DRUSEN TAKE PLACE IN DRY AMD, ARE YELLOWISH, ROUND AND DEEP IN THE RETINA.

Stuff tagged as DRY

• Atrophic
• Drusen
• Geographic (kinda 'islands' of atrophy)
• RPE atrophy, changes

Stuff which is involved w/WET

• Exudative - stuff exudating out of blood vessels
  
• Disciform (round shaped fibrous scarring)
• Neovascular
• Choroidal Neovascular Membrane - network of all sorts of aberrant BV all over the place. More like a net/mesh

Exudates ain't drusen. They are higher up, hard edged and whiter. Another area of confusion is the Chorodial Neovasc Membrane. This membrane can either be

• Occult - hidden beneath the RPE so nothing visible to zap with PDT
• Classic - membrane has broken through the RPE and is visible

These days now lucentis is the main treatment that's replaced the laser so whether the membrane is occult or classic doesn't matter as much.

Various Things - To Refer Or Not

Oedema

• There are lots of causes of swelling at the macula, central serous retinopathy, cystoid macular oedema etc
• It's difficult to distinguish
• Which layer of the retina is raised?
• Try to avoid using oedema as a primary indicator of wet AMD

Amsler Chart - Distortions

• Distortion is a good indicator, but when the px mentions it before the amsler as opposed to when you're testing for it - the amsler is a very sensitive test. Drusen can raise the macula a bit causing a bit of distortion, as do PED and central serous retinop. In fact any macular disease can cause distortion.
• If the px is reading 6/9 N6 or better then they are highly unlikely to have treatable macular disease. No referral in that case, monitor!

Drusen

• Can be soft/hard
• More a risk factor for ARMD

Blood

• Shouldn't be any visible - leakage if there is - aberrant vessels
• Different from the background diabetic spots

Exudate

• Not good - indicates leaking aberrant vessels
• Could be present with or without visible blood
• Exudate is not treated directly, it's just a sign of potentially treatable new vessels

Exudates/Blood, refer!

Smoking & The Eye

The whole lecture centered around the 'brief advice' that us, GPs etc should be giving to smokers. Evidence shows that brief advice given by GPs to all known smokers leads between one and three percent to stop smoking for at least six months. That doesn't sound like a lot but it's above those that would've quit anyway. Anyway doing this brings health gains in the population for a modest spend and will reduce hospital costs long term.

Smoking is still prevalent throughout the uk

• 26%+ in Scotland
• 25% in England
• 23% in Wales
• 26% in NI

It's 37% in the greater Glasgow area and 50% in some of the more deprived areas. There's 277 hospital beds in Glasgow taken up each day with px suffering from smoking related illnesses. Out of 1000 lifelong smokers, 1 will be murdered, 6 will die in road traffic accidents and 500 will die from a smoking related illness. Here ends the stat parade.

Cigarettes contain 4000 chemicals and 60 of them are known carcinogens. Nicotine is the addictive bit, Carbon Monoxide binds to haemoglobin and causes hypoxia/vascular problems and Tar is the thick sticky ming that causes pulmonary problems. Also you have arsenic, cyanide, ammonia, acetone, formaldehyde etc etc etc! Horrible. Cigarettes aren't allowed to be called light or mild these days because they aren't. Cutting down leads to compensation. So although 'cutting down' seems to do nowt it should still be applauded as the px clearly wants to quit and is making an effort.

How Smoking Affects the Eye

• AMD - risk is increased 2-3times. Smoking is the only proven cause of AMD that's actually avoidable. Out of 500k people in the uk with AMD 54000 have it because of smoking. This is the kind of info you need to give to px because apparently only 7% of people are aware of the link. Furthermore the yoof of today are more worried about losing their eyesight than they are getting cancer or some ting! 9/10 people said they would quit at the first sign of a problem with eyesight.
• Cataracts - smoking doubles the risk of nuclear cataract and the risk increases with the amount smoked
• DR - smoking accelerates development or worsens the existing condition
• Thyroid Eye Disease - people who have Graves disease and smoke have 4 times the risk of developing eye problems (puffy lids, bulging eyes, squint, gritty feeling, sometimes swelling behind eyeball pressing on ON and disrupting vision). The risk increases with the amount smoked.
• Optic Neuropathy - caused by reduced blood flow to the eyes. 16x increased risk of developing it w/smoking and developing it at a young age to boot. Like at 51 instead of 64. Not nice
• Smoking can cause a more serious glaucoma with earlier onset due to again the reduced blood flow to the eyes
• Children born to smoking mothers are prone to developing squinting, learning disability, smaller size

Other problems

• Aesthetics - premature ageing, bad breath, smelly, fatter round the middle, crap at sports, yellow fingers
• Stroke, gum disease/tooth loss, Cancer of lips, tongue, throat, larynx, oesophagus, narrowed arteries, heart attacks, coronary heart disease, chronic obstructive pulmonary disease, bronchitis, emphysema, chest infections, asthma, lung cancer, stomach ulcers, stomach cancer, kidney cancer, bladder cancer, pancreatic cancer, wrinkling of skin, osteoporosis, impotence, reduced fertility, testicular cancer, miscarriage, Sudden Infant Death Syndrome, gangrene, peripheral vascular disease.
• Quite a few
• Secondhand smoke also proven carcinogenic in 2002 - ask if anyone in household smokes

Health Effects Again

• Immediately you have eye irritation, headache, dizziness, sore throat, nausea, cough, reduced coronary blood flow
• Increases CHD risk 25-35%
• Increases lung cancer risk 20-30%
• Risk of acute stroke 82%!!!!!

