You have an implant fitted
for high myopia

What are we talking about

If you were treated for high myopia between the late 1990s and the early 2010s, an implant may have been placed inside your eye, in front of the iris, without your natural crystalline lens being removed.

This is what is called a phakic implant. “Phakic” simply means that the crystalline lens is preserved.

The names you will find them under

The models fitted in Belgium during that period belong to a single family: iris-fixated implants. A small lens, held by two haptics closed onto a fold of iris on either side of the pupil.

• Artisan — the rigid model, in PMMA;
• Verisyse — the same implant under a different trade name;
• Artiflex or Veriflex — the foldable version, which reached the market later.

The indication was precise: eyes for which laser surgery was not a reasonable option, most often because the myopia was too high or the cornea too thin. For those eyes, the implant was the appropriate answer given the means of the time.

Why I monitor these eyes for life

A reserve that is not replenished

The posterior surface of your cornea is lined with a single layer of cells: the endothelium. Its role is that of a pump. It draws off the water that tends to build up in the corneal tissue, and so maintains its transparency.

These cells do not renew themselves. Their number falls slowly over a lifetime, in everyone, and those that remain spread out to compensate. As long as the density remains sufficient, the cornea stays clear.

What an anterior chamber implant changes

The implant sits between the cornea and the iris, a short distance from the endothelium. That proximity, the micro-movements of the implant and a chronic very low-grade inflammation can accelerate cell loss.

This acceleration is neither systematic nor uniform. It depends in particular on your anterior chamber depth and on the exact position of the implant.

This loss is silent. Your vision may remain excellent long after the safety margin has narrowed — which is why I rely on a measurement, and not on how you feel.

When the reserve becomes insufficient, the cornea retains water. Vision is blurred on waking and improves during the day, halos appear, then the loss of vision settles in. This is called endothelial decompensation. At that stage, only a graft of the endothelial layer restores transparency.

How often I see you

One check a year. Sometimes one every two years, when the measurements prove very stable over several years.

The most useful criterion is neither your age nor how long the implant has been in place: it is the date of your last endothelial cell count. If you do not know it, or if it is more than two years old, a check is warranted.

What thresholds are worth

You will read, in the literature and sometimes on your own reports, that a density below 1,500 cells per square millimetre constitutes a zone of concern. That is correct, and it is not enough.

There are three reasons for this:

• the rate of loss counts for more than the isolated value — a density stable for ten years does not read like a density falling every year;
• the shape and regularity of the cells say what the figure does not;
• advances in endothelial surgery have shifted the balance between the risk of waiting and the risk of intervening.

I do not decide on a threshold. I decide from your current vision, from how your measurements are changing, and from where you yourself place the risk.

What makes me reconsider an implant

Two situations predominate, and they are often encountered together.

Endothelial decline

It produces no sign and is detected only by measurement. When the density falls steadily, removing the implant preserves the remaining reserve.

The aim is not to bring the cell count back up — that is impossible. It is to stop the fall.

Cataract

Your crystalline lens was preserved: it ages normally and clouds over time, as it does in everyone. In highly myopic eyes, this readily happens earlier.

The usual signs: a return of myopia, a gradual decline, difficulty driving at night, unusual glare.

This situation has a direct consequence. Operating on the cataract requires removing the implant, which occupies the space through which the procedure is performed. The two steps are therefore carried out at the same time — in practice this is the most common reason for explantation.

The rarer situations

• disenclavation of one haptic, with mobility or decentration of the implant;
• progressive distortion of the pupil, or dispersion of iris pigment;
• an isolated progression of the myopia, leaving the implant’s correction insufficient.

There is another outcome, and it is the most frequent of all: change nothing. A stable implant, on a stable endothelium, in an eye that sees well, calls for nothing but a date for the next check.

What I look at in consultation

My aim is not to decide the fate of your implant that day. It is to establish a complete picture on which a decision can be built — at a second consultation if need be.

Your documents

Bring what you have: operative reports, later checks, even partial ones.

Four pieces of information are valuable to me — the date of implantation, the model, the power, and above all any endothelial cell counts already carried out. These last allow a trend to be established, which no isolated measurement can do.

Their absence blocks nothing. It simply changes what I can conclude straight away: without a history, this first assessment becomes the starting point of a curve rather than a point on an existing one.

The cornea first

This is the heart of the examination. Three measurements complement one another.

• Specular microscopy. It counts the cells and analyses their shape. An adequate density on very irregular cells does not read like an adequate density on regular ones.
• Pachymetry. It measures corneal thickness. Progressive thickening signals water retention, well before any loss of vision.
• Slit-lamp examination. Position of the implant, soundness of the two fixation points, appearance of the pupil, pigment deposits.

