Blood is thicker than water

Mr C is an old patient of mine. I first met him 3 years ago, soon after moving to Singapore from Penang.

His is a story of survival, of successfully battling leukemia and unfortunately then losing vision in one eye from complications of graft vs host disease. At the time of his leukemia treatment, he was fortunate enough to receive a bone marrow transplant from one of his sisters, and he subsequently went into remission. The bone marrow unfortunately produced cells which started attacking parts of his body. Some scarring developed in his mouth, but it was his right eye which bore the brunt of it. Treatment with high doses of steroids produced steroid induced glaucoma in the eye, for which he underwent transscleral cyclodiode laser treatment. Unfortunately, that eye became phthisical.

When I first met him, he was just starting to develop inflammation in his other eye. We managed to control that with oral steroids at the beginning, but soon a tongue of fibrovascular tissue started growing inexorably towards the centre of his cornea from under his upper eyelid.

We got him a haematology referral, put him on other immunosuppressants, searched the literature for graft vs host disease, and got nowhere. His vision was soon obscured by the fibrovascular ingrowth. At first, I did a simple excision of this tissue, but ominously it grew back within a matter of months.

I had read reports of oral mucosal transplantation to the ocular surface, but had up to this time been somewhat skeptical of the reported benefits. For this patient, there were not many alternatives. The superior fibrovascular tissue had obliterated the superior conjunctival fornix, and at a minimum I would need some tissue to resurface that. There was no significant tissue to take from his other, phthisical eye. I got my plastic surgeon brother and together we worked on Mr C. He harvested a rectangle of oral mucosa, following which I dissected Mr C's upper lid free of the cornea. I then transplanted the oral mucosa to the uppermost part of the tarsal surface of the upper lid. The surface of the eyeball I covered with a layer of amniotic membrane.

It was with dismay that I noticed fibrovascular tissue creeping across the amniotic membrane a few weeks after surgery. Before long we would be back to square one!

I took Mr C to the treatment room, and slightly out of desperation took a very thin layer (split thickness, see pic below) of the transplanted oral mucosa from the superior forniceal area and retransplanted this to his superior limbal area, hoping that this would act as a barrier to further fibrovascular ingrowth. Amazingly, it did just that! The fibrous tissue regressed into a small red granuloma (see below), which I easily excised in clinic. Epithelium from the oral mucosa in the limbal area also started growing over the cornea, which was soon epithelialised. Amazing, and here we are with so much research done trying to grow oral mucosal epithelium in the lab.

And we all live happily forever after? Unfortunately, no.

After about a year, it became apparent that things were still unstable. Firstly, blood vessels started growing into the superior part of the cornea (see below). Obviously, the oral mucosal cells do nothing to stop blood vessels from growing in. Anytime I tried to reduce his oral steroids and immunosuppression, his conjunctiva and even cornea would get inflamed, with epithelial defects and even more alarmingly, slowly progressive corneal thinning. Secondly, his long term usage of oral steroids had caused a very dense posterior subcapsular cataract. We got by, by keeping him dilated with atropine so he could still see out of the less affected peripheral lens.

But we knew that things were not getting any better. And I was worried that one day his cornea would melt and perforate (as has happened to one of my Stevens Johnson patients before). What he really needed was limbal stem cells that were immune to attack from the transplanted bone marrow. A light bulb went off-I would use limbal tissue from the sister who had donated the bone marrow in the first place! As the immune cells and the limbal tissue are from the same donor, the limbal tissue would naturally be immune from attack!

We discussed this a number of times, and finally about a month ago I sat down and spoke to quite a few of the siblings (they are a large family). As expected, the sister involved wanted to know how the limbal stem cell harvest would affect her. I replied that it was a very safe procedure that would cause very temporary and mild discomfort, although it could cause some changes in spectacle power/astigmatism.

Last week I performed the operation to remove the cataract as well as transplant the limbal stem cells from the sister to Mr C. Both are doing great. The limbal stem cells are taking well and today donor corneal epithelium had grown to cover most of the corneal stroma. Hopefully this is the last operation I have to do for Mr C!

Even though Mr C was unfortunate to get leukemia and then graft vs host disease, he was very lucky to have such a supportive family and sister. You really know who are the people you can count on when the going gets tough!