Benefits of Quitting

• Start almost straight away - blood pressure goes back to normal after 20 minutes
• Better wound healing, less likely to have complications during surgery
• Halts progression of existing conditions eg COPD
• Mental/financial benefits
• MED/LONG TERM increases life expectancy if before the onset of serious disease, even if px has serious disease does better job of fighting it

Addiction

• The compulsive physiological and psychological need for a habit-forming substance
• Nicotine's actually more addictive than heroin and cocaine and has higher relapse rates
• It takes 7 seconds to reach the brain. You're looking at about 200 hits per day.
• In high levels nicotine is a potent nerve poison. It stimulates adrenal glands and thus produces adrenalin which increases heart rate, BP & breathing
• It also acts on ACh receptors establishing the 'reward pathway'. There's a rush of ACh and new receptors are developed. Dopamine is release and pleasure/enjoyment results
• Nicotine withdrawal involves urges to smoke, depression, sleep probs, GI upset, headache, restlessness, cravings, increased appetite, poor concentration, irritability & anxiety.

Brief Questioning Tactix

• Open questions to help them explore the issue
• How do you think you'd cope w/out a cigarette for a day? What would help you in that situation? What do you like about smoking? What don't you like?
• Have you ever thought about quitting? Have you tried before, how did that go?

Stuff that works

• Nicotine replacement therapy
• Zyban
• Health professional advice
• Individual counselling
• Behavioural support groups
• Pharmacist
• No smurking day
• Workplace tobacco policy
• Smokeline

Not proven to work

• Brand switching
• Cutting down
• Low tar
• Alternative therapies
• That Alan Carr book

In Glasgow

• Intensive smoking cessation groups citywide as well as one to one brief support at 200+ pharmacies, Breathe (for pregnant women) & Hospital Inpatient Service
• Intensive support is 1hr/week groups, weeks 1&2 info, week 3 =quit and 4-7 group support. Stops 16-20% of people after a year. Difficult cos it's a chronic relapsing condition. The group is relaxed/informal and can actually be fun
• Groups don't suit everyone so the pharmacy does trained 1 to 1 counselling ("Starting Fresh") 5-10 minutes once a week and NRT dispensed regularly for up to 12 weeks
• Groups have shown to be twice as effective as Starting Fresh
• Heavier smokers find it harder to quit. If smoking within one hour of wakening px needs intensive support.
• Breathe project launched in May 2004. 4 weeks support and NRT.
  

Nutrition & The Eye

Nutrition is a risk factor in developmental and age-related eye conditions.

Fish Oil

• Contains the lipid docosahexanoic acid (DHA) which is an essential polyunsaturated fatty acid. It's found in the body as a structural component of membranes (1-4%) and is highly concentrated in nerves and photoreceptors (up to 50%).
• The DHA increases membrane fluidity (there's a constant need to make new membranes) and improves the efficiency of membrane functions including phototransduction & synaptic transmission

Antioxidants

• Reminder - oxidation is loss of electrons. When biological molecules are oxidised first an unstable free radical results and then the electron is lost/bond is broken.
• Free radicals are caused by high energy light and toxins like the ones in pollution, drugs and smoking. The concentration of free radicals in the body is exacerbated by high oxygen levels, poor diet and ageing.
• Lipids in membranes, proteins (both in enzymes and structural) and DNA (protein synth) are susceptible to oxidation. If the free radicals become too numerous you will get cell damage
• Antioxidants neutralise free radicals and limit oxidative damage
• Examples of antioxidants include carotinoids (fruit/veg), Flavinoids (fruit/bilberries/gingko/tea), Vitamin E (seed oils/fruit), Vitamin C (fruit/veg), Zinc & Selenium (meat/fish/nuts/seeds/cereal)
• Important carotinoids include beta carotene found in carrots and apricots, lutein and zeanthin (found in corn, leafy veg & egg yolk) and lycopine from tomatoes/fruits.

Special Protection for the Macula

Special protection for the macula is useful because the macula is of course always being bombarded by light, has a high metabolic rate (it's constantly transmitting info) and the highest concentration of oxygen in the entire body.

Antioxidants in the macular pigment xanthophyll are lutein and zeanthin and you can get em from corn, cabbage, kale, egg yolk as well as some other fruits and vegetables. Obviously nutrition alone ain't goin' to save ya - MD is multifactorial - genetic risk, race/pigment, vascular health, oxidative damage.

Four age related studies (see P102 shared care book) showed that high doses of an antioxidant zinc substance reduced progress of nuclear cataract and decreased progression of ARMD in those with intermediate or high risk ie those with large drusen and pigment abnormalities.

