By Dr Robert Bourke MBBS, FRANZCO
There is a simple…
Answer from Dr Simon Chen, retinal specialist, MBBS, BSc, FRCOphth,…
By Dr André Horak MBChB, MMed, FRCSEd, FRANZCO
By Dr Devinder Chauhan MBBS, FRCOphth, MD, FRANZCO
Dr Frank Howes: Any patient with a corneal ectatic disorder is suitable for CXL, although the strong indications for CXL become less as patients age because the cornea crosslinks naturally with the ageing process, this is indeed the very reason why keratoconic progression slows with time. Results from CXL can therefore be variable and occasionally more than one episode of CXL may be necessary to stabilise the ectasia, particularly in the younger age group or in the post laser group.
CXL can be done in different ways, with different forms of riboflavin constituent and with different intensities of ultraviolet light exposure. The different modalities of treatment can have different durations of treatment and variable levels of postoperative discomfort. The patients’ surgeon will determine what treatment is most suitable for each individual patient or cornea.
CXL is also proving to be useful, not only for corneal ectatic disease, but also for corneal infections that are not responsive to antibiotics or where identification of the offending organism proves difficult. Under certain rare circumstances some patients with oedematous corneas and secondary epithelial disease from endothelial malfunction may benefit from CXL. The cross linking process is the same irrespective of the condition with current knowledge.
Dr Colin Chan: There is no age limit for crosslinking. I find that parents are usually more concerned about the potential side effects of crosslinking the younger their child is. However, keratoconus deteriorates more rapidly the younger a patient is and he/she is more likely to end up needing a corneal transplant. Therefore crosslinking to prevent further deterioration is actually more justifiable the younger a patient is.
At Vision Eye Institute, we have been performing crosslinking on patients younger than 18 since 2006. To date, we have not seen any unexpected long-term complications in this group. A large study by the Siena group in Italy demonstrated good safety and efficacy in children over 3 years of follow up.
There is no upper age limit either, but the natural history of keratoconus means that the condition usually stabilizes in the late 20s or early 30s. Therefore it is uncommon to need to do crosslinking in patients above the age of the 30. One reason for this may be that as the cornea ages, crosslinking occurs naturally.
Dr Frank Howes: Early, in any patient with high astigmatic correction, particularly if they are young (10 – 25years) with progressively increasing cyl, with a scissors retinoscopy reflex, or with reduced best corrected acuity, especially if there is a family history of keratoconus. CXL can stabilise progressive corneal ectatic change minimising loss of BCVA and the chances of needing corneal grafting at a young age, always worth avoiding if possible. If keratometry or corneal topography is available in the referring practice, then any K value over 49D or topography pattern suspicious of keratoconus should be referred in, in this age group. Older than this, patients with normal BCVA, even with the above mentioned signs, may be observed, until progressive changes are noted in refraction, keratometry or topography. Referral in this age group with the above mentioned changes is particularly important in those patients who have had corneal excimer laser refractive surgery or radial keratotomy. CXL is capable of stemming change and in some instances, capable of improving the topography, the keratometry and the astigmatism and vision. There are also other procedures, beyond CXL, which may improve these factors, particularly the vision. This is of course what the patients are after, so referral is worthwhile.
Professor Gerard Sutton: My recommendation is that each eye is treated separately. Whilst collagen cross linking is a safe procedure, it is not perfectly safe. My preference is always to separate the treatments by one month. In most circumstances keratoconus progresses asymmetrically and as such the need for bilateral simultaneous surgery rarely arises.
Professor Gerard Sutton: Following crosslinking treatment the eye will be irritable and sensitive to light for at least five days. Once the contact lens is removed this improves significantly but the vision will remain blurred for two weeks. Normal activities can recommence at that point including swimming, but visual improvement can occur up to one year and beyond.
Dr Abi Tenen: After surgery the treated eye may be sore and photophobic (particularly with epithelium-off procedures). A bandage contact lens is instilled for several days, until the first post-op visit, and the patient has drops to use regularly (antibiotic, steroid, NSAID, optional local anaesthetic). Oral pain medications plus sleeping pills are prescribed in case they are required. Similar to recovery post ASLA/PRK, the patient should expect to have a week at home to recover although only the first 2-3 days are uncomfortable.