Update (13 August 2014)
Mr C continues to do well with clear corneas and vision of 6/12 unaided. Driving vision!

Can spectacle power return after LASIK?

LASIK changes the power of the eye by changing the shape of the cornea, the clear window at the front of the eye. Besides transmitting light, this window is also responsible for much of the focusing power of the eye, giving doctors a great opportunity to 'build a contact lens' into the eye itself.

LASIK works by removing minute amounts of corneal tissue from the surface of the eye. By doing so, certain parts of the cornea can be flattened, and other parts steepened. For example, in shortsighted patients the central part of the cornea is flattened, the amount of flattening corresponding to the spectacle power of the patient.

Back to the question: Can spectacle power return after LASIK? The short answer is yes. This can happen for a few reasons:
1. The corneal shape slowly regresses towards its original shape (It can never regain its original shape, but the 'healing' process sometimes causes the corneal curvature to become a little more like how it was before the LASIK)
2. The eyeball changes in length, usually by becoming longer in very shortsighted people
3. Some other unrelated eye disease, such as cataract

The higher the spectacle power of the eye to begin with, the more likely this is to happen. However, overall the risk is low as has been shown in a number of studies.

Am J Ophthalmol 2008;145:46–54. 

The above graph from an article in the American Journal of Ophthalmology shows that even after 10 years, the average spectacle power of the eyes of a group of patients was only about 50 degrees, or 0.50 dioptre of shortsightedness.

If the spectacle power returns, what next?

It depends on how much power has come back, how much cornea is left, and how keen the patient is on having a LASIK enhancement/adjustment.

Generally speaking, an enhancement is not recommended if the residual spectacle power is 50 degrees or less than targeted. Some patients are also quite happy if the power is higher than that, and there is no need to repeat surgery for all these patients.

When the power gets to 75 degrees or higher though, more and more people find that it affects their daily activities. They may need glasses, for example, when driving. If so, the inconvenience may drive them to seek an enhancement. This can be considered if the remaining cornea is thick enough.

In recent times it has been found that a LASIK flap can be lifted again many years after the original surgery. As such, an enhancement surgery is very much 'half an original LASIK operation', since it does not involve making another flap. Using topography guided techniques, enhancements can be done not only to correct residual short/long sightedness and astigmatism, but also aberrations like spherical aberration and coma. The picture below shows topographies (corneal maps) of a patient who had coma and residual shortsightedness before (left most map) and the subsequent healing after enhancement. Note how the blue area has shifted from the right side (left map), over to the centre (right map).

If the cornea under a LASIK flap is already too thin for further treatments, alternative techniques would include PRK on the flap, or even ICL surgery if the anterior chamber of the eye is deep enough.

Atropine eyedrops for the control of shortsightedness

Shortsightedness is a huge problem in Singapore and many big cities around the world. More than half of Singapore schoolchildren are already wearing glasses for shortsightedness by the age of 12 years. What is worrying is that the earlier one starts out becoming shortsighted, the higher the final spectacle degree tends to be. Very highly shortsighted people are at increased risk of eye problems like cataract and retinal problems at a younger than average age.

It is important therefore that we try to slow down the increase of shortsightedness as much as possible. Ensure that a child spends 1-2 hours outdoors in sunlight each day. Take regular breaks from near work when reading or with computer use. Apart from these, using Atropine eyedrops is the only method proven in big studies (randomised controlled trials) to slow down the rate at which shortsightedness increases.

What is Atropine?

This is a chemical obtained from plants in the same family as the nightshade plant. Owing to the presence of extremely high levels of atropine and other chemicals, the berries and leaves of the plant are poisonous. 

Interestingly, the nightshade plant is also called ‘belladonna’ (meaning beautiful woman in Italian) as people in the past used atropine to dilate the eyes for a cosmetic effect! It achieves its effects in the body by blocking a special receptor molecule that among other things controls the action of muscles as well as the growth of the eyeball.

Atropine is available in many forms, but for eye conditions it is used as an eyedrop. Various concentrations have been tried but the commonly available concentrations are 1%, 0.125% and 0.01%.