Nutritional Advice to Px re: eye disease

• Eat fruit and veg (corn, carrots, spinach)
• Routine supplements aren't justified if your diet is pretty good already
• Supplements may benefit those at high risk. If you aren't then they aren't going to do any harm but don't think subbing them for stopping smoking works
• Other factors like smoking and vascular health may have a greater impact
• Bear in mind that you aren't a nutritionist - if the px is thinking of taking a load of supplements best to refer them to one
• Good articles here

Developing Visual System

• The foetus/neonate needs a lot of DHA for photoreceptors and synaptic membranes and Vit A for photopigments. These are provided by the mother.
• Preterm infants are especially vulnerable due to low fat levels / limited nutrient stores and receving little or no breast milk
• Fish? WHO now says 3 servings of oily fish are good every week especially if you're pregnant. Pregnant women transfer the DHA to the baby and can leave their own supply depleted. So if the woman takes supplements then they have a good amount of DHA for both them and the baby. The baby takes only as much as it needs so the supplements don't make much difference to them
  

Gonioscopy

To view the angle. It's Greek. Specifically it's to view the iridocorneal angle. The primary use of gonioscopy is in glaucoma. There are a few other uses that i'll cover later. Barkan defined the different types of glaucoma with the help of gonioscopy as well as being the first to notice that the superior angle was narrower than the inferior angle. He classified glaucoma into closed and open angle. You can't view the angle with slit lamp alone. The originator of this whole thing was Maximillian Salzmann in 1915. He realised that total internal reflection obscured the anterior angle. He used a Fick type contact lens with radius smaller than that of the cornea. Then in 1919 with the development of the slit lamp a magnified view of the cornea could be obtained and with it a magnified view of the angle. In 1938 after a few less exciting developments that I can't be bothered to cover Goldmann introduced the first indirect gonioscopy mirror lens.

When I say an 'indirect' lens that means a truncated prism which has a surface that basically fits the cornea. Light from the anterior angle comes out, hits a mirror and is reflected into your own human eye via the slit lamp. The difficulty involved in viewing the angle is due to the critical angle of reflection at the cornea/air interface. The lens replaces the eye/air interface and the critical angle is eliminated by the steeply curved outer surface of the lens. Direct gonioscopy (using eg the Koeppe lens) produces an image round to the side of the lens which is much less easy to observe.

Direct Gonioscopy - Koeppe Lens

The Koeppe lens resembles a very thick high plus lens. It only has x1.5 magnification so has to be used in conjunction with another magnifying device like a hand slit lamp. The image produced is erect and virtual

Advantages - panoramic binocular view, good view of narrow angles, transillumination, can be used on bedridden patients, wide fov for teaching purposes

Disadvantages - time consuming, requires large working area as px really needs to be supine. You would have to walk all the way around the patient in order to see the full 360 degree view the lens provides. You might even need an assistant. It needs separate mag and illum, mag is low and it's not great for fine detailed view (eg you aren't going to see schwalbe's line)

Indirect Gonioscopy

Advantages - focal illumination allows the location of schwalbe's line. If you can't see schwalbe's line then you have a very narrow angle. The view is magnified and is excellent for picking out fine detail. It's technically simple to use and useful for lazer treatment.

Disadvantages - stereopsis is difficult, requires coupling fluid which can be a bit messy, observation is reversed and fov is small. An anaesthetic (eg proxymetacaine) is used.

Grading System

There have been many over the years and to analyse them all now would cause me great confusion. So we're going to go with the classic one - Schaffer.

• Grade 4 = wide open = 40 degrees
• Grade 3 = open = 30 degrees
• Grade 2 = just about showing trab meshwork = possible closure = 20 degrees
• Grade 1 = 10 degrees = eventual closure
• Grade S = <10>
• Grade 0 = closed angle

The Schaffer grades correlate well with Van Herick's slit lamp grades for anterior depth. When doing gonioscopy there is a 'goniogram' which is a generic sheet on which you can mark the appearance and grades along with what's visible. This is great to reduce confusion between optom and ophthal or whoever.

Structures

From Cornea

• Schwalbe's Line
• Non Pigmented Trab Meshwork
• Pigmented Trab Meshwork
• Scleral Spur
• Ciliary Body
• Iris Root/Insertion

Optometric Management of Cataract Px

Prevalence

• Increases with age. Approaches 100% if lens opacities are included
• Patient defines whether it's visually significant

Risk Factors

• Exposure to UV light
• Smoking
• Heavy drinking
• Family/Genetic
• Race (higher in indian population)

Vision in Cataract

• Decreased light transmission of short wavelength light esp if the cataract is nuclear
• Refractive change - myopic shift, cyl changes
• Light scatter - glare, decreased contrast sensitivity, decreased VA

Management Pathway

• Px attends optom, cataract diagnosed and discussed, risks and benefits of surgery discussed. Px wishes to proceed and info given. Px offered choice of hospital and appointment agreed
• Px attends HES outpatient appointment w/ophthalmologist, pre-assessment w/nurse, date for surgery arranged/agreed. Details of current medication received from the optom/GP/Px
• Patient attends HES and day case surgery undertaken
• Patient attends HES or optom for final check, sight test. Px discharged or 2nd eye discussed and appt arranged
  

Optometric Management of Low Vision Px

Current Management

• Optoms are trained and qualified & NHS pays (usually in hospitals only)
• Low Vision shared care pays for community based Low Vision

Proposed Pathway

• START: Px referred to LV service from secondary care, GP, social worker, rehab officer, community nurse, occupational therapist, self referral. Px may have RVI, LVI, CVI. All px contacted by LVS within 10 days
• Px attends LVS - service seamless across health, social care and voluntary sector. Full sight test forms part of assessment. Px given info on eye condition, entitlements etc as well as local services. Counselling and advice on employment/education available. LVAs, advice and home adaptation discussed and made available. Referral to other areas of health and social care as needed. This includes certification.
• Px has followup visits as needed that may take place in home or elsewhere
  