The geometry of the anterior segment

Imaging measures your anterior chamber depth and the distance between the optic of the implant and the posterior surface of the cornea.

That distance is a recognised factor in the rate of cell loss. Where relevant, it also bears on whether a posterior chamber implant (ICL type) might be considered.

The crystalline lens

I look for the beginnings of clouding, however slight. Corneal topography and biometry complete the assessment.

These two examinations do not serve diagnosis alone: they prepare the calculation of the implant that would be fitted if lens surgery were to be decided upon. In a long eye, already operated on, whose cornea has already received an incision, that calculation calls for anticipation.

And the rest of the eye

High myopia concerns the whole globe, not just its correction. I therefore look systematically at:

• intraocular pressure and the optic nerve — glaucoma is more frequent and harder to detect in these eyes;
• the retina after dilation, with particular attention to the periphery;
• the macula on tomography, looking for myopic maculopathy.

These three elements are not an additional assessment. They determine what a procedure can reasonably bring you — and therefore the decision itself.

The four possible outcomes

They are not equivalent in frequency, and the first is by far the most common.

Monitoring

A well-positioned implant, a stable endothelium, a clear crystalline lens: no intervention is warranted. My conclusion is then a date, that of the next check.

This is what I propose to most of the patients who come to see me — including those who arrive with the idea that something will have to be done one day.

Doing nothing is a recommendation in its own right here, not an absence of recommendation.

Removing the implant and operating on the crystalline lens

This is the most frequent of the situations that lead to intervention. It becomes necessary once a cataract has set in, and I favour it when an endothelial decline coincides with a lens beginning to lose its transparency.

The two steps are carried out in the same operating session. Removing the implant frees the access needed for lens surgery, and a permanent implant is placed in the capsular bag, in the posterior chamber, far from the endothelium. Your myopia is built into its calculation.

This procedure removes accommodation, that is, focusing at near without correction. In a patient who is already presbyopic, that loss is in practice already accepted. In a younger patient, whose crystalline lens is still clear, it is a serious argument — and it is what motivates the next option.

Removing the implant and replacing it with a posterior chamber implant (ICL type)

This option is uncommon. I discuss it when the anterior chamber has to be freed — an endothelial decline, or a fixation problem on the iris making re-fixation inadvisable — while the crystalline lens is still perfectly clear and you are too young for its removal to be warranted.

The implant is then replaced by another one, placed behind the iris and in front of the crystalline lens, at a distance from the endothelium.

This solution is not always feasible: it requires precise anatomical conditions, notably a sufficient chamber depth, which I verify during the assessment. When it is not, the discussion returns to lens surgery and to the trade-off over accommodation.

Removing the implant, operating on the lens and grafting the endothelium

This option concerns eyes whose endothelial reserve is already too depleted for the cornea to recover its transparency on its own, or in which decompensation has already set in.

A graft of the endothelial layer — which replaces the failing layer alone, without touching the rest of the cornea — then completes the two preceding steps.

The question of timing always arises: to graft in the same session, or to wait and see how the cornea behaves after the implant is removed. Both strategies have their merits; I discuss this with you case by case, according to the state of the cornea before the procedure.

What decides between these four outcomes

None is better in absolute terms. Four elements, examined together:

• the state, and above all the trend, of your endothelium;
• the transparency of your crystalline lens;
• your age and your situation regarding near vision;
• the state of your retina and your optic nerve.

A procedure only makes sense if the expected gain is proportionate to the risk taken. In an eye whose macula is damaged, this reasoning may lead me to defer a step that the corneal figures would seem to justify. This discussion belongs to you as much as it belongs to me.

What removal involves

If we decide to remove the implant, a few particularities are worth knowing in advance.

They do not make the procedure riskier in the usual sense of the word. They explain why it unfolds differently from ordinary cataract surgery, and why recovery calls for more patience.

A wider incision

The Artisan is a rigid implant, which does not fold. Removing it requires an opening of 5 to 6 millimetres, where contemporary cataract surgery is performed through an incision of about two millimetres. The foldable models allow an intermediate opening, of 3 to 4 millimetres.

This incision is sometimes closed with sutures. It has two direct consequences.

• An induced astigmatism. Opening then closing the eye alters the curvature of the cornea. The result is a distortion that makes vision imprecise at all distances until it is corrected — and whose magnitude and orientation I cannot fully predict at the time of surgery.
• Slower stabilisation. Where conventional cataract surgery gives stable vision within a few weeks, here it takes longer. The cornea continues to change during healing, and removing any sutures alters it further.