Traditional treatment (Atropine 1%)

Traditionally, to reduce the rate at which shortsightedness increases, 1% Atropine eyedrops were used once a day or even once a week. In a study at the Singapore National Eye Centre, 1% eyedrops used once a day reduced the progression of shortsightedness from an average of 100 degrees a year to less than 25 degrees a year. Our experience suggests that using it even once a week has a very similar effect.

Side effects of traditional Atropine treatment

Atropine 1% dilates the pupil and relaxes the muscle used for near focusing inside the eye. As a result patients feel very sensitive to bright lights and with normal glasses on have difficulty with close up work such as reading. If this concentration is used, special glasses which turn dark outdoors (‘Transitions’ lenses) and which have progressive lenses (having a near section below for near focus) are required. All of these side effects are temporary and disappear when the patient stops using the drops.

Newer treatments (Atropine 0.125% and 0.01%)

In an effort to do away with the side effects of Atropine, lower concentrations of Atropine were tried. When used once every day, 61% of those using 0.1% and only 6% of those using 0.01% Atropine felt a need for special ‘Transitions’ and progressive lenses. Therefore, normal glasses or contact lenses can usually be worn while the 0.01% Atropine concentration is used.

However, the lower concentrations are not as effective as the 1% concentration at slowing progression of shortsightedness. On average, the myopia progression over 2 years for 1% Atropine was 28 degrees, for 0.1% 38 degrees, and for 0.01% 49 degrees. This was still better than the 120 degree increase seen in those who were not using the Atropine eyedrops.

General pointers about using Atropine for shortsightedness

Whether 1% or 0.01% Atropine is used, the eyedrops must be used for a long period of time. Although the shortsightedness increases at a slower rate while Atropine is used, the rate increases again when it is stopped. The idea is therefore to use the Atropine during the period of time when the shortsightedness is increasing fastest. Usually by about 18 years of age, the rate of increase of shortsightedness would have already slowed down naturally.

This means that on average, most children who use the eyedrops would be using them for several years. The longer the eyedrop is used, the bigger its potential effect. For example, if a child had shortsightedness that was increasing by 100 degrees every year, using the 1% eyedrop for 3 years would reduce the final power by 300 degrees. This might mean that instead of having 500 degrees of shortsightedness as an adult, he/she would only have 200 degrees of shortsightedness finally.

In trying to slow the progression of shortsightedness, a number of decisions have to be made. Should Atropine be used or not? Should the 1%, 0.125% or 0.01% concentration be used? How long should the child continue with the eyedrops?

These decisions should be made after a discussion of the pros and cons of each decision with your eye doctor. For example, if the shortsightedness is increasing very fast and is already of a high degree, one would favour using the 1% eyedrop despite the side effects. On the other hand, if the side effects cannot be tolerated and one is willing to give up some of the stabilizing effect of the 1% eyedrop, then the 0.01% concentration is a good option.

EDIT 7 MAY 2018
Please note that I do not run an online pharmacy, and these are illegal in many parts of the world. Do not request Atropine from myself, or any other doctor, unless you or your child have seen the particular doctor and it has been determined after a proper consultation that Atropine is necessary. Requests for Atropine will be deleted in the future to avoid cluttering up the comments section in this post.

P/S.
Have you ever seen pinhole glasses? I heard that they are available at Watsons. Do NOT waste your money on these gimmicks. They do nothing to help the eyes or vision. Have a look at this link: Case Watch report on settlement of charges of misleading claims

How is glaucoma treated?

As was discussed earlier, glaucoma refers to damage to the optic nerve cells. There may be many factors important in causing this, but the biggest factor shown in studies is the level of pressure in the eye. (IntraOcular Pressure, or IOP)

Hence, the main aim of treatment in glaucoma is to lower the eye pressure. Sometimes, the eye pressure may be in the ‘normal’ range of 10-21mmHg, but the nerve continues to deteriorate. In such cases, the eye pressure is lowered further still. Lowering the eye pressure of most glaucoma patients starts with eyedrops (right).

Fortunately there are many medicines available now to reduce eye pressures. If using one does not lower the pressure enough, the doctor may change the eyedrop to a different one, or a second eyedrop may be added. In patients with very high pressures, an oral medicine called Diamox may also be used.