Optometric Management of ARMD

Prevalence

• 350,000-500,000 in the uk 'blind' from ARMD
• Most of the impairment is due to wet ARMD
• Most of that is untreatable

Incidence

• 21,000 new cases every year
• 10% added risk/year to fellow eye

Non modifiable Risk Factors

• Age
• Genetic predisp
• Gender (females 2xrisk)
• Race
• Iris colour (light pig)
• Type I diabetes
• Rx
• Cataract (can vary w/UV exposure)
• Handgrip strength ('weak' px)
• OD appearance
• Size @ birth

Modifiable Risk Factors

• Smoking
• Drink
• Socioeconomic factors
• Nutrition
• Body Mass Index
• Dietary Fat Intake
• CV disease
• Hypertension
• No statin usage (if you have cholesterol more likely to get it)
• Aspirin
• Type II diabetes
• Sunlight exposure
• Birth of child (px weaked if had 5 or 6 kids)

Optometric Assessment of the ARMD Px

• History - co-morbidity; hypertension, diabetes, hyper cholesterol, smoking, excessive alcohol
• Acuity - If poss use logMAR - more immediate steps so can spot disease early
• Contrast sensitivity
• Amsler - History of metamorphopsia, give copy to put on fridge
• Refraction
• Dilated assessment w/Volk lens
• Decisions - if WET refer. Will see vasc changes, exudate, haem, oedema, neovasc
• Decisions - if DRY monitor especially if they have large confluent drusen

Medical Management of the ARMD Px

• Flu Ang exam to clarify/make diag of wet/dry
• Treat: Laser Photocoagulation - leakage away from the fovea
• Treat: Anti VEGF treatment - intraocular injection which blocks neovasc and causes shrinkage of existing vessels
• Macular translocation - surgery for ppl w/huge scars
• Future: retinal implants. Currently only for ppl who are totally blind
  

Diabetic Retinopathy

Background

• Microaneurysms
• Retinal haemorrhages +/- any exudate

Pre-Prolif

• Venous Beading
• Venous looping
• IRMA
• Multiple deep round haemorrhages
• Cotton Wool Spots

Prolif

• NVD
• NV Elsewhere
• Pre-retinal/vit haem
• Pre-retinal fibrosis/tractional ret det

Photocoagulation

• Focal/grid macular
• Peripheral scatter
• Pain
• No driving that day
• Loss of visual field

Maculopathy

• Exudate within a disc area centred on fovea
• Circinate/group of exudates within macula
• Retinal thickening within a DA centred on fovea (seen on stereo photo)
• Microaneurysm/haem within a DA centred on fovea if assoc with best VA of 6/12
  

Optometric Management of DR

History

• before insulin DR wasn't recognised and insulin dependent diabetics died early. Type II were diet controlled
• 1950s-1970s diabetes becomes a controlled disease and DR was recognised. Hypoxia was recognised as the trigger for the neovascular process
• Laser treatment - pan retinal photocoagulation - focal treatment to stop specific leaks
• Newest development c.2000 - intensive diabetic control via continuous control, slow release insulin, insulin pumps

There were two big trials

1. Diabetes control and complications trial - type I diabetes (insulin cells destroyed)
   
2. UK prospective diabetes study - type II diabetes (high blood glu, relative insulin def)

Glucose tests for diabetes

• Fasting blood sugar = >7.8mmol/litre
• Random blood sugar = >11.1mmol/litre
• Two hour post load = >11.1mmol/litre = you're diabetic
• Two hour post load = >7.8mmol/litre = you have impaired glucose tolerance

Glycosylated Haemoglobin = Glu bound to haemoglobin. Measuring it is good because it correlates w/blood sugar average over 6-8 weeks:

• Normal <6% (corr w/ 7.6mmol/l)
  
• Controlled diabetic = 9% (corr w/10mmol/l)
  
• Intensive control = <7%>

If you're intensively controlled then there's only a 7% chance of you developing DR after nine years and if you're 9% controlled then it's around 20%. So intense control is way beneficial.

Initial Adverse Effects - sudden intensive control leads to increased DR in 6/9 months. Phase it in!

Factors which aggravate DR

• smoking
  
• hypertension
• hyperlipidaemia
• obesity
• renal disease
• pregnancy
• puberty

The challenge currently is to get 100% of diabetics an annual eye exam w/high level of accuracy (or every 6 mths for the high risk people) Strategies for screening include

• GP w/ophthalmoscope - good recruitment but poorest accuracy
• Special screenings + photo
• Optom - good accuracy but poorest recruitment. Optom has skill, equipment, accuracy and knowledge

Scottish National Screening Program

• Want to detect referable sight threatening retinopathy to reduce the risk of sight loss
• To detect lesser degrees of DR

This was launched April 2002. Target px were everyone >12yrs old, both type I and II, excluding everyone that already has ophth. care, the irreversibly blind and the medically untreatable. Working out national register of all diabetics, system of appts/feedback/followup. The whole thing is audited and coordinated

Screening process

1. Digital camera - 80% can have non-dilated. Pic stored for analysis
2. Digital photo w/mydriatics
3. Volk

Photos are then graded by technicians or optoms

The importance of screening must be stressed to ppl. Remember tell em not to drive after mydriasis/light sensitivity

Results

• Retinopathy yes/no?
• Follow-up (screen or referral)
• GP and ophthalmologist informed

Flu Angiography #2: Abnormalities

Abnormalities can either involve hypofluorescence or hyperfluorescence. Defects are sub-classified according to

• type of defect (leakage, blockage etc)
• Location (retina, choroid, optic nerve)
• depth
• whether in inner retina (sharp focus) or outer retina/choroid (blurred cos you're looking through retina)

Also timing of defect. Autoflu before injection can occur if there are drusen. Drusen fluoresce a bit even without NaF. Sclera and gliomas can too. Then you have early arterial filling defects, later arterio-venous leaks and late phase abnormal staining and leaks (lack of staining indicates non-perfusion).

