From the History of IOL Implantation

HISTORICAL PERSPECTIVE

From the History of IOL Implantation* C.D. BINKHORST Axelsestraat 54, 4537 AL Terneuzen, The Netherlands

I have been involved in intraocular lens (IOL) implantation since 1952, stimulated by the work of Harold Ridley, and I am still active as an IOL surgeon in an out-patient location. I thank the Organizing Committee of this 5th Congress of the EIIC for their request to give a kind of warming-up, with a talk about the evolution of IOL surgery. In honour of Harold Ridley, who is present here, I want to show a short film demonstrating how I did a Ridley operation in 1955. In the meantime, let us start with the eye that receives an IOL, the recipient eye. It is interesting to know that, in the beginning, IOLs were used in sick or otherwise inferior eyes. This was not always fair for the IOL. Then there was the choice between intracapsular and extracapsular cataract extraction (ICCE and ECCE). Long before the first IOL, some 60 years ago, ICCE had become the routine of choice and had developed into a nearly perfect operation. Imagine what it was for Ridley and his followers to do an ECCE! It i~ not even a secret that Ridley tried out his IOLs in a small series of intracapsular cases. After a relatively successful series of 15 Ridley lenses, I decided that the Ridley operation was not an operation for general use. The Ridley IOL finally was abandoned. With the exception of some AC anglesupported lenses, there was a world-wide calm in the implantation field and even a hostile attitude developed. Epstein and myself worked, still in the 1950s, and independently, on a method of iris fixation that could be used following ICCE. After 1958, I implanted an increasing number of iris clip lenses for many years when hardly anybody still believed in IOLs. The iris clip lens made a breakthrough for the IOL! In 1963, however, I started to experiment with ECCE again and with an adapted IOL design, the iridocapsular IOL, I could prove that ECCE was the better method to stabilize an IOL, and also that ECCE was a better method for the eye itself. Today, most IOL surgeons will tell you that ECCE is to be preferred, this despite

*The Binkhorst Lecture, 5th Congress of the EIIC, Jerusalem, 13-18 September 1987. 0955-3681/89/010055+03 $03.00/0@ 1989 Bailliere Tindall

the fact that the secondarj cataract problem is not yet completely solved. That the ICCE and iris fixation with the iris clip lens is certainly not bad, is proven by the many long-time wearers among my patients. Two years ago in Harrogate, England, Roper Hall also reported his long-term results with iris clip lenses after ICCE that were also definitely not inferior. Clearly, the iris clip lens after ICCE had caused an inevitable interest in IOLs! I still owe you an explanation as to why the ECCE method is superior and not just a safer operation. In an intracapsular aphakic eye deprived of its stabilizing lens-zonule diaphragm, as a rule, the vitreous is detached and degenerated. With every eye movement, oscillations occur in the anterior as well as in the posterior segment. In the anterior segment, vitreodonesis causes an ongoing change in the depth and the shape. The eye is characterized by 'endophthalmodonesis' as I have called it. An IOL in such an eye can easily hurt surrounding tissues. A capsular membrane has a stabilizing function and also the vitreous is often normal and there are no such wild oscillations, more stability for the IOL, and consequently less chance of lesions of the eye. The extracapsular aphakic eye is a safer eye than the intracapsular aphakic eye, also without an IOL. Oscillations always cause turbulences and these can hurt the corneal endothelium and the retinal capillaries: a turbulence endotheliopathy, a corneal decompensation and retinal oedema. This may be the reason that the incidence of corneal decompensation and of retinal complications has always been higher after ICCE than after ECCE. I think that the intracapsular aphakic eye is a sick eye, suffering from what I have called 'the barrier deprivation syndrome'. The next subject is how to do 'atraumatic' surgery, because this is necessary to obtain good results with IOLs! Let me illustrate this with the corneal endothelium. For a long time, breakdown of the cornea was the most dreaded complication of IOLs, and at a certain point the high frequency of corneal complications caused an almost complete abandonment of IOLs. Also 'good' surgeons appeared to experience corneal oedema regularly, when they added an IOL to