Medicines used to lower the eye pressure either reduce the production of fluid inside the eyeball, or they help the fluid to drain out of the eye more easily. Medicines that do the former include beta blockers such as Timolol, Brimonidine (Alphagan), and Dorzolamide (Trusopt). Others that help with drainage include the prostaglandin analogues Latanoprost (Xalatan), Travaprost (Travatan) and Bimatoprost (Lumigan).

In most cases of glaucoma, long term use of the medication is required. When the medication is stopped, the pressure starts to rise again, and optic nerve damage gets worse with enlargement of blind spots. It is very important therefore, that glaucoma patients do not stop using their eyedrop unless their doctor says it is OK to do so.

As with any medication, glaucoma medicines may have side effects. The most interesting concern the prostaglandin analogues. They do not cause any serious life or sight threatening side effects, but often make the eye redder than normal. This effect can persist for some months, and then often gets better by itself. They also make the eyelashes longer, an effect which has been exploited in the eyelash lengthening treatment called Latisse.

Another cosmetic side effect that is often undesirable is the changing of the iris colour, usually from a lighter blue or green colour to a browner colour, as seen below.

In cases of glaucoma where the front of the eye is narrow, a laser procedure called a laser peripheral iridotomy may be performed (See figure below-the two black dots are small holes in the iris made by a laser; the video below shows the procedure being performed with an Nd:YAG laser). This is a simple procedure performed in the clinic and may take 15 minutes to complete. It helps to improve fluid flow out of the eye despite the narrowness of the anterior chamber.

In some patients, medical or laser treatment fails to lower the eye pressure, necessitating surgery. In the most common operation, a new channel is created for fluid to drain out of the eyeball. This operation is called a ‘trabeculectomy’. To facilitate drainage, sometimes a metal tube (called the ExPRESS shunt) is used as well. In some patients where trabeculectomies have previously been performed but eye pressures have increased again, silicone drainage tubes may be implanted for better fluid flow out of the eye and pressure control.

Glaucoma in the long term

Many people with glaucoma are worried about blindness. However, most glaucoma patients do not become blind. The most important factor is control of the eye pressure, which is achieved either with the use of eyedrops or surgery. If eyedrops are regularly instilled, and eye pressures are well controlled, vision is usually well preserved.

However, patients should realise that damage to the nerve before treatment was started cannot be reversed. The aim in glaucoma treatment is to stabilise the condition, and in most patients vision is maintained for life.

What is glaucoma?

Glaucoma is a fairly common condition affecting the eye. It generally occurs when the pressure within an eye is too high, causing the nerve fibres that carry signals from the retina to the brain to be damaged.

A few issues arise here. The most common questions I get asked-there’s a pressure within the eye? How high is too high? Is it better to have a very low eye pressure?

The eyeball is rather like a football or a car tyre. As an analogy, a football or tyre is pumped to a certain pressure with air. In the eye, pressure is generated and maintained by the production of a liquid called aqueous, rather than air. The aqueous is produced continuously, but fortunately there is also a drainage channel for the aqueous to leave the eye. The pressure within the eye (IntraOcular Pressure, or IOP) is therefore dependent on a fine balance between aqueous being ‘pumped’ into the eye, and aqueous leaving the eye. The IOP tends to increase when there is an imbalance between fluid production and how fast it can leave the eye. Therefore, when there is a blockage of the drainage channels, the fluid tends to build up and so does the IOP.

Without a certain pressure, however, the eyeball becomes soft and squishy, causing vision to fluctuate with every blink. Indeed if the pressure is too low a number of other problems show up to blur the vision-the retina swells and the eyeball may even shrink (phthisis bulbi).

On the other hand, when the IOP is too high, nerve fibres within the retina and optic nerve get damaged. Vision is lost gradually, with blind spots (scotomata) developing, coalescing, and eventuating in complete loss of vision in the most advanced stages.

Most people have an IOP between 10-21mmHg (millimeters of mercury), and traditionally those IOPs above 21mmHg were considered 'high'. Nowadays, we know that while very high IOPs like 30 and 40mmHg will definitely damage nerves in the eye, those between about 21-24mmHg do not always result in visual loss. In order to determine whether these patients with somewhat high IOPs need treatment, the doctor will look at other tests such as the visual fields and also the optical coherence tomogram (OCT), which can display the retinal nerve fibre layer around the optic disc or perform an en face analysis via the ganglion cell complex display.