Dr Colin Chan: The primary purpose of crosslinking is to stop the progression of keratoconus, not to improve vision. Therefore patients should not expect to see any improvement in their vision. However, nearly all international studies on crosslinking show that about 50% of patients will have a 2 diopter reduction in keratometric readings and a one line improvement in best corrected visual acuity. It is not possible to predict which patients will have this gain in vision and therefore I always tell patients not to expect any improvement. Also it may take months or years for this visual improvement to become apparent, as healing can be quite slow and prolonged post crosslinking.
Dr Abi Tenen: Refractions can fluctuate and shift quite quickly following a cross-linking procedure. Often the shift is not noticeable to the patient but their old contact lens may no longer be suitable. Sometimes vision and refraction worsen before they start to improve. On average, most of the changes occur within the first three months. Most patients have a stable refraction by six months although some keep shifting up until 12 months.
Today cataract is readily treatable with modern surgery, and while the surgery has evolved over time, far more progress has been made in the last fifty years than in the preceding two thousand.
The surgery has evolved from intra-capsular cataract surgery where the whole lens was removed, to extra-capsular where the capsule remains in order to support an intraocular lens. This better technology has seen significant improvements in visual outcome and most importantly, safety. Routine suturing of surgical wounds has become a thing of the past by performing the surgery with phacoemulsification through a 3 mm or less wound, followed by the implantation of a foldable intraocular lens.
In the last decade we have seen similar advances in laser technology. Lasers of varying wavelengths are used in medical practice, and design has been adapted for use in the eye. There is now an argon laser for retinal disease, and the YAG laser for posterior capsular thickening and iridotomies. The excimer laser has been developed for corneal refractive surgery and SLT laser for glaucoma.
The advantages of the femtosecond laser for laser vision correction were initially seen as minimal (less likelihood of a hole or tear in a flap, a more precise depth of cut and a lessened risk of epithelial ingrowth) because complications were already rare and the new technology was expensive. However, with the improved safety and flap quality ensured today, nearly all refractive laser surgeons use the femtosecond laser to create LASIK flaps.
It is this femtosecond laser technology that has now been adapted for cataract surgery in the Laser Cataract operation.
Is this new technology worth adopting? Can the increased expense be justified, and finally does it represent a significant improvement in precision and safety?
Ophthalmologists by nature are cautious and averse to changes in their operating habits. This was apparent when we moved to phacoemulsification and smaller incisions, followed by intraocular lens implantation.
Currently Laser Cataract surgery (LCS) has a relatively short clinical history with the majority of the 30,000 procedures to date having been undertaken in the last year. While there are other femtosecond cataract lasers entering the market, most of these cases have been performed with the LenSx. Considerable data has been gathered to date and the learning curve shortened.
The first cataract laser in Australia was installed at Vision Eye Institute (VEI) in Sydney in April 2011. Significantly the centre now has the largest published series of laser cataract cases in the world.
How is Laser Cataract Surgery different?
Are there any problems associated with the laser?
Is everyone suitable?
No, there are certain eyes that are not suitable; for example those with smaller pupils or with a lens that is tilted, or if there are significant corneal opacities which the laser is unable to penetrate. However the laser excels in previously high risk situations when done mechanically. For example, if the patient has a white mature cataract, pseudo exfoliation, dense cataract, the ability to perform the initial part of the procedure with the laser is extremely beneficial.
Current manual cataract surgery will still be an acceptable alternative for those patients not suitable or for those surgeons without access to the Cataract Laser. But as our experience grows and more of the published data confirms the apparent benefits it will be clear that LCS is a significantly safer and more precise procedure.
Finally, it is with great excitement that the surgeons Drs Lewis Levitz and Joe Reich who consult at VEI Camberwell, VEI Blackburn South and Coburg, together with Dr Abi Tenen at VEI Blackburn South, VEI Coburg and VEI St Kilda Rd and Dr Raj Pathmaraj at VEI Blackburn South now have this technology available for their patients.
There is a simple answer, or alternatively, a more complex answer based on an understanding of retinal anatomy and physiology and let’s face it, the pragmatism of the real world.
Simple answer – straight away (or within 72 hours, because most macular problems will respond beautifully to treatment that is instituted within 72 hours).
Complex answer – it depends on some features
• Is the loss of vision of rapid onset or has it slowly evolved
• The nature of the vision loss – central distortion only (metamorphopsia) with no peripheral vision involvement, or loss of peripheral vision, painless or painful.