This is the point I make a matter of principle from the consultation onwards: the visual result is not judged at three weeks. This slowness is expected, and it is not a bad sign.

The fixation points on the iris

The implant is held by two haptics closed onto a fold of iris. Releasing them leaves, at those two places, a small remodelled zone.

The pupil may keep a slightly oval shape, and increased sensitivity to light or halos may persist. These sequelae are most often subtle and well tolerated; they are more pronounced when the iris was already distorted before the procedure.

The cell cost of the step itself

Removing an implant that sits close to the endothelium consumes cells in itself.

Waiting has a cost in cells, and so does operating. It is the weighing of those two costs that underpins my decision — more than the figure reached at any given check.

Intervening early on a still comfortable endothelium and intervening late on a depleted one do not present the same balance.

In practice

The procedure is carried out as a day case, one eye at a time.

The second eye, when it has to be operated on, follows after an interval that lets me check how the first behaves. That interval is all the more useful here because the astigmatism induced in the first eye tells me what to expect in the second.

Removal of an intraocular implant falls under care reimbursed by the statutory health insurance scheme, as does the lens surgery accompanying it. The exact terms are set out at the preoperative consultation.

Your vision after the procedure

You do not become short-sighted again

This is a worry I often hear: that of returning to the myopia you had before the implant.

That is not what happens when the crystalline lens is operated on at the same time. The permanent implant builds your correction into its calculation: the power carried by the implant removed is taken over by the one replacing it.

The calculation nonetheless remains less precise than in an ordinary eye. A very long eye, with a wider incision, partly escapes the formulas. A residual deviation is possible, and I would rather you knew that beforehand than discovered it afterwards.

Residual astigmatism

This is the most frequent limitation of this surgery. The astigmatism linked to the incision often persists, to a variable degree, once healing is complete.

In practical terms: a residual correction often remains necessary, at least for certain activities.

Several options are then discussed — selective removal of sutures, simple optical correction (spectacles or contact lenses), or additional refractive surgery if the astigmatism is significant and the cornea allows it. None is decided before stabilisation.

Choosing the permanent implant

The question arises as it does in any lens surgery, with one additional reservation.

Implants that extend the depth of focus, to reduce reliance on spectacles, require a retina in good condition and a regular cornea. In a highly myopic eye, whose macula often carries the marks of the myopia and whose cornea will be remodelled by the incision, those two conditions are not always met.

A monofocal IOL, combined with a correction for near, is frequently the safest choice in these eyes. This is not a renunciation: it is matching the objective to what the eye can actually deliver.

Follow-up afterwards

Removing the implant puts an end to the cause of the cell loss. It does not put an end to monitoring — that simply changes its object.

The first months

The close checks concern the transparency of the cornea, the healing of the incision and the course of the astigmatism.

A cornea that takes time to clear is not unusual when the endothelial reserve was low to begin with. It is during this period that the need for a deferred endothelial graft is decided, where relevant.

Clouding of the capsule

The permanent implant is placed in the envelope that contained your crystalline lens. That envelope, the capsule, is preserved: it holds the implant in position.

Over time, its posterior wall may cloud over — a gradual decline, glare, a sense of a veil. The symptoms resemble those of a cataract, which earns this phenomenon the misleading name of “secondary cataract”. It is not a recurrence: the crystalline lens, once removed, does not grow back.

Treatment consists of opening this membrane with a laser, in consultation, without an incision. The step is brief and painless.

In a highly myopic eye, I add two reservations: I wait for the refraction to stabilise, and I take into account that it slightly increases the risk of retinal detachment, already higher in long eyes. This is why I do not carry it out as soon as clouding appears, but when the difficulty warrants it.

Then a rhythm set by the retina and the optic nerve

Once healing is over, it is no longer the cornea that governs follow-up, but two elements particular to high myopia.

• The macula. High myopia weakens the central zone of the retina, independently of any surgery. What you see at the end of the journey depends on it directly.
• The optic nerve. Glaucoma is more frequent in these eyes and more delicate to detect, the very shape of the myopic optic nerve making early signs difficult to interpret. This follow-up is lifelong.

The rhythm is therefore individual: annual in most cases, closer together if either of these two elements calls for particular attention.

What should prompt you to seek advice without delay

• the sudden appearance of numerous floaters, or of flashes of light;
• the sense of a veil or a fixed shadow in part of the field of vision;
• a rapid loss of vision.

Intraocular surgery increases the risk of retinal detachment in long eyes. That risk remains low, but I would rather you knew these signs than discovered them.

In an eye that has carried an implant for twenty years, follow-up is not what comes after the procedure. It is the only genuinely continuous element of the journey.