HYPOFLU - FILLING DEFECTS

• Indicate not enough circ. Occlusion or insufficiency of artery/vein
• @Retina - central or branch occlusion of art/vein OR hypoflu showing optic nerve atrophy
• @ON - normally there's a bright flush @ arterial phase and venous phase & late staining. In cases of ON atrophy you get hypoflu and only late staining present. This could happen in glaucoma
• Choroidal

HYPOFLU - BLOCKED TRANSMISSION

• Retinal vessels not visible eg pre-retinal haemorrhage - blockage in media or anterior retina
• Choroidal vessels not visible indicates deep retinal/subret haemorrhage

HYPERFLU - ABNORMAL VESSELS

• Dilated and or tortuous, wide & bright
• Neovascular vessels - wide, leaky, high density
• Tumour Vessels
• Aneurysms/leaks

HYPERFLU - LEAKS

• Microaneurysms - initially contained, then hazy leaks. EG Background DR
• Inflammation causing leakage like ischaemic optic neuropathy
• Choroidal Pooling - breaks in the RPE and NaF pooling in subret space eg central serous retinop.

HYPERFLU - PRE-INJECTION FLU

• Autoflu - drusen
• Pseudoflu - not really fluorescing, just bright reflective surfaces - hard exudates, coloboma

HYPERFLU - TRANSMITTED FLU

• lack of pigment, retinal atrophy
• choroidal background brighter 'window defect'
  

Flu Angiography #1

Assessment of retinal circulation is important in oc. disease. Loss of circ is the main cause of visual loss in the western world - diabetic retinopathy, ARMD etc. The flu angio reveals vascular dysfunction that you can't see and make the extent/severity more visible

NaF is non-toxic and maintains good flu. in biological tissues. 60% of it binds to protein in blood and 40% is in solution. The flu absorbs short wavel. light (blue) and emits longer (yellow/green)

Retinal flu

• Central Retinal Vessels - tight junctions in the epithelium, no NaF leaves the vessels normally
• Choriocapillaris - fenestrated epithelium. The NaF in solution passes straight out into the extracellular space and the NaF that's bound to the proteins will stay inside the capillaries
• Ciliary Body - Unbound NaF can leave vessels, join the aq. and colour the anterior chamber
• Optic Nerve - served by central retinal circulation (no leakage) but leakage in the choroid nearby will stain glial tissue and this is late staining which occurs after a few circulations of flu through the bloodstream
• Sclera - collagen is stained by flu from the choroid

Methods of Angiography

• Injection - IV, rapid concentrated inj. Arm --> Heart --> Lungs --> L Heart --> Arteries --> CRA (takes 7 secs to get there)
• Observation w/fundus camera fitted with cobalt blue filter
• Risks/side fx - staining of skin and urine, 5-10% of px nausea and vomiting, rarely serious allergic reaction

Normal Flu Angiogram

• Arterial Phase - 7-9 secs after injection. This is the arm --> retina circulation time. The stained blood appears to be flowing up the middle of the arteries ("lamellar flow"). The choroid fills in a patchy way giving background flu.
• Venous Phase - 10-12secs --> 15secs. Arteries contain NaF, the capillaries are filled and the veins also begin to flow. The flu flows along the sides of the veins. Bright background from the choroid, bright filled arteries, veins w/lamellar filling, maximal brightness @ 14-18secs
• Late Phase - diffuse NaF in the blood, veins and arteries equal in brightness, background will be diffusely stained, staining of the optic nerve and sclera. This is 4-5 minutes after injection.
  

Glaucoma Mega Brief Version

Progressive optic neuropathy associated with elevated IOP. Has characteristic field defects - nasal step, arc scotoma etc. Lowering IOP is protective even in normal tension glau.

Fluid in the eye is produced and drained away at a certain rate. Glaucoma doesn't involve a problem with increased production, it's a drainage issue. You can help by lowering the production though. Normal IOP is considered to be 21 or less. Ocular hypertension is when pressure is higher than normal but the px doesn't have glaucoma. There's a diurnal fluctuation - usually higher in the AM.

Goldmann/Perkins is used if optom is unsure whether to refer or not. History can give clues - hyperopes are more prone to closed angle glaucoma whereas myopes are more prone to open angle. If the patient has had refractive surgery then the change in rigidity/flatness of the cornea could lead to underestimation of the pressure. Also side effects of asthma treatment could increase chance of glau.

Damage may progress as follows - if some nerves are damaged then the surrounding nerves can follow. It's thought that using some drugs the surrounding nerves can be spared. Research into this is in progress the noo.