• Is it a sudden loss of vision or merely a sudden awareness of a more chronic loss of vision (quite common). (the take home message here being that more people should use the Amsler grid to facilitate earlier detection of unilateral decreased vision)
The basic anatomic feature to remember is that we’re issued with approximately 25,000 cone photoreceptors at our fovea, the majority of which will have to last us our lifespan to enable us to have useful central vision. Unfortunately, submacular fluid inevitably causes a loss of photoreceptor mosaic and our cone photoreceptors are not replaceable.
Obviously the entire set of cone photoreceptors don’t die immediately and the damage that is done to the photoreceptors depends on how rapid the onset, the severity of the condition and the duration of the condition. E.g. macular fluid associated with an aggressive blood vessel growth (SRNVM) or with peripheral loss of vision (i.e. serous macular detachment secondary to rhegmatogenous retinal detachment) will experience a more rapid loss of photoreceptors than a more benign Central Serous Retinopathy. But, ALL these conditions do lead to loss of valuable cone photoreceptors if given enough time.
Also, to further confuse the issue, many patients have a sudden onset of awareness of central vision aberration. It is all too common to see patients that have been developing severe macular pathology in one eye that has been there for up to twelve months but the patient has not noticed this because the vision in the other eye has been sufficient to carry them through.(Let’s encourage use of the Amsler grid as a public eye health strategy)
Here’s the common clinical scenario:
Rapid onset metamorphopsia (over a few days) – metamorphopsia (i.e. straight lines appearing wavy or kinked) of rapid onset should be seen within 24 – 72 hours. Although it would most likely be wet macular degeneration in the older age group, it’s still possible that it could be a retinal detachment developing. Obviously symptoms of significant loss of peripheral vision will favour a retinal detachment (or other more extensive retinal pathology such as branch retinal vein occlusion).
Slow onset Metamorphopsia - If the symptoms had come on slowly, e.g. over a period of many weeks or months, I still think it’s useful to review these patients relatively quickly – i.e. within a fortnight. If these patients could monitor their vision during that fortnight and if the symptoms are getting markedly worse quite quickly, then the appointment could be brought forward 24 – 48 hours.
Other less common scenarios:
Sudden painful loss of vision – review straight away. Ask about Giant cell Arteritis symptoms, trauma, CVA etc. It would be very rare for it to be a macular problem, but I have seen SRNVM present as severe subretinal and suprachoroidal haemorrhage with severe pain due to stretching of the choroidal nerves (or high pressure or both).
Summary – treatment of submacular and/or intraretinal fluid from SRNVM, retinal vein occlusions, diabetic retinopathy, CSCR, retinal detachment within 72 hours will result in excellent recovery of macular cone photoreceptors. Other ILM and vitreous related maculopathies such as Macular Hole, Macular pucker, Vitreo-macular traction, will also respond beautifully to restorative Vitrectomy and epiretinal membrane peel within a time frame of a few weeks.
Please note that you can help the patient not only with the urgency of your referral but also with your selection. The referral can be made rapidly, but please keep in mind that retinal subspecialists who see many second opinion cases, witness the fact that the patient’s visual outcome heavily depends on the correct diagnosis, rapid facilitation of appropriate investigations and rapid movement from clinic assessment to actual treatment. An incorrect diagnosis or a treatment plan that consists of too-little-too-late macular treatment will be more damaging to the patient’s macula than a one day delay to see the retinal subspecialist. Our Vision Eye Institute Retinal subspecialists’ clinics are geared up to rapidly accept add-on patients experiencing metamorphopsia and to get their treatment started straight away.
Firstly, I would question the accuracy of the diagnosis.
AMD is typically a bilateral condition with symmetrical clinical features, so it would be unusual to have advanced AMD in one eye but no sign of AMD in the fellow eye. Conditions that mimic AMD (e.g. myopic, traumatic, post-inflammatory or post-central serous chorioretinopathy maculopathies) should be excluded.
