ICL (Implantable Collamer Lens) is a posterior chamber phakic intraocular lens widely used for refractive correction of high myopia. It is made of collamer (collagen-HEMA copolymer) and fixed between the iris and the lens (ciliary sulcus). Indications include myopia with spherical equivalent of 6D or more; moderate myopia of 3D to less than 6D and high myopia exceeding 15D require careful consideration1). The surgical age range is generally 21 to 45 years, and age-related changes in the lens must be fully considered1).
In Japan, only posterior chamber collamer ICL is approved, and since its approval in 2010, it has become widely used as a correction method for high myopia. Recent guideline revisions allow cautious use in cases of mild keratoconus that has not progressed and in moderate myopia. Astigmatism correction of 1D to 4D is also possible.
Glaucoma associated with ICL surgery is a general term for secondary glaucoma caused by abnormal positional relationships between the ICL and intraocular structures (iris, lens, angle) or related to postoperative management. The Refractive Surgery Guidelines (8th edition) list “transient postoperative intraocular pressure elevation and steroid glaucoma” and “angle-closure glaucoma” as postoperative complications of phakic intraocular lens surgery 1).
With conventional ICLs, preoperative laser peripheral iridotomy (LPI) was mandatory. This was because the ICL closely contacted the posterior surface of the iris, obstructing aqueous humor flow into the anterior chamber and posing a risk of pupillary block. Subsequently, the central hole ICL (Hole ICL / EVO ICL) was developed with a small hole (KS-AquaPORT) in the center of the lens, allowing aqueous humor to flow into the anterior chamber through the central hole 5). This made preoperative LPI generally unnecessary and reduced the risk of intraocular pressure elevation due to pupillary block 5, 6). However, even with the central hole type, risks of angle-closure due to excessive vault and pigment dispersion glaucoma remain, so regular postoperative monitoring continues to be important.
Intraocular pressure elevation after ICL surgery can be broadly classified into the following three categories based on pathogenesis.
In addition, transient intraocular pressure elevation due to residual viscoelastic material may occur immediately after surgery, but it usually resolves conservatively 1).
The exact incidence of intraocular pressure elevation after ICL surgery varies depending on the ICL generation (conventional vs. central hole), sizing method, follow-up period, and definition in reports. With conventional ICLs, intraocular pressure elevation due to pupillary block was occasionally reported despite preoperative LPI, but after the widespread adoption of central hole ICLs, its frequency has significantly decreased 7). Transient postoperative intraocular pressure elevation is a relatively common complication, and guidelines recommend observation for at least 2 hours after surgery 1). In a review by Packer, the risk of acute intraocular pressure elevation with central hole ICLs was reported to be significantly lower than with conventional ICLs 7). In the long term, attention should also be paid to chronic angle narrowing due to excessive vault and gradual intraocular pressure elevation due to pigment dispersion.
Glaucoma can develop after ICL surgery. The main mechanisms include angle closure due to ICL size mismatch, pigment dispersion from friction between the ICL and iris, and steroid-induced glaucoma from postoperative eye drops. Although the risk of pupillary block has decreased with the widespread use of central-hole ICLs, regular measurement of intraocular pressure and vault is essential 1). Appropriate ICL size selection and postoperative management can minimize the risk.
The symptoms of glaucoma associated with ICL surgery vary greatly depending on the mechanism and acuity of the course. While angle-closure type presents with acute and severe symptoms, pigment dispersion type and steroid-induced type often progress asymptomatically.
When angle closure due to excessive vault progresses rapidly, symptoms similar to acute glaucoma attack appear.
If the vault remains chronically high, peripheral anterior synechiae (PAS) may form with few subjective symptoms, leading to chronic angle-closure glaucoma.
Similar to primary open-angle glaucoma, it often progresses asymptomatically. However, some patients may notice blurred vision associated with intraocular pressure fluctuations. In particular, pigment dispersion is promoted after exercise, so some patients report blurred vision or eye pain immediately after exercise. As it progresses, visual field defects may be noticed, but they are often unnoticed in the early stages.
There are almost no subjective symptoms, and it is often discovered incidentally during intraocular pressure measurement at regular checkups. When severe intraocular pressure elevation occurs, blurred vision and eye pain may occur.
When intraocular pressure elevation is observed after ICL surgery, the cause is differentiated based on the following three types of clinical findings.
Angle-closure type
Excessive vault: Excessive vault of 750 µm or more on anterior segment OCT or UBM.
Shallow anterior chamber: The iris is displaced forward by the ICL.
Angle closure findings: Widespread angle closure confirmed by gonioscopy.