The optic disc is imaged mostly with the direct ophthalmoscope but indirect biomicroscopy is becoming more widespread in practice. Also fundus photography, stereo imaging and computerised topography. Disc assessment concerns the cup and disc size. The disc should follow the ISNT rule, if it doesn't then suspect glaucoma. The NRR should be thickest at the inferior, then superior, then nasal, then temporal. Also look for focal loss of ON fibre tissue and disc haemorrhages.

Assessment of the anterior chamber angle can be with Van H's on the slit lamp, ultrasound, Gonioscopy - shaffer grades.

There are various types of glaucoma - open and closed/narrow angle, chronic and acute, primary and secondary, congenital, juvenile and adult.

With pseudoexfoliative glaucoma small flecks of white material are noticed in the pupil (on the edge of the lens). They are very easily seen if the pupil is dilated. Other types include pigmentary, uveitic, steroid induced and rubeotic.

Angle Closure glaucoma assessment. As I typed before closure is more likely in a hypermetropic patient. Ask if any headaches/intermittent blurred vision, haloes around lights (corneal oedema), whether taking anti-deps, drugs for asthma etc. If px has IOP of 60 or something could do gonioscopy, instil pilo, acetazolamide, peripheral iridotomy, surgery (trabeculectomy/lens extraction)

Angle closure typically involves small eyes, a mid-dilated fixed pupil, iris atrophy, ON cupping/field loss

Normal Tension Glaucoma - 10-30% of glaucomas are actually normal IOP. This is mostly older PX. If you can lower pressure more still by using medication or surgery then you can slow down progression.

Pilocarpine causes constriction of ciliary muscle fibres, opens trabecular meshwork, increases outflow, causes miosis, headache and low vision in dim light, also contributes to myopia, cataract and accommodative spasm. Instilled 4x/day

Adrenergic type drugs like epinephrine increase aqueous drainage. They can cause adrenochrome deposits (black granules in conj), mydriasis (angle closure glau), rebound hyperaemia and allergic reaction

Alpha-2 agonists like apraclonidine are not often used. They decrease production and increase drainage but cause dry mouth, allergy, headache and fatigue.

Beta Blockers - beta receps in eye moderate aq production so blockers decrease secretion. They become less effective over time and can cause bronchospasm which in asthma px could actually cause respiratory failure and even death if given enough drops. Preps inculde timolol, betaxolol

Prostaglandins increase outflow via trabecular and uveoscleral routes. eg latanoprost. 50% of px are on this. Can cause increased iris pigmentation, thicker eyelashes and hyperaemia. It's expensive too.

Carbonic Anhydrase Inhibitors like acetazolamide are used in the short term for px w/uveitis. Side effects include nausea, lethargy, metallic taste, kidney stones, all. reaction. Combos of the above are also used.

Surgery could involve iridotomy, iridectomy, laser trabeculoplasty. Probs include plain old failure of it to work, accelerated cataract, endophthalmitis

Shared Care: Optometric Management of Glaucoma

The glaucoma prevalence for europeans - one percent of ages 40-60, 2% of over 60s and >3% of those over 80. The risk factors are as follows

• Age, gender (F), race (african/afro-carribean)
• IOP, ON Head, Myopia/Hypermetropia
• Diabetes, systemic hypertension
• Family History (FH)
• Smoking, alcohol, socio-economic factors

If IOP is less than 15 glau is very unlikely. Anything between 15 and 25 is low tension. 25 upwards the risk of POAG goes up from 10% to about 35%

People with high diurnal variation are more likely to have glaucoma also. A glaucoma patient also has poor VA in mid range contrast sensitivity. You wouldn't normally spot this as most optoms just use a normal snellen w/high contrast. You could spot it w/a pelli robson though. Blue/Yellow fields are more sensitive when spotting the early visual loss.

There is ganglion cell damage in glaucoma. There are two theories behind this

1. Magno vulnerability where selective loss of magno cells (concerned w/good flicker/motion perception and more sensitive to low contrast stuff
2. Redundancy whereby magno and parvo cells are lost at the same rate but the larger number of parvo cells means the effect is less pronounced at high contrast

Glaucoma Management Pathway

1. Patient attends optom, has sight test. IOP = >21 w/applanation tonometry and/or vfd and/or suspicious discs. This results in the patient/optom making an appointment with an optom with a specialist interest in glaucoma or an OMP
2. Px attends that person and a full assessment is carried out according to protocol. A decision is taken whether the patient has ocular hypertension (OSI/OMP reviews) or can be discharged (return to optom) OR has glaucoma (treat or refer to HES). The px is advised and given further info
3. OSI/OMP relays data to HES and the HES reviews the data, advises regarding management and sets up review at HES if needed
4. OSI/OMP manages px in community setting w/regular reviews set in place. OSI/OMP relay data to the hospital if there's significant progression for HES review if req

Each different shared care scheme has its own recruitment, testing and re-referral criteria. Varies. eg Bristol - people who are included have stable POAG, pigmentary or pseudoexfoliative glaucoma but other glaucomas (ie stuff that needs surgery) is going to be excluded.

Referrals in Optometry

The quality of yr referral letters is a major determinant of your REP as well as being crucial for effective px care and to your reputation in the community.