Assuming the diagnosis is correct, the decision whether or not to commence anti-VEGF treatment is complex. I would base my decision upon consultation with the patient, her family and carers, and careful consideration of the following questions:
1. Is treatment likely to improve or maintain her quality of life?
This depends upon multiple factors, including;
a) the extent of permanent structural macular damage present
- this is related to the duration and severity of wet AMD
b) the risk of further loss of vision if treatment is withheld
- this depends upon the current visual acuity (VA) e.g. if the VA of
the affected eye is hand movements, it cannot deteriorate much further,
but if it is 6/9, it is likely to deteriorate markedly without treatment
c) the risk of the fellow eye losing vision due to wet AMD or unrelated ocular disease
- based upon prospective data from the Age Related Eye Disease Study
(AREDS), her risk of developing advanced AMD in the fellow eye
approximates 12% within 5 years and 25% within 10 years (assuming
that she currently has no signs of AMD in the fellow eye).
d) The presence of ocular co-morbidity (e.g. cataract, glaucoma, diabetic retinopathy or amblyopia).
- this will influence her visual potential and prognosis
2. What is her life expectancy?
According to actuarial life tables, the life expectancy of a 94-year-old Australian woman is between 3 to 4 years. This may be longer if she is in excellent health or reduced if significant medical morbidity is present e.g. cancer or cardiovascular disease.
Age per se is not a reason to withhold treatment because good vision is increasingly important to maintaining independence with increasing age. However, life expectancy does influence the likelihood of developing visual loss in the fellow eye, an important consideration when weighing up the risks and benefits of anti-VEGF therapy.
3. What is her social situation?
This is relevant to the logistics of attending for anti-VEGF treatment e.g. does she have family or social support to help her attend for regular anti-VEGF treatments and eye examinations, does she live in an urban centre or rural setting located a long way from ophthalmic care?
Social habits also determine visual demands e.g. someone who enjoys needlework, drives and has an active lifestyle has greater binocular visual demands than someone who has dementia, is housebound and spends their time listening to the radio.
Ultimately, my decision on whether or not to commence anti-VEGF therapy would be highly dependent upon the desires of the patient after she has been provided with sufficient information to enable her to make an informed decision.
Retinal toxicity from Plaquenil has a low incidence, 6.8/1000 users, and the prevalence is dependent on duration of use (cumulative dosage >1000g). Toxicity from these drugs is however of serious ophthalmologic concern because even after cessation of the drugs, there is little if any visual recovery and sometimes progression of visual loss.
Screening by a retinal specialist is recommended for all individuals taking the drug. Following a baseline evaluation, screening for toxicity should be initiated annually, no later than 5 years after starting the medication.
Routine screening test should include: A thorough ophthalmic examination with documentation of visual status and ocular findings. Automated threshold visual field testing with a white 10-2 pattern. The finding of any reproducibly depressed central or parafoveal spots can be indicative of early toxicity. At least one or more of the following objective tests should be considered, spectral domain-OCT (can show localized thinning in the parafoveal region), fundus autofluorescence (may reveal subtle RPE defects or areas of photoreceptor damage before visual field loss) and a multifocal electroretinogram (can objectively document localized paracentral depression in early toxicity). Amsler grid and color vision testing can be used as supplemental tests but are not consistent and specific enough as screening tools.
Particular risk factors for developing visual loss include the elderly, drug usage for more than 5 years, exceeding the recommended daily dosage and suffering from existing macular, kidney or liver disease.
The goal is to recognize early signs of paracentral field loss, or paracentral tissue damage, before the development of visible bulls eye maculopathy. Screening can recognize toxicity early and minimize visual loss, but cannot necessarily prevent all toxicity or guarantee there will be no visual loss.
The commonest macular diseases in patients with cataract are age-related macular degeneration (AMD), diabetic retinopathy (DR), epiretinal membranes (ERM) and vitreomacular adhesion (VMA) syndromes.
When considering cataract surgery in the presence of such conditions, several factors come into play. Foremost is the visual prognosis; if, for example, there is a large, dense disciform scar and only mild to moderate nuclear sclerosis, surgery is unwarranted. In most cases, however, such decisions are more difficult and are informed by an understanding of the risks of surgery worsening the macular disease. The two basic mechanisms by which cataract surgery may adversely affect the macula are inflammation and mechanical.
The inflammation induced by cataract surgery causes worsening of diabetic macular edema (DME), which can result in permanent visual loss. Surgery should be delayed until resolution of the DME is achieved and, even so, an intravitreal injection of steroid or anti-VEGF agent may be given perioperatively to ‘protect’ the macula. The same is probably true for all causes of macular edema, such as retinal vein occlusion.