Types of glaucoma

In general terms, we can separate glaucoma into 2 main groups: Acute and chronic.

• Acute glaucoma

In this form of glaucoma, pressure in the eye rises quickly to very high levels. These pressures are often higher than 40mmHg (twice normal). In this situation the patient will experience sudden onset of severe eye pain and headache on the affected side. Vision in that eye will also be very blur. Sometimes nausea and vomiting occur as well.

• Chronic glaucoma

This is the most common kind of glaucoma. Chronic glaucoma does not cause any symptoms in the early stages. There is no pain, no redness, not even a little irritation. As the nerve is progressively damaged, however, vision is affected. Eventually, only ‘tunnel vision’ may be left, meaning that the patient can only see what is directly ahead with loss of the ‘side’ vision (see below). In the most advanced stages, even tunnel vision is lost and the patient may become blind. This is why glaucoma is sometimes known as the ‘silent thief of sight’.

Causes of glaucoma

In most cases, glaucoma arises without an obvious cause or is age related, ie drainage channels for aqueous don't flow as well as they used to and the IOP slowly builds up.

Acute glaucoma and some unusual types of chronic glaucoma occur because the front part of the eye (called the anterior chamber) is narrow (see picture below, and note how close the 2 beams of light are). This narrowness is partly inherited, however, it tends to become worse with age because of the development of cataract.

Other less common causes of glaucoma include the sometimes seen side effect of medications like steroids, eye injury, and eye inflammation (uveitis).

In the next post, I will discuss how glaucoma is treated. Feel free to comment and let me know if anything is not clear.

EpiLASIK, ICL or LASIK?

In recent years, LASIK has become one of the commonest operations performed. Its popularity and success are understandable, given the good outcomes experienced by the majority of patients. Still, there are potential side effects with any procedure, and LASIK also has its limitations especially for those with very high spectacle degrees. 2 commonly mentioned alternatives are epiLASIK and ICL (implantable collamer lens), and in Singapore these 2 procedures have been marketed quite heavily as well. Some of their proponents would have you consider undergoing these ops rather than LASIK, and in their reading material sometimes emphasise the potential side effects of LASIK. So, what's the deal with these alternatives and are they really to be preferred over LASIK?

There are pros and cons with each procedure. With epiLASIK, the advantage (which is also a disadvantage, as you will see later) is that no corneal flap is created, so theoretically the eye is stronger and perhaps at somewhat lower risk for a complication called corneal ectasia.

Having said that, the vast majority of cases that we do are LASIK rather than epiLASIK. Visual recovery following LASIK is much faster than after epiLASIK. In comparison, vision the second day after LASIK is already pretty good (usually in the region of 6/6 and 6/7.5), but for epiLASIK, to reach a comparable level of vision you might need to wait several weeks. We also take precautions not to go below 250 microns of residual stromal thickness and this avoids ectasia in normal LASIK patients (the risk being in the region of 1 in 5000 cases or so).

The problem with epiLASIK/LASEK/PRK procedures is that the corneal epithelium is removed (see below). Healing of this to provide a smooth surface will take from several weeks up to a couple of months or so. Because the surface is ablated, there is a chance of corneal scarring, but this is much less nowadays since we use mitomycin C at the end of epiLASIK/LASEK/PRK. 

I have grouped epiLASIK/LASEK/PRK together since they are essentially the same procedure. The difference is in how the epithelium is removed. In epiLASIK, a special blunt blade (tissue separator/microkeratome) cleaves the epithelium from the stroma. There is a risk that the blade may cut into the corneal stroma sometimes, resulting in an uneven surface, and because of this risk we don't do epiLASIK in our clinic. LASEK uses alcohol to loosen the epithelium, and this is our method of choice if we decide on surface treatment for a particular patient. The LASEK we do is 'epithelium-off', or 'alcohol assisted PRK' (see below in italics). Traditional PRK used a toothbrush type scrubber and we think the alcohol is gentler to the eye. In our clinic we currently reserve LASEK for patients with corneas that are too thin for conventional LASIK. The number of patients who have this done is probably less than 5%. The others all have LASIK with a 'bladeless' technique ie. using a femtosecond laser to create the flap and then the excimer laser to reshape the cornea.