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their cataract surgery. The reason was not the IOL, but that they were 'not good enough' surgeons! The vitality of the endothelium of the cornea (or shall we say the capacity of the aqueous pump) decreases throughout life, as a rule without clinical consequences. If cataract extraction is performed, the pump capacity decreases sharply, but rarely with clinical consequences. This represents the work of a so-called 'good' cataract surgeon. If the same surgeon also performed lens implantation on the same eye, the decrease would become so marked that sooner or later the endothelium would decompensate and corneal dystrophy appear. If, however, the loss had been less during the cataract extraction, and also during lens implantation, nothing would have happened with the cornea. The conclusion is that the endothelium, from the beginning to the end of surgery, has to be handled with the utmost care, more than is generally done. The total damage done to the endothelium is a summation of all sorts of lesions, including mechanical lesions caused by instruments or by the lens, and also lesions caused by folding of the cornea, by the irrigation stream, by the use of cold irrigation fluids, by the use of toxic drugs in the anterior chamber (AC), and by prolonged hypotension of the eyeball. Endothelial breakdown is a multifactorial process. Over the years, measures to prevent corneal lesions have been advised: no folding of cornea, no contact instrumentation (Healon), air ( = deep chamber technique), temperature, irrigation stream, no drugs. The availability of the specular microscope has certainly helped in this respect. Only those surgeons who have listened or will listen to this cry for perfection become really good implant surgeons. Today, the cornea is no longer a serious problem in IOL implantation. The time spent on a cataract patient, however, has increased enormously. We come now to the lens implants. One aspect that has played a role from the very beginning is the degree of toxicity oflenses. The toxicity can clinically be measured, roughly, by the postoperative reaction of the eye. A so-called toxic lens produces a severe postoperative uveitis. Sometimes this reaction is recurrent. A non-toxic lens produces hardly more reaction than cataract surgery alone. The early implants regularly produced a terrible reaction, sometimes leading to loss of the eye. When I became interested in lens implants, I found that the reason for this toxicity was two-fold: (a) remnants of the polishing material that still stuck to the lens, and (b) the chemical sterilization procedure. Before I did my very first case I had started my own, very primitive, cleaning of the lenses and sterilized them by treating them with bactericidal ultraviolet radiation. This explained my fairly good results with the Ridley lenses

C.D. Binkhorst

also. It was clear that the sterilization had to be non-toxic and this became for many years the case with the Ridley method, the so-called 'wet-pack' method. I am not aware of accidents with this sterilization procedure in Europe. In any case, the FDA of the USA, have since 1978 ordered ETO gas sterilization to be used in America. This was certainly the reintroduction of the toxicity factor. At first, ETO lenses often produced hypopyons. Today, an occasional hypopyon still occurs. I personally, and also many other implant surgeons, use German-made Morcher lenses, which during the past six years have been sterilized by gamma radiation. This method is quick, reliable and non-toxic. So for the toxicity of lenses. Of great importance is where the lens has physical contact with the eye. The site of fixation should very carefully be chosen. By 1967 I had already stated: 'It is the site of fixation that determines the fate of an eye with an artificial lens, and not the position of the optical part.' The site of fixation of course is the place of a potential lesion inside the eye. A little now about classifying lenses. Various classifications have been proposed over the years. The most widespread is the classification in AC and PC lenses. This does not mean a lot. For instance, a lens in the capsular bag is in no way in the PC. The terms prepupillary and retropupillary lenses instead of AC and PC sound a little better, but this also does not define the site of fixation. Retropupillary lenses can be supported in the ciliary sulcus, which is actually the angle of the PC, or in the capsular bag. These two support systems, ciliary sulcus and capsular bag, are completely different and so can be the long-term behaviour of the eye. This today is the big issue! A classification of all lenses that does justice to the clinical merits of a lens, is the following:

AC angle-supported lenses; Iris-supported lenses; Capsule-supported lenses; PC angle (ciliary sulcus) supported lenses. The lesions caused by touching uveal tissue are the most important. Ellingson has introduced the term UGH syndrome. Personally, I found a greater variety of lesions, all caused by touching the uvea, and I would prefer to speak of the uvea-touch syndrome. For more than 30 years I have observed my own lens designs and lens designs of others. I have used the four-loop iris clip lens (1958) and the two-loop, eventually three-loop, iridocapsular lens (1963). These two designs were used for many years and only abandoned as routine lenses about 7 years ago. Both lens designs were successful in my hands and in the hands of many others. Why then change? We have seen lesions inside the eye caused by continuous or intermittent contact with the lens; perhaps small but Eur J Implant Ref Surg, Vol1, March 1989