Similarly, ‘wet’ macular degeneration is best controlled prior to performing surgery and the operation may be performed with an intravitreal injection of anti-VEGF at the same time or beforehand. Whilst there is currently consensus that cataract surgery does not induce choroidal neovascularization, some uncertainty persists as to whether the surgery causes progression of ‘dry’ macular degeneration through a phototoxic effect from the operating microscope light.
In all patients, but particularly those at risk of phototoxicity (eg. AMD, Stargardt’s disease, retinitis pigmentosa), every effort is made to minimize light exposure through measures aiming for shorter surgery, using dimmer lighting and switching off the operating light at all possible times during the surgery. The increasing use of blue-filtering intraocular lenses is predicated on concerns regarding the chronic photochemical effects of long-term exposure to blue light after implantation of a clear IOL; most retinal specialists who perform cataract surgery use blue-filtering IOLs.
There is little high-quality evidence available on the effect of cataract surgery on epiretinal membranes. For symptomatic ERMs, in the presence of significant cataract, the operation of choice is a combined vitrectomy with ERM peel and cataract extraction. Here, the cataract extraction is necessary primarily to improve the surgeon’s view for the epiretinal membrane peel. Considering the fact that the vitrectomy itself accelerates cataract formation, many perform combined surgery to reduce the number of procedures required. This can sometimes, however, result in variable refractive outcomes for patients due to the unpredictability of the effective lens position within the eye.
Asymptomatic ERMs often require no particular attention and cataract surgery alone may readily be performed with a guarded prognosis- some patients only notice the effects of the ERM after their cataract surgery. Considering the low additional surgical risk of addressing the ERM, it may be worth performing combined surgery for ERMs that distort the fovea markedly.
Most ERMs are associated with a posterior vitreous detachment. In this case, the anterior shift in the vitreous that follows the replacement of the (thick) crystalline lens with a (thin) IOL has no effect on the macula. However, some ERMs are part of a disease spectrum known as vitreomacular adhesion (VMA), in which there is an extramacular posterior vitreous detachment but persistent attachment of the posterior vitreous face to all or part of the macula. In this situation any anterior shift of the vitreous body following cataract surgery may result in a forward mechanical pull on the point of vitreomacular adhesion. If the VMA is broad, affecting much of the macula, the result may be a thickening of the whole macula, but if there is vitreofoveal traction alone, a macular hole may result. In VMA, therefore, there is a very strong case for either performing the vitrectomy first or concurrently.
A significant part of vitreoretinal surgeons’ practice in the past was spent ‘salvaging’ disappointed cataract surgery patients. Macular disease can be very subtle and is often difficult or even impossible to detect on fundoscopy alone and even more so in the presence of cataract. Nowadays, though, this aspect of our practice is less common due to a greater understanding of the importance of macular assessment by general ophthalmologists, better treatments for macular diseases and (above all) the use of optical coherence tomography routinely before cataract surgery. Many retinal specialists would recommend this as a routine part of any cataract assessment.
In surgery it is hard to try before you buy. It is therefore important to assess the patient’s true visual needs prior to embarking on cataract surgery or lens exchange, for an incorrect decision can be difficult to rectify. Not all patients seek emmetropia and many are happy with spectacle correction for reading following cataract surgery or even being left myopic. It is after all what most in that age group have been used to. Monovision in the non-dominant eye, particularly a low minus of 1D or less, has a pseudo-accommodative effect giving more bang than expected for the buck. Many patients then find they need readers only for fine print, much to our surprise.
Having been an early adopter of both the multifocal lens technology and the accommodative lens where do I feel we are at present? My initial experience with the Restor Multifocal was a series of highs and lows. Some wonderful results, grateful patients then a few grumblers, including some in whom lens removal and exchange was required and many more requiring refractive laser correction than I would have suspected. That was back some 7 years ago and after a first 100 back then I implanted very few Restor lenses until the last year.
What has changed? The new Restor is aspheric, has a decreased reading add giving a more comfortable reading distance and most importantly has incorporated a toric correction allowing for astigmatism correction down to 0.6D. The result has been significantly fewer comments from patients about haloes at night and I have had no issues with those who drive at night. The improved lens formulae and the toric lenses have meant 40% of my patients have a toric lens implant. No lenses have been explanted so far.