Peripheral anterior synechiae (PAS): Formed in chronic cases.
Pigment dispersion type
Krukenberg spindle: Vertical pigment deposition on the posterior corneal surface.
Angle pigmentation: Circumferential heavy pigmentation on gonioscopy.
Posterior bowing of the mid-peripheral iris: Concave deformation of the iris.
Iris atrophy: Increased transillumination due to depletion of the pigment epithelium.
Steroid-induced type
Open angle: No angle closure or pigmentation.
Normal vault: ICL position is appropriate.
Steroid use history: Confirmation of postoperative eye drop history is important.
In the excessive vault type, quantitative evaluation of the vault using anterior segment OCT or UBM (ultrasound biomicroscopy) is essential. Generally, if the vault exceeds 750 µm, the ICL size is likely too large, and if it is less than 250 µm, the risk of cataract increases 8, 9). Schmidinger et al. reported that the vault of posterior chamber phakic intraocular lenses changes over time, and long-term monitoring is necessary even if it is appropriate immediately after surgery 12).
In the pigment dispersion type, suspect this condition if, in addition to elevated intraocular pressure, there is posterior displacement of the mid-peripheral iris, pigment dispersion findings in the anterior segment (pigment deposition on the cornea, lens, and angle), and iris atrophy.
Blurred vision after exercise in eyes with ICL implantation is an important symptom suggesting pigment dispersion glaucoma. Exercise increases friction between the ICL and the iris, promoting pigment dispersion and potentially causing a transient rise in intraocular pressure. If such symptoms occur, it is necessary to evaluate the degree of pigment deposition by measuring intraocular pressure and performing gonioscopy immediately after exercise. It is advisable to see an ophthalmologist early for a thorough examination.
The causes and risk factors of glaucoma after ICL surgery differ depending on the mechanism of onset.
The most important factor is ICL size mismatch.
For safe ICL surgery, preoperative evaluation including glaucoma risk assessment is essential. The Guidelines for Refractive Surgery (8th edition) stipulate that the following examinations should be performed for phakic intraocular lens surgery 1).
In addition to standard preoperative examinations for refractive surgery (visual acuity, refraction, corneal curvature radius, slit-lamp microscopy, corneal topography, corneal thickness, tear film, fundus, intraocular pressure, pupil diameter, corneal diameter), the following are added.
For intraocular pressure management after ICL surgery, the following examinations should be performed regularly.
If pigment dispersion type is suspected, the following additional tests are useful.
In cases of intraocular pressure elevation in eyes with ICL implantation, differentiation from the following diseases is necessary.
| Differential Disease | Key Points for Differentiation |
|---|---|
| Primary angle-closure glaucoma | Confirm presence of ICL (UBM) |
| Malignant glaucoma | High intraocular pressure with extremely shallow anterior chamber |
| Pigmentary glaucoma (idiopathic) | Onset in eyes without ICL |
| Uveitic glaucoma | Presence of inflammatory cells and flare |
| Steroid-induced glaucoma | Check history of steroid use |
Differentiation from secondary glaucoma due to uveitis is particularly important. Inflammatory reactions after ICL surgery and uveitis are distinguished by the degree of anterior chamber flare and cells.
After ICL surgery, check-ups are generally recommended the day after surgery, at 1 week, 1 month, 3 months, and 6 months. Thereafter, regular check-ups at least once a year are necessary. At check-ups, intraocular pressure measurement, vault evaluation, corneal endothelial cell examination, and visual acuity testing are performed to check for ICL malposition and early signs of glaucoma. If symptoms such as eye pain, blurred vision, or decreased vision occur, you should see a doctor immediately without waiting for the next regular check-up 1).
Treatment of glaucoma associated with ICL surgery begins with identifying the mechanism of onset, as the treatment strategy differs greatly depending on the mechanism.
If elevated intraocular pressure is observed after ICL surgery, the mechanism is differentiated and treatment is selected according to the following flow.
In acute angle-closure attack due to excessive vault, emergency intraocular pressure reduction with medication is performed first.
If the ICL is too close to the lens, there is a risk of cataract development; if it is too far and the lens protrudes forward, angle closure and elevated intraocular pressure may occur. If improvement is not expected, lens size should be reconsidered and lens exchange performed.
ICL size exchange is a procedure to replace the ICL with an appropriately sized one based on remeasurement of the ciliary sulcus (e.g., UBM), and is a definitive solution for excessive vault.
Pharmacological treatment for pigment dispersion type follows that for primary open-angle glaucoma 3).