A little bit of history: Why, might you ask, did people invent different ways to remove the epithelium when it could very easily be rubbed off with any instrument at hand? Well, it turns out that once people realised how long an eye took to recover from PRK, they tried to keep the thin epithelial cell layer intact and replace it at the end of the operation rather than throwing it away. The 2 ways of separating the epithelium while keeping it intact were 1) using alcohol to loosen the epithelium (LASEK) and 2) using a special blunt blade (epiLASIK). It turns out that once the epithelium is peeled away, whether by alcohol or the blunt blade, it dies. If this dead layer of cells is replaced, it slows healing down even more! Therefore, nowadays, usually even when LASEK or epiLASIK is done the epithelium is thrown away rather than replaced. So that makes it identical to PRK, doesn't it? Why spend money on an epiLASIK blunt blade when you can simply peel away the epithelium, perhaps with alcohol to loosen it first? There just doesn't seem to be a role for epiLASIK...and furthermore when you use a blade, even a blunt one, you run the risk of cutting into the stroma when you don't want to...

The ICL (above) is similarly different, with different pros and cons. When LASIK is done for patients with very high spectacle degrees or thin corneas, the area of cornea treated (optical zone) is smaller, so that the cornea does not get too thin. Unfortunately, when the area treated is small, the risk of halos in the dark and poorer quality vision also rises. The good thing about the ICL is that halos, even if present, are usually very mild even when the spectacle power corrected is high. It is also true that after ICL, the eye does not get as dry as after LASIK.

However, potential intraocular (inside the eye) complications exist with the ICL, of which cataracts and glaucoma are the 2 main (but rare) ones. The main thing about reducing complications with the ICL is to achieve accurate sizing, and at our clinic we do 'sulcus to sulcus' measurements for all ICL patients. What is the sulcus? This is the little nook in the eye just behind the iris (coloured part of the eye) and in front of the original crystalline lens where the ICL will sit. If the ICL is too big for this space in a particular eye, it will be 'squashed', bend forwards, and narrow the drainage angle of the eye (increasing the risk of glaucoma). If the ICL is too small for this space, it will sink backwards and touch the crystalline lens, thus causing a cataract. Although there is no perfect way to measure this sulcus diameter down to the last micron, we have found the Artemis VHF ultrasound biomicroscope (above) to be very accurate and allows us to choose an appropriate size ICL. The figure below shows a measurement made by the Artemis.

I would say that for my patients with lower spectacle powers, LASIK provides excellent clarity of vision including night vision (and without the risk of any intraocular complications). I have performed ICL surgery for a number of patients with excellent results, but I think bearing in mind the potential seriousness of problems with the ICL my preference is still an extraocular (outside the eye)  procedure like LASIK in cases where I judge that the outcome will be good. Extraocular means zero chance of causing cataract or glaucoma. Actually, I think the ICL is wonderful, but I prefer to use it for patients with very high powers or thin corneas, where I feel that the risks of intraocular problems are outweighed by the better visual quality that can be obtained with the ICL in such cases compared with LASIK. Although a lens is implanted into the eye in both ICL as well as cataract surgery, an ICL op is quite different from a cataract op, not least because when an ICL is implanted the patient's original crystalline lens/cataract is left alone while during a cataract op the crystalline lens/cataract is removed and is replaced by an intraocular lens implant (IOL). This has implications because there are some doctors out there who perform 'clear lens extractions' to correct high spectacle degrees. If a 'clear lens extraction' (which is like a cataract operation) is done in a younger person less than 45 years old or so, then they will immediately lose the ability to focus for near ie develop immediately the maximum amount of presbyopia/LaoHua. ICL surgery will not affect the development of presbyopia, nor can it cure this problem. ICL surgeons can offer monovision with the ICL, just like with LASIK or contact lenses. On the other hand, if somebody has a cataract then he/she should have a cataract op, not an ICL op. The ICL surgery doesn't do anything about a cataract, which would continue to blur the vision.  Overall I would say, go for LASIK if your cornea is thick enough because the theoretical advantages of epiLASIK probably do not bear out clinically for the majority of patients. ICL surgery is a great option for those who would otherwise be at risk for visual or other side effects from LASIK.