There are other manufacturers of lens implants that also offer multifocality but not all have a toric option. The particular acrylic material and lens design makes the Restor toric very stable from the moment of implantation with little likelihood of lens rotation off axis, a key to a predictable outcome.
Whom do I exclude from consideration of a multifocal lens today? The myope whose expectations re near vision are so much greater, any difficulty in lens power estimation (Keratoconus, high astigmatism, previous refractive surgery) and any suggestion of macula disease, including any diabetic retinopathy and amblyopia. Care must be taken to reduce the likelihood of CMO post operatively and for these patients especially there is a role for the NSAID drugs (Voltaren or Acular) postoperatively.
Personally, I will not use a multifocal on an emmetrope looking for presbyopic correction. I don’t believe the risk justifies the end result and would still prefer a monovision refractive laser in this situation.
Who does best? The initial hypermetropes appear to enjoy the benefits, especially those greater than +2D. So far I have not required a refractive laser top up in these more recently implanted eyes but expect with the refractive surprises that occur from lens positioning that they will be needed for some. I also feel patients do best with bilateral implantation and plan for this a week apart or as soon as the patient can schedule the second surgery.
My current practice involves less than 20% Restor multifocal lens implantation in my cataract patients and over 80% (in the refractive lens exchange grou)p are Acrysof Spherical or toric with a few Raynor Toric for very high astigmatism.
Presbyopia is a frustrating phenomenon reaching everyone eventually, some people more than others, some earlier in life and some later in life, but eventually everyone. Solutions from past to present have revolved around scleral expansion techniques to retain natural accommodation, to corneal inlay techniques, producing pinholing, around monovision induction using corneal steepening techniques, with holmium laser and conductive heating but mostly with the excimer laser ablation. There have been lens based techniques, usually lensectomy or cataract surgery, with low myopia induction, and in appropriately selected people, using multifocal intraocular lenses (piggy back or bag – multifocal phakic IOLs have been available in the past and may be so in the future). This myriad of options suggests that none are perfect, and some simply don’t work! This also confirms the necessity for the surgeon or optometrist to perform some sort of simulation trialing in most patients (contact lenses, loose lenses, or whatever is deemed closest to the effects of the intervention) to demonstrate both the positive and negative attributes of the technology and the all important permanency of the intervention.
While all ophthalmologists have their preferred surgical approach to presbyopia (as is outlined by the different views of my colleagues within this newsletter), my choice is usually a refractive lens exchange. As IOL technology improves and our understanding of optics and optical aberration improves newer options for presbyopia will potentially become available:
The cause of presbyopia relates, in the majority, to progressive inelasticity of the crystalline lens with ciliary accommodative effort no longer achieving the quantum of lenticular power change required to bring a near focal point into sharp focus. The crystalline lens shows an almost linear loss of elasticity, and hence accommodative power, from birth to approximately age 65 when the lens becomes motionless, ie a decline in accommodative power from approximately 18 diopters at the age of 5years to zero at the age of 65 years, with approximately 3 diopters left at age 45years; 3 diopters of focal power provides a focal point at 33cms, a comfortable ‘arms length’ for reading in an average sized person. So when arms become too short – Presbyopia has arrived.
Now, not only do we lose elasticity in our crystalline lenses with time, so does the optics of the lens change, with a shift of the youthful negative asphericity (which balances the usual positive corneal asphericity, thus providing the excellent ‘High Definition’ vision of youth), to the more positive asphericity which accompanies the ageing lenticular nuclear sclerosis. The loss of this balance degrades the quality of vision as we get older.
The discussion above refers to the average. As usual there are outliers to the general rule on both sides, with some people showing presbyopic symptoms earlier than others and some showing symptoms later. There is information emerging that seems to demonstrate that the shift in the asphericity balance spoken of above to more net positive asphericity in an eye with time (or high base corneal positive spherical aberration) may lead to early presbyopia and vice versa. More retained negative spherical aberration (SA) may promote the retention of a form of accommodation dubbed pseudo-accommodation (probably in this case an increase in depth of field, supplementing pupil size). This status quo is aside from the base myopic and hyperopic prescriptions and pupil size which, as is well known, retards or advances presbyopic symptoms.