The main intraocular pressure-lowering drugs are listed below.
| Drug class | Representative drug | Dosage |
|---|---|---|
| PG-related drugs | Latanoprost 0.005% eye drops | Once daily at bedtime |
| Beta-blockers | 0.5% timolol maleate | Twice daily |
| CAI | 1% dorzolamide eye drops | Three times daily |
| CAI | 1% brinzolamide eye drops | Twice daily |
| Alpha-2 agonists | 0.1% brimonidine eye drops | Twice daily |
Prostaglandin-related drugs (latanoprost 0.005%, tafluprost 0.0015%, etc.) are often used as first-line therapy. Mydriatic agents are contraindicated because they can cause pigment dispersion and worsen aqueous outflow 3).
If intraocular pressure control is insufficient with medication and laser therapy, consider the following surgeries.
Removal of the ICL can eliminate the cause of angle closure due to excessive vault and pigment dispersion. In the angle-closure type, ICL size exchange or removal is the definitive treatment. In the pigment dispersion type, removal reduces pigment dispersion, but increased outflow resistance due to pigment deposited in the trabecular meshwork may persist 3). Therefore, continued use of intraocular pressure-lowering medications or surgical intervention may be necessary even after ICL removal. If glaucomatous optic neuropathy has already progressed, ICL removal cannot restore lost visual field.
The pathophysiology of glaucoma associated with ICL surgery is understood primarily through the physical impact of the ICL on aqueous humor dynamics and the iris-lens relationship within the eye.
Aqueous humor is produced by the ciliary epithelium, flows from the posterior chamber through the pupil into the anterior chamber, and exits via the trabecular meshwork into Schlemm’s canal. Since the ICL is positioned between the iris and the lens (in the posterior chamber), it physically affects this aqueous flow pathway.
In the central-hole ICL (EVO ICL), the 0.36 mm micro-hole in the center of the lens allows aqueous humor to flow from the posterior chamber to the anterior chamber, reducing the risk of pupillary block 5). However, around the periphery of the ICL (near the haptics), contact between the ICL, iris, and lens within the ciliary sulcus cannot be completely avoided.
When the ICL size is too large relative to the width of the ciliary sulcus, the following cascade occurs:
This mechanism is similar to the pupillary block mechanism of primary angle-closure glaucoma, but differs in that the presence of an ICL as a physical structure is the cause. Gonvers et al. reported a dilemma: if the distance between the posterior ICL surface and the anterior lens surface is too small, the risk of cataract increases; if too large, the risk of angle closure increases 8).
Longitudinal changes in vault are also an important factor. In a long-term follow-up by Schmidinger et al., the vault tended to change after ICL implantation compared to the early postoperative period. While age-related lens thickening contributes to a decrease in vault, in some cases the vault increases, raising the risk of angle closure 12).
Pigment dispersion in ICL-implanted eyes occurs through the following mechanisms:
This mechanism is similar to the reverse pupillary block mechanism in idiopathic pigment dispersion syndrome/pigmentary glaucoma. In pigmentary glaucoma, the mid-peripheral iris is displaced posteriorly (reverse pupillary block), and the posterior iris surface contacts the zonules, promoting pigment dispersion 4). In ICL-implanted eyes, the lens itself provides a physical contact surface with the iris, resulting in similar pigment dispersion.
Krukenberg spindle is formed by pigment granules floating in the anterior chamber depositing on the corneal endothelium, along the convection pattern of aqueous humor (boundary between rising warm aqueous and descending cold aqueous), resulting in a vertical spindle-shaped deposit.
The phenomenon of pigment dispersion being promoted by exercise is thought to be due to increased friction among the iris, lens, and ICL caused by pupillary dilation/constriction and accommodative changes.
Steroid eye drops act on the trabecular meshwork structure, causing the following changes.
Steroid responders have a genetic predisposition. Although ICL surgery patients are not particularly more sensitive to steroids, they are given steroid eye drops as postoperative anti-inflammatory treatment, creating an opportunity for onset 1).
Long-term contact of ICL haptics with the ciliary sulcus may lead to the formation of iridociliary cysts. Zhang et al. reported a case where an iridociliary cyst near the haptics ruptured after ICL implantation, causing hyphema 2). UBM confirmed the positional relationship between the cyst and the ICL haptics. The hemorrhage was absorbed over 17 days with conservative treatment using 0.1% tobramycin-dexamethasone eye drops (4 times daily) and 1% atropine sulfate eye ointment (twice daily) 2). Hyphema itself poses a risk of inducing glaucoma (trabecular meshwork obstruction by blood cells).