As well as the referral letter other stuff that comes under referral includes verbal and written communications with the patient and other health care profs allowing transfer of care based on your examination. The referral letters need to be complete, accurate and useful (clear concise and understood)

Info for the Px (verbal or written - both if poss)

• Reason for referral - diag, risk - "the pressure in your eye is a bit high so you might have glaucoma". Use technical term and description
• Expected Management - when, who, what
• Appropriate time course - when expected/followup, what to do if followup is missed

Info for the professional

• Who is the patient - complete identification and contact deets - phone no. important if it's urgent
• Reason for ref - heading Re: , the key points, complete and concise relevant supporting info. brief history and test results if relevant. GOS18
• Identify Yourself - Name, posn, tel no, supervisor if pre-reg, stamp (esp if locum)
• What you expect/plan to do - recall/monitor/await discharge from hopital
• Authorisation - was verbal, signature best

Types of ref. out

• direct referral / shared care scheme
• ref to consultant via GP
• ref to optoms who specialize (keratoconus)

Ref Stats - How Well We Are Doin'

• 2.5% optoms no name on letter, 6% no postcode
• eg glaucoma - 85% give disc app, iop, field plot. which is good
• 80% good on the routine info - VA, refraction, symptoms, poor info on previous VA, fundus info, media, onset and duration of symptoms
• 57% no legible name, no practice address 7%

Types of referral "in"

• Individual professionals - optoms, GPs, Other health care providers - health visiting nurses, physios, occupational therapists
• Screening programs - schools, special needs
• Informal - patient referrals (cos of your good rep - build the good rep and acknowledge this stuff!)
  

Formal Co-Management Schemes

Currently in the uk there are around

• >65 diabetic schemes
• >35 cataract
• >20 glaucoma/ocular hypertension
• 13 low vision
• 10 referral/prioritisation

There are also some broad schemes like the one on the south side of Glasgow.

The Crown Report of 1999 recommended optoms as independent prescribers. The govt decided that supplemental prescriber status would come first. The New Prescribing Advisory Commitees drafted the legislation for that stuff in 2000, including a drug list, specific training and associated ongoing CET.

The New(est) Optom Legislation

• In 2005 the prescribage became no longer confined to 'in an emergency'. Also the drug list was updated
• Section 60 Order: student registration is now required, new registration for misconduct, new requirement for malpractice insurance, CL supplies regulated, optometric specialities defined, CET requirement
• Supplementary Prescriber - this involves a voluntary association with an independent prescriber (w/medical qual) managing cases according to set management plans
• Independent Prescriber - establishes diagnosis, directs clinical management and is responsible for prescribing

The NHS goals for co-management are as follows:

• Shorter waiting lists, greater px accessibility and more efficient use of the hospital eye services and the consultants

The benefits to optometry are thisssss

• Px continuity and advancement of the profession mainly - more variety, interest
• Increased REP
• Income to a certain (small) extent
  

Co Management / Shared Care Intro

Optoms should have an in-depth knowledge of diseases that are the focus of current co-management schemes, the necessary skills required for the schemes and understanding of their current state in UK optometry

There was a change in how shared care related to optometrists in the year 2000. Before then it only involved the optician spotting an injury/disease of the eye and referring the person to a medical practitioner. In 2000 the GOC put forward the following:

If in the pro. judgement of a registered optician there is no justification to refer a person consulting him to a registered medical practitioner the registered optician may at his discretion decide not to refer that person but in that event:

• He shall record a sufficient description of the injury or disease in his records
• his reason for not referring
• details of advice tendered
• if appropriate and with the consent of the px inform the GP

Legal posn - The NHS (General ophthalmic services amended 1986)

Optom having accepted persuant to the regs an application for the testing of sight make such examination of the patient's eyes as may be required and in doing so exercise proper care and attention. Where a contractor is of the opinion that a patient whose sight he has tested

• Shows on examination signs of injury or disease in an eye or in its immediate vicinity or any other abnormality of the eye or the rest of the visual system which may require medical treatment
• If px not likely to attain a satisfactory standard of vision notwithstanding the application of corrective lenses he shall so inform the px's doctor

Optoms have always been involved in px management, they are actually often the initial point of contact for a patient in the community. There are four levels of management which the optom is involved in

1. Detection with non-specific referral of the abnormality. This is like basic entry level!
2. Detection with informed referral for advice/management - this is where you're indicating diag/diff diag with maybe some signs and symptoms, level of urgency, suggest what will be done/who will do it. Ideally this is what you're aiming for. Doing (1) is just weak mang. Acceptable, but weak.
3. Detection w/a directed management plan in which you (a) advise the GP of the status of an ocular condition that you plan to monitor - diagnosis/plan or (b) advise the GP of an ocular condition and provide prioritized referral advice - w/diagnosis/plan, referral pathway and urgency and a note of where you participate in the scheme (maybe later on - like post cataract check)
4. Formal Shared Care Scheme - this is set up thru the health board/NHS and involves specific training, criteria for px inclusion, examination requirements and criteria for referral and monitoring. This can include delegation of medical management to the optometrist
   

LV: Types of Telescope

Basic types

• Hand held
• Clip on
• Spectacle mounted
• Monocular versus binoc
• Focus/Afocal

Specials

• Autofocus
• CL telescope
• IOL lens scopes
• BTLT - Behind the lens telescopes. These offer cosmetic adv but great care must be taken obvs. Increased risk of eye injury if the patient bumps into something while wearing them. Also v expensive
• Bioptic - for px who fulfil certain requirements driving with bioptics is legal in some US states, not here. Px can resolve fine detail like road signs

Contact Lens Telescopes

• These use a galilean system where the obj lens is a high plus spec lens and the eyepiece is a high powered -ve CL. The vertex dist of specs is equal to the sum of the focal lengths (length of the telescope)
• The FOV is better than with a conventional telescope cos the exit pupil is really close to the eye but it also depends on the objective diameter (use a blended aspheric to avoid a ring scotoma)
• Has many practical and cosmetic disadvantages though so is rarely used.
• EG a +20DS spec lens and a -40DS contact lens. Px is emmetropic.