If we can harness this status with more understanding we would be able to provide people with greater near function without excessive distance function loss by this phenomenon of psuedoaccommodation. This would allow multifocal vision (or shall we use the catch phrase blended vision), without the penalty of multiple retinal imagery of multifocal lenses, or the excessive monovision induction which increases anisometropia and asthenopia and avoids the corneal risks of laser and inlays.
Are we there yet? Yes!! With the new range of aspheric monofocal IOLs which are available with asphericity values from +0.4um RMS SA to -0.3um RMS SA in 4 steps, we have the capability of restoring youthful total eye asphericity. The obvious target for Hi Def vision is Oum SA (perfect asphere) to +0.1um RMS of spherical aberration (this is the spherical aberration measured in the sharp shooting US fighter pilots), a great place for our dominant eyes to be in for distance vision. However, by measuring the total corneal asphericity and selecting an IOL with the appropriate asphericity value, we can now target greater degrees of negative asphericity thus enhancing depth of field and psuedoaccommodatino. By this mechanism, small degrees of monovision (eg -0.75DS) can provide greater near vision in the nondominant eye without significant loss of distance acuity!
This type of correction still provides excellent contrast sensitivity and MTF (modulation transfer function) – good, sharp, ‘nonhaloed’ vision, as opposed to some other forms of presbyopic correction. The question remains whether targeting a similar ‘defocus’ in the positive spherical aberration range will provide a similar effect. With these new aspheric monofocal lenses discussed above now available we should be able to find this out. Obviously the usual risks of surgery still apply, but the safety, speed, techniques and technology of microincisional surgery in this day of modern surgery are exceptional.
Roll on Refractive Lens Exchange!
Speaking from personal experience, I can say that presbyopia is a frustrating condition. For emmetropes especially, who have never required spectacles, the new found dependency can be very frustrating. Those patients looking at surgical options to reduce or eliminate the need for reading glasses, are faced with a myriad of choices. It is an old but true adage that in medicine, whenever there are numerous options for the treatment of a condition, you can be sure of one thing; none of them is perfect.
In my practice, based on the current evidence in the peer-reviewed literature, the only surgical options that I consider for the treatment of presbyopia are blended vision (monovision) or a Restor multifocal intraocular lens. The Kamra Inlay and Intracor femtosecond treatments are currently investigational techniques, with inadequate numbers in the peer-reviewed literature to date to warrant their general use. In my opinion their safety and efficacy have not yet been established and patients (and surgeons) should approach their use with caution.
Why risk these new unproven modalities when we have two proven and safe options? My preferred surgical option is blended vision. This is often poorly understood by patients who consider that having one eye which is better focused for distance and one for near will make the patient feel unsteady or create headache issues. Indeed a small percentage of patients (<10%) will not be suitable and that is why it is important to create the effect of the blended vision with a contact lens trial prior to any surgery. In my experience if the contact lens trial is successful the patient will be very happy with the surgical outcome. It is important not to try for too much near correction.
Finkelman et (JCRS 2009) showed that if the induced myopia was less than 1.5Dioptres there was no loss in stereoacuity or contrast senstitivity. Depending on a patient’s age this degree of anisometropia would allow good intermediate ( shopping prices, computer screens ) and adequate near vision ( newspapers, restaurant menus, mobile phones) for most activities. The compromise is that reading glasses may still be required for finer activities such as sewing and for reading in poor illumination.
In patients undergoing LASIK surgery, blended vision is the preferred presbyopic treatment option. In patients undergoing cataract or refractive lens exchange surgery, a good multifocal IOL (Restor; Alcon) is a reasonable option as well.
So how do we decide between a multifocal lens and a blended vision correction? In a recent study Zhang, Sugar and colleagues (JCRS May 2011) compared these two options. They found that for uncorrected distance and near visual acuity the two groups were identical. However for intermediate vision (computer) the blended vision group did statistically better. They also performed better in terms of their overall satisfaction score and had fewer complaints about night vision.
Other advantages of blended vision over multifocal intraocular lenses are that they are not sensitive to intraocular decentration and they do not have a negative impact in patients with macular disease. It is a fact often overlooked that in patients with a multifocal IOL, the modulation transfer function (MTF) which is an indication of how much light is getting to the retina, is reduced by up to 50%. In patients with any macular disease this can severely reduce visual function. Patients with multifocal IOLs are also very sensitive to any residual astigmatism or posterior capsular opacity. The incidence of refractive surgical touch ups and yag capsulotomies are therefore higher.
