Sunday 26 April 2009

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

Thursday 16 April 2009

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

Sunday 5 April 2009

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

Saturday 4 April 2009

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!