From the History of IOL Implantation

sometimes severe lesions. The incidence of these complications may not be so high, but we are at a point to combat the last percentage of complications. It became apparent first with AC angle-supported lenses: haemorrhages, uveitis and glaucoma occur regularly. Also iris-supported lenses, although rarely, can cause haemorrhages, uveitis and glaucoma. Lately, the UGH syndrome has also been reported with ciliary sulcus-supported lenses. Any contact of the lens with the uvea is likely to cause an even wider scale of symptoms than described in the UGH syndrome. Apart from uveitis, glaucoma and haemorrhages, we have also seen atrophy and necrosis, pupil distortion, pigment dispersion, vascular obstruction, and as far as there is a nerve supply, sphincter paralysis, and finally soreness of the eye. Here are a few examples: destruction in the AC angle, deep into the iris and into the ciliary body, caused by a foot-plate of a rigid angle-supported lens; erosion of the iris stroma caused by the optical portion of an angle-supported lens; the common aspect of an eye with a rigid angle-supported lens-the oval pupil; erosion of the pupillary border caused by an iris-supported lens. Metal loops especially can cause vast iris atrophy. In the ciliary sulcus it is difficult to show lesions during life. The fact that you cannot see so well behind the iris was, and still is, part of the explosive popularity of the so-called 'PC lenses'. However, pigment dispersion from this region betrays the presence of lesions. Lenses with haptic parts in contact with the pupillary border (four-, three- and two-loop prepupillary lenses) can cause inflammation. This contact is likely to cause iritis, with a tendency to form adhesions and precipitates, not forgetting fibrosis of the posterior capsule. From my experience with the two-loop capsular lens, I know how painstaking it can be to treat this peripupillary iritis. Actually, it was largely due to this problem of after-care that I finally decided to abandon this lens as a routine lens. Fluorescein angiography of the iris nicely illustrates what sometimes is going on at the pupillary border. It is well known that there is also a correlation between the uvea and the retina in pathology. Leakage of uveal vessels often goes hand in hand with leakage of retinal vessels. Possibly, this is a remote effect of prostaglandins that are released from the iris. Anyhow, macular oedema often accompanies the uveal lesions. I hope that I have made it clear that all uvea-supported lens systems are potentially dangerous systems. Constant pressure against the uvea can do harm, but intermittent pressure or intermittently intensified pressure even more so. In this respect it is good to remember that, even when blinking, the shape ofthe eyeball changes and also that there is an Eur J Implant Ref Surg, Vol1, March 1989

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ongoing muscle activity in the iris and also in the ciliary body. The other structure that is available for lens support is the capsule of the crystalline lens. The capsule is free from the reactions that the uvea may show. For nearly 20 years the capsular bag was used by me for lens support. The loops of a prepupillary lens were placed between the anterior and the posterior capsule. When, almost 12 years ago, retropupillary lenses were initiated, it was also the intention to place the haptics into the capsular bag (which would have been the correct method). The advocates of retropupillary lenses, however, soon found that the capsular bag was often missed. So they started to praise the ciliary sulcus. It was literally said that it hardly matters where lens loops landed, in the sulcus or in the capsular bag, and that it is also not critical whether one loop is in the sulcus and the other loop in the capsular bag. We know now that this is not correct. Nowadays, a rehabilitation of the capsular bag is in the air and that is mainly because reports of long-term complications with sulcus-fixated lenses are arriving. The same situation is now dawning with the PC angle lenses, as earlier was the case with AC angle lenses. It is clear that safe and guaranteed placement into the capsular bag depends on how the capsular bag is opened. This is even more critical when one intends to place more than mere lens loops into the capsular bag. A large circular capsulectomy is surely not the most adequate. The small rim of anterior capsule that is left usually retracts underneath the iris and also easily 'sticks' to the posterior capsule. This makes it hard to find the fornix ofthe capsular bag. It may be of help to place some visco-material in the fornix, but the same facilitates luxation out of the fornix in the early postoperative period. The chances of finding the capsular bag and staying in the capsular bag are much better if only capsulotomy is performed and initially nothing of the anterior capsule is removed. If the incision is made in the upper part of the anterior capsule as an envelope, the chances of entering the capsular bag and staying there are optimal. This technique has been suggested by Sourdille, practised a few times by Baikoff and further studied by Galand and by myself. It is called the envelope technique. During all of the surgery, including cataract removal and lens insertion, the anterior capsule remains intact-real intercapsular surgery. In this way, we have an IOL nearly completely covered with lens capsule and an eye that is protected against the IOL. Received August 1988