Despite these limitations, I believe that the Restor multifocal IOL is an excellent choice in patients without macular disease, who don’t spend a lot of time driving at night and who wish to achieve vision that will allow them to read comfortably without glasses.
Finally it is is essential to remember and to tell all patients, that these surgical procedures will reduce but not necessarily eliminate the need for spectacles.
Blended (mono) vision and multifocal IOLs are the safest and best options for the treatment of presbyopia. In LASIK I will use some form of blended vision in almost all presbyopes. In intraocular surgery, I give the patients an option of blended vision or a multifocal lens and customize the surgery to their visual needs and lifestyle.
So as a 48 year old Professor of Corneal & Refractive Surgery what surgery did I chose when the dreaded dependency on reading glasses became too great? Blended vision of course. I have typed this article without the need of any reading correction and next week I will go fishing and tie on my hooks without them as well.
Reading glasses offer a wonderful solution for presbyopia for many patients but for those who would prefer to be less dependent on glasses there are a number of surgical options that will improve unaided near vision. None of these is perfect and each involves some compromise.
Perhaps the most difficult group has been the emmetropic presbyope; the 50 year old who has never needed glasses but now finds reading glasses unavoidable. Kamra is the only surgical intervention specifically tailored for this patient and offers significant reduction in dependence upon reading glasses.
Corneal Inlay uses pinhole effect
Kamra offers a unique solution for the emmetropic presbyope being appealing both for preservation of distance vision and its reversibility; as an implanted device it can be readily removed in the future, restoring the eye to its pre operated state.
An Intracorneal Inlay KAMRA (Acufocus) as a treatment for presbyopia acts as a small aperture to increase depth of focus by selectively allowing passage of the central light rays and blocking the less well focused peripheral rays. It has no refractive effect so does not change the overall focusing of the eye.
The intracorneal inlay is fully registered in Australia with the TGA and available to patients in Sydney and Melbourne. Two clinics in Australia participated in the early FDA clinical studies demonstrating the safety and efficacy of the implant.
The implant is made of a synthetic material with a thickness of just 5 um – similar to the size of a red blood cell. The central aperture measures 1.6mm and the overall size of the device is 3.8mm. Whilst the device acts optically as a simple small aperture its design is sophisticated. Nutrition of the overlying cornea is maintained by more than 8,000 nutrient holes passing through the device to allow flow of nutrients through the implant. Evolution of the devices design has optimised the size and direction of these nutrient channels to enhance the health of the overlying cornea whilst minimising the passage of stray light. The device material is well tolerated by the cornea with good biocompatibility. Confocal analysis shows minimal keratocyte activation or elaboration of inflammatory markers.
Although implanted unilaterally the inlay does not create monovision. The eye with the implant remains emmetropic so retains normal unaided distance vision and both eyes continue to work together (binocularity is preserved). As there is no refractive change to the implanted eye image magnification does not occur and there is no aniseikonia. Examination and imaging of the eye with the inlay is unaffected and there is no change to visual field testing.
Surgery – Implanting the inlay
Only one eye ( the non dominant eye) is implanted. The inlay is implanted into a femtosecond ( laser) created corneal pocket at a depth of 200um. Some centres create a corneal flap of 200um but there are clear advantages to avoiding a thick flap. The pocket technique minimises post surgery dry eye effects and there is minimal impact on corneal biomechanical stability. Flap problems such as striae can not occur. A new system of surgical alignment (Acutarget) has been developed to facilitate predictable positioning of the inlay on the patients line of sight.
Surgery is performed using anaesthetic drops and takes around 10 minutes to complete. Eye movement and rubbing is not a problem as there is no flap to disturb. The patient is advised to go home and sleep for a few hours. Improved near vision occurs by day 1 and continues to improve for up to 12 months after surgery.
Pooled data from various arms of the clinical trials demonstrates that patients are capable of achieving N5 unaided near vision and distance vision within one line of pre operative measurements. Near vision is light dependant and patients need to know that they will continue to need reading glasses under some conditions – poor lighting, reduced contrast or very small print.
While acknowledging that all my colleagues have their own approaches to treating presbyopia, Kamra is my preferred option for the emmetropic presbyope. Surgery is straightforward and patients achieve functional vision for both near and far with high rates of spectacle independence. There is minimal if any compromise to distance vision so for many patients this is a better option than monovision.