Eye doctor trivia

In Ophthalmology, as in many other fields, "innovation" is always regarded as a golden word and there are countless doctors/researchers at any time looking for better ways to treat a given eye condition. True innovation requires a number of qualities on the part of the "innovator", and perhaps it's as good a time as any to re-visit the stories behind some of the greatest inventions of the twentieth century.

He came from a family of doctors and clergy, and once was a lapchild of Florence Nightingale.

His father was an ophthalmologist, and following a distinguished stint in medical school received the FRCS (Fellowship of the Royal College of Surgeons) at the tender age of 25. Even around this time, before formal training in eye surgery, he had begun discussing the possibility of replacing crystalline lenses after cataract surgery with his father and close associates.

In 1940, Flight Lieutenant Gordon Cleaver was returning from a sortie in his Spitfire. In his haste to get into the plane that morning, he had forgotten his flight goggles, so when a bullet smashed through the canopy of his fighter, bits of perspex plastic from the canopy were blown straight into his eyes. In the end, he underwent 18 operations on his eyes and face, many of which were performed by this doctor.

It used to be said (something to the effect of) 'Thou shalt not have a foreign body in the eye'. And yet, it was quite clear in this particular patient that some of the remaining plastic pieces in the eye were not causing any problems even years after the original injury.

So this young doctor spoke with some spectacle manufacturers and eventually a small perspex disc similar in shape to the original crystalline lens was produced. This was implanted into the eye of a patient on 29 November 1949. It wasn't long before he felt the full force of hostility (and some might say jealousy) from his peers. For several decades, the topic was not even given a section for presentation and discussion at conferences. By the 1970s, though, the unquestionable benefits of implants over thick aphakic glasses were apparent and with improving lens designs, better results were also being seen around the world.

Today, it is the unusual patient who does not get a lens implant. The question has become 'why didn't this patient get an implant?' rather than the other way round. And of course, this was the story of Harold Ridley and the intraocular lens implant, which has revolutionised eye surgery in fundamental ways.

He was a bit of a maverick, but a persistent one at that.

Finding himself unable to get into medical school in the United States, he applied and got accepted into the University of Geneva Medical School in Switzerland, where for a time he was spending more time composing music than on his medical studies. But fortunately for all of us, graduate he did, and became heavily involved with research into better ways of doing cataract surgery.

In the mid 1960s, he was given US$299,000 to find a way to remove cataracts through a small incision (cut). Going through more than 40 different ways of doing so, including a meat grinder (!) type of device, he failed every single time and was close to despair. " I thought I might face defeat better if I looked better, and so I prepared," this doctor wrote in his 1985 autobiography Through My Eyes. "The haircut came first, then a shoeshine, and finally, the dentist." 

At the dentist's, he was very taken with the then also new method of removing calcified plaque with an ultrasonic cleaner. After many hundreds of modifications later, including refinements in technique from many other surgical experts, we now have almost one day visual rehabilitation, with many patients achieving better than 6/9 vision on the first day after surgery.

Of course, I'm talking here about Charles Kelman, the legendary inventor of phacoemulsification, which is the gold standard for cataract surgery nowadays.


A common thread that runs through these innovators seems to have been a long standing conviction that something was not quite right and could be done a whole lot better. Although it seems so obvious to us nowadays, it took long and winding roads before conviction was translated into innovation. But for serendipity, sometimes, nothing might have come of it.

It has been said (on Ming Thein's blog and perhaps others) that he who tries 99 times and fails is seen as a fool, while success on the 100th time is a sign of great persistence in the face of adversity. Perhaps the frustration and fear of failing just before success is as good a motivating force as any!

For all the success that we see sometimes, I think the respect we accord to these pioneers should include a great dose of not just awe for their genius and intellect, but also their willingness to risk everything (peer respect and sometimes even careers) and to persist in the face of great adversity. In fact, it seems like the greater the uproar created, the greater the invention! The ability to think laterally and to find uses for seemingly unconnected things is also priceless. And to this end, I have viewed the increased sub and sub-sub specialization of the medical specialties with some concern, since the narrower world view could discourage cross-discipline exchange of ideas and methods.

As always, it is the devil in the details, finding the right balance between craziness of an idea and potential for success, and decisions regarding the distribution of limited funds, that will determine the success or failure of future endeavours.