The fitting of

• check that normal scope improves VA as expected
• Check nystagmat for oscillopsia
• Fit CL, maximise vd of trial frame, perform over-refraction
• CL must be stable
• Vergence amplification means separate reading specs are required
• Account for uncorrected ametropia - +10D hypermetrope with -30CL effective eyepiece is -40 and -10 myope with -30 CL effective eyepiece is -20.

Advantages of

• In theory px could drive under uk law if visual requirements were met
• Can get acuity much better than expected in congenital nystagmus
• IOL could be used instead of CL giving a longer vd so better magnification but IOL can't be changed if acuity worsens

Disadvantages of

• Low magnification so only works for moderate acuity loss
• Patient has to be adapted to CL wear & it's difficult to insert contact lenses
• Need to wear the system regularly for long periods
• Adaptation to spatial distortion required
• Poor cosmesis with high vd and big fat plus lenses
  

Telescopes: Depth of Field

If you do calculations it appears that plus lenses and telescopes have the same depth of field, but px feel it to be less in telescopes. This could be because the dept of focus for the telescope represents a smaller portion of the working space. Anyway here are some more lovely calculations

Ok, the px has 0.5D depth of focus. What change in incident vergence or object distance could the px tolerate:

a. With a plus lens mag of 10D

f = 10cm if obj at focal point

let emergent vergence = +0.5D
L' = L+F = 0.5-10 = -9.5cm

let emergence vergence = -0.5D
L' = L+F = -0.5-10 = -10.5cm

So overall there's a 1cm range

b. With a 2.5x scope with a +4.00

Emergent vergence Ltel = L'tel/M2 = +/-0.5/2.52 = +/- 0.08m

The incident vergence at the reading cap is of course -4D to match up with it so

delta l = (1 / -4D+0.08D) - (1 / -4D + 0.08D) = (1 / -3.92) - (1 / -4.08) = 1cm

NB Aberrations may also have an effect on the depth of field.

NB2 Changing the obj posn can alter the vergence of light entering the eye. This could create a refractive correction for spherical ametropia

• Move obj closer to magnifier: light divergent leaving magnifier so uncorrected myopes need to hold material closer
• V.V. ie uncorrected hyperopes need to hold material further away
• The effect is similar for both plus lenses and telescopes but because of vergence amplification the effects will be much more severe for telescopes
  

LV: Compensating Telescopes for Ametropia

Again there are three methods for this

1. Full correction for refractive error behind eyepiece

This is the simplest method in which the telescope is clipped onto or held over the spec correction. You could also fit a correcting lens into a holder behind the eyepiece if required. This method doesn't have any effect on the magnification of the system because the telescope is still afocal (unmodified).

2. Partial correction for Rx over objective lens

This achieves some divergence or convergence of light entering the telescope which is then amplified by the telescope to give the correct amount. This is complex to work out and rarely attempted.

3. HERE WE GO MORE F'IN CALCULATIONS: Changing the separation of Fe and Fo

• Shorten the scope to correct myopia and lengthen for hypermetropia - how much depends on Rx
• Changing the length has an effect on magnification

Astro Example

Work out the magnification and length of a 3x astro (Fe +60, Fo +20) used by a -10.00 myope with the correction behind the eyepiece. NB With a myope you want divergent light coming out of the eyepiece which can then bend into the patient's eye thru the specs

a. The magnification is as for an emmetropic user as the telescope is afocal so = -Fe/Fo = -3x
b. t = fo' + fe' = 50mm + 16.7mm = 66.7mm

Ok that was easy, but what about if the guy was uncorrected and the telescope was focussed to compensate?

t = fo' + fe' = 1/20 + 1/60-(-10) = 64mm

it's like a part of the Fe power has been borrowed to correct the ametropia leaving it as +70D
So to correct for myopia you need to decrease the sep between the lenses w/Astro
And to correct for hyperopia you need to increase the sep between the lenses w/Astro
the Fe in that case will go down to +50D and the length will increase to 70mm.

Galilean Example

3x Fe = -60, Fo = +20 fixed for -10 myope

t = fe' + fo' = 1/20 + 1/(-60+10) = 0.05 - 0.02 = 0.03m = 30mm
Mtel = Fe / Fo = 50/20 = -2.5x

Conclusion

Myopia

• Higher mag with focussing astro
  
• Increase length of astro telescope to correct
• Higher mag with correction behind eyepiece for Galilean
• Decrease length of Gal to correct

Hypermetropia

• Higher mag with corr.behind eyepiece with astro
• Decrease length of astro to correct
• Higher mag with focussing Gal
• Increase length of Gal to correct

These egs used large ametropias so effect less pronounced usually. Any big cyls >2.00 will have to be corrected behind the eyepiece. Removing spec correction = shorter v.d. and wider field of view but if the scope is going to be used for spotting then it may not be practical to remove specs. Telescopes are mainly used for near vision due to the increase in working space which is usually needed for manipulative tasks like writing or sewing or some ting. The problem is the fov is far smaller so this counteracts that whole thing a bit.